# disease info

info:
What is infertility?
Infertility is a condition or disease affecting the reproductive system that prevents successful pregnancy. It is typically diagnosed after a couple has had 6 to 12 months of unprotected, well-timed (around the time of ovulation) intercourse without a pregnancy occurring or when a woman has been unable to carry a pregnancy that results in a live birth.

Problems in fertility can occur at any point in the process of conception – in the development or release of the egg or sperm, in fertilisation or transport of the fertilised egg from the fallopian tube to the uterus, in implantation of the embryo in the uterine lining (the endometrium), even in the timing of intercourse or physical conditions after conception. In the female, the reproductive system consists of the vagina, cervix, uterus, fallopian tubes, ovaries, and vulva (the external structures). The male genital organs include the testicles, vas deferens, seminal vesicles, prostate gland, and penis. Hormones controlling reproduction and metabolism (produced by the hypothalamus, pituitary, and thyroid glands as well as the ovaries and testes) also play an important role.

In the UK approximately 1 in 7 couples have impaired fertility. The source of the infertility problem may be in either partner. Age can play an important role ― especially in women, but also in men. Endometriosis and the effects of sexually transmitted diseases may be factors in infertility. The presence of other diseases or infection in either partner can be a source of the problem. Nutritional, health, lifestyle choices, and environmental factors also have an effect. The most common defects reported are sperm disorders in men, and damaged or blocked tubes or ovulation problems in women. No cause is identified in up to one third of cases.

Infertility testing can be complex, expensive, and time-consuming. Often, both partners are required to undergo extensive physical examinations, blood tests, evaluation of lifestyles, and/or ultrasound testing to determine the source of the problem.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests of Female Fertility
A woman’s fertility declines substantially by age 35 and even more so after age 40. Infertility occurs because an egg may not be produced, or once released, it may not get to the womb, sperm may not reach it, or a fertilised egg may fail to develop. Common reasons for female infertility include blocked fallopian tubes, polycystic ovary syndrome (PCOS interferes with egg release), fibroids, Endometriosis, autoimmune disorders (producing antibodies against fetal tissue), diabetes, hypothyroidism, eating disorders, excessive smoking and alcohol intake, and gluten intolerance (coeliac disease). A woman’s fertility may also be affected by factors such as fluctuating or diminished hormone levels; inconsistent ovulation; or a poor reproductive environment that does not support proper fertilisation of the egg, interferes with the sperm’s transport, or impairs retention of a fertilised egg.

The initial evaluation of a woman’s fertility includes a personal and family history with a thorough physical examination. A number of tests can be used to help diagnose the problem and aid in treatment.

Initial investigations may include some blood tests, such as measuring the levels of hormones involved in reproduction: luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (PRL), oestradiol, and progesterone. Other measurements which can help include thyroid function tests (TSH and/or T4) and steriods such as  testosterone and DHEA-S (dehydroepiandrosterone sulphate is used in creating androgens and oestrogens). These tests help to check the health of the pituitary, thyroid and adrenal glands which can themselves affect the menstrual cycle and ovulation. Further investigations may be undertaken in specialist clinics and may include additional blood tests such as anti-Müllerian hormone (AMH) to assess ovarian reserve, or  imaging techniques such as ultrasound (US) to look at individual reproductive organs.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests of Male Fertility
A man’s fertility can be affected by factors such as a low sperm count, poor sperm movement (motility), clumped (or agglutinated) sperm (unable to swim to the egg), abnormally shaped sperm, enlarged veins around the testes (varicoceles), obstructions that prevent sperm from being released during ejaculation, and genetic or congenital conditions that impair the reproductive environment. The most common anatomic abnormality in men is varicoceles.

A history of having mumps, testicular injury, exposure to chemicals or toxins, acute illness or prolonged fever, drug or alcohol use, and ingestion of anabolic steroids can negatively impact male fertility. Temperature also affects sperm efficiency. Age-related problems include decreased testosterone production; declining sperm mobility or production; prostate, erectile, or ejaculation problems; and excessive alcohol use.

For the male, a medical history and physical examination to detect anatomic abnormalities may be all that is necessary to diagnose an infertility problem.

Semen analysis. Semen analysis is the mainstay of male testing. Collection and prompt evaluation of an ejaculate can quickly determine any abnormalities in the number of sperm, their shape, and ability to swim toward the egg.

Blood tests. Measurements of the levels of some hormones in blood may contribute to understanding in male reproductive disorders: testosterone, luteinising hormone (LH), follicle-stimulating hormone (FSH), and prolactin (PRL).

In some instances a biopsy of testicular tissue may be required to identify the problem.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What are they?
Inflammatory bowel diseases (IBD) are chronic disorders that affect approximately 1 in 350 people in the UK. Characterised by swollen and damaged tissues in the lining of the intestinal tract, these conditions vary in severity from patient to patient and change over time. During a flare-up, a patient may experience frequent bouts of watery and sometimes bloody diarrhoea, abdominal pain, weight loss and fever. Between these flare-ups symptoms frequently diminish. Many patients may go through extended periods of remission before another flare-up occurs.

The cause of IBD is not known, but these diseases are thought to be due to an autoimmune process that has been triggered by a viral illness or an environmental factor in persons with a genetic predisposition. IBD affects slightly more women than men and is seen most frequently in Caucasians who live in industrialised countries. The most common inflammatory bowel diseases are Crohn’s disease and ulcerative colitis. In the UK, ulcerative colitis is twice as common as Crohn’s disease. Both diseases can start at any age, but the majority are first diagnosed in patients between the ages of 15 and 30 and a smaller number between 60 and 80. Children affected by either disease may experience delayed development and growth retardation in addition to gastrointestinal symptoms.

A serious complication of these disorders is toxic megacolon. Toxic megacolon is a rare condition, arising due to severe inflammation and paralysis of a section of colon. This leads to rapid dilation (widening) of the colon, which can cause abdominal pain, fever, and weakness. It is life threatening condition if left untreated.

Patients who are diagnosed with IBD at a young age are also at an increased risk of developing colon cancer later in life.

Crohn’s disease can affect any part of the gastrointestinal tract from the mouth to the anus, but is most commonly found in the last part of the small intestine (the ileum) or the colon (large intestine). Intestinal tissue may be affected in patches with normal tissue in between. Over time the inflammation caused by the Crohn’s disease can damage the digestive tract. This may cause narrowing of the colon, ulcers (painful sores on lining of intestine) or fistulae (tunnels through the intestinal wall into another part of the gut or another organ). Other complications of Crohn’s disease include bowel obstruction, anaemia from bleeding tissue, and infections. About 80% of patients with Crohn’s disease require surgery at some stage, either to remove damaged sections of the intestine or to treat an obstruction or fistula.

Ulcerative colitis primarily affects the surface lining of the colon. Although the symptoms may be similar to those seen with Crohn’s disease, the tissue inflammation is continuous, not patchy, and usually starts from the anus and extends up the colon. Ulcerative colitis tends to present more frequently with bloody diarrhoea. 

About 5% of patients with IBD affecting the colon cannot be classified because they have some clinical, radiological, endoscopic and pathological features of both Crohn’s disease and ulcerative colitis.

Inflammatory bowel disease is not the same as irritable bowel syndrome (IBS). IBS is a more common but poorly understood condition that causes symptoms such as bloating, abdominal discomfort, and change in bowel habits (diarrhoea and/or constipation). IBS is not associated with inflammation or change in structure of the bowel.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests
The diagnosis of an inflammatory bowel disease (IBD) is primarily made with non-laboratory tests, but laboratory testing is an important tool for ruling out other causes of diarrhoea, abdominal pain, and colitis (inflammation of the colon). These causes can include viral or bacterial infections, parasites, medicines, abdominal or pelvic radiation, colon cancer, and a variety of other chronic conditions such as coeliac disease and cystic fibrosis.

Laboratory Tests
Tests that may be requested to exclude other causes of diarrhoea and inflammation include:

Stool culture to look for bacterial infection

Ova and parasite examination of the stool

Clostridium difficile to detect toxin created by bacterial infection; may follow antibiotic therapy

Stool white blood cell count (WBC) to detect the presence of WBC

A screen for Coeliac disease tests


Tests that are not specific for IBDs but help to distinguish them from non-inflammatory causes of diarrhoea such as irritable bowel syndrome (IBS) include:

White blood cell count as part of a full blood count (which also checks for anaemia)

ESR (erythrocyte sedimentation rate)

CRP (C-reactive protein)

Faecal calprotectin


Calprotectin is a protein found in cells associated with inflammation. It is the most abundant protein present in neutrophils (white cells blood cells), and is released from these cells when they die.

The concentration of calprotectin in faeces correlates with the level of bowel inflammation present. The concentration of faecal calprotectin therefore tends to be increased in IBD (a disease characterised by inflammation), but not in IBS (Irritable bowel syndrome, a disease which is not characterised by inflammation). A negative faecal calprotectin result supports the diagnosis of IBS.

In October 2013 the National Institute for Health and Care Excellence (NICE) recommended that faecal calprotectin testing could be used to support clinicians in differentiating IBD from IBS. Importantly, faecal calprotectin analysis may avoid the need for more invasive tests (such as endoscopy) to distinguish between these two disorders.

Calprotectin may also be useful to help monitor IBD and alert your doctor to a flare-up.

Non-Laboratory Tests
These tests are used to help diagnose and monitor IBDs. They can be used to look for characteristic changes in the structure and tissues of the intestinal tract and to detect blockages. Care must be taken during an acute attack or flare-up of an IBD as there is a slight chance of perforating the bowel during testing.

Barium meal and follow through: after swallowing barium contrast dye, abdominal Xrays picture the small intestine

Sigmoidoscopy: a slender tube is used to examine the last two feet of the colon

Colonoscopy: a slender tube is used to examine the entire colon; it includes a light and camera and can be used to take biopsies

Capsule endoscopy: may be used in selected patients. A small pill shaped camera is swallowed so that it travels through the digestive system. The camera records images of the digestive tract which can be viewed by the doctor. 

Biopsy: tissue samples taken from the colon are evaluated for inflammation and abnormal changes in cell structure




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatment
Treatment of inflammatory bowel diseases is targeted at reducing inflammation, relieving symptoms such as pain and diarrhoea, controlling and healing damage where possible, identifying and addressing complications, and supplementing any nutritional shortages. Since the course of an IBD is usually one of flare-up followed by remission, the treatment often changes over time.

Patients with Crohn’s disease or ulcerative colitis need to be regularly monitored and should work with their doctors to become educated about their condition. While lifestyle changes, such as diet modification, rest and stress reduction, may help improve a patient’s quality of life and extend a remission, they cannot prevent an IBD flare-up. Acute symptoms are treated with a variety of medicines. These drugs are effective but many can only be given for short periods of time because of their side effects.

Current therapies include the use of, anti-inflammatory drugs, steroids (to control and to suppress inflammation), immunosuppressive drugs, and antibiotics. Infliximab, an anti-TNF monoclonal antibody with potent anti-inflammatory effects, may be used in active, fistulating Crohn’s disease if other treatment options have not worked. In addition to drug treatment, one or more surgical procedures may become necessary to remove damaged tissue, to treat fistulae or to relieve obstruction. Guidance on the use of treatments in the management of patients with Crohn’s disease was published by the National Institute of Health and Clinical Excellence (NICE) in October 2012.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Also known as: Flu; Avian flu; Swine flu; H1N1; Influenza A; Influenza B


                                                
                                            

What is influenza?
Influenza (the flu) is a viral respiratory infection that spreads from person to person through coughing, sneezing, and contact with contaminated surfaces. The flu is caused by types A, B, or rarely C influenza virus. The most common cause is influenza A, the viral culprit behind flu pandemics and most epidemics. In colder climates, influenza is seasonal, occurring primarily in the winter. In warmer regions of the world, it may be present year-round. During each flu season, there are multiple strains of influenza present, but typically one or two strains predominate as that year`s ``seasonal flu.``

Influenza A and B viruses change over time. Seasonal influenza strains can undergo a series of genetic changes so that people no longer have immunity from prior infections or vaccination, which is why annual flu vaccination is recommended for persons at increased risk of severe flu-related symptoms. When a large number people are susceptible to the virus, it can cause an influenza epidemic. In addition to this, influenza A can undergo a major genetic change that can make a virus strain much more lethal and/or easier to transmit. Flu vaccines that are developed each year to prevent flu infection are based upon medical experts` opinions as to which strains are likely to circulate in the community and usually contain attenuated or inactivated virus targeting two influenza A strains and one influenza B strain.

Influenza viruses cause illness in humans and in many animals, including birds, pigs (swine), dogs, and horses. Human influenza strains pass easily from person to person, but most strains of animal influenza only rarely infect humans. When they do, it is almost exclusively when there is significant close animal contact, such as a person that raises chickens or pigs, and the subsequent infection is only rarely transmitted from the infected person to another person.

The ongoing worry for the world`s medical communities is that an influenza strain that is infecting animals such as birds or pigs will mutate sufficiently that it will cause serious illness and death in humans (who have no protective antibodies against it) and that it will become a strain that is transmitted easily from human to human.  Once this happens, a new worldwide flu pandemic could spread across the world.

Influenza A virus can be further sub-typed based on two unique protein antigens, H (hemagglutinin) and N (neuraminidase). The most common influenza A viruses currently infecting humans have the subtypes H1N1 and H3N2. New flu virus strains are named according to the place where the virus was first observed, strain number, and year. For instance, the predominant strain during the 2003-2004 flu season was influenza A/Fujian/411/2002 (H3N2).

In most cases, the specific name of the influenza virus is only relevant to the medical community and those charged with influenza surveillance, but in recent years there has been news and focus on first avian (bird) flu and then H1N1 (swine) flu.

Avian (Bird) Flu
 One of the most predominant recent avian flu strains, an influenza A, H5N1virus was first described in Hong Kong in 1997. It caused an epidemic in birds in Southeast Asia in 2004, and since then it has caused illness and deaths in birds and in some people in parts of Asia. So far this strain of influenza has remained a bird-to-human infection. In 2013, avian influenza H7N9 was first reported to have infected humans in 2013 in China.  Reported cases of human infection have resulted in severe respiratory illness.

H1N1 (Swine) Flu
 The 2009 H1N1 flu virus was originally called ``swine flu`` but it is now known to be a combination of human, swine, and avian flu genes. First reported in Mexico and the U.S., it is a new influenza A, H1N1, virus. It is currently the predominant influenza A virus and is causing influenza infections throughout the world.

So far, the 2009 H1N1 flu appears to have had a greater effect on those younger than 65. Between April and December 2009, about 90% of influenza-related hospitalisations and 88% of estimated deaths were in people younger than 65. However, if infected, very young children, pregnant women and the elderly are at increased risk of severe or fatal flu.

Estimating the actual numbers of flu cases is difficult because many of those who get the flu do not seek medical treatment and, of those who do, only a small number are tested. Testing is more common in people who are hospitalised, but overall, laboratory-confirmed cases of influenza only represent a small percentage of those in a community who actually have the flu.

For comparison with the 2009-2010 flu season, the most lethal pandemic in recent history, the 1918-1919 H1N1 influenza A pandemic, infected about one third of the world`s population (an estimated 500 million people) and killed an estimated 20 to 50 million persons, with more than 500,000 deaths in the U.S. alone.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
For most people, the seasonal flu is a moderate illness that causes symptoms such as fatigue, fever, chills, stuffy nose, sore throat, headache, muscles aches, weakness, a cough and, with some strains, even diarrhoea and vomiting. These symptoms may also be seen with a variety of other conditions and seasonal viral infections.

Influenza can be severe and lead to complications such as viral pneumonia or secondary bacterial pneumonia (see Pneumonia) in the very young, the elderly, in those who are pregnant, and in those with underlying conditions such as asthma, lung disease, heart disease, diabetes, kidney disease, liver disease, and in those with compromised immune systems as with cancer or HIV/AIDS.

The incubation period for influenza is about two days. This is followed by several days of illness and then a resolution of symptoms. People shed virus and are infectious about a day before symptoms emerge and then for about five to seven days, or until about 24 hours after their fever ends.

Children and those with compromised immune systems may be infectious for longer periods of time.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
Influenza tests are performed to diagnose the flu, to distinguish it from other viral infections or other causes of symptoms, to guide treatment, and to monitor the spread of influenza through communities and throughout the world.

Many individuals with the flu are not tested. They either do not seek medical treatment or their doctor makes the diagnosis of probable-flu based upon the person`s symptoms, the fact that it is the flu season, and based upon the presence of influenza in the community. This is partially because rapid influenza tests will not detect every case of influenza and partially because more sensitive tests take too long to be useful to guide treatment. If it is to be useful in helping doctors make decisions about treatment, testing must be done within 48 hours of the onset of symptoms.

When rapid test results are negative, doctors may request follow-up testing but they will not wait for the results to initiate treatment. Testing is primarily performed on those who are seriously ill (hospitalised) and on those who are at risk for a severe case of influenza or for complications.

Laboratory Tests
 Several different types of influenza tests may be used to detect an infection. These include:

Real-time polymerase chain reaction (RT-PCR) – a sensitive test that detects viral genetic material. A specific version of this test has been developed to detect the 2009 H1N1 influenza virus.  This is the test most commonly used in the UK with testing done in hospital laboratories.

Rapid influenza antigen test – used to detect influenza A or influenza A and B and to guide antiviral treatment.. These tests are not currently widely used in the UK.

Direct fluorescent antibody stain (DFA) – more sensitive than rapid testing but requires specialised training to interpret.  This test is only performed in hospitals on young children in the UK.

Viral culture – considered the gold standard for diagnosing influenza but can take 3 to 7 days. Can detect influenza A and B and determine the strain of influenza.  This test, although useful for epidemiology and vaccine production is used rarely in the UK.

Influenza A or B antibody test – blood tests performed to detect the body`s immune response to an influenza infection. These tests are typically done for research or public health purposes.


For more on these, see the article Influenza Tests.

Non-Laboratory Tests

Chest X-ray - sometimes done to evaluate the lungs of a person with symptoms of pneumonia.




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Insulin is a hormone produced by the beta cells in the pancreas. Small amounts of insulin are normally released into the bloodstream after each meal and help transport glucose into the body’s cells where it is needed for energy production. Insulin resistance is a decreased ability of the body to respond to the effects of insulin especially by muscle and adipose (fat) tissues. Since cells must have glucose to survive, the body compensates for insulin resistance by producing additional amounts of the hormone. This results in a state of hyperinsulinaemia in the blood and over-stimulation of some tissues that have remained insulin sensitive. Over time, this process causes an imbalance in the relationship between glucose and insulin and can have adverse effects in the body.  

Hyperinsulinaemia and insulin resistance can affect the proportion of the body’s lipids, significantly increasing the amount of triglycerides and sdLDLs (small dense lipoproteins) in the blood and decreasing the amount of HDL (high density lipoprotein) cholesterol level, (the “good cholesterol”). It may also increase a person’s risk of developing a blood clot, cause inflammatory changes, and increase a person’s sodium retention, which can lead to increased blood pressure. It is also a vascular risk factor, increasing the likelihood of disease in arteries.

Insulin resistance is not a disease or specific diagnosis, but it has been associated with conditions such as cardiovascular disease (CVD), hypertension, polycystic ovarian syndrome (PCOS), type 2 diabetes, obesity and non-alcoholic fatty liver disease. Some researchers also believe that there may be a link between insulin resistance and some forms of cancer. The mechanisms of these associations, however, are not well understood. It is important to remember that many of the people who have these conditions do not have insulin resistance and, likewise, many of the people who have insulin resistance will never develop these conditions. These are just patterns of association that have emerged. They are frequently seen together and it is thought that insulin resistance may contribute to their development and exacerbate them when it is present.

Metabolic syndrome and insulin resistance syndrome are two terms that have been used to characterize some of the abnormalities associated with insulin resistance and to recognize them as risk factors for future disease. Although both terms are often used interchangeably, metabolic syndrome is more of a subset of the insulin resistance syndrome. It is a worldwide effort to identify patients who are primarily obese and sedentary and who are beginning to experience alterations in lipid levels and impaired glucose processing. The focus is on educating them about their increased risk of developing CVD and/or type 2 diabetes and on working with them to lower that risk through lifestyle changes. Since obesity and lack of exercise are known to exacerbate insulin resistance and exercise is known to increase the body’s sensitivity to insulin, identifying and treating those with metabolic syndrome also improves their insulin resistance. The insulin resistance syndrome term is broader. It’s intent is to define and catalogue the abnormalities and conditions that have been associated with insulin resistance and hyperinsulinaemia.

The cause of insulin resistance is not fully understood. It is thought to be due partly to genetic factors, including ethnicity, and partly to lifestyle, such as excessive caloric intake and inadequate exercise. Most patients with insulin resistance do not have any symptoms and they do not realize that this process is taking place in their bodies. In most cases, the body is able to keep pace with the need for extra insulin production, and the effects of it on the body are subtle and years in the making. If or when the body’s insulin production fails to keep up with demand, then hyperglycaemia will occur. Over time, hyperglycaemia can progress and become type 2 diabetes, which can damage body organs. At this stage symptoms may be present.

 



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests
There is no one test that can directly detect insulin resistance. Instead, a doctor will look at a patient’s entire clinical picture and may suspect that the patient has insulin resistance if he has increased blood glucose levels, increased levels of triglycerides and LDL cholesterol, and decreased concentrations of HDL cholesterol. Laboratory tests most likely to be ordered include:

Glucose. This is usually performed fasting but, in some cases, a doctor may also request a GTT (glucose tolerance test – two glucose tests that are taken before and 120 minutes after a glucose challenge). The goal of glucose testing is to determine whether a patient has an impaired response to glucose i.e. whether the blood glucose level climbs higher than it should under normal circumstances. 

Lipid profile. This measures the HDL, LDL, triglycerides, and total cholesterol. If the triglycerides are significantly elevated, a DLDL (direct measurement of the LDL) may need to be done. 


Other laboratory tests that may be used to help evaluate insulin resistance and provide additional information include: 

Insulin. The fasting insulin test is variable, but insulin levels will usually be elevated in those with significant insulin resistance. 

hs-CRP. This is a measure of low levels of inflammation that may be done as part of an evaluation of cardiac risk. It may be increased with insulin resistance. Mild inflammation is a feature of metabolic syndrome.

sdLDL. This is a measurement of the number of small dense low-density lipoprotein molecules a patient has. This test is not ordered frequently but may be measured as part of a lipoprotein subfractions test. 

Insulin tolerance test (ITT). Not widely used but is one method for determining insulin sensitivity (or resistance), especially in obese individuals and those with PCOS. This test involves an IV-infusion of insulin, with subsequent measurements of glucose and insulin levels. 


Specific insulin suppression tests may also be requested in a research setting to study insulin resistance but are not generally used in a clinical setting. An intravenous glucose tolerance test can be carried out where the glucose load is given into a vein rather than by mouth but again this test tends to be used for research purposes only rather than in a clinical setting.

 



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatment
Treatment of insulin resistance primarily involves changes in diet and lifestyle. This life style and dietary change will include losing excess weight, taking regular amounts of moderate-intensity physical activity, and increasing dietary fibre to lower blood insulin levels and increase the body’s sensitivity to it. Weight loss and exercise can:

Decrease blood pressure levels 

Increase insulin sensitivity (ie decrease insulin resistance)

Decrease triglyceride and LDL cholesterol levels 

Raise HDL cholesterol levels (with regular exercise)  


Patients who are identified by their doctors as having insulin resistance should work with their doctor and with other medical professionals to develop an individualised treatment plan and to monitor its effectiveness. Drug treatments may also be necessary to control any existing, underlying, associated conditions and diseases.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Jaundice is a yellowing of the skin, whites of the eyes and body fluids. It is caused by an increase in the amount of bilirubin in the blood. Bilirubin is a yellow pigment that is produced from the breakdown of haem, mostly from haemoglobin in red blood cells (RBCs). Bilirubin is transported by the blood to the liver, where an enzyme links it to a sugar, a process called conjugation. The conjugated bilirubin is excreted from the liver as bile, eventually reaching the small intestine. Jaundice may arise from an increase the breakdown of red blood cells, from liver disease or from a problem with the excretion of bile.

Examples of common conditions that may cause jaundice

Haemolytic anaemia: may be caused by an abnormal haemoglobin variant in the red blood cells, malaria, an autoimmune process, haemolytic disease of the newborn or any other condition that lead to a significant increase in the destruction of red blood cells and to an increase in the production of bilirubin. The jaundice is mild and due to unconjugated bilirubin.

Physiological (normal) jaundice: mild jaundice is seen in more than 50% of newborns due to the immaturity of the baby`s liver enzyme which is needed to conjugate bilirubin. It usually appears at 2 to 4 days and disappears by 7 to 10 days. If the jaundice appears early, persists or is severe the infant will be investigated for other causes and is likely to need treatment.

Gilbert’s syndrome: about 3% of the UK population have this condition. It is associated with decreased bilirubin conjugation in the liver due to an inherited decrease in enzyme activity and therefore reduced excretion in the bile. Those affected may have temporary mild jaundice during times of illness or stress caused by increases in their blood  unconjugated bilirubin levels.

Acute hepatitis: liver inflammation due to a variety of causes including hepatitis A, B, C, D, and E viral infections, alcohol abuse, and some medicines and toxins. More than half of the bilirubin in the blood is conjugated and bilirubin appears in the urine.


Obstruction of the bile ducts inside or outside the liver may be due to liver damage and scarring in the late stages of cirrhosis, cancer in the liver or biliary atresia, a congenital  condition with abnormal development of the bile ducts. Gallstones can block bile ducts and pancreatic cancer can sometimes lead to a blockage of the main bile duct. Back-up of bile behind an obstruction leads to the appearance of conjugated bilirubin in the blood and urine. If the obstruction is severe, the stools become pale. 


Examples of more rare conditions that may cause jaundice

Wilson’s Disease: an inherited disorder of copper metabolism which results in excessive deposits of copper in the liver, causing cirrhosis and jaundice, as well as in the brain and cornea of the eye.

Alpha 1 Antitrypsin Deficiency: an inherited condition in which defective alpha 1 antitrypsin accumulates in the liver cell causing liver damage and jaundice. The severe form of alpha 1 antitrypsin deficiency is the most common genetic cause of liver disease in babies and children

Crigler-Najjar syndrome: an inherited condition that may lead to high bilirubin concentrations; a gene mutation leads to a deficiency in the enzyme necessary for bilirubin conjugation.

Dubin-Johnson syndrome: an inherited disorder that impairs the secretion of bilirubin from liver cells after it has been conjugated; patients may have intermittent jaundice.

Rotor’s syndrome: an inherited cause of mild intermittent jaundice; similar to Dubin-Johnson without the retention of bilirubin in the liver cells.

Pseudojaundice: the skin of a person may turn yellowish when they eat large quantities of carrots, pumpkin or melon due to the presence of beta-carotene; a temporary and benign condition not related to bilirubin or bile




                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests
The goal of testing is to determine the cause of the jaundice and to evaluate the severity of the underlying disease. Initial testing is usually focused on the liver. Specific additional tests, such as viral hepatitis testing or testing to evaluate increased RBC destruction, may be requested with or following the initial tests based on the patient’s clinical findings and the doctor’s suspicions of the cause of the jaundice.

Laboratory Tests

Tests may include:

Liver function tests, which usually include total bilirubin, ALT (alanine aminotransferase), ALP (alkaline phosphatase), total protein and albumin

Conjugated and unconjugated bilirubin

AST (aspartate aminotransferase)

GGT (gamma-glutamyl transferase)

Copper (serum and/or urine)

Caeruloplasmin

Alpha 1 antitrypsin level (pheno/genotype if indicated)

Hepatitis A

Hepatitis B

Hepatitis C

FBC (Full blood count)

Reticulocyte count (if FBC is abnormal)

PT (prothrombin time)


Less commonly requested tests include G6PD (glucose-5-phosphate dehydrogenase), haemoglobin variants, ASMA (anti-smooth muscle antibodies) and ANA (anti-nuclear antibodies).

Non-Laboratory Tests

Imaging tests and liver biopsies may be used to help evaluate the status and structure of the liver, gallbladder, and bile ducts. Tests may include:

Abdominal ultrasound

Computed tomography (CT)

Cholangiography (an imaging of the bile ducts)

ERCP(endoscopic retrograde cholangiopancreatography, imaging of the pancreatic and bile ducts)

Liver biopsy




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatments
Jaundice in newborns must be treated if it becomes severe, usually by exposure of the skin to blue light, because high unconjugated bilirubin levels can cause permanent brain damage. In all other cases it is not the jaundice that needs to be treated but the underlying condition. Should the condition resolve, then the jaundice will resolve as well. If an obstruction is present surgery may be necessary.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Juvenile Rheumatoid Arthritis (JRA), also sometimes called Juvenile Idiopathic Arthritis (JIA) or Juvenile Chronic Arthritis (JCC), affects about 1 in 1000 children in the UK.  It is a chronic condition that causes joint inflammation, pain, swelling, redness, and stiffness.  It may also affect the eyes and internal organs.  About one-fifth of those with JRA have an enlarged spleen.

There are three main types of Juvenile Rheumatoid Arthritis:

Pauciarticular or Oligoarticular – about 50%.  It affects four or less joints and is most common in girls less than 8 years old.

Polyarticular – about 30%.  It affects five or more joints, especially in the hands and feet but also other larger joints.

Systemic – about 20%.  It affects both joints and internal organs.  Children with this type may have frequent fevers and rashes that can come and go rapidly.  Also known as Still’s disease.

Each patient’s symptoms will differ and will frequently change over time, with flare-ups and remissions.  In a few children the symptoms may be persistent, in a few others they may permanently disappear.

Doctors consider the diagnosis of JRA in patients who have had symptoms for at least 6 weeks.  These symptoms may include morning stiffness, limping, reluctance to move an affected joint, joint pain and swelling.  Patients with systemic JRA may have intermittent fever, rash, swollen lymph nodes, and in some cases liver, spleen, and (very rarely) lung involvement.

Complications of JRA may include eye inflammation and problems related to joint growth.  The disease may cause the affected joints to grow either too quickly or too slowly, causing one arm or leg to be shorter or longer than the other.   It may also cause uneven growth in the joint itself.  General growth may also be affected by JRA.

Testing 
The goals with testing are to help diagnose juvenile rheumatoid arthritis, to distinguish it from other forms of arthritis and conditions with similar symptoms, and to evaluate its severity.  Testing can be used to monitor the condition, its potential complications, response to treatment, and to monitor for potential side effects associated with some treatments.   

Laboratory Tests 

Full blood count (FBC) – to check for anaemia and to check for a normal response to infections 

Erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) – to detect inflammation 

Antinuclear antibody (ANA) – to detect the presence of autoantibodies; about 80% of those with eye involvement will test positive for ANA 

Rheumatoid factor (RF) – may be positive (present) or negative (absent) depending on the type of JRA 

Urea and Electrolytes – to assess the patient’s kidney function 

Liver function tests – to assess the liver function 

Histocompatibility antigens (HLA) – may show the presence of antigens specific to autoimmune diseases 

Synovial fluid analysis – Fluid from an affected joint may be examined to detect crystals and to look for signs of joint infection 


Other tests of diagnostic use include joint and chest X-rays to identify the presence of joint inflammation or fluid build-up around the heart or lungs, and ECG to detect inflammation of the heart.

Non-Laboratory Tests

X-rays of the joints and chest, to identify the presence of joint inflammation or fluid build-up around the heart or lungs 

Eye exam to detect the development of eye inflammation

ECG, to detect inflammation of the heart 


Treatments 
There is no cure for juvenile rheumatoid arthritis.  The goals with treatment are to decrease pain and inflammation, maintain mobility and joint function, and to minimize joint damage and complications.  Treatment will vary from patient to patient and frequently varies over time.

Medications may include pain relievers, disease-modifying antirheumatic drugs (DMARDs), immunosuppressants, steroids and biologic agents.

Physiotherapy and regular exercise are very important.  They can help maintain flexibility, range-of-motion, muscle strength and joint mobility.  Splints may be used in some cases to help keep a joint in the proper position.  Hot and/or cold treatments may help relieve morning stiffness.  

Some changes may need to be made at school and at home for a child with JRA but in most cases they can lead and should be encouraged to lead relatively normal lives.

Laboratory tests that can aid in the diagnosis of JRA and in ruling out other disorders, are:

The cause of JRA is unknown, but it is thought to be an autoimmune disorder.  The tendency to develop it may be inherited but it is believed that a triggering event is required for it to emerge.  It usually begins between the ages of 2 and 5 years or between 9 and 12 years. More girls than boys develop JRA.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Tests:
What is it?
Juvenile Rheumatoid Arthritis (JRA), also sometimes called Juvenile Idiopathic Arthritis (JIA) or Juvenile Chronic Arthritis (JCC), affects about 1 in 1000 children in the UK.  It is a chronic condition that causes joint inflammation, pain, swelling, redness, and stiffness.  It may also affect the eyes and internal organs.  About one-fifth of those with JRA have an enlarged spleen.

There are three main types of Juvenile Rheumatoid Arthritis:

Pauciarticular or Oligoarticular – about 50%.  It affects four or less joints and is most common in girls less than 8 years old.

Polyarticular – about 30%.  It affects five or more joints, especially in the hands and feet but also other larger joints.

Systemic – about 20%.  It affects both joints and internal organs.  Children with this type may have frequent fevers and rashes that can come and go rapidly.  Also known as Still’s disease.

Each patient’s symptoms will differ and will frequently change over time, with flare-ups and remissions.  In a few children the symptoms may be persistent, in a few others they may permanently disappear.

Doctors consider the diagnosis of JRA in patients who have had symptoms for at least 6 weeks.  These symptoms may include morning stiffness, limping, reluctance to move an affected joint, joint pain and swelling.  Patients with systemic JRA may have intermittent fever, rash, swollen lymph nodes, and in some cases liver, spleen, and (very rarely) lung involvement.

Complications of JRA may include eye inflammation and problems related to joint growth.  The disease may cause the affected joints to grow either too quickly or too slowly, causing one arm or leg to be shorter or longer than the other.   It may also cause uneven growth in the joint itself.  General growth may also be affected by JRA.

Testing 
The goals with testing are to help diagnose juvenile rheumatoid arthritis, to distinguish it from other forms of arthritis and conditions with similar symptoms, and to evaluate its severity.  Testing can be used to monitor the condition, its potential complications, response to treatment, and to monitor for potential side effects associated with some treatments.   

Laboratory Tests 

Full blood count (FBC) – to check for anaemia and to check for a normal response to infections 

Erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) – to detect inflammation 

Antinuclear antibody (ANA) – to detect the presence of autoantibodies; about 80% of those with eye involvement will test positive for ANA 

Rheumatoid factor (RF) – may be positive (present) or negative (absent) depending on the type of JRA 

Urea and Electrolytes – to assess the patient’s kidney function 

Liver function tests – to assess the liver function 

Histocompatibility antigens (HLA) – may show the presence of antigens specific to autoimmune diseases 

Synovial fluid analysis – Fluid from an affected joint may be examined to detect crystals and to look for signs of joint infection 


Other tests of diagnostic use include joint and chest X-rays to identify the presence of joint inflammation or fluid build-up around the heart or lungs, and ECG to detect inflammation of the heart.

Non-Laboratory Tests

X-rays of the joints and chest, to identify the presence of joint inflammation or fluid build-up around the heart or lungs 

Eye exam to detect the development of eye inflammation

ECG, to detect inflammation of the heart 


Treatments 
There is no cure for juvenile rheumatoid arthritis.  The goals with treatment are to decrease pain and inflammation, maintain mobility and joint function, and to minimize joint damage and complications.  Treatment will vary from patient to patient and frequently varies over time.

Medications may include pain relievers, disease-modifying antirheumatic drugs (DMARDs), immunosuppressants, steroids and biologic agents.

Physiotherapy and regular exercise are very important.  They can help maintain flexibility, range-of-motion, muscle strength and joint mobility.  Splints may be used in some cases to help keep a joint in the proper position.  Hot and/or cold treatments may help relieve morning stiffness.  

Some changes may need to be made at school and at home for a child with JRA but in most cases they can lead and should be encouraged to lead relatively normal lives.

Laboratory tests that can aid in the diagnosis of JRA and in ruling out other disorders, are:

The cause of JRA is unknown, but it is thought to be an autoimmune disorder.  The tendency to develop it may be inherited but it is believed that a triggering event is required for it to emerge.  It usually begins between the ages of 2 and 5 years or between 9 and 12 years. More girls than boys develop JRA.



                                        
                                        
    
        
            
                

                

                
                    <a title=``


info:
Also known as: Renal Disease, Kidney Failure; Chronic Kidney Disease; CKD; Acute Kidney Injury; AKI; Acute Renal Failure; ARF; End Stage Renal Disease; ESRD; Nephrotic Syndrome


                                                
                                            

What are the kidneys?
The kidneys are part of the body`s urinary tract. The urinary tract consists of two kidneys, two tube-like ureters that drain urine from each kidney into the bladder (a storage sac), and the urethra, another tube that carries the urine out of the body. Muscles help control the release of urine from the bladder.

The kidneys are a pair of bean-shaped organs that are located at the bottom of the ribcage in the right and left sides of the back. Within them are about a million tiny blood filtering units called nephrons. In each nephron, blood is continually filtered through a microscopic cluster of looping blood vessels, called a glomerulus. The glomerulus allows the passage of water and small molecules but retains blood cells and larger molecules. Attached to each glomerulus is a tiny tube (tubule) that collects the fluid and molecules that pass through the glomerulus and then reabsorbs what can be used by the body. The remaining waste forms urine.

The kidneys control the quantity and quality of fluids within the body. They also produce and release erythropoietin (EPO), which stimulates the bone marrow to make red blood cells, renin, which helps control blood pressure, and calcitriol, the active form of vitamin D, which is needed to maintain calcium for teeth and bones and for normal chemical balance in the body. Among the important substances the kidneys help to regulate are sodium, potassium, chloride, bicarbonate, calcium, phosphorus, and magnesium. The right balance of these substances is critical. When the kidneys are not working properly, waste products and fluid can build up to dangerous levels in the blood, creating a life-threatening situation.

Although the body is equipped with two kidneys, it can function with one reasonably healthy kidney if the other is damaged or removed. However, when kidney – or ``renal`` – function drops below 25% (people with two healthy kidneys have 100% of their kidney function), serious health problems occur, and when function drops below 10-15%, critical intervention in the form of dialysis or kidney transplant becomes necessary to maintain life. This is called end stage renal disease (ESRD or kidney failure).

A sudden loss of kidney function, such as over a few hours or days, is called acute kidney injury (AKI, formerly called acute renal failure or ARF). When kidney damage and decreased function occurs over time and/or lasts longer than 3 months, it is called chronic kidney disease (CKD). The

Sym:
What is kidney disease?
Kidney disease occurs when the kidneys are damaged and cannot function properly. Numerous conditions and diseases can result in damage to the kidneys, thus affecting their ability to filter waste from the blood while reabsorbing important substances. Generally, kidney disease may present or develop in a few different ways:

Acute kidney injury (AKI) is the rapid loss of kidney function. It may be recognised when a person suddenly produces urine much less frequently and/or has a dramatic increase in the level of waste products in the blood that the kidneys normally filter out. AKI is often the result of trauma, illness, or a medication that damages the kidneys. It is most common in people who are already hospitalised, such as those who are critically ill and in the intensive care unit. If the damage caused by AKI persists, it can eventually progress to chronic kidney disease.

Chronic kidney disease (CKD) occurs over time and is usually defined as lasting over 3 months. The most common causes are diabetes and high blood pressure (hypertension). Approximately 1 in 10 people in the UK have CKD. In some cases CKD is preventable or, if detected early enough, treatable to prevent or delay progression to kidney failure.

Nephrotic syndrome is characterised by the loss of too much protein in the urine. It is caused by damage to the glomeruli and can be a primary disorder of the kidney or secondary to an illness or other condition, such as cancer or lupus. Along with a high amount of protein in the urine, signs and symptoms of nephrotic syndrome include a low amount of albumin in the blood, higher than normal lipid levels in the blood, and swelling (oedema) in the legs, feet, and ankles. The condition may be acute or chronic, and the outcome can vary.

Kidney failure, also called end-stage renal disease or ESRD, is the total or near total loss of kidney function and is permanent. Treatment with haemodialysis, peritoneal dialysis or kidney transplantation is the only option at this stage of kidney disease to sustain life.


Various factors can cause different patterns of injury to the kidneys and can affect kidney function. Some factors affect the blood-filtering units, the nephrons, or parts of the nephrons, such as the glomeruli or the tubules. Some factors affect the passage of urine from the kidney while others cause damage to the kidney(s) as a whole.

The most common causes of and main risk factors for kidney disease are:

Diabetes: a sustained high level of blood glucose from uncontrolled diabetes can over time damage the nephrons in the kidneys. This can be avoided by maintaining good glucose control.

High blood pressure (hypertension): can damage blood vessels within the kidneys, preventing them from filtering wastes from the blood as they should. Hypertension can therefore cause CKD, but having CKD can cause high blood pressure as well.

Family history of kidney disease: for example, polycystic kidney disease (PKD) is an inherited disorder in which cysts grow in the kidneys, reducing kidney function over time and eventually leading to kidney failure.


Some other examples of factors affecting the kidneys or patterns of kidney disease include:

Glomerulonephritis (also called chronic nephritis or nephritic syndrome): a group of diseases that cause inflammation and damage to the blood filtering units of the kidneys (glomeruli) and the third most common type of kidney disease. As blood filtering becomes impaired, urine output decreases, water and waste products accumulate in the blood, and blood appears in the urine. Because the blood cells break down, urine often becomes brown instead of red. Certain body tissues swell with the excess water (a condition called oedema). Outcomes can vary: the condition may go away in a few weeks, permanently reduce kidney function, or progress to kidney failure.

Obstruction: the urinary tract can become blocked, or obstructed, from such things as a kidney stone or tumour and, in men, enlargement of the prostate gland. The blockage can lead to infection and injury of the kidney.

Autoimmune disease: in autoimmune diseases, the body`s immune system mistakenly attacks and damages its own tissue and organs, including the kidneys. Sometimes an autoimmune disorder such as systemic lupus erythematosus or Goodpasture syndrome can lead to glomerular disease and affect the kidneys.

Infections: certain bacteria and viruses can infect the kidneys and cause damage. Repeated urinary tract infections (UTIs) that spread to the kidneys is an example.

Immune response: infections in other parts of the body can stimulate an immune response that has an adverse effect on the kidneys. Examples include streptococcal infection of the throat or skin, the skin infection impetigo, an infection inside the heart (endocarditis), or viral infections such as HIV, hepatitis B, or hepatitis C.

Congenital defects: defects present at birth, such as those that impede the normal flow of urine.

Injury: trauma to the kidneys can cause AKI that can lead to chronic kidney disease.

Toxins: some contrast dyes used for imaging procedures and certain medications can have toxic effects on the kidneys.

Drugs: use and/or overuse of non-steroidal anti-inflammatory drugs (NSAIDS), such as over-the-counter ibuprofen, and various prescription drugs can damage the kidneys. Use of analgesics (pain killers) has been associated with two different forms of kidney damage: acute renal failure and a type of chronic kidney disease called analgesic nephropathy. Certain antibiotics can be directly toxic to the kidneys if their levels are too high. Other drugs may trigger an immune response by the body that subsequently causes kidney damage.

Pre-renal azotaemia: any situation in which there is severe blood loss or reduced blood flow may prevent the kidneys from working properly, such as a blood clot, severe burn, severe dehydration, or septic shock.

Interstitial nephritis: a kidney disorder in which the spaces between the kidney tubules become inflamed and swollen. It may be acute or chronic. Causes include side effects of certain medications, certain autoimmune disorders, and having a low blood potassium level or a high blood level of calcium or uric acid. It is associated with decreased urine output, blood in the urine, and oedema. Usually, this is a short-term condition.

Acute tubular necrosis (ATN): a kidney disorder involving damage to the tubules in the kidneys. It is one of the most common causes of kidney failure in hospitalised patients. It is caused by a lack of oxygen to the kidney tissues or from damage to the kidneys by toxic substances such as contrast dyes used for x-ray studies and certain medications. In most cases, ATN is reversible.




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Signs and symptoms
Chronic kidney disease (CKD) can progress silently over many years, with no signs or symptoms or with ones that are too general for a person to suspect as related to kidney function. For that reason, blood and urine tests are especially important allowing the detection of blood or protein in the urine and abnormal levels of certain waste products in the blood, such as creatinine and urea, which are early signs of kidney dysfunction. The following problems may, however, be warning signs of kidney disease and should not be ignored. Prompt medical attention is required when any of these are present:

Swelling or puffiness, particularly around the eyes or in the face, wrists, abdomen, thighs or ankles

Urine that is foamy, bloody, or coffee-coluored

A decrease in the amount of urine

Problems urinating, such as a burning feeling or abnormal discharge during urination, or a change in the frequency of urination, especially at night

Mid-back pain (flank), below the ribs, near where the kidneys are located

High blood pressure (hypertension)


As kidney disease worsens, symptoms may include:

Urinating more or less often

Feeling itchy

Tiredness, loss of concentration

Loss of appetite, nausea and/or vomiting

Swelling and/or numbness in hands and feet

Darkened skin

Muscle cramps


Acute kidney injury (AKI) is a sudden loss of kidney function and can be fatal. It requires prompt treatment. Symptoms may include:

Urinating less frequently

Fluid retention, causing swelling in the legs, ankles or feet

Drowsiness, fatigue

Shortness of breath

Nausea

Confusion

Seizures or coma

Chest pain




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Also known as: Lactase Deficiency; Carbohydrate Intolerance; Disaccharidase Deficiency; Congenital Alactasia


                                                
                                            

What is lactose intolerance?
Lactose intolerance is a condition that occurs when there is decreased ability of the body to digest a type of sugar called lactose. Lactose is found in the milk of mammals such as cows and goats as well as in human breast milk. It is also an ingredient in other dairy products such as cheese, cottage cheese, yoghurt, ice cream, and butter. People who are lactose intolerant can develop abdominal symptoms within 30 minutes to 2 hours of consuming dairy products. The severity of symptoms depends on the type and amount of dairy product consumed and often varies from person to person, changing as a person ages.

Lactose is a sugar with a complex structure. It is a disaccharide, which means it is composed of two simple sugars joined together. Before it can be absorbed and used by the body, lactose must be broken down into its simpler sugars of glucose and galactose monosaccharides). This digestion step is initiated by lactase, an enzyme produced by cells lining the small intestine.

Production of the enzyme lactase begins in a developing baby during pregnancy and peaks near birth. Normal lactase production mirrors an infant`s need for the enzyme when milk is the primary source of nutrition. Almost all babies can digest milk, although premature infants may initially have some degree of intolerance. Lactase levels naturally decrease after the first couple of years i.e. when the diet is less reliant on milk and dairy products. Levels continue to decline as an individual ages.

If an individual does not produce enough lactase (they are lactase deficient), then the undigested lactose passes through the small intestine to the large intestine. In the large intestine, bacteria break down the lactose producing excess hydrogen gas and lactic acid and drawing extra fluid into the gut. Combined, these factors result in the typical symptoms of lactose intolerance; diarrhoea, flatulence and abdominal cramps.

Lactose intolerance can be divided into three clinical syndromes: primary adult lactase deficiency (hypolactasia), congenital lactase deficiency (alactasia),  and secondary lactase deficiency.

Primary Adult Lactase Deficiency

This is the most common form of lactose intolerance and is associated with the decreased production of lactase in adults. The decreased production of this enzyme renders an individual less likely to properly digest lactose.

The incidence of primary adult lactase deficiency varies based on racial and ethnic distribution. Some people, primarily northern Europeans, have an inherited gene mutation that leads to persistence in the ability to digest lactose into adulthood. People without this mutation lose the ability to produce lactase as they age, resulting in lactose intolerance.

Asians, Africans and Native Americans have the highest incidence of lactose intolerance in adults. This is because, traditionally their diets do not contain much lactose, and so the ability of their digestive system to produce lactase has declined.

Ethnic Group or Race
% of Adults with Lactose Intolerance
Northern Europeans
4-11%
Eastern and Southern Europeans
14-38%
Southern and Eastern Indians
77%
Hispanics
50-80%
Africans
80%
Asian and Native Americans
95-100%
Congenital Lactase Deficiency

Congenital lactase deficiency is a rare form of lactose intolerance that begins at birth and severely inhibits a baby`s ability to digest milk or milk-based formulas. It is caused by mutations within the gene that controls lactase production (the LCT gene). Congenital lactase deficiency will occur if a mutation in the gene is inherited from each parent – it is an autosomal recessive inherited condition.

Secondary Lactose Intolerance

In addition to the natural decline of lactase production with age, a variety of diseases and conditions can cause a secondary form of lactose intolerance. Damage to the small intestines and/or causes of general malabsorption may lead to the inability to absorb lactose properly. In some individuals, stomach contents move more rapidly than usual through the small intestine. They too may experience decreased lactose absorption due to insufficient time for lactose digestion to occur.

Secondary causes of lactose intolerance include:

1.	Coeliac disease

2.	Chemotherapy or radiation therapy

3.	Inflammatory bowel disease (IBD)

4.	Infections caused by parasites

5.	Overgrowth of bacteria

6.	Short bowel syndrome

Testing is important to differentiate the various conditions that have similar signs and symptoms, but have different prognoses and treatments. Treatment of the underlying condition may reverse the lactose intolerance.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
Signs and symptoms associated with lactose intolerance are due primarily to undigested lactose reaching the large intestine. Extra fluids are drawn into the large intestine, where bacteria break down the lactose, producing hydrogen gas and lactic acid. This can cause:

Abdominal pain and cramps

Abdominal bloating

Excessive gas, flatulence

Nausea

Diarrhoea

The type and severity of symptoms vary by individual and by the amount and kind of dairy products consumed. Many people with lactose intolerance can consume small amounts of dairy products with few to no symptoms.

Lactose intolerance should not be confused with an allergy to cow`s milk. A milk allergy involves a reaction by the immune system and is directed against a protein in the milk, not a sugar. Although some of the symptoms may be similar, a person with a milk allergy can have a mild to severe or even life-threatening reaction within minutes to hours after drinking milk. In addition to digestive symptoms, those with a milk allergy may experience hives and wheezing.

Lactose intolerance is more common in adults than in children. Milk allergies are common in young children but are also frequently outgrown.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
Tests of lactose intolerance are not always needed. If a doctor suspects a patient has lactose intolerance, then a trial of a lactose free diet may be recommended. If the symptoms improve then this is consistent with lactose intolerance (although it is not diagnostic), and further testing will often not be necessary.

 Laboratory Tests 

The goals of testing are to diagnose lactose intolerance and distinguish it from other conditions with similar symptoms. Testing may include:

Lactose tolerance tests, including  
Hydrogen breath test – currently, this is the most reliable test used to diagnose lactose intolerance. Breath samples are taken before and at timed intervals after a patient drinks a fluid containing a standard amount of lactose. With lactose intolerance, undigested lactose is broken down by bacteria in the large intestine, producing excess hydrogen gas. The hydrogen moves to the circulation and is eventually exhaled by the lungs. Increasing levels of hydrogen in the breath samples over time strongly indicates lactose intolerance.

Lactose tolerance blood test – sometimes performed to help diagnose lactose intolerance; blood samples are collected and tested for glucose at timed intervals after a standard oral dose of lactose is given. If glucose levels do not rise, then lactose intolerance may be present.




Stool acidity (pH) test – rarely performed, usually on infants or children who cannot undergo other types of testing; stool can be acidic with lactose intolerance.

Additional specialist testing that is rarely requested includes: 
Lactase activity performed on a biopsy from the small intestine

Genetic testing of the LCT (lactase) gene







                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Lead poisoning is a preventable condition that results from environmental or occupational exposure to lead. This exposure can result in permanent health damage, especially among children.

Lead poisoning can affect almost all parts of the body, including the central nervous system, kidneys, and reproductive organs. It commonly causes weakness and abdominal discomfort and less often causes abdominal pain, vomiting, constipation, foot and wrist drop and anaemia. In children especially, it impairs cognitive development, which can lead to learning disabilities and behavioural problems. At very high levels, it can even result in hallucinations, coma, seizures, and death.

Environmental lead exposure comes from inhaling or ingesting lead laden dust. This can come from sources such as deteriorated paint containing lead found in older houses. Drinking water can also be contaminated if plumbing parts, such as pipes, are made of lead. Recent reports have included exposure from imported folk remedies, health foods, cosmetics and toys that have been contaminated with lead. Children are especially vulnerable to lead poisoning as they have an increased hand to mouth behaviour which may include ingestion of lead contaminated items such as soil and paint chips. There is also an increased risk of lead exposure to a developing foetus if pregnant women are exposed.

As poisoning from lead became known as a problem, lead began to be removed from paint products and unleaded petrol was introduced. Following these and other measures, there has been a significant reduction in blood lead concentrations in the general population of the UK and many other countries.

Adult lead exposure is usually either from the workplace or from hobbies. Children may be affected if contaminants are brought home from the workplace on clothing. Examples of situations potentially leading to lead exposure are listed below:

Work Settings

lead smelting plants

construction work

steel welding

bridge reconstruction

firing range instructors and cleaners

remodelling and refinishing

foundry work

scrap metal and battery recycling

auto repair work

cable splicing and 

battery, glass and ceramic ware manufacture


In England and Wales the Health and Safety Executive requires some 15,000 workers to be regularly monitored for lead poisoning.

Hobbies

casting bullets, lead shot or fishing sinkers

home remodelling

target shooting at firing ranges

lead soldering

auto repair work

stained glass work and 

glazed pottery work




                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests for Lead Poisoning
A simple blood lead test can be done to detect the level of lead in your body. Sometimes a second test, called a zinc protoporphyrin (ZPP) test, is requested. The ZPP result increases when lead interferes with red blood cell’s ability to make haemoglobin. Some experts question the value of ordering both tests at once, and the ZPP test is not reliable for screening children for lead poisoning. 

In 1997, the Centers for Disease Control and Prevention (CDC) issued revised screening guidelines for all children for elevated blood lead, except those in communities or neighbuorhoods found not to be at risk. The CDC released guidelines for action, including testing intervals, for blood lead levels in children.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatment
Treatment of lead poisoning depends on the concentration of lead in the blood and symptoms. The most common treatment is to identify the source of lead and to eliminate or reduce further exposure.  Efforts to reduce exposure to lead may include wet mopping living areas frequently and flushing water from the tap before drinking if lead pipes are present. Lead abatement of a house is the process of methodically removing lead paint or other lead sources from a building or area and is usually performed by trained professionals. Workers exposed to lead in their jobs may have to wear respirators. If lead is still building up in their bodies, they may be transferred to a job with lower levels of lead exposure. Abatement at the work site may be required if blood lead levels are very high among employees.

Chelation therapy is a last resort treatment to rid the body of high amounts of lead. Chelation involves giving a patient a chemical which lead will preferentially bind to and then be excreted in the urine. Sodium calcium edetate is effective but has to be given into a vein. Dimercaptosuccinic acid has the advantage that it can be given by mouth and is often used in small children. Chelation treatment can be dangerous because the chemical-lead combination can damage kidneys.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Overview
Leukaemia is a cancer of the white blood cells (WBCs) originating in the bone marrow. Over 7000 people are diagnosed with leukaemia annually in the UK, making it the 10th most common cancer in men and 9th in women. While exposure to radiation, benzene, and some anticancer drugs have been shown to increase the risk of developing leukaemia, and a few cases are associated with genetic disorders or rare viral infections, the cause of most leukaemias is not known.

What is it? 
 Leukaemia is a bone marrow disorder that arises when one abnormal white blood cell begins to continuously replicate itself. Except in the case of chronic myeloid leukaemia (CML), leukaemic cells do not function normally, i.e. they do not fight infection as they should and they do not die at the same rate as other WBCs. As they accumulate, the cells inhibit the production of the other normal blood cells in the marrow, leading to anaemia, bleeding, and recurrent infections. Over time, the leukaemic cells spread through the bloodstream where they continue to divide, sometimes forming tumours and damaging organs such as the kidney and liver. Since the spleen is responsible for filtering the blood and destroying old cells, it may become enlarged and swollen with the abnormal cells, as can the liver and lymph nodes. If the cells reach the central nervous system and build up in the cerebrospinal fluid that surrounds the brain and spinal column, they can cause headaches and seizures.

The bone marrow, located in the soft centre of the body`s larger bones, produces precursors (immature versions) of red blood cells, platelets, and various kinds of white blood cells. The most immature recognisable precursor is called a blast cell. Most of these blood cells mature in the bone marrow before being released into the bloodstream. The WBCs created are grouped into two main categories: lymphoid and myeloid. Myeloid cells (which include neutrophils, basophils, eosinophils, (collectively known as granulocytes due to granules visible inside them) and monocytes) circulate in the blood, killing and digesting bacteria. Lymphocytes, which are found in both the blood stream and the lymphatic system, coordinate the immune response and produce antibodies. Leukaemia arises from any one of these white blood cells. It is categorised both by the type of WBC involved and by how quickly it progresses. Although expanded classifications of the disease exist, the main types of leukaemia can be grouped as:

Acute lymphocytic leukaemia (ALL). Affects approximately 200 adults each year in the UK. This is a rapidly developing disease that is characterized by large numbers of immature lymphocytes (lymphoblasts). It is the most common type of leukaemia found in children, although it affects both children and adults (usually adults age 65 and older).


Chronic lymphocytic leukaemia (CLL). This disease progresses more slowly and is characterized by an excess of mature lymphocytes. It tends to be found in those over the age of 55 or 60 and is almost never found in those under 40


Acute myeloid leukaemia (AML).  Affecting people of all ages, although it becomes increasingly common with age and is predominantly found in those over 60, this disease is characterized by production of large numbers of immature granulocyte myeloid cells (myeloblasts) that replace other normal cells in the marrow.


Chronic myeloid (or granulocytic) leukaemia (CML or CGL). Chronic myeloid leukaemia affects approximately 700 people (mostly adults) in the UK each year. It is an acquired condition that begins in an immature stem cell in the bone marrow when pieces from two chromosomes (9 and 22) break off and switch places (translocation). This results in an altered, fused gene (bcr-abl) on chromosome 22 that produces an abnormal which affects cell growth regulation. This leads to an overproduction of myeloid white blood cells, and the presence of both mature and immature cells in the bloodstream.




                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
Acute leukaemia is often diagnosed because the patient feels ill. They may have symptoms related to not having enough normal cells, such as:

Weakness, shortness of breath and anaemia due to a lack of red blood cells (which carry oxygen to the body`s tissues)


Bleeding and bruising due to a lack of platelets (which are cell fragments that the body uses in the clotting process to plug holes in leaking blood vessels)


Recurrent infections due to a lack of normal infection fighting WBCs.


Those with acute leukaemia may also have signs and symptoms related to accumulations of immature white blood cells, such as: bone and joint pain; enlarged lymph nodes, spleen, liver, kidneys, and testicles; and headaches, vomiting, confusion, and seizures (when excess cells collect in the brain or central nervous system). They may also experience fever, weight loss, and night sweats.

Chronic leukaemias often progress slowly and may be found by the doctor during a routine check-up before any symptoms are noticed, or they may cause milder forms of the same symptoms noticed with acute leukaemia. The rate at which they progress depends on the patient. CLL may be monitored for decades and never require treatment, but usually progresses slowly to cause symptoms and may do quickly. CML always requires treatment when diagnosed. The abnormal cell that is producing the chronic leukaemia may also become unstable. Further changes in the cell may cause a blast crisis (becoming an acute leukaemia) leading to the production of only immature cells and a rapidly worsening condition.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Laboratory Tests
Full blood count and differential
These are routine tests that are requested to count the number and relative proportion of each of the different types of cells in the blood stream. They give your doctor information about the relative maturity of the blood cells present and they can provide the first evidence that a person has leukaemia. Irregularities in cell counts, such as elevated WBC counts or low red blood cell counts may be due to leukaemia or to a variety of temporary or chronic conditions, but blasts (very immature WBCs) are not normally seen in the blood. If they are present, some kind of leukaemia is likely, and follow-up testing is indicated. The FBC and differential are used to help diagnose leukaemia and are important tools to monitor the effectiveness of treatment and to detect recurrence.

Bone marrow aspiration/biopsy
 Bone marrow exists as a matrix of fibrous supporting tissue, fluid, undifferentiated stem cells, and a mixture of blasts and maturing blood cells. If your doctor suspects leukaemia, they will often request or perform a bone marrow aspiration or biopsy to look directly at the fluid and tissue in the marrow. A specialist then examines the marrow sample (bone and/or fluid) under the microscope, evaluating the number, size, and shape of each of the cell types, as well as the proportions of mature and immature cells. If leukaemia is present, the type and severity of the disease can be determined.

For more information, see Bone Marrow Aspiration and Biopsy.

Spinal tap (lumbar puncture)
 If leukaemia is found in the bone marrow a lumbar puncture may also be done to look for leukaemia cells in the cerebrospinal fluid around the brain and spinal cord.

Cytogenetic analysis and fluorescent in-situ hybridization (FISH) 
 This is a molecular cytogenetic test used to investigate chromosomal abnormalities associated with leukaemias, other cancers, and genetic disorders. It is used for diagnosis and differentiating the leukaemias: there are translocations such as t(8;21) and many others for acute myeloblastic leukaemia t(15;17) for acute promyelocytic leukaemia and t(9;22) for chronic myeloid leukaemia. These techniques can also detect deletions associated with AML or myelodysplastic syndromes (5q, 7q) and trisomies (trisomy 12) for chronic lymphocytic leukaemia. Karyotyping and/or FISH helps diagnose different leukaemias that may look similar but have different genetic abnormalities and therefore may require different treatment.

Polymerase chain reaction (PCR) 
 This test amplifies DNA mutations, that are associated with certain leukaemias and may help with determining the prognosis for a certain leukaemia. Classic PCR tests look for for the promyelocytic leukaemia mutation PML-RARA (due to the chromosomal translocation t(15;17)(q22;21)], for the AML1-ETO fusion product (chromosomal translocation t(8;21)(q22;q22)) associated with acute myeloid leukaemia [and for (BCR-ABL (translocation t(9;22)) characteristic of chronic myeloid leukaemia. PCR screening tests look for a large number of known mutations.

Non-Laboratory Tests
Computerized tomography (CT), magnetic resonance imagine (MRI), or positron emission tomography (PET) scans are sometimes used to look for signs of the disease (tumours and masses of cells) in areas such as the chest. Other imaging scans may also be used to evaluate the status of body organs such as the spleen, liver, and kidney.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Overview of the Liver
The liver is a vital organ located in the upper right-hand side of the abdomen. It performs numerous functions for the body: converting nutrients derived from food into essential blood components, storing vitamins and minerals, regulating blood clotting, producing proteins and enzymes, maintaining hormone balances, and metabolising and detoxifying substances that would otherwise be harmful to the body. The liver also makes factors that help the human immune system fight infection, removes bacteria from the blood, and makes bile, which is essential for digestion.

National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health



Bile, a greenish-yellow fluid consisting of bile acids (or salts) and waste products, such as bile pigments, flows through small bile ducts inside the liver. The bile flows from these small ducts into larger ones, like streams into a river, eventually leading to the common bile duct. The cystic duct connects the common bile duct to the gallbladder. After eating, the gallbladder, an organ that sits

Sym:
What is liver disease?
Liver disease can result from acute or chronic damage to the liver, usually caused by infection, injury, exposure to drugs or toxic compounds, an autoimmune process, or an inherited defect. The disease can be classified by the effect it has on the liver and its functions.  The following table summarises the main categories of liver disease

Liver Disease
Examples of Causes
Description
Hepatitis
 An inflammation of the liver causing liver cell damage
 

Infection
In the UK the most common causes are hepatitis A, B & C viruses
Infection by one of the hepatitis viruses causing inflammation and damage to liver cells. The damage may be cause quickly (acute hepatitis) or slowly (chronic hepatitis) which depends on the virus.
Drugs or Chemicals
Acute or chronic exposure to alcohol or paracetamol
Many substances are processed and eliminated by the liver that may come from normal metabolism or ingested compounds such as drugs or alcohol. Some of these substances are potentially toxic.
Inherited
Alpha 1 antitrypsin deficiency, Haemochromatosis, Wilson’s disease.
Some gene mutations result in diseases that may cause problems with depositions that result in damage to the liver.
Autoimmune
Type 1 diabetes, Sjorgren’s syndrome
In these conditions, antibodies are produced which are directed against the liver causing damage.
Non-alcoholic fatty liver - Metabolic syndrome
Increased deposits of fat in the liver can lead to decreased amounts of healthy liver tissue.
Cirrhosis
Prolonged damage to the liver replaced by scar tissue affecting liver structure & function
Alcohol, hepatitis, biliary obstruction, congestive heart failure, inherited cause, drugs and sometimes unknown.
Prolonged and persistent damage to the liver can lead to the accumulation of excess connective tissue in the organ. This is called fibrosis of the liver. Over a period of time fibrosis can progress to liver cirrhosis. In cirrhosis the structure of the liver changes with nodules of liver cells surrounded by fibrous tissue that does not function like healthy liver tissue.
Obstruction
Can be either within the liver or outside the liver in the main bile duct
Gallstones, tumours, trauma, inflammation or infection.
Tumours, trauma, inflammation or gallstones of a sufficient size can cause blockage or obstructions in the ducts draining the liver (bile ducts). Bile and bilirubin then accumulate in the blood and the patient becomes jaundiced. Tumours or blood clots may also obstruct the vein from the liver. This may be chronic with few symptoms or acute and life threatening.
Fatty Liver
Fat is deposited in the liver which can reduce the amount of healthy liver tissue
Alcohol, obesity, diabetes
Fatty liver causes liver enlargement, tenderness and abnormal liver function. The most common cause is excessive intake of alcohol. Another cause is NASH (non-alcoholic steatohepatitis) which may progress to cirrhosis. It is seen most commonly in overweight and diabetic individuals.
Cancer
Tumours can damage healthy liver tissue and affect liver function
Primary liver cancer or secondaries from another primary cancer spreading to the liver
Hepatitis and cirrhosis may lead to liver cancer in some cases but cancer from other parts of the body that spreads to the liver (secondaries) is more common. People who have chronic hepatitis or cirrhosis may be checked on a regular basis for cancer, often with an alpha-fetoprotein (AFP) test and/or an ultrasound scan.
Inherited
Genetic defects can prevent vital liver functions and by depositing damaging substances
Haemochromatosis, Wilsons disease, cystic fibrosis, alpha 1 antitrypsin deficiency
Haemochromatosis is a genetic disorder resulting in excess iron storage in the liver, usually diagnosed in adults. Genetic diseases affecting children may involve a structural defect (biliary atresia), a missing enzyme or protein leading to damaging deposits such as galactose build-up in galactosaemia and copper accumulation in Wilson’s disease.

                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Signs and Symptoms
Liver disease is often discovered during routine testing. It may not cause any symptoms at first or the symptoms may be vague, like weakness and loss of energy. In acute liver disease, most commonly symptoms related to:

problems handling bilirubin, including jaundice (yellowing of the skin and eyes), dark urine, and light stools

loss of appetite

nausea

vomiting

diarrhoea


Chronic liver disease symptoms may not be present until the disease has reached an advanced stage. They include:-

jaundice, dark urine

abdominal swelling due to the accumulation of fluid (ascites)

pruritus (itching)

unexplained weight loss or gain

abdominal pain




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Overview of the lungs
The lungs are part of the respiratory (breathing) system and are located in the chest, inside the rib cage and above the diaphragm. Lungs are complex organs that consist of spongy, elastic tissue that is designed to transfer oxygen from the air we breathe into our blood stream and remove carbon dioxide from our blood.


Oxygen in air enters the lungs when we take a breath. It is distributed throughout the lungs by a system called the bronchial tree. It is easiest to imagine the bronchial tree as an upside-down tree starting at our mouth and spreading out across the upper part of our chests. The first tube (airway) is called the trachea or wind pipe. This is similar to the trunk of a tree and guides the oxygen down through our neck from our mouths towards our lungs. The trunk of this tree then splits in two and becomes the left and right bronchus which supplies the left and right lung respectively. These two branches then spread further and as the branches spread out they become thinner until their width is less than 1 mm. These thin branches are called bronchioles.

These brioncholes carry air to small sacs calledalveoli deep within the lungs which are responsible for the exchange of gas between the blood stream and the lungs. In the alveoli oxygen moves from the lungs into the blood stream which is then carried around to supply our body with oxygen.    In addition, carbon dioxide, a waste product of our metabolism, moves from the blood into the lungs to be exhaled (blown out) so that we can get rid of it from our body. The mechanics of breathing in oxygen and delivery to tissue in blood is necessary for all of the cells in our body to function. Removal of carbon dioxide is necessary to prevent the body becoming too acidic which could stop the cells in our body from functioning.

The lungs are covered by a thin layer of tissue called the visceral pleura. This layer continues on to the chest wall and around the heart and is called the parietal pleura. There is a thin layer of fluid between these two layers which allows movement between these two layers. The small space between these two layers is called the pleural space.  Any increase in this level of fluid between the two layers can cause pressure on the lungs and affect the function of the lungs.

The air we breathe contains many dangerous particles from the environment such as dust, pollens, bacteria, viruses, smoke, and damaging chemicals. Our lungs maintain a system of defence against these potentially toxic invaders. This includes immune cells and secretion of mucus to trap and remove these unwanted substances from the lungs. Every time we cough up sputum we are also coughing up thousands of microscopic particles that could have damaged our lungs.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Lung Diseases
Lung diseases can affect all parts of the lung. In some cases the alveoli are damaged and this impairs the transfer of gases from the air sacs (alveoli) to the blood (and vice versa). In other cases the problem is that not enough air gets to the air sacs. This could be due to blockages in the bronchial tree or weakness in the muscles that expand the chest. In some cases the lungs struggle to remove or detoxify dangerous substances – this could be due to problems with mucus such as cystic fibrosis or due to overwhelming toxins such as smoking.

Common Lung diseases include:

Asthma is a chronic lung disease where inflammation of the bronchi and bronchioles prevent enough air getting to the air sacs. Asthma often happens as an attack which can be triggered by many things. Triggers can include:


cigarette smoke




moulds and pollens




infections




exercise




cold air 




During an attack, the lining of the airways swell and the muscles surrounding the bronchi contract, narrowing the airway. Mucus secretion lining the airways increases and this can slow the movement of air making breathing difficult. All these mechanisms contribute to causing a narrowing of the airways and this often causes a wheezing sound. Most episodes do not cause long-term lung damage but it is often necessary to see a doctor since lack of oxygen and build-up of carbon dioxide can be life-threatening. Patients use inhalers to help open up the airways. According to Asthma UK, 1 in 5 households in the UK have a person with asthma.

COPD (chronic obstructive pulmonary disease) is a term used for both emphysema and chronic bronchitis. With chronic bronchitis, the bronchial tubes become inflamed and scarred. This reduces air flow within the lungs and can result in more mucus production. With emphysema, the air sacs in the lungs are slowly destroyed.  The combination of these changes often results in the typical symptoms of cough, shortness of breath and increased sputum production that is found with COPD. Patients with COPD find it hard to breathe and have long term problems getting enough oxygen to the blood and carbon dioxide out due to the damage to the air sacs and the narrowing of the airways. The main cause of COPD is smoking. Other risk factors include repeated exposure to air pollution fumes, dust and genetic disorders, but these are rare. It is estimated that COPD causes around 25,000 deaths a year in the UK.

Pneumonia is a complicated inflammation of the lungs usually caused by bacteria or a virus. This infection and inflammation causes the small air sacs of the lungs to fill up with fluid impairing the exchange of gases.  Pneumonia can affect one area of a lung or both lungs (bilateral). A patient may cough up sputum, have a fever, and feel tired. Doctors can sometimes hear signs of pneumonia when listening with a stethoscope. X-rays can help by showing areas of inflammation (consolidation). Antibiotics are used to treat bacterial pneumonia. The most common cause of pneumonia is a pneumococcal infection caused by a bacteria called Streptococcus pneumoniae. As pneumonia can be life threatening, people at high risk of pneumonia may be offered a vaccine against the pneumococcal bacteria.

Influenza more commonly known as flu, is an acute illness caused by a virus that affects the whole body and often causes respiratory problems such as a sore throat or cough. It usually attacks the upper respiratory tract which involves the nose and throat and causes inflammation in these areas. It may also however affect the bronchi and the lungs itself which may cause breathing difficulties or lead to pneumonia.  In the UK people who are particularly vulnerable to infection can be given the flu vaccine which may reduce symptoms. Antibiotics will not help to treat a viral infection.

Tuberculosis (TB) and nontuberculous mycobacteria (NTM) are chronic bacterial infections most commonly seen in patients with weakened immune systems (such as patients with HIV/AIDS). However, in the last 20 years TB cases have gradually increased, particularly among ethnic minority communities who are originally from places where TB is more common. The infections caused by mycobacteria develop slowly and can affect the whole of the body as well as the lungs. Treatment for TB requires long term antibiotics usually for 6 months. Symptoms usually include a cough, weight loss and night sweats. The BCG vaccine is used to help protect against TB. Currently it is only offered to those at high risk of TB such as health care workers and children living in areas with high rates of TB or those who have close family members from countries with a high TB rate.

Pleuritis often known as pleurisy is caused by inflammation of the lining of the lungs (pleura). It is particularly painful when taking deep breaths or coughing. It can occur with bacterial and viral infections as well as diseases such as pneumonia, TB or pulmonary emboli. It can also be caused by other inflammatory conditions such as rheumatoid arthritis and inflammatory bowel disease. Occasionally it may also be associated with lung cancers particularly mesothelioma. However, pleuritis can also occur spontaneously where the lungs become inflammed for no apparent reason. Treatment of pleurisy therefore depends on the underlying cause.

A pleural effusion is a collection of fluid in the pleural space (the lining of the lungs). This then compresses the underlying lung tissue affecting breathing and the function of the lungs. There are many causes including infections in the lungs such as  pneumonia and TB.  Cancer may also be a cause as well as other conditions such as rheumatoid arthritis and SLE ( systemic lupus erythematosus). Heart  failure can also cause a pleural effusion by causing increased pressure in the blood vessels in the lungs that may cause fluid to leak out into the pleural space. A low level of protein in the blood can also cause blood to seep out from the blood vessels into the lung tissue. Low levels of protein are often found in people with liver diseases such as cirrhosis, so liver disease can also cause a pleural effusion. A pleural effusion is usually confirmed on a chest X ray.  In most cases the doctors will insert a chest drain to drain the fluid from the lungs if there is a large amount of fluid present. A sample of the fluid is then sent to the laboratory for analysis and can help doctors to find out what caused the fluid accumulation.

Lung cancer is the uncontrolled growth of malignant cells in the lungs. The main risk for developing lung cancer is smoking. There are two main types, small cell and non-small cell lung cancers. Non-small cell cancer is the most common type and accounts for about 87% of all cases.  It is divided into 3 types of cancer: adenocarcinoma, squamous cell carcinoma and large cell carcinoma. Squamous cell carcinoma is the most common form of non-small cell carcinoma and is usually caused by smoking. Small cell lung cancer is usually always caused by smoking also. Other cancers may spread to the lungs and are described as metastatic, because the cancer cells do not come from lung tissue originally. Mesothelioma is another type of lung cancer that develops in the pleura (the lining of the lung). This is usually caused by exposure to asbestos. Symptoms of lung cancer include coughing up sputum with small amounts of blood, a long term cough which doesn’t go away, unexplained weight loss and worsening shortness of breath.

A pulmonary embolism is a blockage in the pulmonary artery which is a blood vessel that carries blood from the heart to the lungs. This is normally caused by a blood clot that originated in the veins of the legs (also known as a deep vein thrombosis or DVT) but travelled up through the blood vessels and got stuck in the lungs. Pulmonary embolisms cause chest pain (which is usually worse on breathing in), sudden shortness of breath, and coughing (sometimes of blood). This condition can be life-threatening and requires urgent medical attention. Treatment is usually to thin the blood to stop the clot getting bigger whilst the body breaks down the original clot.

Pulmonary fibrosis is a disease with damage and scarring to the tissues between the air sacs, inflammation of the air sacs, and stiffening of the lungs. This impairs the elasticity of the lungs so that the lungs cannot expand and contract as well during normal breathing so that air cannot flow into and out of the lungs as easily. As the air sacs are also damaged gaseous exchange cannot occur as well as it normally does.  Therefore this may cause shortness of breath, a lack of oxygen in the blood which may cause cyanosis (where the lips may turn blue) and a chronic cough. Pulmonary fibrosis is usually diagnosed on a chest X ray or CT scan of the chest and has many causes.  Causes of pulmonary fibrosis include:

Exposure to small particles (often at work). This includes repeated exposure to substances such as asbestos, coal, beryllium, and silica

Repeated exposure to organic substances such as mouldy hay, animal droppings, and grain dust. This can cause an allergic inflammation pneumonitis) and eventually lead to pulmonary fibrosis

Chemicals and drugs that are toxic to the lungs e.g. amiodarone, methotrexate.

Previous radiation treatment

Sarcoidosis and other granulomatous diseases.

Systemic sclerosis, other autoimmune disorders and connective tissue disease such as SLE and rheumatoid arthritis.

Inherited causes – e.g. neurofibromatosis, tuberous sclerosis, familial idiopathic pulmonary fibrosis.

Other illnesses, including hepatitis C, inflammatory bowel disease, acquired immunodeficiency syndrome.

Idiopathic – cause unknown. This is the most common cause.


Pulmonary hypertension is a rare lung disorder. This is caused by increased pressure within the pulmonary artery which is a blood vessel that transports blood from the right side of the heart to the lung to collect oxygen, This increase in pressure means the heart has to work harder to transport blood into the lungs. This can in turn cause damage to the heart, as the heart may become weaker from this increased work load and cause heart failure. Pulmonary hypertension can occur by itself but often happens with other problems such as heart and lung disease. It may also occur with pulmonary emboli and  rare conditions such as systemic sclerosis which thickens and stiffens the walls of the pulmonary artery.

Bronchopulmonary dysplasia (BPD) is a lung disease that develops mainly in premature babies who have had long-term oxygen and/or been on a ventilator. It may also be seen in those who have experienced oxygen toxicity or had pneumonia such as term babies who have required aggressive ventilation for lung disease. With this disorder airways are inflamed, do not develop normally, and may be damaged.

Respiratory Distress Syndrome (RDS) of the newborn is a life-threatening breathing problem that may develop in babies born before 34 weeks. These premature babies’ lungs are not developed enough to be able to produce much of the protective liquid called surfactant. Without surfactant, the lungs are not able to expand properly and babies have difficulty breathing in enough oxygen. It can occur within a few hours of premature birth.

Acute Respiratory Distress Syndrome (ARDS) is a rapid, severe breathing difficulty due to extensive lung inflammation and the lungs filling with fluid. ARDS can be fatal and may be brought on by many types of injury to the lungs including serious viral or bacterial infection, sepsis, trauma, multiple transfusions, drug overdose, or inhaling substances such as salt water or smoke.

Cystic fibrosis is an inherited disease that affects the lungs, pancreas, and other body systems such as liver, nose, reproductive organs and sweat glands. This is due to a defect in a gene which causes sticky mucus to build up in the lungs and digestive system. In the lungs this thick sticky mucus can trap bacteria in the small airways leading to frequent chest infections and a productive cough. . Diarrhoea and low weight are due to pancreatic problems preventing absorption of nutrients. Cystic fibrosis commonly causes infertility in men. 1 in 25 people in the UK have 1 cystic fibrosis gene, but the disease doesn’t occur unless both parents pass the gene onto a child. According to the Cystic Fibrosis Trust 5 babies are born with cystic fibrosis in the UK each week.

Bronchiectasis is a condition where the airways of the lungs become abnormally enlarged. This causes a build- up of mucus in the airways which causes a chronic cough and can trap bacteria predisposing to infections. Treatment includes regular physiotherapy to help bring up the extra mucus and courses of antibiotics to treat any infection.

Alpha-1 antitrypsin deficiency is an inherited lack of a protein that provides protection to the lungs. This protein is produced in the liver. However in the alpha-1 antitrypsin deficient patient there is a problem with the structure of the chemical so that it cannot leave the liver into the blood stream to get to the rest of the body. Without this protection the lungs slowly become damaged and the elastic walls of the lung can be broken down. This puts  the patient  at an increased risk of COPD especially if they also smoke. In addition the build-up of the protein in the liver can causeliver disease at a young age. 

Other disorders do not affect the lungs directly, but can impair a person’s ability to breathe properly. These disorders may affect the chest cavity, muscles, nerves, and heart. They include a variety of conditions, such as nerve and muscle (neuromuscular) diseases like muscular dystrophy, polio, myasthenia gravis, Guillain-Barré syndrome, and amyotrophic lateral sclerosis (ALS, or Lou Gehrig`s disease). Bony problems that result in abnormal spine formation or rib cage movement can restrict lung expansion. [Note: specific testing and treatment for these disorders is not covered in this article.]



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
Tests can help doctors to choose the best treatments by finding what the problem is. Tests can look at the structure of the lungs (e.g. X-ray or CT scan), how well the lungs are working (e.g. blood gases), or test for infection.

Laboratory Tests:

Blood gases– an arterial blood sample is collected to evaluate blood acidity, oxygen and carbon dioxide levels.

FBC (Full Blood Count) – to look for signs of infection or for anaemia (which causes shortness of breath)

D-dimer – To look for signs of clotting which might suggest a pulmonary embolism

Cystic Fibrosis Tests (CF Gene Mutation Testing, Sweat chloride, Immunoreactive trypsin (IRT)) – to look for the genetic changes causing cystic fibrosis, and to diagnose the condition

Alpha-1 antitrypsin – to determine if a patient lacks alpha-1 antitrypsin

Sputum culture and sensitivities – to grow infectious bacteria and test which antibiotics work against them

AFB smear and culture – to diagnose tuberculosis and nontuberculous mycobacteria (NTM)

Blood cultures –to diagnose bacteria and sometimes yeast infections that have spread into the blood

Influenza tests – not needed normally as doctors can diagnose flu from your symptoms

Lung Biopsy – a sample of tissue from the lung which can be examined under the microscope for diseases such as cancer

Sputum cytology – to look for cells with abnormal changes that might show cancer

Drug screen—to detect drugs in overdoses that lead to breathing difficulties


Lung Function Tests (Pulmonary Function Tests, PFT)

A few of the more common tests are listed below.For more complete information visit the website for John Hopkins Medicine, Pulmonary Function Laboratory 

Spirometry – measures the amount and rate of air as a patient blows out through a tube and looks at how well you breathe in and out. It looks for narrowed or obstructed airways that may be found in asthma or COPD. It is most commonly used to diagnose COPD. 

Peak Flow Meter – measures the rate of exhalation. It can be used at home by patients with asthma to help monitor their condition and can also be used to diagnose asthma.

Lung Volume – the quantity of air a person takes into their lungs and how much is left in the lungs after exhalation. Helps test the elasticity of the lungs, the movement of the rib cage, and the strength of the muscles associated with respiration.

Diffusing Capacity Measurement or lung diffusing testing– assesses the transfer of gases from the lung air sacs to the bloodstream by evaluating how much of a tracer gas (usually carbon monoxide) is absorbed when a small quantity is inhaled (not enough to harm). The exhaled gas is then tested to see how much of the tracer gas was absorbed during the inhaled breath. Abnormal results indicate that gases are not moving normally across the lung tissues which may be due to diseases such as pulmonary fibrosis.


Imaging studies

Chest X-ray – to look at lung structure and chest cavity

CT (Computed Tomography) scan – a more detailed evaluation of lung structure most commonly used to diagnose pulmonary fibrosis and bronchiectasis.

MRI (Magnetic Resonance Imaging) – detailed pictures of organs and vessels in the chest

Ultrasound – used to detect fluid between the pleural membranes

Nuclear lung scanning – used to help detect pulmonary embolism and rarely, to evaluate the effectiveness of lung cancer treatment

PET (Positron Emission Tomography) scans – used to help diagnose lung cancer.


Other tests

Electrocardiogram (ECG) – to look at heart rhythm, to determine if heart disease may be affecting breathing

Sleep studies – usually performed at special sleep centres to determine whether a person is breathing normally during sleep




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Also known as: Lupus; disseminated lupus erythematosus; lupus erythematosus; SLE; LE


                                                
                                            

What is it?
Lupus (SLE) is a chronic, inflammatory autoimmune disorder that may affect many organ systems including the skin, joints, blood cells and internal organs, especially kidneys, and sometimes the brain. SLE affects women nine times more often than men and it usually occurs between the ages of 20-40 years. There is an increased incidence of lupus in persons of African, and Asian descent.  The cause of lupus is not fully understood.  It is thought to involve both an inherited component and a trigger that may be related to environmental factors and/or to hormones.  Certain drugs may also cause SLE. 
Lupus may co-exist with other autoimmune disorders, such as Sjögren’s Syndrome, thyroid disease, and the antiphospholipid syndrome.

Symptoms and signs of lupus are highly variable and include: 

Arthritis-like pain in one or more joints (but no or little joint damage)

A red rash – particularly one resembling a butterfly across the nose and cheeks; sensitivity to ultraviolet light

Fever

Persistent fatigue

Mouth ulcers

Muscle pain

Hair loss

There may also be inflammation and damage to organs and tissues including the kidneys, lungs, heart, lining of the heart, central nervous system, and blood vessels. 

Kidney disease is a frequent occurrence in patients with lupus.  Lupus causes glomerulonephritis, a condition that affects the kidney’s ability to filter toxins, which can lead to kidney failure if untreated.  

Sometimes involvement of the nervous system may occur and can lead to complications including headaches, seizures, depression, or even psychosis.


Symptoms of SLE come and go, vary over time, and vary from patient to patient.  They may worsen abruptly with flare-ups and then improve.  Flare-ups may be triggered by changes in the patient’s health status, such as physical or emotional stressors and/or by outside stimulants such as exposure to ultraviolet light (many affected persons are sensitive to sunlight), infections, and sometimes exposure to oestrogens such as in the combined oral contraceptive pill. It is important not to stop contraception abruptly, but to discuss with your doctor. Pregnant women may experience flare-ups during pregnancy or shortly after giving birth.

Some patients with lupus may also be affected by the antiphospholipid syndrome, where the blood becomes more prone to clot: this can lead to clots in arteries leading to strokes, and in veins such as deep vein thrombosis in the legs, or pulmonary embolism (blood clot in the lung). The antiphospholipid syndrome also leads to an increased risk of miscarriages. Antiphospholipid syndrome can also occur in the absence of underlying lupus.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests
Diagnosis is made by, clinical evaluation of patient symptoms and examination findings, as well as the results of investigations. The following laboratory tests may be useful in the diagnosis of SLE:

Testing for autoantibodies: 

Anti-nuclear antibody test (ANA) is positive in almost all patients with SLE

anti-double stranded DNA antibodies are frequently present, and the level can fluctuate with disease activity

anti-Sm (specific to lupus, but only seen in 10-30% of cases)

anti-SSA (Ro) and anti-SSB (La) antibodies may also be positive

antiphospholipid antibodies

Urine analysis– may show blood, microscopic casts of kidney cells, or protein 

Full blood count (FBC) – decrease in some cell types, including platelets 

Serum protein electrophoresis – increased immunoglobulins 

Erythrocyte sedimentation rate (ESR)  – increased

C-reactive protein (CRP) is typically normal, unless coexistent infection is present

Complement 3 (C-3) – may be decreased; the level can fluctuate with activity of the disease




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatment
There is currently no cure for lupus, although many patients may experience remissions of symptoms between flare-ups, often with the help of treatment.  The goals of treatment are to alleviate symptoms, to minimise the occurrence of flare-ups and to minimise and address the development of complications associated with SLE.  To help decrease the number of flare-ups, patients should get sufficient rest, maintain a degree of exercise, and should minimise stress and avoid exposure to ultraviolet light.  

Patients should work closely with their doctor and with their specialist (often a rheumatologist, a specialist in joint disease) to develop a treatment plan that is effective for them.  This plan is likely to change over time with changes in the patients’ symptoms, their general state of health and as new treatments become available.  Women wanting to become pregnant should talk to their doctor about their health and their medications.  Some treatments are safer than others for the fetus during pregnancy.  

The types of treatment that are used depend on what symptoms and complications the patient is experiencing at that time and their severity.  Patients may take non-steroidal anti-inflammatory drugs (NSAIDs) to help alleviate pain and inflammation, though caution is needed if there is kidney disease.  Antimalarial drugs such as hydroxychloroquine, and chloroquine may be given to help ease lupus skin and joint symptoms and to help inhibit flare-ups.  For more severe symptoms, corticosteroids (such as prednisone) and immunosuppressants (such as azathioprine, cyclophosphamide, mycophenolate mofetil or methotrexate) may be given  - despite their associated side effects. It is important to discuss and assess the risks and benefits associated with these drugs with your healthcare professional before starting.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Overview
Lyme disease is an infection caused by a spiral bacterium, Borrelia burgdorferi, carried by a tick the size of the head of a pin. The tick is found in woods and heathland areas where it infests small animals and birds. People bitten by an infected tick which is not removed within a day or two may develop Lyme disease. An expanding rash called erythema migrans appears at the site of the bite within 3 to 30 days in a large proportion of those infected. Some develop flu-like symptoms with aching joints and muscles. The disease can later affect the nervous system, joints and other body systems.

The best defences against Lyme disease are wearing protective clothing, using an insect repellent, and checking for (and carefully removing) ticks at regular intervals.  Tests that can help diagnose Lyme disease detect antibodies that the body develops against the Borrelia burgdorferi bacterium. They appear some weeks after being bitten, so the tests may be negative if done too early and may need to be repeated a few weeks later.

Since August 2000 there has been a single Health Protection Agency laboratory in England and Wales offering a wide range of specialised tests for Lyme disease. In the UK in 2010 there were 972 laboratory-confirmed cases reported (1.73 per 100,000 of the population) of which a fifth were acquired overseas. The disease is more common in the US and in central and northern Europe than in the UK.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Symptoms
The first symptom of Lyme disease in 80% of those infected with Borrelia burgdorferi is a rash that appears a few days to a month after a tick bite that is usually painless. (In Europe, a third of those with the rash do not recollect a bite.) The characteristic rash, called erythema migrans, is flat, round or oval, pink or red and typically grows outward from the bite site for several weeks. It is usually becomes larger than 5 cm across and can be as large as 1 metre. Most develop a central clearing area and begin to look like a ``bulls-eye.`` Some people may develop multiple red rashes and others may not have, or remember having, a rash. Flu-like symptoms sometimes develop with fever, headache, tiredness, nausea, vomiting and aching joints and muscles.

If left untreated, additional symptoms may emerge after several weeks or months:

Nervous system symptoms in up to 15%, including temporary paralysis of facial muscles on one or both sides, numbness and pain in the limbs, difficulty concentrating and poor memory. A few develop meningitis with headache, neck stiffness and sensitivity to light

Heart symptoms including fainting or chest pain

Joint symptoms of arthritis with repeated brief attacks of joint swelling in one or more large joints, often the knee.

In a minority of untreated patients, persistent nervous system or joint disorders may develop many years after infection.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
Laboratory tests are unnecessary if you have had a tick bite that becomes red and swollen when the tick is still attached or shortly after it drops off or is removed, but you have no other symptoms. This is a tick hypersensitivity reaction, not Lyme disease.

If you develop the characteristic spreading rash of Lyme disease (erythema migrans) 3 to 30 days after a tick bite or possible exposure to ticks, your GP is highly likely to make a clinical diagnosis. You will be treated with antibiotics without having had any laboratory tests, and should make a complete recovery.

However, if you see your GP without a characteristic rash but with other symptoms that occur in early or later Lyme disease, the information that you have had a tick bite or possible exposure to ticks may be very helpful.

The first test done is an enzyme-linked immunosorbent assay (ELISA) blood test for antibodies to Borrelia burgdorferi. The antibodies take time to develop so the test may not be requested until a few weeks after the onset of symptoms. Although it is a sensitive test, it has a high false positive rate, giving positive results in glandular fever, rheumatoid arthritis and other autoimmune conditions for example.

If the initial ELISA result is borderline or positive, the laboratory will retest the same sample using a more specific test, a Western blot, to confirm the diagnosis.

Another specific test, the polymerase chain reaction (PCR), detects the DNA of Borrelia burgdorferi. It is used to confirm the presence of the bacterium in joint fluid in Lyme arthritis and in cerebrospinal fluid (CSF) in Lyme meningitis.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Lymphatics and Lymph Node Structure
The lymph system consists of a series of vessels, similar to blood vessels, and nodules called lymph nodes. The lymphatic vessels are spread throughout the body and carry lymph, a milky fluid filled with lymphocytes, the cells that control the immune system. The lymphatics pass through lymph nodes as they circulate through the lymphatic system. The lymphocytes can also leave the lymphatics to enter the blood stream and tissues and return to the lymphatics at any time. 

Lymph nodes can be found throughout the body, including in the neck, armpits, middle of the chest, and back of the abdomen. Additional lymphoid tissue can be found in the tonsils, adenoids, thymus, bone marrow, spleen, lung, and areas in the gastrointestinal tract.

What is lymphoma?
Lymphoma is a tumour of lymphocytes. There are several different types of lymphocytes, the major types being the B-lymphocyte and the T-lymphocyte.

T-lymphocytes can be thought of as the controllers of the immune system. They initiate the immune response, control how big or small it should be, and shut it down when it’s not needed. In addition, they can neutralize several different types of foreign attackers. B-lymphocytes make antibodies. It is these cells that are activated when a person is vaccinated against diseases such as measles, mumps, or hepatitis. Natural killer (NK) cells make up about 10-15% of total lymphocytes in the blood. NK cells attack and “kill” abnormal cells such as cancer cells or those infected with viruses.

Any one of these cells or a combination of them can be involved in lymphoma. Lymphoma usually begins with the production of one or more abnormal cells in one or more of the lymph nodes, areas where lymphocytes congregate. These cells reproduce uncontrollably, begin to outnumber normal cells in the node, lead to the enlargement of the lymph node, and eventually travel to one or more other lymph nodes. They may also spread to and from other lymph-system-related organs including the spleen, bone marrow, tonsils, adenoids, and thymus.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
Patients who have lymphoma may experience painless swelling of the lymph nodes in the armpits, neck, and/or groin. They may experience fatigue, fever, unexplained drenching night sweats, unintended weight loss, a loss of appetite, or itchiness. If the lymph node is in the chest, it may affect the person’s breathing; if it is in their abdomen, it can cause abdominal discomfort. Lymphoma can sometimes be difficult to diagnose because the signs and symptoms are often mild or non-specific. Some patients may have no noticeable signs while others might have a low-grade fever. Usually, there are swollen lymph nodes, but the node may not be visible or felt by the patient or physician.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Types of Lymphoma
There are two primary types of lymphoma: Hodgkin lymphoma (HL, also called Hodgkin’s disease), which is characterized by the presence of large distinctive cells called Reed-Sternberg cells, and non-Hodgkin lymphoma (NHL), a large group of about 30 other lymphomas.

Hodgkin Lymphoma
Hodgkin lymphoma is most prevalent in two age groups: in those between about 25 and 35 years of age and in those over 55.

Historically, Hodgkin lymphoma was divided into several subtypes (nodular lymphocyte-predominant, nodular sclerosing, mixed cellularity and lymphocyte-depleted). Nowadays the important distinction is between classical HL (cHL), which has some distinctive features, and nodular lymphocyte-predominant HL (nodular LPHD). LPHD behaves quite differently from cHL, and could be thought of as a low-grade non-Hodgkin lymphoma.

Non-Hodgkin Lymphoma
Non-Hodgkin lymphoma is the sixth most common cancer in the UK. The incidence of NHL increases with age and is higher in patients with HIV/AIDS and in patients whose immune systems are suppressed. According to Cancer Research UK, in the UK, about 10,000 people are diagnosed with non-Hodgkin lymphoma in one year.

There are about 30 different types of non-Hodgkin lymphoma. Over the years, different classification systems have been used to describe the different types of non-Hodgkin lymphoma as knowledge about the condition has grown. New methods of evaluating the cells involved in non-Hodgkin lymphoma have led to changes in classification systems.

The Revised European American Lymphoma (REAL) looks at the function that the cell should be providing. Some lymphocytes (B-lymphocytes) are responsible for producing antibodies while others (T-lymphocytes) are responsible for cell-to-cell interactions. The newest method, the World Health Organization or WHO Classification, tries to combine all of these characteristics with genetic studies of the cells. Click here to view a table of classifications.

Some Types of Non-Hodgkin Lymphomas 
Classification of non-Hodgkin lymphomas can be confusing because there are so many different types and because of the various classification systems that have been developed and amended over the years. B-cell non-Hodgkin lymphomas are much more common than T-cell. About 85% of non-Hodgkin lymphomas involve mature B lymphocytes with about 15% affecting T-lymphocytes.

Some of the more common forms of B-Cell lymphomas include:

Diffuse large B-cell lymphoma (DLBCL): this form constitutes about 33% of all non-Hodgkin lymphomas. It is a fast growing lymphoma and can affect anyone of any age but occurs mostly in people over 60.

Follicular lymphomas: these make up about 16% of non-Hodgkin’s lymphoma in the UK. This may be a very slow growing lymphoma.

B cell chronic lymphocytic leukaemia (CLL) and small lymphocytic lymphoma (SLL): these are identical diseases because they affect the same cell. CLL is found mainly in the bone marrow and the circulating blood while SLL is found mainly in the lymph nodes. These two together make up approximately 24% of all lymphomas.


Some of the more common forms of T-Cell lymphomas include:

Precursor T-lymphoblastic lymphoma (leukaemia): a disease that can be considered either a lymphoma or leukaemia depending on whether affected cells are found in the blood or whether a certain percentage of bone marrow cells are abnormal. About 1% of all lymphomas are this type.

Mature or peripheral T-cell lymphomas: there are many different kinds of mature T-cell lymphomas that all together make up about 4% to 5% of all lymphomas.

Mycosis fungoides (Sézary syndrome), are types of cutaneous T-cell lymphoma: These are less common forms of lymphoma, unusual because, while most lymphomas begin in lymphoid tissue or internal organs, they start in the skin.




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is malabsorption?
Malabsorption is a condition caused by the decreased ability to digest and/or absorb nutrients from food. It is seen with a variety of diseases and can lead to general malnutrition or to symptoms associated with deficiencies in specific nutrients.

The body requires a steady supply of nutrients to build, repair, and maintain itself, to produce energy, enzymes, hormones, proteins, cells, tissues and bone, and to fight infections. Nutrients come from the diet and include many essential vitamins and minerals (micronutrients).

Food that is eaten is digested in three stages:

Proteins, fats, and complex sugars (carbohydrates) are broken down by stomach acids, enzymes produced by the pancreas, and bile from the liver. This process also releases micronutrients.

Nutrients are absorbed primarily by cells in the small intestines.

Nutrients are transported throughout the body and used or stored.


Any disruption or interference with this process can lead to malabsorption. The type and severity of deficiencies seen and the symptoms experienced depend on whether the problem affects general digestion and absorption or affects one or more specific nutrient.

Digestive problems

Fat, proteins and carbohydrates cannot be properly digested without bile and pancreatic enzymes. Insufficiencies in these substances can occur, for example, with liver and pancreatic diseases that limit their production, and with conditions such as cystic fibrosis that prevent pancreatic enzymes from reaching the digestive tract.

Absorption problems

If the intestines are unable to or prevented from absorbing nutrients, then the nutrients are eliminated from the body in the stool. This can happen when there is damage to the intestinal cells and tissues from disease or when the intestines have been shortened, such as due to surgery, reducing the surface area and the amount of time available in which nutrients can be absorbed from food as it passes through the digestive tract.

As an example of a specific deficiency, vitamin B12 absorption requires both stomach acid and intrinsic factor, a substance produced by parietal cells in the stomach. Stomach acid separates vitamin B12 from proteins and intrinsic factor binds with vitamin B12 enabling its intestinal absorption. A lack of either one prevents intestinal absorption and can lead to vitamin B12 deficiency. This can happen with advancing age, with medications that suppress stomach acid production, with gastric bypass surgeries, and with diseases that damage parietal cells or cause general malabsorption.

Transport problems

Once absorbed in the intestines, nutrients may be hindered from being transported throughout the body. This may be caused by problems with the lymphatic system such as lymphoma or the rare inherited disorder, abetalipoproteinemia.

Within these categories, there are a number of conditions and diseases that can cause malabsorption and the associated signs and symptoms. Below is a list of just some of these:

Narrowing, closure or absence of bile ducts (biliary atresia) or blockage of bile flow (cholestasis) causing a lack of bile for digestion

Cancers, including pancreatic cancer, lymphoma, stomach cancer

Coeliac disease—an autoimmune disease that causes damage to the lining of the intestines (intestinal villi)

Cystic fibrosis—a genetic condition that affects the pancreas and the transportation of pancreatic enzymes to the site of digestion

Damage to the intestines, such as from radiation treatment

Decreased intrinsic factor production

Diseases that affect circulation, such as congestive heart failure

Food intolerances and enzyme deficiencies

HIV and AIDS

Hyperthyroidism

Inflammatory bowel disease (Crohn’s disease and ulcerative colitis)

Liver diseases

Medications, such as phenytoin and those that inhibit stomach acid production

Pancreatic diseases and pancreatic insufficiency—can cause decreased amounts of pancreatic enzymes

Parasitic infections of the digestive tract, such as Giardia lamblia or a tapeworm

Scleroderma

Surgery, such as a bowel resection or gastric bypass

Zollinger-Ellison syndrome—a rare condition causing tumours in the pancreas and/or intestines




                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
The signs and symptoms of malabsorption depend upon the underlying cause as well as the type and severity of nutrient deficiencies. They may become evident quickly or develop slowly and worsen over time. Some nutrients, such as vitamin B12, are stored by the body and symptoms only emerge when stores become depleted. Symptoms associated with insufficient pancreatic enzymes may not emerge until about 90% of the body`s production capacity is disrupted.

Some of the most common signs and symptoms seen with general malabsorption include:

Persistent diarrhoea

Fatty stools that are loose and foul-smelling (steatorrhoea)

Failure to thrive (in children)

Abdominal pain, cramps, bloating, and gas


Other signs and symptoms may be due to general ill health or to specific deficiencies caused by malabsorption. They may include:

Weakness, fatigue

Fluid build-up in the abdomen (ascites)

Dry and scaly skin, rash

Inflammation of tongue (glossitis)

Muscle wasting, unexplained weight loss

Nausea and vomiting

Swelling of the hands, feet and legs (peripheral oedema)

Inflammation of mouth (stomatitis)

Easy bruising, bleeding gums

Numbness and tingling in feet and hands

Paleness

Muscle or bone pain


The following are some complications that can develop over time as a result of chronic malabsorption:

Anaemia

Delayed growth and development in children

Difficulty concentrating, confusion, and sometimes personality changes

Malnutrition

Osteoporosis

Deficiencies of micronutrients such as vitamin A, vitamin D, vitamin K and trace minerals




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Testing
The purpose of testing may be to:

Screen those at risk for malabsorption because of an underlying condition such as cystic fibrosis

Detect malabsorption, identify its underlying cause(s), and evaluate the types and severity of nutrient deficiencies present

Detect complications such as anaemia

Monitor the effectiveness of treatment in people with malabsorption


There is no single test that can identify malabsorption or the underlying cause. Typically, a doctor will take into account many factors when requesting tests, including results from a physical examination, family history, medical history, and signs and symptoms. Testing will often be performed in steps with results leading toward a diagnosis while ruling out other possible causes. Testing typically involves ordering:

An initial set of general tests that evaluate body organs, cells, and digestion and that look for a cause for a person`s persistent diarrhoea, one of the most common symptoms of malabsorption

Specific follow-up tests that are used to detect or exclude diseases associated with malabsorption and to identify specific deficiencies and/or complications


Laboratory Tests

Initial testing may include:

Full blood count (FBC) – to evaluate red blood cells to detect anaemia and white blood cells to detect infections

Renal and liver function tests – to evaluate proteins, electrolytes, and organ function, including the liver

Erythrocyte sedimentation rate (ESR) – to detect inflammation in the body which may be caused, for example, by inflammatory bowel disease

Stool culture – to detect bacterial infection or bacterial overgrowth as cause of persistent diarrhoea

Ova and parasite examination (OCP) – to detect parasites as cause of persistent diarrhoea

Stool white blood cells – present in some inflammatory intestinal diseases

Thyroid stimulating hormone (TSH) – to detect or rule out thyroid disease


Based upon initial testing results, the person`s symptoms, and the doctor`s suspicions, follow-up testing may include one or more of the following:

Faecal occult blood test – to detect bleeding in the digestive tract

Vitamin B12, vitamin D, vitamin A – to detect deficiency

Prothrombin time (PT) – to detect vitamin K deficiency

Coeliac disease tests – to help diagnose this condition

Cystic fibrosis tests – to detect this disease

Faecal elastase, trypsinogen, amylase, lipase – to evaluate pancreatic function


Tests sometimes ordered include:

Methylmalonic Acid (MMA) – to detect early vitamin B12 deficiency

Hydrogen breath test – to detect lactose intolerance and bacterial overgrowth in the digestive system (carbohydrate malabsorption)

Xylose absorption test – to evaluate carbohydrate digestion

Lactose absorption test – though this test is primarily used to detect a deficiency in the enzyme lactase (lactose intolerance), it may sometimes be used to identify malabsorption

Biopsy of the intestine


Non-Laboratory Tests

Testing to examine the digestive tract, liver, and/or pancreas is sometimes necessary and may include imaging investigations such as:

Abdominal ultrasound scan

CT scan

Endoscopy

Endoscopic retrograde pancreatography (ERCP)


Learn more about these imaging procedures at Radiologyinfo.org.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Malnutrition is a disparity between the amount of food and other nutrients that the body needs and the amount that it is receiving. This imbalance is most frequently associated with under nutrition, the primary focus of this article, but it may also be due to over nutrition.

Chronic over nutrition can lead to obesity and to the metabolic syndrome, a set of cardiovascular risk factors characterised by abdominal obesity, a decreased ability to process glucose (insulin resistance), dyslipidaemia, and hypertension. Those with metabolic syndrome have been shown to be at a greater risk of developing type 2 diabetes and cardiovascular disease. Another relatively uncommon form of overnutrition is vitamin or mineral toxicity. This is usually due to excessive supplementation, for instance, high doses of fat-soluble vitamins such as vitamin A rather than the ingestion of food. Toxicity symptoms depend on the substance(s) ingested, the severity of the overdose, and whether it is acute or chronic.

Under nutrition occurs when one or more vital nutrients are not present in the quantity that is needed for the body to develop and function normally. This may be due to insufficient intake, increased loss, increased demand, or a condition or disease that decreases the body’s ability to digest and absorb nutrients from available food. While the need for adequate nutrition is a constant, the demands of the body will vary, both on a daily and yearly basis.

During infancy, adolescence, and pregnancy additional nutrition is crucial for normal growth and development. A severe shortage of food will lead to a condition in children called marasmus that is characterised by a thin body and stunted growth. If enough calories are given, but the food is lacking in protein, a child may develop kwashiorkor – a condition characterised by oedema (fluid retention), an enlarged liver, apathy, and delayed development. Deficiencies of specific vitamins can affect bone and tissue formation. A lack of vitamin D, for instance, can affect bone formation – causing rickets in children and osteomalacia in adults, while a deficiency in folic acid during pregnancy can cause birth defects.

Acute conditions such as surgery, severe burns, infections, and trauma can drastically increase short-term nutritional requirements. People who have been malnourished for some time may have under functioning immune system and a poorer prognosis. They frequently take longer to recover from surgical procedures and spend longer in hospital. Malnutrition is common in patients admitted to hospital but it is easily overlooked by hospital staff. For this reason, many hospitals screen and monitor the nutritional status of their patients. This approach is recommended by the National Institute for Health and Care Excellence  (NICE). Patients having surgery are frequently evaluated both prior to surgery and during their recovery process. 

Chronic diseases may be associated with nutrient loss, increased nutrient demand, and with malabsorption (the inability of the body to absorb one or more available nutrients). Malabsorption may occur with chronic diseases such as coeliac disease, cystic fibrosis, pancreatic insufficiency, and pernicious anaemia. An increased loss of nutrients occur in chronic kidney disease, diarrhoea, and haemorrhaging. Sometimes conditions and their treatments can both cause malnutrition through decreased intake. Examples of this are the decreased appetite, difficulty swallowing, and nausea associated both with cancer (and chemotherapy), and with HIV/AIDS (and its drug therapies). Increased loss, malabsorption, and decreased intake may also occur in patients who chronically abuse drugs and/or alcohol.

Elderly patients are often less able to absorb nutrients due in part to decreased stomach acid production and are more likely to have one or more chronic ailments that may affect their nutritional status. At the same time, they may have more difficulty preparing meals and may have less access to a variety of nutritious foods. Older patients also frequently eat less due to a decreased appetite, decreased sense of smell, and/or mechanical difficulties with chewing or swallowing. For these reasons, elderly patients are often malnourished and require nutrutional support.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
General malnutrition often develops slowly, over months or years. As the body’s store of nutrients is depleted, changes begin to happen at the cellular level, affecting biochemical processes and decreasing the body’s ability to fight infections. Over time, a variety of symptoms may begin to emerge, including: 
Anaemia

Weight loss, decreased muscle mass, and weakness

Dry scaly skin

Oedema (swelling of limbs, due to build-up of fluid)

Hair that has lost its pigment

Brittle and malformed (spooned) nails

Chronic diarrhoea

Slow wound healing

Bone and joint pain

Growth retardation (in children)

Mental changes such as confusion and irritability

Goitre (enlarged thyroid gland)

Specific nutrient deficiencies may cause characteristic symptoms. For instance, vitamin B12 deficiency can lead to tingling, numbness, and burning in the hands and feet (due to nerve damage), a lack of vitamin A may cause night blindness and increased sensitivity to light, and a lack of vitamin D can cause bone pain and malformation. The severity of symptoms depends on the intensity and duration of the deficiency. Some changes, such as to bone and nerves, may be irreversible. 



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
Malnutrition will often be noticeable to the doctor’s trained eye before it causes significant abnormalities in laboratory test results. During physical examinations, doctors will evaluate the patient’s overall appearance: their skin and muscle tone, the amount of body fat they have, their height and weight, body mass index and their eating habits. In the case of infants and children, doctors will assess development and rate of growth.

If there are signs of malnutrition, the doctor may request general laboratory screening tests to evaluate a patient’s blood cells and organ function. Additional individual tests may be requested to look for specific vitamin and mineral deficiencies. If general malnutrition and/or specific deficiencies are diagnosed, then laboratory testing may be used to monitor the response to therapy. A person who has malnutrition because of a chronic disease may need to have his or her nutritional status monitored on a regular basis.

Hospitalised patients should have their nutritional status assessed at the time of admission. This is usually done using a nutritional screening tool such as the MUST (Malnutrition universal screening tool) which involves assessing the patient’s body mass index (BMI), recent weight loss and presence of acute illness. If screening suggests that the individual is malnourished or at risk of developing malnourishment they should have a more detailed nutritional assessment which may include dietetic assessment and laboratory tests. If the results of these tests indicate possible nutritional deficits, patients may be provided nutritional support prior to a surgery or procedure and be monitored regularly during recovery. Nutritional support encompasses oral nutritional support (providing nutritional supplements to be taken by mouth), enteral nutrition (feeding through a tube directly into the gut) and parenteral nutrition (feeding into a vein).

Laboratory tests may include:

For general screening and monitoring:

Lipids

FBC (Full Blood Count)

Metabolic screen

For nutritional status and deficiencies:

Prealbumin (is decreased in malnutrition and in acute illness. It’s level in the blood rises and falls rapidly in response to changes in nutritional status and can be used to detect short-term response to treatment). This test is not routinely performed in the UK.

Iron tests (such as Iron, TIBC, and Ferritin)

Vitamin and minerals (such as vitamin B12 and folate, vitamin D, vitamin K, calcium, and magnesium)

Trace element levels such as copper, zinc, selenium and manganese

The results of these laboratory tests should always be considered in clinical context because they can be influenced by many conditions other than malnutrition. Laboratory tests are not a substitute for clinical assessment by a health professional.

Non-Laboratory Tests
Imaging and radiographic scans may be requested to help evaluate the health of internal organs and the normal growth and development of muscles and bones. These tests may include:

X-rays

CT (Computed Tomography)

MRI (Magnetic Resonance Imaging)



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Menopause is the time in a woman`s life when her normal menstrual periods stop and a woman`s ovaries, the organs that produce eggs, stop making female hormones. Menopause occurs at an average age of about 50, but the usual range is anytime in the late 40s to the early 50s. It can occur much earlier (35-40 years) or be delayed (55 years or greater).

Two important hormones, oestradiol and progesterone, are made by the ovaries (the organs that produce eggs) in a cyclical fashion and help to maintain a normal menstrual cycle. When a woman reaches menopause, cyclical hormone production from the ovaries stops, leading to a cessation in monthly menstrual periods and of egg production.

The menopausal change is slow and usually takes two to five years to complete. During this so-called peri-menopausal phase (also sometimes referred to as ‘the climacteric’ or ‘the change’), hormone levels can fluctuate from high to low and from one month to the

Sym:
Symptoms
A woman’s body goes through several changes during menopause. Some of the more common symptoms of menopause occur when oestrogen levels start to drop. Women may experience:

hot flushes;

rapid mood swings ranging from depression to euphoria

decreased libido and sex drive

increased frequency or sudden urge to urinate

vaginal dryness with pain during intercourse


In addition, bone loss, which occurs naturally with age, is accelerated after menopause due to the lack of oestrogens. Excessive bone loss can lead to osteoporosis and a higher incidence of fractures of the hip and spinal column. A higher risk for heart disease is also seen after menopause because the levels of LDL ``bad`` cholesterolin the blood may rise.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
The diagnosis of menopause is usually made on clinical grounds, i.e. symptoms and history. The following biochemical investigations may be performed on blood when menopause is suspected but the diagnosis is not clear:

Follicle-stimulating hormone (FSH), to learn whether she is approaching or has gone through menopause

Oestradiol, to measure ovarian production of oestrogen and to further assist in determining menopausal state

Thyroid function testing (T4 and TSH tests) to assess the function of the thyroid gland

Assessment of liver and kidney function




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Metabolic syndrome is a set of cardiovascular risk factors that includes: central abdominal obesity, a decreased ability to process glucose (increased blood glucose and/or insulin resistance), dyslipidaemia, and hypertension. Patients who have this syndrome have been shown to be at an increased risk of developing cardiovascular disease and/or type 2 diabetes. Metabolic syndrome is a common condition that goes by many other names (dysmetabolic syndrome, syndrome X, insulin resistance syndrome, obesity syndrome, and Reaven’s syndrome). Most people identified as having this syndrome have been educated about the importance of checking their lipid levels, watching for symptoms of diabetes, having their blood pressure monitored, and exercising – but there has been little to tie all of these factors together except pursuit of a ``healthier lifestyle.``  

It is estimated that around 25% of adults in the Western World have metabolic syndrome. It can affect anyone at any age, but it is most frequently seen in those who are significantly overweight - with most of their excess fat in the central abdominal area - and physically inactive.

While several national and international organisations use certain criteria to define metabolic syndrome, others, including the American Diabetes Association (ADA), question the value of the specific diagnosis of metabolic syndrome. They point out that the criteria, taken together, are no more useful at predicting risk of cardiovascular disease or diabetes than the individual criteria considered separately. The science needs to be clearer, suggests the ADA, before metabolic syndrome be considered a definable syndrome. There is therefore an ongoing debate about the scientific validity of the term ‘metabolic syndrome’. However, most clinicians are agreed that it is a clinically useful term as it alerts the clinic to the increased cardiovascular risk and risk of the patient developing diabetes.

The World Health Organization (WHO) was the first to publish an internationally accepted definition for metabolic syndrome in 1998, but the criteria that have received the most widespread acceptance and use in the United States are those established as guidelines in the ATP III (the third report of the National Cholesterol Education Program expert panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults).

The American Heart Association (AHA) in conjunction with the NHLBI also released a scientific statement regarding metabolic syndrome that includes a set of criteria that defines the condition. The table below summarizes the three sets of criteria:

Criteria for Clinical Diagnosis of Metabolic Syndrome
clinical measure WHO1 ATP III2 AHA/NHLBI3 Waist Circumference
≥102 cm in men,
≥88 cm in women
Same as ATP III
BMI
BMI >30 kg/m2
Triglycerides
≥1.64mmol/L
Same as WHO
Same as WHO
HDL-C
<0.9mmol/L in men,
<1.0mmol/L in women
<1.0mmol/L in men,
<1.2mmol/L in women
Same as ATP III
Blood Pressure
≥140/90 mm Hg
≥130/85 mm Hg
Same as ATP III
Glucose
IGT, IFG, or T2D
Fasting >6.1mmol/L (IFG)
Fasting >5.6mmol/L (IFG)
Insulin Resistance
YES
NO
NO
Microalbuminuria
YES
NO
NO
References:
1. Alberti KG, Zimmet PZ. Diabet Med 1998;15:539–553.

2. National Cholesterol Education Program (NCEP) Adult Treatment Panel III final report. Circulation 2002;106:3143–3421.

3. Grundy, SM, et al. Circulation 2005;112:2735–2752.

Notes: WHO requires insulin resistance plus two additional risk factors for diagnosis; ATP III requires three of five risk factors for diagnosis. AHA/NHLBI recommends that triglycerides, HDL-C, and blood pressure should be considered abnormal when drug treatment is prescribed.

Abbreviations: BMI=Body mass index; IGT=Impaired Glucose Tolerance; IFG=Impaired Fasting Glucose; T2D=Type 2 Diabetes

Adapted from: Pizzi, R.,  Agreeing to Disagree: ADA, AHA Publish Opposing Views on Metabolic Syndrome, Clincal Laboratory News, January 2006 Volume 32, No. 1

Also frequently seen with metabolic syndrome but not included in the ATP III criteria are pro-thrombotic (blood clotting) and pro-inflammatory tendencies. While overt disease symptoms may be absent, these features are a warning of an increased likelihood of clogged arteries, heart disease, stroke, diabetes, kidney disease, and even premature death. If left untreated, complications from diseases associated with untreated metabolic syndrome can develop in as few as 15 years. Those patients who have metabolic syndrome and also smoke tend to have an even poorer prognosis.

Another feature commonly present in metabolic syndrome but not included in the diagnostic criteria is hyperuricaemia (an increased level of uric acid in the blood). In many patients this does not cause any symptoms but excessive amounts of uric acid can be associated with gout.

The root cause of most cases of metabolic syndrome can be traced back to poor eating habits and a sedentary lifestyle. Some cases occur in those already diagnosed with hypertension and in those with poorly controlled diabetes; a few are thought to be linked to genetic factors that are still being researched.

All of the factors associated with metabolic syndrome are interrelated. Obesity and lack of exercise tend to lead to insulin resistance. Insulin resistance has a negative effect on lipid production, increasing VLDL (very low-density lipoprotein), LDL (low-density lipoprotein – the “bad” cholesterol), and triglyceride levels in the bloodstream and decreasing HDL (high-density lipoprotein – the “good” cholesterol). This can lead to fatty plaque deposits in the arteries which, over time, can lead to cardiovascular disease and strokes. Insulin resistance also leads to increased insulin and glucose levels in the blood. Excess insulin increases sodium retention by the kidneys, which increases blood pressure and can lead to hypertension. Chronically elevated glucose levels in turn damage blood vessels and organs, such as the kidneys.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests
A doctor may suspect that a patient has metabolic syndrome if he has central/abdominal obesity and a sedentary lifestyle. In order to make a diagnosis of metabolic syndrome the criteria in the above table must be met therefore both laboratory and non-laboratory tests are important in establishing the diagnosis. Recommended laboratory tests include:

Laboratory Tests

Glucose. Usually a fasting glucose test is performed but, in some cases, a doctor may also order a post prandial glucose (after a meal) or a GTT (glucose tolerance test – several glucose tests that are taken before and at timed intervals after a glucose drink. The commonest form of the test involves a fasting level and another glucose level 2 hours after the glucose drink). The goal of glucose testing is to determine whether a patient has an impaired response to glucose resulting in elevated blood glucose concentrations.

Lipid profile. Measures total cholesterol, HDL cholesterol, LDL cholesterol and triglycerides. If the triglycerides are significantly elevated, a DLDL (direct measurement of the LDL cholesterol) may need to be done.


There are other laboratory tests that are not recommended for diagnosing metabolic syndrome but that may requested by some doctors to provide additional information. They include:

C-peptide. A reliable indicator of endogenous (by the body itself) insulin production.

Urine albumin : creatinine ratio. An early indicator of kidney disease, this test is used to help monitor patients with diabetes and is recommended under the WHO criteria.

hs-CRP (highly sensitive C-reactive protein). A measure of low levels of inflammation that may be tested as part of an evaluation of cardiovascular risk. This test is not performed by many laboratories.

sdLDL. A measurement of the number of small dense LDL particles a patient has. LDL particles vary in size, and the smaller denser ones, which tend to form when elevated triglycerides and VLDL are present in the blood, are thought to be more aggressive in causing atherosclerosis. This test is not performed by many laboratories and is not requested frequently. Its ultimate clinical utility has yet to be determined. May be evaluated in a lipoprotein subfractionation test.

Insulin. The fasting insulin test is considered too variable to be clinically useful in diagnosing metabolic syndrome and is not currently recommended by guidelines for this purpose.  However, if measured it will usually be elevated in those affected.


Tests for which the clinical utility in diagnosing metabolic syndrome has not yet been established include plasminogen activator inhibitor-1 (PAI-1) and proinsulin.

Non-Laboratory Tests

Blood pressure. To check for hypertension

Weight and waist circumference. To document abdominal obesity

BMI (Body Mass Index). An alternate measure of obesity that is used by many doctors. It is calculated by taking: (Weight in pounds X 705) / (height in inches squared); for example: (150 pounds X 705) / (67 inches X 67 inches) = a BMI of 23.5. If you prefer to use kilograms for weight and metres for height BMI can be calculated by (weight in kilograms)/(height in metres squared); for example: (62kg)/(1.70m x 1.70m) = 21.5 kg/m2. An adult with a BMI greater than 30 kg/m2 is considered obese. This calculation does not, however, describe where the excess weight is on the body.




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatments
The primary “treatments” for metabolic syndrome are for patients to lose excess weight, exercise regularly, and stop smoking. Weight reduction and exercise can:

Decrease blood pressure levels

Increase insulin sensitivity

Decrease triglyceride and LDL cholesterol levels

Raise HDL cholesterol levels

Decrease risk of cardiovascular disease and stroke


Drug treatment may be necessary to address hypertension and high cholesterol and triglyceride levels. Some doctors also recommend aspirin to decrease the risk of clotting, and a few doctors prescribe medications to increase insulin sensitivity (although there is not widespread agreement on this).

Patients with metabolic syndrome should work with their doctor and develop an individualised treatment plan and to monitor its effectiveness.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Overview
Staphylococcus aureus, also called S. aureus or “staph,” is a bacterium that frequently colonises the human skin and is present in the nose of about 25-30% of U.K. adults. S. aureus can exist in this form without harming its host or causing symptoms. However, if there is a break in the patient’s skin from a wound surgery or indwelling device (including intravenous catheters), or if there is a depression in the person’s immune system, then colonising S. aureus can cause an infection. S.aureus frequently causes localised skin infections, such as folliculitis, furuncles, and impetigo. It can also cause abscesses and spread into the bones (osteomyelitis), lungs (staphylococcal pneumonia), blood (bacteraemia or sepsis), heart (endocarditis – which can damage the heart valves), and other organs. S.aureus may also be transmitted to close contact from both infected and colonised people to other people through inadequate hand hygiene or throughsharing contaminated objects, such as towels or razors.

Hospital-acquired infections (Healthcare-associated infections, HAI)
S.aureus infections acquired while a patient is in a hospital, long-term care facility, or other health care setting have been a challenge for many years. Hospital conditions, including the widespread use of antibiotics, have selected for antibiotic-resistant strains of S. aureus. These strains are called Meticillin Resistant Staphylococcus Aureus (MRSA), named after the antibiotic treatment that was developed in 1960 to treat penicillin-resistant strains. MRSA is inherently resistant to flucloxacillin and most other antibiotics belonging to a class of antibiotics known as the `beta-lactams`, which includes penicillin. MRSA is also frequently resistant to a wide variety of other antibiotics. Infections are associated with significantly higher rates of morbidity and mortality, higher health care costs, and longer hospital stays than infections caused by methicillin susceptible S. aureus.

Risk factors for MRSA infection in the hospital include surgery, prior antibiotic therapy, admission to intensive care, close contact with MRSA-colonised patients and health care workers, being in the hospital more than 48 hours, and having an indwelling catheter or other medical device that goes through the skin. The risk of spread of MRSA is reduced through adequate hand hygiene amongst all close contacts, particularly healthcare professionals.

One strategy that may be used in an effort to control the spread of MRSA includes active surveillance for the detection of MRSA infection or colonisation amongst patients admitted to intensive care units (ICUs) and other high risk areas. Another approach is to screen all patients admitted to a health care facility. Public Health England (PHE; formerly the Health Protection Agency) actively manages mandatory surveillance of MRSA on behalf of the Department of Health. In 2014, the latest figures show that the total number of MRSA blood stream infections reports have decreased compared to the same period last year.

Community-acquired infections
MRSA infections have been associated with outbreaks and deaths in non-medical settings where individuals are in close contact, including  prisons, day care facilities, military units, and contact sports. These infections are occurring in people who do not have classic MRSA risk factors as described above. A significant number of those affected have had to be hospitalised for what appears to be a simple but persistent skin infection or for pneumonia that develops after a bout of influenza.

There is increased awareness of community-acquired MRSA (CA-MRSA) amongst the medical community and the community at large. With CA-MRSA, conventional therapy options have frequently failed. Investigations of outbreaks have revealed that the CA-MRSA was spread from infected or colonised patients to those around them through skin contact (such as sports-related cuts and abrasions), through droplets from the respiratory tract, or through exposure to contaminated objects, such as shared sports equipment, towels, toys, or playground equipment. Investigations have also revealed that the S. aureus strains involved in CA-MRSA are genetically different from those that have been causing hospital-acquired MRSA.  Effective treatment is usually readily available.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Laboratory Tests
The purpose of culturing wound infections is to identify the bacteria causing the infection and to determine the susceptibility of the microorganism to available antibiotics. If an infection is due to MRSA, it should be investigated to determine the primary source of the infection. This is especially important in CA-MRSA to break the chain of infection and prevent further cases from occurring.

The primary laboratory tests performed are:

Cultures of the affected areas. Fluid or pus from a wound, sputum, blood, joint fluid, or even breast milk (in the case of an infected breast) is collected and spread onto a thin layer of nutrient gel (agar) and/or grown in a nutrient broth. Sometimes, multiple samples are collected to evaluate different body sites or to attempt to detect bacteria that may be present in small numbers. 

Nasal (collected by inserting a swab inside the nose), throat, axilla and groin cultures may also be requested to determine whether someone is colonised with MRSA. The cultured samples are incubated and examined for the growth of characteristic S. aureus colonies, often on agar plates that change colour in the presence of MRSA. If suspicious-looking organisms are isolated on culture, susceptibility testing is usually performed to confirm that the strain is MRSA and determine appropriate treatment options, should these be required. 

Nasal swabs may be collected to detect MRSA colonisation by means of rapid molecular tests, which do not grow the bacteria but detect the genes responsible for the meticillin resistance. 


Identifying MRSA can sometimes be challenging. The population of S.aureus that a person is colonised with tends to be mixed. This means that even if a patient has CA-MRSA or hospital-acquired MRSA, not all of the S.aureus present will be equally resistant. Since resistant strains may grow more slowly than susceptible strains, laboratories may employ additional methods for detection.

A variety of methods may be used to monitor the spread of MRSA. These are used in the investigation of the spread of MRSA within a community or region but are not used in the treatment of an individual patient.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatments
Prevention of infection is the most important target for the UK healthcare system. National efforts are underway to raise awareness of MRSA and to encourage the adoption and maintenance of preventative measures, particularly adequate hand hygiene. For more on the proper way to wash your hands, visit the Health Protection (Scotland) and Public Health England (PHE) websites.

Many institutions have put procedures in place to more rapidly recognise and address MRSA infections. Health care providers are being urged to request cultures and susceptibility testing with outpatient skin and wound infections, to monitor them carefully for effectiveness of treatment, and to be alert for the possibility of CA-MRSA. Outbreaks of CA-MRSA are being investigated and traced back to their source in order to identify the cause, to determine whether other patients may have unrecognised MRSA infections or colonisation, and to reduce the potential for additional cases.

There are multiple treatment options for patients with MRSA infections. Some antibiotics may be given orally, whilst others must be administered intravenously (IV), often for several weeks’ duration.  Treatment options for significant MRSA infections include, but are not limited to, vancomycin, teicoplanin, linezolid, daptomycin, ceftaroline, ceftobiprole and chloramphenicol. .



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Overview
Myeloma is a cancer that develops in cells of the bone marrow called plasma cells. Plasma cells develop from B lymphocytes and are an important part of the immune system. Their primary function is to produce antibodies – targeted immunoglobulin proteins that help protect the body against infections. Normally, plasma cells are produced as needed. When B cells are exposed to pathogens, they mature into plasma cells and begin to produce antibodies. They share space in the bone marrow with maturing red blood cells (RBCs), platelets, and several types of white blood cells (WBCs). Sometimes, however, a plasma cell may become malignant and begins to divide uncontrollably, forming tumours in the bone marrow, eroding the surrounding bone and producing producing soft spots and holes known as lytic lesions. Myeloma can develop wherever there is bone marrow, including the pelvis, spine and ribcage. As it can occur in several places in the body, it is often called multiple myeloma.

Since the malignant cells are derived from a single plasma cell, they all produce an identical antibody – an abnormal monoclonal immunoglobulin (also termed an M-protein) that is released into the blood and sometimes excreted in the urine. The abnormal antibody does not work properly and is not able to fight infections while the proliferation of malignant cells can affect the production of normal antibodies (immunosuppression), causing susceptibility to infection.

Normally, the body makes five different types of immunoglobulins - IgG, IgA, IgM, IgE and IgD - that have slightly different immune system functions. Each type of immunoglobulin is composed of four protein chains - two identical heavy (long) protein chains and two identical light (shorter) protein chains. The light chains consist of one of two different types called kappa and lambda. Within a plasma cell, two heavy chains of one type and two light chains of one type become attached to form one intact immunoglobulin. Each particular plasma cell will produce only one type of immunoglobulin.

In patients with multiple myeloma, the malignant plasma cells produce only one type of intact (whole) immunoglobulin in large amounts. However, in about 75% of myeloma patients, the balance in production of light and heavy chains is disturbed and light chains are produced in excess. The surplus free light chains are released into the bloodstream and, because they are relatively small molecules, they are filtered by the kidneys and excreted into the urine, as a protein known as Bence-Jones protein. Rarely, the monoclonal protein produced consists only of light chains or, very rarely, heavy chains. Though the type of M protein produced by malignant cells may vary from one patient to the

Sym:
Symptoms and Signs
Many patients with multiple myeloma may show no symptoms for many years. Eventually, most patients develop some evidence of the disease either related to weakened bones (bone pain), decreased numbers of red or white blood cells (anaemia, infections), or kidney failure. As bones weaken, soft spots and fractures may develop. Destruction of the bone frequently increases the level of calcium in the blood, leading to symptoms of hypercalcaemia such as loss of appetite, nausea, thirst, fatigue, constipation, and confusion. A decrease in the number of normal white blood cells, red blod cells and platelets can result in recurrent infections, anaemia, bleeding, and bruising. Bence-Jones proteins can lodge in the kidneys and may permanently damage them. In some cases, an increase in the thickness (viscosity) of the blood may lead to headaches.

 Risks
 Multiple myeloma is relatively uncommon. According to Cancer Research UK, Myeloma is the 17th most common cancer in the UK (2009 data), accounting for around 1.5% of all new cases of malignancy. This equates to around 8 cases for every 100,000 people in the UK population. The cause of multiple myeloma is not yet known. The risk of developing it increases with age, with the majority of cases being diagnosed in patients 60 years or older. There is evidence of increased risk associated with a decrease in immune system function (e.g. HIV, post organ transplant). It has been suggested that occupational exposure to certain chemicals may increase risk but the International Agency for Research on Cancer (IARC) states that the evidence is limited. Genetic factors may also play a role; people with a parent, brother, sister, or child with myeloma or MGUS are 2 or 3 times as likely to develop myeloma or MGUS compared to people with no close family members with these illnesses.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
The goals of testing for multiple myeloma are to diagnose the condition, determine its severity and spread, monitor its progress, detect complications as they arise and monitor the effectiveness of treatment. There is no one single test that can diagnose multiple myeloma. Typically, the disease is diagnosed using a combination of patient’s signs and symptoms, medical history, physical examination, laboratory tests, and/or imaging tests.

 Laboratory Tests
 Multiple myeloma may first be suggested during routine blood testing, with the finding of an abnormal total protein level, an elevated calcium level, a low white or red blood cell count, an elevated erythrocyte sedimentation rate (ESR) and / or moderate to large amounts of protein in the urine. Findings such as these may raise suspicions but are not diagnostic as similar abnormalities may be seen with a variety of other conditions. They simply indicate the need for further testing.

Tests used as a follow-up to help diagnose the disease may include one or more of the following:

Serum Protein Electrophoresis: This test is used to diagnose and monitor multiple myeloma. Protein electrophoresis separates the proteins in a blood sample into several groups based on their electrical charge and size. In most patients with multiple myeloma, large amounts of an abnormal immunoglobulin protein (M-protein) will show up as an abnormal band on the electrophoresis strip. The amount of normal immunoglobulins in the sample may be visibly decreased. Usually, both a blood and a urine sample will be tested during the diagnosis of multiple myeloma because some proteins, such as the Bence Jones proteins (free light chains), may not show up in significant quantities in blood samples, while those with only intact immunoglobulins may not have the abnormal protein in urine.

 Immunofixation: is a technique used to identify the specific type of abnormal protein that is being produced by the malignant plasma cells. The amount of protein produced may vary throughout the course of the disease, but the type will remain the same.

 Bence-Jones protein (free light chains) can be detected in the urine of some patients with multiple myeloma. Usually the qualitative detection of Bence-Jones protein in an early morning urine sample is adequate, though occasionally, quantitation in a 24-hour urine collection may be requested.

 Serum free light chains (SFLC):This test measures the amount of free light chains in the blood. Even in normal circumstances (and for unknown reasons), plasma cells produce an excess of light chains compared to heavy chains and there is usually a small amount of light chains that do not become incorporated into intact immunoglobulins. These remain as free light chains and are released into the bloodstream. Most patients with multiple myeloma produce increased amounts of either kappa or lambda free light chains, which can be measured in blood. Consequently, the ratio of kappa to lambda light chains is abnormal in most patients and is a sensitive indicator for this disease. This test may be used to monitor progression and/or treatment.

Quantitative Immunoglobulins: Each of these tests measures amounts of a different type of immunoglobulin. The multiple myeloma protein will be an IgG, IgA or, rarely, an IgD or IgE immunoglobulin. Patients with a monoclonal IgM immunoglobulin may have a related but different disease (Waldenstrom’s macroglobulinaemia). IgG, IgA, and IgM may be requested to help diagnose multiple myeloma and to monitor the course of the disease and its effect on the production of normal immunoglobulins.

Bone marrow aspiration and biopsy: Multiple myeloma is a disease of the bone marrow. Patients usually require a bone marrow evaluation to confirm the diagnosis, evaluate how many malignant plasma cells are present in the marrow, and to what degree they have affected the production of normal white or red blood cells and platelets.

 Beta2-microglobulin: is a protein on the cell surface of myeloma and other cells. Increased levels may indicate a poorer prognosis, but this protein may also be elevated in other diseases.

 Other Laboratory Tests
 Other tests that may be done as part of an initial diagnostic workup, to monitor the progress of the disease, and to help detect and address complications include renal profile, calcium level, uric acid level and full blood count.

 Non-Laboratory Tests
 The large numbers of plasma cells being made in the bone marrow can cause damage to the hard outer covering of the bones. Your doctor will ask you to have X-rays of all your long bones, and your spine, pelvis and skull, to find any areas of damage. This is termed a skeletal survey.

MRI (Magnetic Resonance Imaging) can be more sensitive than X-ray for evaluating bone destruction and is occasionally resorted to.

Staging

The stage of a cancer tells your doctor how far it has grown or spread. Staging is based on information obtained from the tests and scans you have when diagnosing your myeloma, such as abnormal immunoglobulin being produced, the serum calcium level, the amount of normal proteins and ß-2 microglobulin in blood and the extent and severity of the bone damage. Staging helps to determine a patient’s prognosis and allows your specialist plan the treatment that is most appropriate for you.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is multiple sclerosis?
Multiple sclerosis (MS) affects the function of the brain, spinal cord and nerves. It is caused by inflammation and destruction of myelin in small patches called plaques. Myelin is a white fatty tissue that surrounds nerve fibres and insulates them against short-circuits that can prevent nerve signals from having their desired effects. The ``demyelination`` process interferes with nerve impulse transmission, causing a wide variety of symptoms affecting sensation, movement and thought. Myelin damage occurs in attacks that usually resolve with time, allowing symptoms to subside, but repeated demyelination can damage the nerve fibres resulting in progressive and persistent disability.

MS is an autoimmune process thought to be triggered by a virus or environmental factors in those with a genetic predisposition. Typically MS is first diagnosed when individuals are between 20 and 50 years of age, although it can occur in young children. It affects women two or three times more often than men, is more common in Northern European Caucasians than other ethnic groups and is seen in greater numbers in people who live in temperate climates than warm ones. Between 2 and 2.5 million people are affected worldwide with about 100,000 in the UK. The risk of developing the disease is estimated to be about 1 in 750 in the general population. In families with an affected member the risk rises to 1 in 40, and it is about 1 in 4 for the identical twin of an affected person, strengthening the notion of a genetic predisposition.

There is no single test that can conclusively diagnose MS. Instead, doctors will consider a patient`s medical and family history together with a variety of clinical and laboratory tests to aid diagnosis. In 2001 an international panel chaired by Dr Ian McDonald recommended that to diagnose MS a doctor must:

Determine that the central nervous system has been damaged in at least two places

Confirm that the damage occurred at separate times, more than one month apart

Rule out other conditions that cause a similar set of signs and symptoms


The McDonald criteria have been regularly updated to include radiological and laboratory tests that can help to make a more rapid diagnosis, for example following a single attack.

Once diagnosed, an individual may be classified as having one of several types of MS based on signs and symptoms, frequency of relapses, rate of disease progression and the number of areas of the central nervous system that are damaged.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
Because MS can attack any area of the central nervous system the signs and symptoms are many and varied. Symptoms of MS may come and go, and they may last from days to months. They include:

Sensory symptoms such as numbness, tingling, pain, burning, itching, facial pain and visual disturbances

Motor symptoms such as speech impediments, weakness, tremor, difficulty walking, lack of coordination, constipation and problems with the control of urination

Psychological symptoms such as mood swings, depression and problems with thinking, learning and memory

Fatigue (occurs in up to 90% of those with MS)

Temperature sensitivity (occurs in up to 60%; symptoms temporarily worsen with heat)


About 80% of those with MS have the relapsing-remitting type (RRMS) at the time of diagnosis. They experience periodic attacks or relapses followed by healing and symptom remission which may or may not leave residual disability. Later in the course of the disease about half develop secondary progressive MS (SPMS). Their symptoms and disabilities worsen as they continue to have relapses but do not fully recover. About 10% of people with MS have a primary progressive form of the disease (PPMS). They grow gradually worse without experiencing remissions.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
Although there is no single test or set of tests that can establish a diagnosis of MS, there are three tests that are generally considered useful:

Cerebrospinal fluid (CSF) analysis

Evoked potentials (EP)

Magnetic resonance imaging (MRI)


 Laboratory tests

There are no laboratory tests that are completely specific for MS, but several are helpful in diagnosing or excluding this disease as the cause of signs and symptoms. The most useful tests look for evidence of immunoglobulin G (IgG) production within the central nervous system.

CSF Electrophoresis and Isoelectric Focusing
Electrophoresis and isoelectric focusing are two methods for separating the proteins in a biological fluid. A patient`s CSF and serum are evaluated side-by-side on a test surface using either of these techniques. Following the separation step, a protein stain is applied to both specimens and the banding patterns that appear in the CSF and serum are compared. The presence of two or more IgG bands in CSF that are not present in serum is a positive test for oligoclonal banding. About 90% of those with MS show permanent oligoclonal banding in their CSF.

CSF Immunoglobulin G (IgG) Index
 Increased levels of CSF IgG can be due to excess production of IgG within the central nervous system, and is seen in MS and several other diseases. It can also be due to leakage of plasma proteins into the CSF that can occur with inflammation or trauma. To discriminate between these two possibilities, the IgG index is calculated from IgG and albumin measurements in CSF and serum:

IgG index = (CSF IgG / serum IgG) / (CSF albumin / serum albumin)

An elevated IgG index indicates increased production of IgG within the central nervous system. It is found in about 90% of MS cases.

Myelin basic protein
 This protein is a major component of myelin. Increased concentrations of myelin basic protein in CSF indicate that demyelination is taking place. This process is not specific for MS because other inflammatory diseases of the central nervous system can also elevate the amount of myelin basic protein in CSF. The test may be used to assess disease activity in established MS but is not widely available.

Doctors may also test for diseases that can cause symptoms similar to MS to determine if they may be responsible for a patient`s illness. Examples include:

Autoimmune disorders (e.g. lupus)

HIV

Lyme disease

Sarcoidosis

Syphilis

Vasculitis

Vitamin B12 deficiency


 Non-laboratory tests

The Evoked Potentials test involves measuring the time it takes for the brain to receive messages by placing small electrodes on the head to monitor the brain wave response to what is seen or heard. Damage to myelin can slow nervous system response time and the tests can reveal evidence of damage along nerve pathways.

An MRI (magnetic resonance imaging) scanner uses a strong magnetic field to create a detailed image of the brain and spinal cord. It is very accurate and can show the exact location and size of both permanent scarring and new lesions. MRI scans confirm the diagnosis in over 90% of people with MS.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Also known as: MG


                                                
                                            

What is myasthenia gravis?
Myasthenia gravis (MG) is a chronic autoimmune disease that affects muscle strength by impeding the communication between nerves and muscles. MG is typically first noticed when it causes weakness in eye muscles and symptoms such as a drooping eyelid and/or double vision. This is often referred to as ocular MG. From the eye muscles, it can spread over time to facial and neck muscles, causing weakness, slurred speech, difficulty chewing and swallowing, and/or difficulty breathing, and from the head and neck to other parts of the body, resulting in generalised MG. Muscle weakness will vary over time; it tends to worsen with sustained effort and improves with rest.

Body movements, including those as small as keeping the head upright and eyes open, are normally carried out by a coordinated series of muscle contractions. These muscle contractions are initiated by chemical nerve signals. On a microscopic level, a nerve impulse travels to a nerve ending and acetylcholine, a neurotransmitter, is released. This chemical travels from the nerve ending to a muscle fibre across a tiny gap that exists at the ``neuromuscular junction`` and it binds to one of many acetylcholine receptors on the muscle fibre. This binding activates the receptor and initiates muscle contraction.

With MG, the body`s immune system produces proteins (autoantibodies) that target a person`s own acetylcholine receptors and block or destroy them. This inhibits the receipt of acetylcholine signals and causes weakness and rapid muscle fatigue.

In the United Kingdom, MG is estimated to affect between 20 and 70 people in 100,000. Anyone can develop MG, but it is most frequently diagnosed in men over 60 years of age and in women under 40. During pregnancy, a woman with MG may pass acetylcholine receptor antibodies to her foetus. This can cause a newborn baby to have symptoms of MG, but the symptoms typically resolve within 2-3 months of birth.

The cause of MG is not known, but about 75% of those affected have an abnormally large thymus gland and some develop thymomas (generally benign tumours of the thymus). The thymus is a small gland located behind the upper breastbone at the base of the neck. It plays an active role in the immune system through young adulthood, but normally begins to shrink after puberty and is essentially nonfunctional in adults. The relationship between MG and the thymus is not fully understood, but some think that the thymus plays an indirect role in triggering acetylcholine receptor antibody production.

Those who have MG are at an increased risk of also developing other autoimmune disorders, such as systemic lupus erythematosus, rheumatoid arthritis, or autoimmune thyroid disease.

A small percentage of those with MG have an affected family member, but most do not. Congenital myasthenic syndrome is an inherited condition that causes symptoms similar to MG, but it is not an autoimmune disorder. Another condition, Lambert-Eaton Myasthenic Syndrome, can also cause similar symptoms, but it involves interference with the release of acetylcholine by the nerve ending, not acetylcholine receptor activity.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
A person with myasthenia gravis (MG) may experience a variety of symptoms. These may vary from day to day, worsen after activity and later in the day, and improve with rest. Symptoms may stay confined to the muscles around the eyes (ocular MG), but in most people they will extend to the face, neck, and other parts of the body within about a year (generalised MG). MG symptoms tend to worsen for several years and then stabilise. Some people may go through extended periods of remission.

Symptoms may include:

Drooping eyelid

Double vision

Decreased eye movement control

Difficulty swallowing, chewing, with choking, drooling and gagging

Slurred speech

Weak neck muscles

Trouble holding up head

Difficulty breathing

Difficulty walking and an altered gait

Specific muscle weakness but normal feelings/sensations


When MG affects the muscles that control breathing, it can cause a medical emergency called a myasthenic crisis that often requires hospitalisation and may require the temporary use of a respirator to assist ventilation.

Heat, stress, illness, and certain medications can cause symptoms to worsen.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
The goals with testing are to diagnose myasthenia gravis (MG), distinguish it from other conditions with similar symptoms, and to guide treatment. Some tests may be performed to monitor a person`s health status over time.

Laboratory tests

Laboratory testing may include the measurement of one or more autoantibodies:

Acetylcholine receptor (AChR) antibodies—found in up to 90% of those with generalised MG and about 50% of those with ocular MG; this is the primary blood test for MG. There are three types of AChR antibodies: binding (most frequently tested), blocking, and modulating.

Anti-MuSK (muscle-specific kinase) antibodies—found in up to 70% of those who are negative for AchR antibodies and have generalized MG.

Anti-Striated muscle antibody test—found in about 80% of those with MG who have an enlarged thymus gland and indicate a significantly increased likelihood of the person having a thymoma.


Other testing that may sometimes be requested:

Rheumatoid factor (RF)—this test may be used to detect or rule out rheumatoid arthritis.

Cyclic citrullinated peptide antibody (CCP)—may also be used to rule out rheumatoid arthritis.

Antinuclear antibody (ANA)—may be used to rule out other autoimmune disorders such as systemic lupus erythematosus.

Thyroid panel—used to rule out Graves disease, an autoimmune condition associated with hyperthyroidism.


Non-laboratory tests

Tensilon test (acetylcholinesterase test using edrophonium)—a person is given a drug intravenously that increases the availability of acteylcholine to see if muscle strength improves for a few minutes (for more on this, see MedlinePlus Medical Encyclopedia: Tensilon test).

Repetitive nerve stimulation and/or single-fibre electromyography—to evaluate neuromuscular response in a specific area.

A chest CT (computed tomography)—to detect an enlarged thymus gland or thymoma.

A brain and eye orbit MRI (magnetic resonance imaging)—this is not routine but can help rule out other causes of eye-related symptoms.




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What are they?
During the first few weeks of pregnancy a baby’s brain, spinal cord and its’ coverings develop. The cells that grow to form these structures do so by first forming into a tube - the neural tube. If the tube does not close fully, the opening that is left is called a neural tube defect (NTD).

Normally, the spinal cord and brain are surrounded and cushioned by cerebrospinal fluid (CSF) and are protected by outer layers of tissue called the meninges. The brain is also protected by the skull, and the spinal cord is protected by the backbone (spine), formed by bones called vertebrae. When someone has an NTD, there are one or more gaps in the brain or spinal cord’s protection. This can affect the brain’s development and can leave the spinal cord vulnerable to damage. Because the spinal cord contains the nerves that control body movement, any damage that occurs can paralyse or weaken associated muscles and organs.

The reason why the neural tube may develop incorrectly is not known for sure, but probably involves both genetic and environmental factors.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Types of Neural Tube Defects
Spina bifida, is the most common type of NTD. It occurs when the neural tube does not close completely somewhere along the backbone/spine. Symptoms vary from person to person and can change over time. They tend to occur below the defect and may range from few or none, to partial or total lower body weakness, loss of feeling, or paralysis. Complications will also vary. Cases of spina bifida are generally classified as either “closed” where the skin covers the defect or as “open” where the skin is not intact. Variants include:

Closed Neural Tube Defects
Spina Bifida Occulta
Spina bifida occulta is often called hidden spina bifida. A small gap may exist in one or more of the bones of the spine, but the spinal cord and tissues are normal. Many people with this condition do not have any symptoms and may never know that it exists unless it is identified during testing that is done for another reason.

Closed neural tube defects are frequently grouped with spina bifida occulta. They consist of a wide variety of spinal defects with malformed bone, tissue, and/or fat deposits at the location of the defect. Often there is a visible sign on the outside of the baby’s skin. This may be a tuft of hair, a dimple, a birthmark, lump, or skin opening. Many patients with this condition will have few symptoms, but some may have nerve damage that affects normal bowel or bladder function and/or can cause lower body weakness and pain.

Open Neural Tube Defects
Meningocele
With this type of spina bifida, cerebrospinal fluid (fluid from around the brain) and meninges (membranes covering brain) have ballooned out of the spinal opening to form a bulge or sac, but the spinal cord is usually in its normal location. This bulge may or may not be covered with a layer of skin. This bulge will be noticeable on the back of the baby. Symptoms are variable.

Myelomeningocele
This is the most severe type of spina bifida. It develops when the cerebrospinal fluid, meninges, and the spinal cord protrude through the opening in the spine. It leaves the spinal cord vulnerable to damage and can cause paralysis in those parts of the body below the opening. Affected patients frequently have bowel and bladder problems. Some will require assistance to walk and others will require a wheel chair. Newborns with this condition are at an increased risk of developing meningitis.

Up to 80 to 90 percent of people with spina bifida will develop hydrocephalus. This occurs when the flow of cerebrospinal fluid is blocked and builds up in the brain. The child’s head becomes larger and there is increased pressure on the brain. Left untreated, this condition can cause mental retardation and learning disabilities and can in some cases be fatal. Hydrocephalus is usually treated by putting in a tube called a shunt that allows excess cerebrospinal fluid to drain into the abdomen (tummy).

Anencephaly is the term used for an NTD that affects the head. The result is the lack of development of a large portion of the brain and skull. Some babies affected are stillborn. Those that are born alive are usually unconscious, unable to feel pain, deaf, and blind. Most of those affected die within a few hours or days.

There are a variety of other, rarer forms of NTDs. All are associated with a lack of proper neural tube formation.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
Laboratory Tests
Laboratory tests used to screen for the presence of NTD during pregnancy may include measurement of alpha-fetoprotein (AFP) in the mother`s blood. This is a protein made by the developing baby that crosses the placenta, into the mother`s blood stream. Levels rise during the first half of pregnancy, but will be particularly high if an open NTD is present as higher amounts cross to the mother. The concentration of AFP in the maternal blood may also be higher than expected in a twin pregnancy, or if the pregnancy is at a later stage than estimated.

Non-Laboratory Tests
Tests include:

Foetal ultrasound – to help diagnose NTDs prior to birth.

X-ray, MRI (magnetic resonance imaging), and/or CT scan (computed tomography) – of spine and vertebrae after birth to look for defects and deformities.

X-ray or CT scans of the head to detect excess fluid when hydrocephalus is suspected.


Regular clinical examinations – to detect and address complications as they arise.

Tests offered during pregnancy vary from region to region, please discuss available tests with your doctor or midwife.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is neuropathy?
Neuropathy is any disease or disorder that affects the functioning of nerves in a person`s body. The nervous system is divided into two parts, the central nervous system (CNS), which includes the brain and spinal cord, and the peripheral nervous system, which branches off from the brain stem and spinal cord to the rest of the body. The peripheral nervous system is further subdivided into the somatic and autonomic nervous systems. The somatic nervous system controls sensation and movement, while the autonomic nervous system controls vital functions, such as heart rate and breathing.


Nerve cells originate in the central nervous system and have long fibres that extend throughout the body and terminate as nerve endings in skin, muscle, and organs. These cells transmit impulses from the brain and spinal cord to other parts of the body.

Sensory nerves relay information about temperature, pressure, vibration, pain, and muscle position from various locations in the body (such as the tip of an index finger) to the brain.

The brain processes impulses from sensory nerves and also sends commands to muscle groups through motor nerves, allowing someone, for example, to walk, sit, run, and grasp objects.

Autonomic nerves send and receive messages that affect internal organs and involuntary functions, such as regulating blood pressure and heart rate, breathing, and digestion.


Neuropathy can develop in a wide variety of diseases and conditions. It may be inherited or acquired, acute or chronic, temporary or permanent. Nerve damage may occur in a single location or may be widespread. It may affect primarily one type of nerve, such as sensory, or multiple types. Anything that damages nerves can interfere with their ability to transmit accurate signals, which can lead to a number of signs and symptoms.

Neuropathy can affect both the central and peripheral nervous systems, this article will focus mostly on peripheral neuropathy, with some discussion of autonomic neuropathy. Peripheral neuropathy is a relatively common condition that affects around 1 in 50 people in England, with 8% of people who are 55 years of age or over being affected by it.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Causes
There are many causes of peripheral neuropathy and  in about 30% of cases; the cause is unknown and referred to as idiopathic neuropathy. Common causes include:

Diabetes –  The longer the duration of diabetes, the greater the chance of developing neuropathy. It is estimated that half of all people who have been living with diabetes for 25 years or more have diabetic neuropathy.

Vitamin deficiencies – especially vitamin B12, but also other  B vitamins such as B1, B6, B3, and vitamin E

Alcoholism – due to nutritional deficiencies and many think as a direct effect of the alcohol

Trauma – physical injury to a nerve; may be seen with repetitive stress and with any condition that traps, compresses, or damages a nerve (e.g., carpal tunnel syndrome).


Other causes include:

Kidney, liver and lung disease, or other chronic illness

Hypothyroidism and pituitary disorders

Autoimmune disorders such as Guillain-Barré syndrome, rheumatoid arthritis, and systemic lupus erythematosus (SLE).

Some cancers, either through production of substances that damage peripheral nerves (paraneoplastic syndrome) e.g. lymphoma, multiple myeloma or lung cancer, or through direct compression of the nerve itself.

A wide range of infections, including: shingles (varicella zoster virus), Lyme disease, HIV/AIDS, cytomegalovirus (CMV), Epstein-Barr virus, syphilis, leprosy, diphtheria, and parasites

Exposure to toxins, such as the heavy metals lead, arsenic, and mercury, or to other environmental toxins.

Some medications can cause peripheral neuropathy as a side effect. These include: antiretrovirals (for treatment of HIV infections), microtubule inhibitors (a type of chemotherapy), metronidazole, thalidomide (used in treatment of multiple myeloma), phenytoin and disulfiram (for treatment of alcohol dependence).

Other rare, inherited disorders such as Charcot-Marie-Tooth disease




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Signs & Symptoms
The symptoms of neuropathy depend upon the nerves affected. Neuropathies often start in the longest nerve fibres, those in the feet and legs, and ascend progressively, to affect the hands and arms and other parts of the body. There may be numbness, tingling, and pain that can range from mild to extremely severe and debilitating. Symptoms may include:

Loss of reflexes, balance, and coordination

Muscle atrophy

Muscle weakness, cramping, paralysis, or twitching

Pain – burning, aching, sharp, jabbing, electric-like, shooting

Extreme sensitivity to touch, even with very light pressure (such as from a bed sheet)

Tingling, numbness, loss of ability to detect touch, pressure, temperature, and vibration


If autonomic nerves are affected, symptoms may include:

Blurred vision; slow pupil reaction, which affects night vision

Decreased or excessive sweating and heat intolerance

Difficulty swallowing or breathing

Dizziness and fainting when standing due to low blood pressure

Erectile dysfunction in males; vaginal dryness in females

Heart rate that does not change appropriately with exercise

Incontinence and difficulty urinating and emptying the bladder

Lack of awareness of low blood glucose

Altered movement of food through the gastrointestinal tract, leading to constipation or diarrhoea, abdominal pressure and bloating, nausea, heartburn




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Also known as: NTM; MOTT


                                                
                                            

What are they?
Mycobacteria are a diverse group of rod-shaped bacteria that include more than 70 different species. Except for Mycobacterium tuberculosis (which causes the disease tuberculosis (TB)), and Mycobacterium leprae (which causes leprosy), most mycobacteria live in the soil and water in both rural and urban settings throughout the world. They can be found in aerosols, rivers and swamps, in treated  water, public swimming pools, hot spas, humidifiers, aquariums, garden soils, food, and many other places. Because they are protected by their waxy lipid-rich cell wall, mycobacteria are resistant to disinfectants and water treatment measures.

There is not a standard naming convention for this group of microorganisms. They may be referred to as nontuberculous mycobacteria (NTM), mycobacteria other than tuberculosis (MOTT), atypical mycobacteria, and/or environmental mycobacteria. The term MOTT is still often used but is an older designation. “Nontuberculous mycobacteria” has come into use more recently so, for the purpose of this article, this group will be referred to as NTM.

Almost half of the NTM species identified are associated with opportunistic infections in animals and humans, and several have caused sporadic outbreaks. NTM are acquired through environmental exposure to water, aerosols, soil, and dust – through inhalation, ingestion, and through breaks in the skin due to injuries, surgical procedures, or IV catheters.

Anyone can become infected, but people with suppressed immune systems (such as AIDS patients and transplant recipients), people with pre-existing lung damage (such as from smoking and previous tuberculosis) and those with lung diseases (such as emphysema or cystic fibrosis) are most likely to be affected. NTM infections can be challenging and time-consuming to treat since the organisms may be resistant to commonly prescribed antibiotics.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Common Species
The table below identifies different NTM species and provides a brief description of each.

Mycobacteria Examples-Many Overlap
M. avium- intracellular complex (MAC)
MAC has become one of the most common infections in patients with AIDS; often in the lungs and disseminated throughout the body; found widely
M. kansasii
Most frequently causes lung infections
M. abscessus
May infect implants, such as pacemakers
M. chelonae
May cause post-surgical infections in artificial heart valves and prosthetic implants
M. fortuitum
May cause post-surgical infections
M. xenopi
Found in hot water systems
M. scrofulaceum
May cause cervical adenitis, especially in children
M. marinum
Found in fresh and salt water, aquariums and swimming pools; infects through breaks in the skin and may cause persistent sores
M. ulcerans
Endemic in the tropics; causes Buruli ulcer, large lesions; the 3rd most common mycobacterial infection in healthy people
M. leprae
Infects mucous membranes and cool areas such as skin; causes nerve damage and numbness and skin nodules; can lead to skin damage and infection

                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Signs and Symptoms
The symptoms associated with non-tuberculous (atypical) mycobacteria (NTM) infections depend on which part(s) of the body are involved. Pulmonary infections may cause TB-like symptoms, including:

Chronic cough, sometimes with bloody sputum

Fever

Chills

Weight loss

Weakness


Skin-related NTM infections may cause persistent sores, boils, ulcers, and granulomas. Those affecting lymph nodes may cause inflammation in the node.

All of these symptoms may also be seen in a variety of other conditions. The diagnosis of most NTM infections depends on the positive identification of mycobacteria in body fluids or tissues. M. leprae cannot be detected with this method. It is diagnosed primarily through clinical signs as this species will not grow on culture media.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Osteoarthritis (OA) is a common joint disease due to wear and tear of  joint cartilage and the formation of new bone (bone spurs) at the edges of the joints. The cartilage of the affected joint wears down until there is none left and the opposing bones rub together. The joints most commonly affected are those of the hips, knees, big toe, and spine. Risk factors for osteoarthritis include age, female sex, obesity and joint injury.

What tests are used? 
Blood tests are not used to diagnose the disease but may be used to monitor side effects of various treatments.
X-rays of the affected joints will show loss of cartilage and narrowing of the joint space. 

What treatments exist? 
Osteoarthritis cannot be cured, but there are several types of treatment available to reduce the symptoms. Exercise, particularly in water, weight loss, good nutrition and the use of heat and cold treatments may increase mobility. Pain due to OA can be treated with pain killers and anti-inflammation drugs. Sometimes steroid drugs are injected directly into the affected joint to help relieve pain. The dietary supplements glucosamine and chondroitin are available `over-the-counter` in many pharmacies though their effectiveness is unproven. Surgical treatment to replace or repair damaged joints may be needed in severe cases.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Tests:
What is it?
Osteoarthritis (OA) is a common joint disease due to wear and tear of  joint cartilage and the formation of new bone (bone spurs) at the edges of the joints. The cartilage of the affected joint wears down until there is none left and the opposing bones rub together. The joints most commonly affected are those of the hips, knees, big toe, and spine. Risk factors for osteoarthritis include age, female sex, obesity and joint injury.

What tests are used? 
Blood tests are not used to diagnose the disease but may be used to monitor side effects of various treatments.
X-rays of the affected joints will show loss of cartilage and narrowing of the joint space. 

What treatments exist? 
Osteoarthritis cannot be cured, but there are several types of treatment available to reduce the symptoms. Exercise, particularly in water, weight loss, good nutrition and the use of heat and cold treatments may increase mobility. Pain due to OA can be treated with pain killers and anti-inflammation drugs. Sometimes steroid drugs are injected directly into the affected joint to help relieve pain. The dietary supplements glucosamine and chondroitin are available `over-the-counter` in many pharmacies though their effectiveness is unproven. Surgical treatment to replace or repair damaged joints may be needed in severe cases.



                                        
                                        
    
        
            
                

                

                
                    <a title=``


info:
Overview
Osteoporosis is a thinning and weakening of the bones, usually associated with the aging process. The bones hold almost all of the body’s calcium – the remaining small amount circulates for use by the body. Bone, like other organs, is constantly breaking down and reforming. With osteoporosis, the amount of calcium present in the bone slowly decreases, causing the bones to become brittle and prone to fracture. Often, the diagnosis of osteoporosis is not made until a fracture (broken bone) occurs with only moderate pressure.

People at increased risk include women who go through early menopause or hysterectomy with removal of ovaries, those who have never given birth and those who are anorexic.  Men at risk include those with decreased testosterone levels due to treatment for prostate cancer, or following surgery for testicular problems. Men or women who have a family history of osteoporosis or who have taken high dose steroid medicines for long periods of time are also at risk.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
To identify whether osteoporosis is present, a test called the DXA scan (dual X-ray absorptiometry scan) is used to measure the thickness (or density) of the bone. Here an x-ray beam is directed at a small area of bone (usually the heel, spine, hip, or wrist). The thicker your bone is, the less x-ray beam will pass through it.
If you are being investigated for osteoporosis, you may have a blood sample taken to measure certain mineral and hormone levels, in addition to identification of risk factors in your personal history and physical examination. Blood calcium levels are usually normal in osteoporosis even if the bones are deficient, making this test useless for diagnosis. Alkaline phosphatase (ALP) is an enzyme that may be elevated in both liver and bone disease, but it is not normally increased in osteoporosis. Tests of thyroid function (TFT) may be performed to identify overactivity of this gland.  Hormones produced by the brain (LH and FSH) and ovaries in women (oestradiol) or testicles in men (testosterone) may be measured to identify any deficiency. Protein levels may be examined in both blood and urine to identify the presence of multiple myeloma, a type of cancer associated with bone breakdown. Products of bone turnover can be found in blood and urine. These `bone resorption` and `bone formation` markers may be measured and are useful when monitoring a person`s response to treatment with drugs which slow down bone breakdown.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Whilst complete prevention of osteoporosis may not be possible, measures can be taken to reduce the level of bone loss. This measures include regular weight-bearing exercise and calcium and vitamin D supplements (or food rich in these), stopping smoking and reducing coffee and alcohol intake. People should not wait until they are older to start these preventive activities.
There is evidence that hormone replacement therapy may lower the risk of osteoporosis in women by increasing bone density, reducing the number of fractures, and improving balance. However, there are risks associated with this therapy, including an increased risk for uterine and breast cancers and blood clots. Other, non-hormonal, treatments available include drugs called bisphosphonates which reduce bone breakdown, and selective oestrogen receptor modulators (SERM). These maintain bone density and reduce risk of experiencing fractures.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Cancer of the ovaries is the sixth most common cancer in women. About 6,500 new cases are diagnosed in the UK each year. It is a more frequent cause of death than the more common, but more easily detected, cancers of the uterus and cervix. 

Women have two ovaries, located in the lower abdomen above and to either side of the uterus. About the size of apricots, the ovaries are connected to the uterus by fallopian tubes. Ovaries have two main functions, they produce oestrogen and progesterone, hormones which are responsible for the development of the features that distinguish women from men, their secondary sexual characteristics. The ovaries also regulate a women’s periods and the development and release of an egg into the fallopian tube once a month during childbearing years.

Ovarian tumours can be either benign or malignant; it is not usually possible to tell them apart until they have been removed unless they have spread to other parts of the body. About 85% of ovarian tumours begin in the cells covering the outside of the ovaries, but they may also arise in the egg-producing cells (germ cells) or more rarely in the tissue that produces oestrogen and progesterone and holds each ovary together. While benign tumours do not spread, cancerous ovarian tumours will do so if left unchecked. They spread first into the tissues around the ovaries, then to the uterus, bladder, rectum, and the lining of the abdomen. Eventually, cancerous cells will reach the lymph nodes and spread throughout the body and invading and damaging other organs, such as the lungs.

The main risk factors for ovarian cancer are increasing age (ovarian cancers are rare before 45 and most occur between 65 and 74) and a family history of ovarian and/or breast cancer. However, less than 10% of ovarian cancer appears to have a family link. Slightly increased risks may be associated with not having children, taking fertility drugs, and with hormone replacement therapy. Slightly decreased risks are associated with having your tubes “tied” (tubal ligation), taking oral contraceptives, having children, and breast feeding. 

It is difficult to detect ovarian cancer early – only about 25% of the cancers are found in the easily treatable stage, before they have spread beyond the ovaries. The symptoms of ovarian cancer are subtle and nonspecific. They include abdominal swelling and pain, indigestion, changes in passing urine and bowel habits, bloating and a feeling of pressure in the pelvis, weight changes, and unexplained vaginal bleeding. Since there are many non-cancerous conditions that can also cause these symptoms, it is important to consult your doctor if you are experiencing any symptoms.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests
Currently there is no ideal screening test for ovarian cancer. However, research there into the development of a reliable method for early detection amongst women without apparent symptoms. In the meantime, it is important that women are awareness of the symptoms of ovarian cancer.

Testing of symptomatic women includes:

CA 125 (Cancer antigen 125) measures a protein in the blood which is high in about 80% of those ovarian cancers which are derived from the surface cells. It may be used in with pelvic examination and a transvaginal and/or pelvic ultrasound to help diagnose ovarian cancer. CA 125 however, it is not specific enough to be used as a general screening test: increases in CA 125 levels are seen in other cancers, in hepatitis, pelvic inflammatory disease, and endometriosis as well as in early pregnancy and menstruation. It is mainly used as a tumour marker to monitor ovarian cancer treatment and to help detect early recurrence of cancer.

AFP (Alpha fetoprotein) and hCG (human chorionic gonadotrophin) levels are increased in some ovarian cancers derived from the germ cells, but they are also elevated during pregnancy. If AFP or hCG are increased in a case of ovarian cancer, the tests can be used to monitor treatment and to detect recurrence of cancer.

BRCA-1 and BRCA-2 are tests for two genetic mutations which have been associated with an increased risk of ovarian and breast cancer. These tests are usually done to screen and/or help diagnose a patient who has a strong family history of breast or ovarian cancer.


Other non-laboratory tests that are used to look for other abnormalities include:

Ultrasound (pelvic and/or transvaginal) uses sound waves to create a picture of the uterus and ovaries. It can help determine whether an ovarian growth is likely to be a cancer or a fluid-filled cyst.

CT scan (computerized tomography)

X-ray of the gastrointestinal tract




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatment
When abnormalities are found and ovarian cancer is suspected, surgery is required to confirm the diagnosis. This may be done by or in consultation with a doctor who specializes in cancers of the female reproductive organs, a gynaecologic oncologist. If cancer is found, the grade (how normal or abnormal cells appear under the microscope) and stage (how far the cancer has spread) will be determined and appropriate treatment decided. If cancer is visible during surgery, the ovary containing it is usually removed along with as much as possible of any tumour that has spread beyond the ovaries. It may also be necessary to remove the other ovary, the fallopian tubes, and the uterus.

Follow-up treatment usually involves chemotherapy, sometimes radiation treatments, and some doctors use CA 125, AFP, or hCG to monitor response to treatment and recurrence. Ovarian cancer treatment is constantly evolving. New drugs, immunotherapies, gene therapies, and bone marrow transplants are being studied for their effectiveness. Your doctor and/or cancer team can help you determine the treatment course that is right for you.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
For an explanation of the pancreas, please see the description under ``What is the pancreas?`` in Pancreatic Diseases.

Cancer is an uncontrolled growth of abnormal cells that form tumours, damage normal tissue and that may eventually spread throughout the body (metastasise). Most pancreatic cancers (95%) are adenocarcinomas that develop in the pancreatic ducts and sometimes in the enzyme-producing cells of the exocrine tissue. Endocrine tumours are usually less aggressive than exocrine tumours and are rarer. They may be benign tumours that do not metastasise (such as an insulinoma) or malignant, including a group of cancers called islet cell cancers. Endocrine cancers are usually detected earlier than exocrine cancers because they often produce excessive amounts of the hormones insulin and glucagon that frequently result in the development of characteristic symptoms.

The remainder of this discussion focuses on exocrine cancer because it is more common and the tumours are more aggressive. Unfortunately, they are hard to detect at an early stage. Since the pancreas is deep in the body, tumours usually cannot be seen or felt during a physical examination and, by the time symptoms develop, the cancer has often spread throughout the pancreas and beyond. One exception to this is a cancer that forms at the ampulla, the point where the pancreatic and bile ducts empty into the duodenum. Ampullary cancer often obstructs the flow of bile from the bile duct and causes jaundice, so it has the potential to be detected earlier than most exocrine cancers.

According to Cancer Research UK, 8500 UK people were diagnosed with pancreatic cancer in 2010. It is the tenth commonest cause of cancer death in the UK, two thirds occurring in those over 70 years of age.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
Early symptoms of pancreatic cancer are often either absent or subtle. They include abdominal pain, back pain, nausea, loss of appetite, unexplained weight loss and jaundice. Since these symptoms can be experienced in conditions other than cancer, they may be ignored or misinterpreted in the early stages. By the time chronic pain, vomiting, impaired digestion of food and problems with blood sugar control surface and are recognised, the pancreatic cancer has often become firmly established.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
Unfortunately, there are no laboratory tests available for the early detection or diagnosis of pancreatic cancer. The diagnosis is usually made using a combination of the results of a clinical examination, clinical history, imaging tests and biopsy. 

Laboratory tests that may be abnormal but are not diagnostic of pancreatic cancer (i.e. can be abnormal as a result of other conditions) include:

Amylase: this may be raised if the tumour obstructs the ducts through which pancreatic juice flows to the intestine

Liver function tests: an elevated bilirubin concentrations suggests the tumour itself or glands it has spread to are blocking the bile duct. A raised ALT suggests that the tumour has spread to the liver

Calcium: this is sometimes raised in pancreatic cancer (as in other cancers), producing symptoms such as weakness, nausea, abdominal pain and thirst. A raised calcium caused by cancer can be treated and the symptoms relieved

CA 19-9 (Cancer Antigen 19-9): a tumour marker that can be used for monitoring response to treatment. It is not useful for detection or diagnosis because it is not elevated in all cases and it is not specific for pancreatic cancer (it may be elevated as a result of  other conditions). If it is raised at diagnosis it may then be used to assess the efficiency of treatment and to monitor for recurrence.

CEA (Carcinoembryonic antigen): a tumour marker that may also be used to monitor the response to treatment and for recurrence, if the concentration is raised at diagnosis.

Other tests such as stool chymotrypsin or elastase, blood immunoreactive trypsin (IRT), amylase, and lipase may be measured to help determine how well the pancreas is functioning and whether pancreatic enzyme supplementation is necessary


Non-laboratory tests that may be used:

CT (computed tomography) scan: useful for detecting pancreatic masses and any cancer that has spread to other areas of the body.

Biopsy: used to confirm diagnosis of cancer, often in conjunction with CT scan

ERCP (endoscopic retrograde cholangiopancreatography): test that uses a flexible endoscope tube inserted through the nose, stomach and into the pancreas which may be used to introduce a dye for X-rays, to place a stent (a metal or plastic tube that can help keep a duct open and functioning) or to take a biopsy

Transabdominal ultrasound

MRI (magnetic resonance imaging)




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is the pancreas?
The pancreas is a narrow, flat organ about six inches long, with a head, middle, and tail section. It is located below the liver, between the stomach and the spine, and its head section connects to the duodenum (first part of the small intestine). Inside the pancreas, small ducts (tubes) feed fluids produced by the pancreas into the pancreatic duct. This larger duct carries the fluids down the length of the pancreas, from the tail to the head, and into the duodenum. The common bile duct also runs through the head section of the pancreas, carrying bile from the liver and gall bladder into the small intestine.

The pancreas consists of two kinds of tissue:

Exocrine  tissue which makes powerful enzymes to digest fats, proteins, and carbohydrates. The enzymes normally are created and carried to the duodenum in an inactive form, then activated as needed. Exocrine tissue also makes bicarbonate that neutralises stomach acids.

Endocrine tissue which produces the hormones insulin and glucagon and releases them into the blood stream. These hormones regulate glucose transport into the body`s cells and are crucial for energy production




                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Common Diseases of the Pancreas
Acute Pancreatitis
The most common cause of acute pancreatitis is blockage of the pancreatic duct by a gallstone. Secretions can back up in the pancreas and cause permanent damage in just a few hours. They also can circulate to other body organs, causing shock and organ failure. Acute pancreatitis can be life-threatening

Chronic Pancreatitis
Chronic pancreatitis, associated most often with alcoholism, can cause painful attacks over a number of years and lead to other problems such as pancreatic insufficiency (see below), bacterial infections, and type 2 diabetes

Diabetes
Type 1 diabetes involves destruction of pancreatic beta cells which produce insulin and a dependence on treatment with insulin; type 2 involves loss of some beta cell function and insulin resistance; treatment is usually with diet and tablets. Diabetes affects many other body organs, especially the kidneys

Cystic Fibrosis
CF is an inherited genetic disorder that disrupts chloride transport at the cellular level. This causes mucous plugs that block pancreatic enzymes from reaching the intestines and leads to digestive problems.

Pancreatic Cancer
Cancer of the pancreas is thought to be the tenth most common cause of cancer death in the UK, being diagnosed in about 8,800 people a year. Risks include smoking, age, chronic pancreatitis and exposure to some industrial chemicals. Most (around 95%) pancreatic cancers are adenocarcinomas, developing in the exocrine tissues. Pancreatic cancer is very difficult to detect in the early stages because symptoms are either absent or non-specific: abdominal pain, nausea, loss of appetite and sometimes jaundice. Only about 10% of the cancers are still contained within the pancreas at the time of diagnosis



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Pancreatic insufficiency is the inability of the pancreas to produce and/or transport enough digestive enzymes to break down food in the intestine and allow its absorption. It typically occurs as a result of long term pancreatic damage - damage that may be caused by a variety of conditions. In children it is most frequently associated with cystic fibrosis less commonly  with a rare inherited condition, the Shwachman-Diamond  Syndrome (SDS).  In adults it may follow pancreatic damage caused by repeated attacks of acute panreatitis or by  chronic pancreatitis; it is less frequently but sometimes associated with pancreatic cancer.  

Pancreatic insufficiency usually results in symptoms of malabsorption, malnutrition, vitamin deficiencies, and weight loss (or in children who do not gain weight at the normal rate) and is often associated with pale, fatty, foul-smelling, floating stools (steatorrhoea). Diabetes may also be present in adults with pancreatic insufficiency. 



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests
Faecal chymotrypsin.  This is a stool test for an enzyme that digests food proteins.  It is produced in the pancreas in an inactive form and then becomes activate when it enters the small intestine.  Low values indicate pancreatic insufficiency.  

Faecal pancreatic elastase. Elastase is a protein-cleaving enzyme produced in and secreted by the pancreas.  It is resistant to degradation by other enzymes and so is excreted and can be measured in the stool.  The amount of this enzyme is reduced in pancreatic insufficiency. The patient’s own (human) enzyme can be measured to assess pancreatic insufficiency even if they are receiving oral (animal) pancreatic supplements that include elastase. 

Serum Immunoreactive trypsin (IRT). Raised values show that  there is obstruction of trypsinogen secretion by the pancreas into the intestine where it is normally converted to trypsin. It is used in many countries as a screening test for cystic fibrosis in newborn babies. Low serum values indicate failure of production in pancreatic disease. 



The excretion of fat in the stools is increased in pancreatic insufficiency, but faecal fat is now very rarely measured in the UK, having been superseded by the enzyme tests described above.

Non-laboratory tests

Endoscopic retrograde cholangiopancreatography (ERCP): a flexible scope is passed through the nose and stomach into the common opening of the pancreatic and bile ducts in the small intestine. It is most often used when an obstruction, for example pancreatic carcinoma, is suspected.

Secretin test (not widely used): a tube is positioned in the duodenum to collect pancreatic secretion of enzymes and bicarbonate stimulated by intravenous (IV) secretin.

Magnetic resonance imaging (MRI ) may be used to examine the structure of the pancreas and bile ducts.





                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatment
Treatment involves dealing with the underlying condition, preventing further pancreatic damage and managing the symptoms. If the cause of the pancreatic insufficiency is chronic pancreatitis, abstention from alcohol is critical in preventing further attacks. To aid digestion patients may be given oral preparations of pancreatic enzymes as a supplement to make up for decreased production. They may also be given vitamin supplements (especially fat-soluble vitamins A, D, E, and K because of impaired fat absorption) and may be put on a diet low in fat and high in protein and calories to help them gain and maintain weight.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Pancreatitis can be an acute or chronic inflammation of the pancreas. Acute attacks typically give severe abdominal pain which extends from the upper stomach through to the back and can cause effects ranging from mild swelling of the pancreas to life-threatening organ failure. Chronic pancreatitis is a slowly progressing disease that may involve a series of acute attacks, causing intermittent or constant pain as it permanently damages the pancreas.

The pancreas is a narrow, flat organ located deep in the abdominal cavity, behind the stomach and below the liver. It has exocrine tissues, which make powerful enzymes that help digest fats, proteins and carbohydrates and bicarbonate that helps neutralise stomach acids. It also has ``islets`` of endocrine tissue that produce the hormones insulin and glucagon, vital for the transport of glucose into body cells.

Normally, the pancreatic digestive enzymes are created and carried into the duodenum (first part of the small intestine) in an inactive form. It is thought that during an attack of pancreatitis these enzymes become activated while still in the pancreas and begin to digest and destroy it.

While the exact mechanisms of pancreatitis are not well understood, it is known to be linked to and aggravated by alcoholism and it can be caused by gallstones blocking the bile duct which joins the duodenum. These two conditions are responsible for about 80% of acute pancreatitis attacks. Alcoholism is the major cause of chronic pancreatitis. In about 15% of episodes the cause of pancreatitis is unknown. Rarer causes include:

Drugs such as sodium valproate or morphine

Viral infections such as mumps, Epstein-Barr or hepatitis A and B

High plasma triglycerides (hypertriglyceridaemia) in diabetes, alcoholism or inherited conditions

High plasma calcium (hypercalcaemia) in hyperparathyroidism or malignant disease

Cystic fibrosis or Reye`s syndrome in children

Pancreatic cancer

Surgery in the pancreas area (such as bile duct surgery) or trauma



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
Acute pancreatitis
About 80% of acute pancreatitis attacks are mild, although they may cause the sudden onset of severe abdominal pain, sickness, vomiting, weakness and jaundice. Attacks cause local inflammation, swelling, and haemorrhage that usually gets better with supportive treatment and does little or no permanent damage. About 20% of the time complications develop, such as tissue necrosis, infection, hypotension (low blood pressure), difficulty breathing, shock, and kidney or liver failure. It is important to see your doctor if you have symptoms that suggest pancreatitis because symptom severity does not necessarily reflect the amount of damage that may be occurring and because other conditions that require different treatments may cause similar symptoms. 

Chronic pancreatitis
Patients with chronic pancreatitis may have recurring attacks with symptoms similar to those of acute pancreatitis; these attacks increase in frequency as the condition progresses. Pain with chronic pancreatitis may be intermittent or become severe and continuous. It may be made worse by eating, drinking particularly alcohol. Over time, the pancreas tissue becomes increasingly scarred and the cells that produce digestive enzymes are destroyed, causing pancreatic insufficiency (inability to produce enzymes to digest fats and proteins). There is often weight loss, malnutrition, ascites, the development of pancreatic pseudocysts (fluid pools and destroyed tissue that can become infected) and fatty stools. As the cells that produce insulin and glucagon are destroyed, the patient may become permanently diabetic. Patients with chronic pancreatitis have an increased risk of developing pancreatic cancer.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
Amylase (the pancreatic enzyme responsible for digesting carbohydrates) is the most common blood test for acute pancreatitis. It increases from 2 to 12 hours after the beginning of symptoms and peaks at 12 to 72 hours. It may rise to 5 to 10 times the normal level and will usually return to normal within a week. Amylase also may be monitored in chronic pancreatitis.  It is often moderately elevated until the cells that produce it are destroyed. 

Lipase (the enzyme that, along with bile from the liver, digests fats) increases in the blood within 4 to 8 hours of the beginning of an acute attack and peaks at 24 hours. It may rise to several times its normal level and remains elevated longer than amylase. As cells are destroyed in chronic pancreatitis and as lipase production drops to less than 10% of the normal level, steatorrhoea (fatty, foul-smelling stools) will result.

An increase in plasma alanine aminotransferase (ALT) and jaundice suggest gall stones are the cause of acute pancreatitis. If the cause is not clear, plasma triglycerides and calcium should be measured.

Stool chymotrypsin tests can be used to exclude pancreatic insufficiency. Immunoreactive trypsin (IRT) is a blood test that may be used to check pancreatic sufficiency in those with chronic pancreatitis. Nowadays faecal fat is rarely used to check for pancreatic sufficiency.

Other tests that may be used to check for complications of acute pancreatitis include:

Full Blood Count (including white blood cell count)

Glucose

Non-laboratory tests may include:

Abdominal ultrasound

ERCP (endoscopic retrograde cholangiopancreatography), a flexible scope used to see and sometimes remove gallstones

CT (computed tomography) scan to look for calcified ducts in chronic pancreatitis

Secretin testing (rarely used) in which a tube is positioned in the duodenum to collect pancreatic secretions stimulated by injection of the hormone secretin into a vein

MRI (magnetic resonance imaging)



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Polycystic ovarian syndrome (PCOS), which used to be called Stein-Leventhal syndrome in its most severe form, is a common condition, affecting 5 to 10% of women of childbearing age. The disorder is probably the most common hormonal abnormality in women of reproductive age and is certainly a leading cause of infertility. Although the underlying cause is not well understood, PCOS is generally characterised by an excess production of androgens (male hormones - usually testosterone), lack of ovulation i.e. anovulation (the egg is not released by the ovary) and absence of menstrual periods (amenorrhoea), and by a varying degree of insulin resistance. The ovaries usually have many fluid-filled sacs (cysts) hence the name of the condition.

Androgens are normally created in small amounts by a woman`s ovaries and adrenal glands. Even a slight overproduction can lead to symptoms such as hirsutism and acne. In extreme cases, they can lead to virilization.

There is frequently increased secretion of luteinising hormone (LH) from the pituitary gland and all these hormone imbalances also affect the menstrual cycle in PCOS, causing infertility problems. Most women with this condition do not have regular monthly periods. Often they have chronic anovulation and amenorrhoea, but they may also experience irregular periods and uterine bleeding. With PCOS, both ovaries tend to be enlarged as much as 3 times their normal size. In 90% of women with PCOS, an ultrasound of the ovaries will reveal cysts (small immature egg-bearing follicles, fluid-filled follicles) that can be seen on the surface of the ovary. These ovarian cysts are often lined-up to form the appearance of a ``pearl necklace.`` When the egg is not released and a woman is not menstruating, sufficient progesterone is not produced. This leads to a hormonal imbalance in which oestrogen acts ``unopposed.`` This can lead to an overgrowth of the lining of the uterus (endometrial hyperplasia) and increases a woman`s risk of developing endometrial cancer. Women with PCOS who do ovulate and become pregnant tend to have an increased risk of miscarriage.

Although the cause of PCOS is not well understood, some think that insulin resistance may be a key factor. Insulin is vital for the transportation and storage of glucose at the cellular level; it helps regulate blood glucose levels and has a role in carbohydrate and lipid metabolism. When there is resistance to insulin`s use at the cellular level, the body tries to compensate by making more.  This leads to hyperinsulinaemia (elevated levels of insulin in the blood). Some believe that hyperinsulinaemia may be at least one cause for an increased production of androgens by the ovaries.

Most women with PCOS have varying degrees of insulin resistance, obesity, and lipid dysfunction. Insulin resistance tends to be more pronounced in those who are obese and do not ovulate. These conditions put those with PCOS at a higher risk of developing type 2 diabetes> and cardiovascular disease.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and symptoms
PCOS is said to be heterogeneous; that is, patients may experience a wide variety of different symptoms to a greater or lesser degree, and vary over time. Also, a uniform and precise definition of the syndrome is lacking. Women often go to their doctor because they are having menstrual irregularities, experiencing infertility, and/or are having symptoms associated with androgen excess. They may experience:

Abnormal uterine bleeding

Acanthosis nigricans

Acne

Amenorrhoea or irregular periods (oligomenorrhoea)

Decreased breast size

Deeper voice (rare)

Enlarged ovaries

hirsutism involving male hair growth patterns such as hair on the face, sideburn area, chin, upper lip, lower abdominal midline, chest, areola, lower back, buttock, and inner thigh

Weight gain/truncal obesity; fat distribution in the centre of the body

Skin tags in the armpits or neck

Thinning hair, with male pattern baldness




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
PCOS is to some extent a diagnosis which is reached after excluding other disorders. PCOS remains a syndrome (a collection of signs and symptoms) with no single clinical feature which can make the diagnosis. Your doctor will carry out tests to rule out other causes of anovulation and infertility. He will usually request a variety of hormone tests to help determine whether hormone overproduction may be due to PCOS, an adrenal or ovarian tumour, or an overgrowth in adrenal tissue (adrenal hyperplasia). Ultrasound is often used to look for cysts in the ovaries and to see if the internal structures appear normal.

Your doctor will use the combination of laboratory results and clinical findings to make a diagnosis. If the diagnosis is PCOS your doctor may then request further tests such as lipid profiles and glucose levels to monitor your risk of developing future complications such as diabetes and cardiovascular disease

Laboratory Tests

FSH (Follicle Stimulating Hormone), may be normal or low with PCOS 

LH (Lutenizing Hormone), may be elevated 

LH/FSH ratio. This ratio is normally about 1:1 in premenopausal women, but a ratio of greater than 2:1 or 3:1 may provide supporting evidence for a diagnosis of PCOS

Prolactin may be normal or mildly elevated

Testosterone, total and/or free, usually elevated

DHEAS (may be measured to rule out a virilising adrenal tumour in women with rapidly advancing hirsutism), frequently mildly elevated with PCOS

Oestrogens, may be normal or elevated

Sex hormone binding globulin, may be reduced

Androstenedione, may be elevated

Anti-Müllerian Hormone is a relatively new test used by some centres and has been found to be increased 2-3 times in PCOS. At present, this test is not routinely used in the investigation of PCOS in the UK, although this could change as a result of ongoing research.

hCG(Human chorionic gonadotropin), used to check for pregnancy, negative

Lipid profile, (collected after a fast), (low HDL, high LDL, and cholesterol, elevated triglycerides) 

Glucose, fasting and/or a glucose tolerance test, may be elevated

HbA1c another measure of diabetes which is carried out in some centres in preference to glucose.

Insulin, (collected after a fast), often elevated 

TSH (Thyroid stimulating hormone) some who have PCOS are also hypothyroid 

Cortisol to rule out Cushing`s syndrome

17-hydroxyprogesterone to exlude adrenal hyperplasia

Insulin-like growth factor (IGF-1) to exlude acromegaly


Non-Laboratory Tests
Ultrasound, transvaginal and/or pelvic/abdominal are used to evaluate enlarged ovaries.  With PCOS, the ovaries may be 1.5 to 3 times larger than normal and characteristically have more than 8 follicles per ovary, with each follicle less than 10 mm in diameter.  Often the cysts are lined up on the surface the ovaries, forming the appearance of a ``pearl necklace.``  These ultrasound findings are not diagnostic.  They are present in more than 90% of women with PCOS, but they are also found in up to 25% of women without PCOS.

Laparoscopy may be used to evaluate ovaries, evaluate the endometrial lining of the uterus, and sometimes used as part of surgical treatment.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
A peptic ulcer is a hole in the lining of the stomach or duodenum (the upper part of the small intestine), usually caused by a bacterial infection with Helicobacter pylori. The stomach produces hydrochloric acid and enzymes, including pepsin, that break down and digest food. A mucus layer coats the stomach and protects it from the acid. Prostaglandins, hormone-like substances involved in muscle contraction and the inflammatory response, also aid in protecting the lining. When these defences are not performing their job properly, acid and pepsin eat away at the lining, forming an open sore called an ulcer.

H. pylori decreases the stomach’s ability to produce mucus, making it more likely that acid will cause peptic ulcers. Although H. pylori infection is found in many people, it does not cause ulcers in all of them. However, of those who have peptic ulcers more than half have this infection.

Long-term use of non-steroidal anti-inflammatory agents (NSAIDs), such as aspirin, naproxen and ibuprofen can also cause peptic ulcers. Rarely, peptic ulcer is caused by the Zollinger-Ellison sydrome in which a tumour in the small intestine or pancreas produces large amounts of the hormone gastrin.

Smoking and heavy alcohol drinking can exacerbate peptic ulcers and slow healing.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Symptoms
The most common symptom is abdominal pain that is dull, comes and goes over a period of time, occurs regularly a few hours after eating or during the night, and is relieved by food and/or antacids. Weight loss, bloating and nausea may also occur.

Peptic ulcers are rarely fatal, but they can be very serious if they go through the stomach or duodenal wall (perforation), break into a blood vessel (haemorrhage) or block food leaving the stomach (obstruction).

Symptoms that require immediate medical attention are:

sharp, sudden, persistent stomach pain

bloody or black stools

vomit that is bloody or looks like coffee grounds




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
The laboratory diagnosis of H. pylori as the likely cause of a peptic ulcer can be made using a number of methods and specimen types. The UK National Institute for Clinical Excellence and Health (NICE) recommends the use of a carbon-13 urea breath test to detect the enzyme activity of H. pylori, a positive result indicating current infection. If the breath test is not available, a stool test to look for the H. pylori antigen should be used. Of least value is a blood test for antibodies to H. pylori because a positive result simply means that you have been infected with H. pylori at some time.

If x-rays of the upper gastrointestinal tract have shown the presence of an ulcer and a stool or breath test is negative, an invasive procedure called endoscopy may be used to detect H. pylori. A tiny camera on the end of a thin tube is fed through the mouth, down the oesophagus to the duodenum and tissue removed (a biopsy) to be examined in the lab for H. pylori antigen and under the microscope for the bacteria. Endoscopy and biopsy allow the diagnosis of other conditions that may be the cause of indigestion, including gastric cancer.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Pelvic inflammatory disease (PID) is an inflammation and infection of a woman’s upper reproductive organs. It occurs when bacteria move from the vagina, upward through a layer of mucus that protects the opening of the cervix, and into the uterus, fallopian tubes, and ovaries. PID can cause an acute illness, chronic pain, or it may be present as an almost silent long-term infection. Left untreated, it can cause scarring and irreversible damage to one or more of the reproductive organs. Scarring in the fallopian tubes can cause infertility and significantly increase the risk of an  ectopic  pregnancy.

Pelvic inflammatory disease is primarily associated with Chlamydia trachomatis and Neisseria gonorrhoeae, two common  microorganisms that cause the sexually transmitted diseases (STDs) chlamydia and gonorrhea. PID may also be caused by bacteria typically found in the vagina or gastrointestinal tract - such as Gardnerella vaginalis or Escherichia coli, and by a variety of other pathogens.

Although PID can affect any woman at any age, with or without sexual transmission, most cases occur in sexually active women of childbearing age. Those at increased risk include women who began having sex at a young age, those with multiple sexual partners, and those who have had a previous STD or PID. A woman with an intrauterine device (IUD) may be at an increased risk for a few months after its insertion. Douching may increase the risk of PID because the practice can change the vaginal normal  flora and can potentially flush bacteria into the uterus. Since the uterus is sealed off during gestation, an occurrence of PID during pregnancy is rare.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
A woman with PID may have no symptoms, mild discomfort, chronic and/or progressive pain, or she may be severely and acutely ill. Many of the signs and  symptoms of PID are nonspecific and may be seen with a variety of other conditions that affect the pelvic area. Symptoms may include:

vaginal or cervical discharge with an unpleasant smell

pain in the lower abdomen – this is the most common symptom

abdominal tenderness

intermittent fever 

painful sexual intercourse and bleeding with sex

painful urination

irregular menstrual bleeding

nausea 

Complications of PID include infertility, long-term pelvic pain, lesions on an ovary or fallopian tube, and an ectopic  pregnancy. Even a small amount of scarring in the fallopian tubes can impair fertility. It can prevent an egg from becoming fertilized or prevent a fertilized egg from reaching the uterus. If a fertilized egg begins to develop in a fallopian tube, it can rupture the tube, causing a life-threatening emergency with internal bleeding and severe pain.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
The aim of testing is to diagnose pelvic inflammatory disease, to discover the microorganism(s) causing it, if possible, and to distinguish PID from other conditions with similar symptoms. There is not one single laboratory test that can definitely diagnose PID. Most cases are diagnosed based on clinical findings. Some are diagnosed when a person is screened for STDs as part of a physical examination. PID may go unrecognized and undiagnosed as frequently as two-thirds of the time because the symptoms are nonspecific. There are several tests that may be performed to help diagnose the condition.

Laboratory Tests
 Some tests that may be requested to determine the cause of PID or rule out other causes of pelvic pain include:

Chlamydia trachomatis test – to detect chlamydia infection as cause of PID

Neisseria gonorrhoeae test – to detect gonorrhea infection as cause of PID 

 Wet prep – a sample of vaginal/cervical discharge is placed on a slide and examined under a microscope. It is primarily performed to count the number of white blood cells (WBCs) in the discharge; often elevated with PID

Cervical culture – requested to help identify causative microorganisms

Urine culture – performed to detect a urinary tract infection 

Tests that are not specific for PID but may be used to detect and evaluate the inflammation and immune response associated with it include:

FBC (Full Blood Count) – performed to evaluate white and red blood cell counts

ESR (Erythrocyte Sedimentation Rate) – nonspecific indicator of inflammation

CRP (C-Reactive Protein) – nonspecific indicator of inflammation

A pregnancy test may be performed to determine whether a woman is pregnant and to help identify ectopic  pregnancy.

Non-Laboratory Tests

Physical examination – an evaluation of the cervix, discharge, and degree of pain or tenderness present. Cervical motion pain and uterine pain are characteristic of PID. A diagnosis may be made based upon clinical findings.

Pelvic or transvaginal ultrasound – may be performed to examine reproductive organs

Laparoscopy – minimally invasive surgery sometimes used to confirm the diagnosis, collect biopsy samples, and evaluate organ status

CT (computed tomography) scan or MRI (magnetic resonance imaging) scan

Power Doppler ultrasound – scan that allows evaluation of blood flow and inflammation 




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What are they?
The pituitary is a pea-sized gland that is attached to an area at the base of the brain called the hypothalamus. The pituitary gland is part of the endocrine system; a system of glands that produce and regulate hormones, affecting processes throughout the body. The hypothalamus communicates with the rest of the brain and nervous system. It senses the body’s need for more or less of a particular hormone and controls the amount of hormone released from the pituitary.

Pituitary disorders are characterised by an excess or a deficiency in one or more of the hormones produced by the pituitary gland. When the disorder is caused by a pituitary tumour, symptoms such as headache and loss of vision may be present due to compression of the surrounding tissues.

The pituitary consists of a front (anterior) and back (posterior) portion. In the anterior pituitary, growth hormone (GH), adrenocorticotrophic hormone (ACTH), thyroid-stimulating hormone (TSH), luteinising hormone (LH), follicle-stimulating hormone (FSH) and prolactin are produced. They affect particular “target” tissues throughout the body, including the thyroid gland, adrenal glands, ovaries (women), and testes (men). In the posterior pituitary, oxytocin and antidiuretic hormone (ADH), produced in the hypothalamus, are stored for release. Some of the normal functions of these hormones are described below.

Prolactin: stimulates breast milk production after childbirth. 

LH and FSH: required for the development of sexual characteristics at puberty; fertility. 

GH: regulates bone growth and muscle mass 

ACTH: regulates the body’s response to stress via stimulation of the production of cortisol by the aderenal glands. 

TSH: stimulates the thyroid gland to produce thyroid hormones, which regulate the rate at which the body uses energy (the metabolic rate) 

ADH: controls the amount of water that the kidneys excrete, which in turn helps regulate the balance of water in the body. 

Oxytocin: stimulates the contraction of the uterus during and after childbirth and is responsible for stimulating the release of milk during breastfeeding.


 



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
What can go wrong?
The most common problem with the pituitary is the development of a tumour. While most are benign, they can produce excessive amounts of a specific pituitary hormone and /or block the production of other pituitary hormones. The tumour can also compress surrounding tissues. Blood vessels and the optic nerves are in close proximity to the pituitary gland. Pressure from a tumour on the optic nerve and the base of the brain can cause headaches, visual disturbances, loss of vision, fatigue, weakness, and seizures, as well as signs and symptoms related to reduced or increased hormone production.

Other causes of pituitary disorders include i) surgical or radiation treatment of a previous pituitary disorder ii) physical accident (trauma) or an impaired blood supply, iii) an autoimmune process iv) inherited genetic mutations, iv) congenital disorders (present from birth), v) malignant tumour (rare), or vi) due to causes that are not yet well understood. The hormone deficiencies and excesses from these disorders can produce a variety of symptoms depending on which hormones and target tissues are affected.

Pituitary hormone production is often affected when the hypothalamus is not functioning properly. Excess or deficient hormone production by the pituitary may also occur if the glands “downstream” from it are not functioning properly. For example, normally the hypothalamus detects low levels of thyroid hormone in the blood and stimulates the pituitary to produce TSH. TSH in turn stimulates thyroid hormone production by the thyroid gland. If the thyroid gland cannot produce adequate amounts of thyroid hormone, then blood thyroid hormone levels will remain below normal even though the hypothalamus and pituitary are promoting production by increasing the amount of TSH in the blood. This results in very high levels of TSH and abnormally low levels of thyroid hormone.

Examples of Common Pituitary Disorders

Pituitary Tumours: may be hormone-secreting or non-secreting; most are benign; may cause visual disturbances and headaches as they grow and compress surrounding tissues; often results in excessive amounts of one pituitary hormone and decreases in others.

Growth Hormone Deficiency: from a variety of causes; in children it causes delayed growth and short stature; in adults it can lead to muscular weakness, fatigue, decreased bone mass, and obesity.

Hypopituitarism: from a variety of causes including tumours, trauma, decreased pituitary blood supply, infection, sarcoidosis, an autoimmune process, radiation, surgical removal of the pituitary, or a side effect of pituitary surgery; results in a general decrease in pituitary hormone production.

Hyperprolactinaemia: a pituitary tumour that secretes prolactin or a tumour that prevents the regulation of prolactin production; in women can cause galactorrhoea (milk secretion from the breasts) and amenorrhoea (loss of menstrual cycles), and in men decreased sex drive and impotence.

Empty Sella Syndrome: the sella is the structure that surrounds the pituitary gland; it may increase in size and put pressure on the pituitary; rarely, the pituitary gland shrinks in response and hormone production decreases, leading to hypopituitarism.

Craniopharyngioma: a type of brain tumour that develops close to the pituitary gland; most commonly occurs in children and adolescents but can also occur in adults over 50 years old; benign but may put pressure on the pituitary, causing hypopituitarism, headaches, visual disturbances, and delayed growth. 


Examples of Rare Pituitary Disorders

Acromegaly and Gigantism: excess growth hormone production, usually due to a tumour; when it occurs in childhood, it causes gigantism associated with excessive bone growth and abnormally tall stature; in adults, it causes acromegaly, with increases in bone thickness, coarsened facial features, enlarged hands and feet, carpal tunnel syndrome (aching, numbness and tingling in hand), headaches, sweating, sleep apnoea (breathing problems at night associated with snoring), fatigue, and hypertension.

Cushing’s Disease: caused by a pituitary tumour that produces excess ACTH and leads to excess exposure by the body to the adrenal gland hormone cortisol; symptoms vary but include: upper body obesity, a rounded face, thin skin, pink streaks on the abdomen, muscular weakness, osteoporosis, high blood sugar, and high blood pressure.

Diabetes Insipidus: decreased production of ADH by the hypothalamus; patient’s kidneys don’t conserve water and concentrate urine; patient is thirsty and has frequent, dilute urination.

Nelson’s Syndrome: may result when both adrenal glands are removed as part of the treatment for Cushing’s Disease; a pituitary tumour develops that produces ACTH and can cause darkening of the skin due to increased production of melanocyte stimulating hormone (MSH).

Multiple Endocrine Neoplasia Type 1 (MEN1): an inherited genetic mutation that increases the risk of developing tumours in the pituitary and in other endocrine glands.

Kallman’s Syndrome: deficient release of GnRH (gonadotropin-releasing hormone) from the hypothalamus leads to lack of FSH and LH production; causes delayed or absent puberty; associated with no sense of smell; occurs only in males.

Pituitary Infarction: restricted blood supply to the pituitary gland; may cause gland tissue damage and lead to hypopituitarism.

Sheehan’s Syndrome: This is a very rare condition caused by pituitary infarction following severe blood loss during childbirth.




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
The goals of pituitary disorder testing are to detect excess or deficient hormone production, determine the cause, and evaluate the severity of the condition. Testing frequently includes measurements of both the hormones that the pituitary produces, such as TSH, and the hormones of other endocrine glands that the pituitary is responsible for stimulating, such as the thyroid hormone thyroxine.

Pituitary hormones are released as needed. Concentrations of some hormones (such as TSH) are relatively constant in the blood, whilst others vary over the course of a day, (GH), or over a cycle (such as FSH and LH, during the menstrual cycle). The concentration of a hormone may also be dependent on specific situations. For example, prolactin is raised in women that are breast feeding. Sometimes, because of these variations, the result from a single blood test does not give enough information. Tests which involve the patient taking medication to either suppress or stimulate hormone production can be used to detect hormonal excess or deficiency respectively. Related tests may also be used as a marker of the hormone under investigation. For example, measurement of IGF-1 (insulin-like growth factor-1) reflects total growth hormone production.

Laboratory Tests

Prolactin

LH and FSH

TSH and Thyroxine

ACTH, Cortisol

Urine and serum osmolality (for investigation of Diabetes Insipidus)

GH and IGF-1


Non-Laboratory Tests

MRI (magnetic resonance imaging)

CT (computed tomography)


Once a diagnosis has been made testing of pituitary function may be requested at regular intervals to monitor the effectiveness of the treatment given. Such tests are necessary as treatments may not completely resolve the condition. Furthermore, treatment may cause additional pituitary dysfunction either immediately (following surgery) or in the future (following radiation). Long term monitoring may also be necessary if a person has an inherited condition that presents a lifetime risk of developing a pituitary disorder.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Also known as: Lower Respiratory Tract Infection; Community-Acquired Pneumonia; Hospital-Acquired Pneumonia; Healthcare-Associated Pneumonia; Walking pneumonia; Double pneumonia; Lobar pneumonia; Atypical Pneumonia


                                                
                                            

What is it?
Pneumonia is an infection of the lungs, an invasion of lower respiratory tract by microrganisms that can cause a disease that ranges from mild to life-threatening. Worldwide, pneumonia kills more people than any other infectious disease, more than 4 million people a year, half of them under 5 years old.

Although anyone can get pneumonia, it is most common and potentially severe in those who are very young, over 65, immune compromised, or who have an another disease or condition that affects their lungs. This group of conditions includes people who have HIV/AIDS or have had an organ transplant and those who are on chemotherapy for cancer, are pregnant, in intensive care (ICU), on mechanical ventilation, have scarred or damaged lungs as occurs from smoking, or who have a lung disease such as cystic fibrosis.

Pneumonia can occur at any time, but the greatest numbers of cases are seen in the late autumn through to early spring. Infection of the lungs can occur in five different ways:

Microorganisms can move downwards from the breathing airways into the lungs

Airborne droplets from a sneeze or cough can be inhaled

Surfaces contaminated with mucus or other respiratory secretions when touched by hands can spread through the mouth or eyes

Microorganisms in a person`s own mouth or stomach can enter the lungs

An infection may spread from another site in the body, through the blood and into the lungs


It takes more than exposure to a potential disease-causing microorganism (pathogen) to get pneumonia. Microorganisms are always present in the environment, and we are exposed to infection daily. In most cases, the lungs can take care of these infections. The body has layers of defences that include mechanical barriers, protective microorganisms (normal flora), and the immune system. Pneumonia occurs when these defences are weakened or damaged and/or when the invading microorganisms are strong enough to overcome them.

A wide range of viruses, bacteria, and (less commonly) fungi or parasites can cause pneumonia, but the majority of cases are due to just a few of these. The most likely microorganism to cause pneumonia will depend upon the age and health of the person and on the time of the year. Those with poor immune systems and those who have been traveling abroard may develop pneumonia that is due to more unusual microorganisms.

Pneumonia may be grouped by the medical community into different categories. These distinctions are most useful in finding a cause of the pneumonia, how best to prevent its spread, and in guiding treatment.

Community-acquired pneumonia—when a person becomes infected during normal daily activities

Hospital-acquired pneumonia—when an infection occurs, for example, after surgery while connected to a ventilator or in an intensive care unit

Healthcare-associated pneumonia—when a person is infected from a healthcare establishment such as a nursing home or dialysis clinic


Hospital-acquired and healthcare-associated microorganisms are more likely to be resistant to first-line antibiotics where as community-acquired pneumonia is more likely to be due to bacteria that are susceptible to commonly prescribed antibiotics or due to seasonal viruses for which antimicrobial agents are not the appropriate treatment.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
Pneumonia symptoms vary, depending on the age and health status of the person affected and on the microorganism causing the infection. Very young infants may grunt and wheeze, breathe rapidly, and be irritable and/or lethargic. The elderly may experience confusion. Bacterial pneumonia may emerge following a viral infection and may just be seen as a lingering or worsening cold or bout of the flu. Common pneumonia symptoms include:

Cough

Fever and chills

Tiredness

Shortness of breath

Headache

Muscle aches

Chest pain

Nausea and vomiting


Complications
Complications that can occur with pneumonia include the build-up of fluid in the lungs, the scarring of lung tissue (which can lead to recurrent infections), respiratory failure, sepsis, and rarely lung abscesses (pockets of pus in lung tissue).



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Types
Pneumonia can be due to a variety of bacteria and viruses, less commonly due to fungi, and rarely due to other microorganisms or parasites. Likely causes are associated with the age of the person, the season, the person`s health status, and/or where the infection was contracted. Some of the more common examples of microorganisms that cause pneumonia are listed in the table below:

Type
Comments
Some Causative Organisms
Viral
Viruses cause about one-third of all cases of pneumonia.
 They are the most common cause of pneumonia in infants, accounting for approximately 90% of all lower respiratory infections.
 Less than 20% of pneumonias in adults younger than 60 years old are viral.
 In those over 60-65 years of age, viral causes become increasingly common.
Viral pneumonia is often mild, requiring only supportive care. However, more serious cases may require admission to hospital. Sometimes bacterial pneumonia may develop following viral pneumonia.
The most common causes of viral pneumonia are influenza parainfluenza, and respiratory syncytial virus (RSV).
 Other less common causes include adenoviruses, human metapneumovirus, and cytomegalovirus (CMV).
RSV is the most common cause in children younger than 1 year old.
Bacterial
Bacteria are the most common cause of pneumonia in adults. There are many different types of bacteria that can cause pneumonia, some more common than others. Sometimes people, particularly those who are elderly or who have other health problems, will develop bacterial pneumonia after having an upper respiratory infection or the flu.
 Bacterial pneumonias in young children are uncommon.
  
 Atypical pneumonias are bacterial lung infections that do not respond to commonly prescribed antibiotics.
Some bacterial pneumonias are relatively rare but may be seen in certain populations or in certain geographic areas. Travellers and people who have moved into the UK may be infected with bacteria that are less common in this country. Those with pre-existing conditions such as decreased lung function or weakened immune systems may be more likely to become infected from types of bacteria not found in the general population.
Most commonly due to Community-acquired Streptococcus pneumoniae. Some other less common causes:
 Group B Streptococcus, Moraxella catarrhalis, Staphylococcus aureus, Haemophilus influenzae type B, Listeria monocytogenes, Escherichia coli, Klebsiella pneumoniae

Atypical pneumonias: 
Mycoplasma pneumoniae
 Chlamydophila pneumoniae
 Legionella (Legionnaire`s disease)
Mycobacterium tuberculosis and nontuberculous Mycobacteria (M. avium-intracellulare, M. kansasii) may be seen, for example, in travellers, prison populations, and those with HIV/AIDS.
Pseudomonas aeruginosa can affect those with decreased lung function due to Cystic Fibrosis (CF).
Fungal
Pneumonias caused by fungi are relatively rare.
 There are some types of fungi that usually cause pneumonia only in people who have weakened immune systems. These people include, for example, organ transplant recipients who are on immunosuppressant drugs, those on chemotherapy, and those with HIV/AIDS. These fungi are referred to as ``opportunistic.``
  
Some types of fungi are pathogenic. This means that they can cause pneumonia in people regardless of their health status. These types are usually found only in certain areas of the US and/or the world.
Some opportunistic fungi include: Pneumocystis jiroveci, Aspergillus species, Candida species, and Cryptococcus neoformans. P. jiroveci is the most common opportunistic infection in the UK in those with HIV/AIDS. It was previously known as P. carnii; thus pneumonia caused by this organism may still sometimes be called Pneumocystis carnii pneumonia or PCP.
 Pathogenic fungi include:
Histoplasma capsulatum
Coccidioides immitis
Blastomyces dermatididis
``Walking pneumonia`` refers to a mild form of the disease that typically does not require bed rest. It is often caused by a virus or M. pneumoniae. Lobar pneumonia describes a form of the disease that affects one lung, while double pneumonia is an infection that affects both lungs.

Pneumonia due to the aspiration of oral or gastric secretions may be due to more than one microorganism and may include anaerobic bacteria. Some more exotic and rare causes of pneumonia may infect otherwise healthy individuals and can be fatal. Some of these include:

The systemic fungus Histoplasma capsulatum (histomplasmosis) — contracted from infected soil in caves

The hantavirus — contracted from infected rodent droppings

The fungus Coccidiodes immitis (coccidioidomycosis)

The bacteria Bacillus anthracis (anthrax) — due to a natural or bioterrorism exposure

The bacteria Yersinia pestis (pneumonic plague)




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
The porphyrias are a group of uncommon diseases that cause either disease affecting the skin, disease affecting the nervous system, or both.

Porphyria results from accumulation of porphyrins either in the skin, which results in sensitivity to sunlight, or in the liver, which results in acute attacks of porphyria. Normally, porphyrins are converted from one type of porphyrin to another, in a sequence of chemical reactions, each one under the control of a specific enzyme. The end product of this sequence is haem, an essential component of haemoglobin, which is responsible for transporting oxygen around our body. If one of these enzymes is deficient or defective, there is a build up of porphyrins which may accumulate to toxic levels. In all, there are seven types of porphyria of which four are acute porphyrias, the others affect the skin predominantly.

Porphyria cutanea tarda
The most common type of porphyria is called porphyria cutanea tarda or PCT. PCT does not usually occur until middle age and affects the skin in sun-affected areas causing fluid-filled blisters. Over time the skin becomes scarred, brown and blotchy and fragile. Sometimes excess hair grows in the affected areas. Unlike the other porphyrias, PCT is rarely inherited and is usually triggered by some other factor or condition. Even in cases where it appears to be inherited from a parent, another factor is usually required before it causes symptoms. The most common factor is excessive alcohol consumption but the presence of other diseases such as haemochromatosis, hepatitis C and HIV infection or some drugs, eg oestrogens may precipitate PCT symptoms.

Acute intermittent porphyria
The

Sym:
Tests
Measurement of porphyrins and porphyrin precursors in blood, urine and faeces are the main tests for assessing patients with symptoms that may be caused by porphyria. Measurement of enzyme activities in cells and DNA testing for mutations are most useful for assessing people who may be affected but do not currently have symptoms and close relatives of affected persons.

Measurement of porphobilinogen or PBG in urine is the most important test for diagnosing an acute neurological porphyria.

Measurement of porphyrins in urine, faeces, red blood cells and blood plasma are used to differentiate the various types of porphyrias that may have the same symptoms.

Measurement of enzyme activity in red blood cells may be used to identify relatives of persons with AIP who also are potentially affected.

Identification of individual porphyrias by specialist biochemical and/or genetic testing is available through Porphyria Specialist Laboratories (see the European Porphyria Network (EPNET) link at the end of this article).




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Prevention and treatment
Once a person is known to have a particular porphyria, or a relative who carries the same gene but has not yet been affected is identified, there are precautions that can be taken to prevent recurrence or a first attack. For the acute neurological porphyrias i.e. AIP (acute intermittent porphyria), VP (variegate porphyria) and HCP (hereditary coproporphyria) the most important precaution is avoiding using drugs that are known to precipitate attacks. Lists of known and suspected drugs are available (see the links at the end of this article). If attacks occur regularly related to the menstrual cycle then hormone manipulation to change the menstrual cycle may prevent attacks. Strict dieting is not recommended in people with one of the acute porphyrias and, in females, avoidance of the contraceptive pill is advised.

Treatment of acute neurological porphyrias involves identifying and removing any precipitating factors, giving an intravenous infusion of a haem derivative such as haematin or haem arginate and supplying enough nutrition, particularly glucose, by intravenous infusion if necessary. Intensive medical care may be required in severe cases. The National Acute Porphyria Service (NAPS) was commissioned by NHS England in 2012 to provide acute care support and clinical advice to patients with one of the acute porphyrias (AIP, VP or HCP).

People with PCT (porphyria cutanea tarda) need to avoid alcohol consumption. Sun protection with clothing and complete sunblock lotions is also very important. Occasionally, venesection, or removal of blood, may be used. Removal of blood removes iron from the body as excess iron exacerbates PCT. People who cannot tolerate venesection may be treated with chloroquine to help remove excess porphyrins.

Children and adults with EPP (erythropoietic protoporphyria) benefit from sun protection using thick clothing. Conventional sunscreens have limited effectiveness. Treatment with beta-carotene reduces sun sensitivity and skin symptoms.

People with VP and HCP need to take the same precautions as people with AIP to avoid neurological symptoms. They also need sun protection with clothing and complete sunblock lotions if they suffer from sun sensitivity.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Description
Prostate cancer is a relatively common type of cancer affecting the small walnut-shaped prostate gland located near the base of the bladder and found only in men. The gland surrounds the upper part of the urethra, the tube that leads from the bladder to the penis. In more advanced stages of the disease the tumour may spread and eventually be carried (metastasise) to other areas of the body.

Prostate cancer is the commonest cause of cancer in men in the UK, accounting for a quarter of all new cases of cancer in males. In the UK there are about 40,000 new cases of prostate cancer each year. It is rare in men under 45 and quite common in men over 80. However, in older men the cancer is often small, restricted to the prostate and without symptom.

Often, the first symptom of prostate cancer is difficulty in urination, as the growing tumour constricts the urethra. Frequent urination (especially at night); a weak or interrupted urine stream; pain or burning upon urination or ejaculation; pus or blood in urine or semen; and discomfort in the lower back, pelvis, or upper thighs, are also symptoms of the disease. Other conditions, such as urinary-tract infections, benign enlargement of the prostate (benign prostatic hypertrophy or BPH), a serious infection of the prostate gland (acute prostatitis)and sexually transmitted diseases can also cause some of these symptoms.

Doctors must determine whether a man`s symptoms are due to prostate cancer, BPH, or to another non-cancer-related condition. They must also determine whether the prostate cancer they have detected is clinically significant. If a prostate cancer is small, localised, and slow-growing, it may never cause significant health problems to the individual. In these cases, the treatments may sometimes be worse than the cancer as they can cause side effects such as erectile dysfunction and incontinence.

Some prostate cancers, however, do grow and spread aggressively into the pelvic region and then throughout the body; and some slow-growing cancers are eventually large enough and troublesome enough that they require intervention. The challenge for the doctor is detecting prostate cancer, evaluating its growth rate and spread, and then deciding, along with the affected person, which treatment courses to follow and when.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests to Diagnose and Monitor the Condition
The tests most commonly used tests to investigate men with symptoms suggestive of prostate cancer are rectal examination and the Prostate-Specific Antigen (PSA) blood test. To perform a rectal examination, the doctor inserts a gloved, lubricated finger into the rectum (back passage) and feels the prostate gland with his or her finger for localised hardness or nodules. For the PSA test, blood is taken and sent to a clinical laboratory. There the blood is examined for an increased level of the blood marker which is associated with prostate inflammation or cancer.

Whilst the PSA level is raised in up to eighty percent of prostate cancers, an abnormal result does not necessarily mean a diagnosis of cancer. In fact, two-thirds of men with a raised serum PSA level do not have prostate cancer, although other abnormalities requiring treatment may be the cause of a raised PSA results. Rectal examination and PSA measurement can also assist in the early detection of benign prostatic hypertrophy (BPH). The current UK NHS policy about the use of PSA to screen men without symptoms for prostate cancer is explained under Screening/Adults 50+.

Should you have symptoms of prostate disease, be sure to let your GP know. If your PSA and/or rectal examination have normal results, your doctor can recommend when re-testing is appropriate. If your results are abnormal, your doctor may recommend further tests, such as a transrectal ultrasound-guided biopsy. This procedure allows a doctor to take a sample from the prostate for further study. It may be necessary to stop taking certain medicines up to ten days before the test. Ultrasound examination helps the doctor to assess the size of the prostate gland.  A few weeks after the time of the biopsy you may also be asked to have an examination of your urinary flow rate and assessment of how much urine is retained in the bladder after urination. If your PSA level is only mildly elevated then your doctor may recommend re-testing after a certain period of time e.g. six months to a year.

Once a diagnosis of prostate cancer is made, doctors may use a variety of tests to monitor the cancer, determine treatment options, and evaluate the effectiveness of a chosen course of treatment. In addition to using rectal examination and PSA for this purpose, tests using X-ray, ultrasound, magnetic resonance imaging (MRI) and tissue sampling may be used.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatments
Treatments for prostate cancer differ and are influenced by how much the tumour has spread outside the prostate (the ``stage`` of the cancer) and by how aggressive or fast growing the tumour is found to be in a tissue sample (the ``grade`` of the tumour). A doctor may use one or more of the tests discussed earlier to find out the stage of the tumour.

The decision to pursue one or a combination of treatments depends not only on the stage and grade of the tumour, but also on other factors such as the age of the patient and the patient`s individual preferences.

Prostate cancer is typically treated using one or more of the following methods: ``watchful waiting``, surgery, radiation therapy and hormone treatment. Chemotherapy is rarely used for prostate cancer, but may be used in advanced cases that are unresponsive to hormone therapy.

Watchful waiting, surgery, and radiation are most often used when the tumour is contained and has not spread to other areas. As many prostate tumours grow slowly, a programme of watchful waiting may result in an unaffected life span that is largely symptom-free and uncompromised by side effects. This programme will be likely to include regular PSA testing and rectal examination.

Surgery can remove the entire tumour in early cases, and may be used to ease urination in more advanced cases. Cryosurgery, a relatively new surgical option, freezes and kills the affected tissue with liquid nitrogen. Radiation may be delivered as targeted rays from outside the body, or by inserting tiny radioactive seeds in the prostate, or by injection. Radiation can also be coupled with hormone treatment to provide pain relief in patients with prostate cancer that has spread to the bones.

Hormone therapy is most commonly used to treat prostate cancer that has metastasized to other areas of the body. While it is not a cure at this stage, the treatment can shrink tumours, relieve symptoms and extend the life of the patient. Hormone therapy is also used to treat less advanced stages of prostate cancer - either in conjunction with radiation therapy or to shrink a tumour prior to surgery. Men with decreased testosterone levels due to hormone treatment for prostate cancer are at an increased risk for developing osteoporosis. Your doctor can tell you whether you should have tests for a loss in bone density, or whether measures or treatments to prevent osteoporosis should be considered.

The side effects of different prostate cancer treatments can range from none to tiredness, hair loss, incontinence and the inability to have an erection. Your doctor can make treatment recommendations based upon your test results and particular circumstances.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Proteinuria is a condition characterised by the presence of greater than normal amounts of protein in the urine. It is associated with a variety of different diseases and is sometimes seen in those who are apparently healthy. Mild or transient proteinuria may become more severe over time.

Plasma, the liquid portion of blood, contains many different proteins. One of the many functions of the kidneys is to retain plasma protein so that it is not excreted along with waste products when urine is produced. There are two mechanisms that normally prevent protein from passing into urine: (1) the glomeruli in the kidney provide a barrier that keeps most larger plasma proteins inside the blood vessels but allows water and small proteins to be filtered out and (2) the small proteins that do get through are almost entirely reabsorbed by the tubule. For additional details on kidneys and how they function, see the page on How Kidneys Work on the Davita website.

Proteinuria most often occurs when either the glomeruli or tubules in the kidney are damaged. Inflammation and/or scarring of the glomeruli can allow increasing amounts of protein and sometimes red blood cells (RBCs) to leak into the urine. Damage to the tubules can prevent protein from being reabsorbed, meaning proteinuria may also develop when the tubules cannot reabsorb all of a small protein which has been filtered from the blood. 

A variety of diseases and conditions can cause kidney damage which can result in proteinuria. Two of the most common causes are:

diabetes

hypertension

Others causes include:

immune disorders (e.g. systemic lupus erythematosus (SLE), IgA nephropathy, Goodpasture’s syndrome)

infections

exposure to toxins

trauma

kidney cancer

pre-eclampsia

multiple myeloma

Pregnant women are frequently screened for proteinuria because its development is associated with preeclampsia (also know as toxaemia), a hypertensive disorder that can cause oedema, nausea, and headaches during pregnancy. Preeclampsia can be dangerous for both the mother and her baby.

Proteinuria due to the presence of excess small proteins in blood may be seen in multiple myeloma (free immunoglobulin light chains) and in conditions that damage red blood cells in the circulation and release of haemoglobin which appears with its red colour in the urine.

Healthy people can have short term or long term proteinuria. It is associated with stress, exercise, fever, aspirin therapy, and exposure to cold. Some people excrete more protein into the urine when they are standing up than when they are lying down (orthostatic proteinuria).

 Signs and symptoms
 Frequently, no symptoms are seen with proteinuria, especially in mild cases. Large amounts of protein may cause the urine to appear foamy. Loss of large amounts of protein from the blood can affect the body’s ability to regulate fluids, which can lead to swelling in the hands, feet, abdomen and face. When symptoms are present, they are usually associated with the condition or disease causing proteinuria.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests
The reasons for looking for protein in the urine include screening those at risk, looking for a cause for proteinuria, evaluating the type and quantity of protein being released, and assessing kidney function. When proteinuria is detected, patients are monitored at intervals to see if it gets better or becomes worse. Both urine and blood tests may be requested to evaluate proteinuria.

 Laboratory Tests

Several tests may be requested on either  24-hour or random urine samples:

Urinalysis– evaluation of a urine sample by visual inspection, chemical testing with a simple dip stick and, in some cases, microscopic examination.

Microalbumin, 24-hour urine – a more sensitive test for proteinuria that is used to detect and monitor kidney function in diabetic patients.

Urine protein, 24-hour urine – measures the amount of protein passed in the urine over a 24-hour period; this is a more accurate assessment of the degree of proteinuria than a random urine measurement.

Microalbumin/creatinine ratio (ACR), random urine - measures albumin in a random sample and corrects for the volume of urine passed by measuring the amount of creatinine in urine (a substance released by the body at a steady rate); this is more convenient than having to collect a 24-hour sample.

Urine protein/creatinine ratio (UPCR), random urine - measures protein in a random sample and corrects for the volume of urine passed by measuring the amount of creatinine in urine;  this is more convenient than having to collect a 24-hour sample.

The following tests may also be requested and are measured primarily on blood alone:

eGFR (estimated Glomerular Filtration Rate) - uses a blood creatinine level to calculate the estimated rate of urine filtration; rate decreases with progressive kidney damage.

Creatinine - a blood test used to evaluate kidney function; less frequently, it may be done on urine. (Note: Although creatinine may be measured in urine samples, it is usually measured to be included as part of a ratio or calculation.)

Total Protein - a blood test that measures all of the protein in the serum.

Albumin - a blood test that measures the concentration of albumin in blood.

A kidney biopsy may also be requested. This is a procedure that is sometimes done to look at a small sample of kidney tissue under the microscope to look for evidence of kidney disease or damage.

Non-Laboratory Tests

Imaging scans of the kidney to detect the presence and determine the severity of kidney disease or damage.

Blood pressure; may be measured as part of investigation of cause of proteinuria; frequently monitored in those who have hypertension or are at risk of developing it.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatments
The goals of treatment are to control the underlying conditions causing proteinuria and to minimise its progression. Treatment for each condition is likely to be different. For example, controlling blood sugar levels in patients with diabetes will help to preserve kidney function. In patients with hypertension, it is important to control blood pressure to prevent progressive kidney damage.  Pre-eclampsia-related proteinuria usually resolves once the baby is born.

In some patients with persistent proteinuria, the doctor may recommend dietary changes such as altering the amount of protein consumed. No treatment may be necessary for mild or transient proteinuria.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Reactive arthritis, which is sometimes known as Reiter’s syndrome or disease, can involve a combination of three symptoms:

Arthritis – pain, redness and swelling affecting a small number of joints. Most often large joints such as the knee.

Uveitis or conjunctivitis – Inflammation of the coating of the eye (conjunctiva) or the front chamber of the eye. Conjunctivitis causes redness and itching. Uveitis is more serious and causes pain and blurring as well as redness.

Urethritis – Inflammation of the tube which connects the bladder to the outside of the body (urethra). This causes discharge which will be seen at the tip of the penis or in the vagina. It also causes pain on passing urine.


Reactive arthritis is so called because it normally occurs as a reaction a few weeks after an infection. The exact mechanism is unclear but scientists believe that either the body reacts against itself (autoimmune) or fragments of the infection get into the joint to cause inflammation.

The most common infection that triggers reactive arthritis is chlamydia. It can also occur after other sexually transmitted diseases or after gastroenteritis (food poisoning).

Most people with reactive arthritis have a gene which makes them susceptible. This is called HLA-B27.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests
Doctors diagnose reactive arthritis based on the patients’ story and on examination. There are a few tests which may be carried out to rule out other diseases:

X-ray or other imaging such as MRI – To examine the joint for any damage or inflammation

FBC – to look for excess white cells which may suggest infection

ESR – may rise with inflammation

CRP – may rise with inflammation

Rheumatoid Factor– to help rule out other diseases such as rheumatoid arthritis

Autoantibodies – may help rule outsystemic lupus erythematosus

HLA-B27- may show that the patient is at risk

Synovial Fluid analysis– examination of joint fluid can show alternative diseases such as infection or crystals within the joint


Doctors may also look for the infection which triggered the reaction:

Throat swab and culture

Genital swab and culture

Urine culture

Stool culture

HIV test




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatments
Treatment of the initial infection with antibiotics may be necessary particularly with sexually transmitted infections.  Painkillers such as ibuprofen and paracetamol are widely used.

Inflamed joints can be injected with steroids or occasionally the fluid can be drained.If the disease is severe and lasts over a couple of months doctors may consider using immunosuppressant drugs.

Often rest is required initially to control the pain and physiotherapy is also used to maintain a full range of movement.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Rheumatoid arthritis (RA) is a long-term disease that usually affects your joints: hand and wrists most commonly, but also elbows, neck, shoulders, hips, knees, and feet. RA causes swelling, stiffness, pain, and loss of function in the joints. Other symptoms include fatigue, fever, and a sense of not feeling well (malaise). Many people with RA develop anaemia. RA also increases the risk of thinning of the bones, osteoporosis, particularly if you are taking corticosteroid drugs such as prednisone. The disease can affect other body organs as well, causing dry eyes and mouth - symptoms of Sjögren’s syndrome. 

Rheumatoid arthritis usually develops slowly between the ages of 20 and 45. More than 75% of patients are women. RA is different from osteoarthritis, in which joint tissue wears down from repetitive use or age. RA usually affects joints in a balanced (symmetrical) way—if one knee is affected, the other knee is also affected. The disease may be partly inherited through genes, but other factors are probably at work, including some kind of a trigger for the gene, perhaps bacteria or viruses. The disease is not contagious, however. Some scientists also think that changes in certain hormones may promote RA in people with particular genes who have been exposed to the triggering agent. 

What tests are used? 
Rheumatoid arthritis is diagnosed from your signs and symptoms. The diagnosis can be supported with a blood test for an antibody known as rheumatoid factor (RF). The RF test for the presence of the RF antibody in blood is positive in about 80% of people with RA. However, this test is also positive about 5% of people without the disease.  A simmilar test known as CCP has recently become available and can help doctors in difficult cases.

Other common tests to support a diagnosis of RA and to monitor treatment for it include:   

Erythrocyte sedimentation rate -  this test (ESR) shows the presence of inflammation in the body and the activity of the disease 

C-reactive protein test (CRP) - this test also indicates inflammation and tests for the activity of the disease 

Full blood count (FBC) - about 80% of people with RA develop anaemia 

X-ray and MRI might also be used to look at particular joints in more detail


What treatments exist? 
Several different types of medication are used to treat RA, including pain relievers, non-steroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs, immunosuppressants, and corticosteroids (also known as glucocorticoids). People with RA can also make beneficial lifestyle changes such as getting more exercise and eating moderate diets, resting, avoiding stress, and taking special care of joints with well-designed tools and other devices that are easy on joints. Surgery is occasionally used for some patients.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Tests:
What is it?
Rheumatoid arthritis (RA) is a long-term disease that usually affects your joints: hand and wrists most commonly, but also elbows, neck, shoulders, hips, knees, and feet. RA causes swelling, stiffness, pain, and loss of function in the joints. Other symptoms include fatigue, fever, and a sense of not feeling well (malaise). Many people with RA develop anaemia. RA also increases the risk of thinning of the bones, osteoporosis, particularly if you are taking corticosteroid drugs such as prednisone. The disease can affect other body organs as well, causing dry eyes and mouth - symptoms of Sjögren’s syndrome. 

Rheumatoid arthritis usually develops slowly between the ages of 20 and 45. More than 75% of patients are women. RA is different from osteoarthritis, in which joint tissue wears down from repetitive use or age. RA usually affects joints in a balanced (symmetrical) way—if one knee is affected, the other knee is also affected. The disease may be partly inherited through genes, but other factors are probably at work, including some kind of a trigger for the gene, perhaps bacteria or viruses. The disease is not contagious, however. Some scientists also think that changes in certain hormones may promote RA in people with particular genes who have been exposed to the triggering agent. 

What tests are used? 
Rheumatoid arthritis is diagnosed from your signs and symptoms. The diagnosis can be supported with a blood test for an antibody known as rheumatoid factor (RF). The RF test for the presence of the RF antibody in blood is positive in about 80% of people with RA. However, this test is also positive about 5% of people without the disease.  A simmilar test known as CCP has recently become available and can help doctors in difficult cases.

Other common tests to support a diagnosis of RA and to monitor treatment for it include:   

Erythrocyte sedimentation rate -  this test (ESR) shows the presence of inflammation in the body and the activity of the disease 

C-reactive protein test (CRP) - this test also indicates inflammation and tests for the activity of the disease 

Full blood count (FBC) - about 80% of people with RA develop anaemia 

X-ray and MRI might also be used to look at particular joints in more detail


What treatments exist? 
Several different types of medication are used to treat RA, including pain relievers, non-steroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs, immunosuppressants, and corticosteroids (also known as glucocorticoids). People with RA can also make beneficial lifestyle changes such as getting more exercise and eating moderate diets, resting, avoiding stress, and taking special care of joints with well-designed tools and other devices that are easy on joints. Surgery is occasionally used for some patients.



                                        
                                        
    
        
            
                

                

                
                    <a title=``


info:
What is sarcoidosis?
Sarcoidosis is a condition in which inflammatory cells produce nodules called granulomas in multiple organs. Granulomas can develop anywhere in the body, but they commonly affect the lungs, skin, lymph nodes, and eyes. Granulomas change the structure of the tissues around them and, in sufficient numbers they can cause damage, inflammation and symptoms and may interfere with normal functions.

The cause of sarcoidosis is not known. The condition is thought to be associated with both a genetic predisposition and the immune system`s reaction to an environmental trigger – such as exposure to a virus, bacteria, allergen, dust, or chemical. Anyone can develop sarcoidosis, but it most frequently occurs in women of African or Northern European descent who are 20 to 50 years of age. It effects about 19 people in every 1,000 in the UK.

Sarcoidosis varies in severity. A person may have the disease without knowing it as mild cases cause no, few, or nonspecific symptoms. It can cause acute illness, resolve on its own within a few years (remission), recur, or continue as a chronic condition. More than half of those affected will go into remission within 3 years of diagnosis, and two-thirds will be in remission within 10 years.

Most people with sarcoidosis will not experience long-term health effects, but about one-third will have some degree of organ damage. Sarcoidosis can cause blindness in rare cases and can sometimes be fatal, primarily in those with severe lung or heart involvement.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
The severity of sarcoidosis and the symptoms a person experiences depend upon the tissues and organs affected. A person may have no symptoms or may have nonspecific findings such as:

Fever

Fatigue

Weight loss

Night sweats

Loss of appetite

Swollen lymph nodes

Joint pain


Signs and symptoms associated with specific organs are listed below.

Lungs

The American Lung Association estimates that as many as 90% of those with sarcoidosis will have lung involvement. Lung tissues may stiffen and scar tissue may develop. Those affected may have:

Dry cough

Wheezing

Shortness of breath

Chest pain


Skin

Up to 25% of those with sarcoidosis have skin problems, including:

Sores on or near the cheeks, ears, nose, and eyelids

A raised, reddish, bumpy rash on the ankles or shins that may itch or be tender and warm

Discoloured skin

Inflammation and nodules around scars


Eyes

Blurred vision

Sensitivity to light

Eye pain and itching

Burning and redness

Tears

Inflammation


Heart

Abnormal heart rhythm

Congestive heart failure


Brain and Nervous System

Headaches

Weakness

Seizures

Decreased coordination and tremors


Muscle and Bone

Pain

Joint stiffness


Sarcoidosis can also cause kidney and liver dysfunction, an enlarged liver or spleen, and swollen salivary glands. It can alter the way the body processes calcium, leading to increased calcium in the blood and urine and the formation of kidney stones. In rare cases, it may cause kidney failure.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
The goals with testing are to diagnose sarcoidosis, evaluate its severity, and to monitor its course over time. Testing is also used to distinguish sarcoidosis from conditions with similar symptoms and from conditions that are also associated with the development of granulomas – such as tuberculosis and some fungal infections.

Laboratory Tests

Tissue biopsy is the primary test used to confirm a diagnosis of sarcoidosis; characteristic changes in the structure of the tissue can be seen under the microscope. Other laboratory tests are not specific for sarcoidosis, but they are helpful in assessing disease activity, looking for damage to individual organs, and ruling out other diseases that may cause similar problems Tests that may be requested include:

ACE (Angiotensin converting enzyme) - often elevated in patients with sarcoidosis but may be increased with other conditions; this test is used to help diagnose sarcoidosis, monitor disease activity, and monitor response to treatment.

Calcium - to detect increases in the blood or urine. Hypercalciuria (increased calcium in urine) occurs in about 50%, while hypercalcaemia (increase blood calcium) can be found in about 5% of patients with Sarcoidosis

ESR (Erythrocyte Sedimentation Rate) - sometimes requested to detect inflammation

Liver Function Tests and/or Renal Profile - a group of tests used to evaluate liver and/or kidney function, to determine if those organs are affected

FBC (Full Blood Count) - may be requested to evaluate red and white blood cell changes

CSF analysis - an evaluation of the cerebrospinal fluid when brain or nervous system involvement is suspected

AFB cultures, sputum cultures, and fungal tests - to help distinguish between sarcoidosis and other conditions associated with the lungs and with granuloma development


Non-Laboratory Tests

X-ray - one of the primary tests used to detect lung involvement; granulomas may be initially detected in people without symptoms who have an X-ray for another reason.

Lung function tests are performed to evaluate lung involvement, lung capacity, and condition severity. (For more on these, visit the Royal Brompton and Harefield NHS Foundation Trust website.)

CT (Computed Tomography), MRI (Magnetic Resonance Imaging), gallium scan, or other imaging scans are sometimes requested to help diagnose and evaluate sarcoidosis. ECG (electrocardiogram) - sometimes ordered when heart involvement is suspected.




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is sepsis?
Sepsis is the name given to a severe and damaging systemic inflammatory response caused by an infection. The infection may begin at one site of the body and then spread to the blood and possibly to other sites. While the terms bacteraemia and fungaemiarefer to the detectable presence of bacteria or fungi in the bloodstream, sepsis refers to the body`s overwhelming response to the infection, which leads to organ dysfunction. (For more on this, see the article on Blood Culture.) The term septicaemia was historically used to describe sepsis with evidence of bacteraemia, but is no longer considered to accurately describe the processes involved.

Sepsis is a serious condition that can progress from sepsis to severe sepsis and then to septic shock with the failure of one or more organs (multiorgan failure, MOF). Successful treatment requires intensive care unit (ICU) support. Although sepsis commonly occurs and is identified in hospitalised patients, it can also develop in non-hospitalised patients who may then present to the hospital accident and emergency (A&E) department. It is more prevalent in newborns and infants and in the elderly but can affect patients of any age. Patients at risk of sepsis include those with trauma, including after major surgery, the presence of invasive medical devices such as catheters, chronic illnesses, and immunocompromised patients.

Sepsis is a major health problem with severe associated morbidity and mortality rates in the range of 25-50%. Comparable figures have been reported for other parts of the world, including the United States and South America.

Normally a person`s immune system targets specific threats and limits the response to the area that is infected. With sepsis, a generalised inflammatory response is initiated by the body. This can cause a significant rise or fall in body temperature, increased heart and respiration rates, and a decrease in blood pressure. If not treated successfully, as noted above, sepsis can progress to severe sepsis and then to septic shock. As the condition progresses to severe sepsis, the amount of oxygen that is carried to tissues and organs decreases, blood clots can form in the capillaries, and fluids can leak from the blood into tissues. This last can cause fluid build-up in the lungs, thereby reducing respiratory function. Overall the body`s acid-base balance becomes disrupted, circulation is impaired, waste products begin to accumulate, tissues are damaged, and organs such as the lungs, kidneys, and liver begin to fail. With the last stage of sepsis, septic shock, there may be MOF and low blood pressure that is resistant to treatment.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
The symptoms that a person experiences depend upon the organs affected, the severity of the condition, and the person`s general health status. They may be nonspecific and, in the very young and elderly, may not be typical. Other medical conditions may cause similar symptoms. It is important to quickly distinguish between these conditions as they are treated differently.

Symptoms of sepsis may include:

Fever (increased body temperature) or coolness (decreased body temperature)

Chills

Rapid breathing

Rapid heart rate

Fatigue

Headache


Additional symptoms may indicate a progression to severe sepsis as organs begin to fail. These may include:

Confusion, mental changes

Anxiety

Decreased urine output (kidney dysfunction)

Abdominal pain

Nausea and vomiting

Difficulty breathing, cough

Chest pain (abnormal function of the heart)

Pelvic or flank pain

Mottled skin


Signs and symptoms of septic shock may include those listed above plus a severe drop in blood pressure.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
Testing is requested to help diagnose sepsis, distinguish it from other conditions, and to evaluate and monitor the function of the affected person`s organs, blood oxygenation, and acid-base balance.

Laboratory Tests

Testing may include:

Blood culture – to detect microorganisms and evaluate their susceptibility to antimicrobial drugs

Urine culture and cultures of other body fluids as indicated – to detect the source and type of infection

FBC (Full blood count) – to evaluate red and white blood cells and platelets

Lactate – increased levels can indicate organ dysfunction

Blood gases – to evaluate oxygen in the blood and acid-base balance

C-reactive protein (CRP) – to detect inflammation in the body

Procalcitonin – marker sometimes used to distinguish bacterial sepsis from other inflammatory conditions that cause similar symptoms

Renal profile – to monitor kidney function and electrolyte balance

Liver function tests – to assess liver status

Blood glucose – to monitor glucose concentrations

Prothrombin time (PT) and/or aPTT or other clotting tests to evaluate clotting status


In addition to the tests listed above, CSF analysis may sometimes be requested if it is thought that the person may have meningitis.

Other tests as indicated may be done to help evaluate health status or to rule out other conditions, such as cardiac biomarkers to detect a heart attack.

Non-Laboratory Tests

May be ordered to evaluate organ status, detect complications, and to detect location of infection:

ECG – to evaluate heart rhythm or injury

X-ray

CT (Computed Tomography) scan

MRI (Magnetic Resonance Imaging)

Ultrasound scan


For more on imaging studies, see the web site Radiologyinfo.org.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Septic arthritis, also called infectious or bacterial arthritis, is not as common as some of the other types of arthritis. However, it needs to be diagnosed and treated quickly because it can destroy joints in a short period of time. Septic arthritis occurs most often following direct injury, such as in an accident, in persons with artificial joints, and in persons with bacteria in the blood (bacteraemia) due to certain infections, such as a skin infection. Additional risk factors include age (older than 80 years), having diabetes or rheumatoid arthritis, and recent joint surgery. The knee and the hip are the most commonly infected joints. The joint becomes hot, red, swollen, painful and difficult to move, and there is often a fever. More than one joint may be affected.

The acute form of septic arthritis is usually caused by bacteria, such as staphylococcus, streptococcus pneumoniae, and group B streptococcus and sometimes by the organisms that cause gonorrhoea and Lyme disease. The rare chronic form may be due to the organism that causes tuberculosis or the yeast Candida albicans. 

What tests are used? 
The following are common tests used to diagnose septic arthritis:  

Blood culture

Full blood count (FBC)

Culture of joint fluid or synovial fluid analysis

X-ray of joint(s) 


What treatments exist? 
Treatment is with antibiotics. The exact antibiotic used may depend on the bacteria, which can be identified from growing the bacteria in a laboratory. Then, the antibiotics can be adjusted depending on the results of the laboratory antibiotic susceptibility tests, which show what antibiotics have been found to work. 

In some cases, the build up of synovial fluid in the joint that occurs because of the infection requires aspiration (using a needle and suction to remove the liquid); in more severe cases, surgery may be needed to drain the fluid.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Tests:
What is it?
Septic arthritis, also called infectious or bacterial arthritis, is not as common as some of the other types of arthritis. However, it needs to be diagnosed and treated quickly because it can destroy joints in a short period of time. Septic arthritis occurs most often following direct injury, such as in an accident, in persons with artificial joints, and in persons with bacteria in the blood (bacteraemia) due to certain infections, such as a skin infection. Additional risk factors include age (older than 80 years), having diabetes or rheumatoid arthritis, and recent joint surgery. The knee and the hip are the most commonly infected joints. The joint becomes hot, red, swollen, painful and difficult to move, and there is often a fever. More than one joint may be affected.

The acute form of septic arthritis is usually caused by bacteria, such as staphylococcus, streptococcus pneumoniae, and group B streptococcus and sometimes by the organisms that cause gonorrhoea and Lyme disease. The rare chronic form may be due to the organism that causes tuberculosis or the yeast Candida albicans. 

What tests are used? 
The following are common tests used to diagnose septic arthritis:  

Blood culture

Full blood count (FBC)

Culture of joint fluid or synovial fluid analysis

X-ray of joint(s) 


What treatments exist? 
Treatment is with antibiotics. The exact antibiotic used may depend on the bacteria, which can be identified from growing the bacteria in a laboratory. Then, the antibiotics can be adjusted depending on the results of the laboratory antibiotic susceptibility tests, which show what antibiotics have been found to work. 

In some cases, the build up of synovial fluid in the joint that occurs because of the infection requires aspiration (using a needle and suction to remove the liquid); in more severe cases, surgery may be needed to drain the fluid.



                                        
                                        
    
        
            
                

                

                
                    <a title=``


info:
Overview
Sickle cell is a condition that is inherited and may occur as a trait (you carry one mutated gene from one of your parents) or as the disease (you carry two mutated genes, one from each of your parents). The trait usually causes little or no problem but can continue to be passed on to your children. The disease may cause significant health problems, called `crises`, throughout life. A crisis is a painful condition brought on by lack of oxygen in the red blood cells, causing them to change shape. They become shaped like a sickle, thus the name of the disease. Infection, dehydration, or change in altitude are among the events that can cause a crisis.  

Haemoglobin in the red blood cells carries oxygen to all parts of the body. In sickle cell anaemia, haemoglobin becomes insoluble, and the red blood cells can become rigid, pointy, and sticky. They can then clog blood vessels, causing pain and damage. A low red blood cell count also may occur due to the destruction of these cells (haemolytic anaemia). Body organs most likely to be severely affected include the spleen, kidneys, and bone marrow. The eyes and top of the femur (thigh bone) are also at risk because there are few arteries in these areas. The sickle cell abnormality is found predominantly in people of African ancestry but may also be found in those who can trace their roots to the Mediterranean area, South and Central America, the Middle East, India, and the Caribbean.

A screen for this condition may include several tests: a haemoglobin electrophoresis to identify the specific types of haemoglobin present, a sickle solubility test, a full blood count (FBC) to detect anaemia, and a reticulocyte count.

Complications of sickle cell disease may include pain, stroke, increased risk of infection, and leg ulcers. Signs of sickle cell crisis include fever, mild jaundice (yellowing of the skin and whites of the eyes), chest pain and shortness of breath. For a more complete list of both complications and signs of crisis, visit NHS Choices: Sickle cell anaemia - Symptoms  

There are different types of sickle cell ‘crisis’: eg. aplastic, haemolytic and painful.

Aplastic – This type is usually due to infection, specifically parvovirus, and results in a decrease in production of red blood cells. It may be self-limiting in 5-10 days but urgent red cell transfusion may sometimes be required.

Haemolytic – resulting from a sudden increase in the destruction of red blood cells. The bone marrow cannot produce cells fast enough to compensate for the loss, resulting in a critical decrease in haemoglobin and haematocrit.      Transfusions are frequently needed to replace the red blood cells. In      children, the spleen sometimes enlarges quickly and causes sudden severe anaemia (usually referred to as a ‘sequestration’ crisis)

Painful – This type is associated with severe pain due to the rigid sickle cells blocking the blood vessels, causing lack of oxygen and damage to cells and organs. It usually lasts 4-6 days, but may persist for weeks.


Newborns with sickle cell disease are often placed on penicillin to prevent pneumonia and other infections. Adults may be treated with hydroxyurea, which has been found to reduce the number of crises and lessen the severity of those that do occur. Intravenous fluids and oxygen are given in crises. Severe crises may be treated with blood transfusion or exchange transfusion to raise the red blood cell count and reduce the number of sickle cells.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Tests:
Overview
Sickle cell is a condition that is inherited and may occur as a trait (you carry one mutated gene from one of your parents) or as the disease (you carry two mutated genes, one from each of your parents). The trait usually causes little or no problem but can continue to be passed on to your children. The disease may cause significant health problems, called `crises`, throughout life. A crisis is a painful condition brought on by lack of oxygen in the red blood cells, causing them to change shape. They become shaped like a sickle, thus the name of the disease. Infection, dehydration, or change in altitude are among the events that can cause a crisis.  

Haemoglobin in the red blood cells carries oxygen to all parts of the body. In sickle cell anaemia, haemoglobin becomes insoluble, and the red blood cells can become rigid, pointy, and sticky. They can then clog blood vessels, causing pain and damage. A low red blood cell count also may occur due to the destruction of these cells (haemolytic anaemia). Body organs most likely to be severely affected include the spleen, kidneys, and bone marrow. The eyes and top of the femur (thigh bone) are also at risk because there are few arteries in these areas. The sickle cell abnormality is found predominantly in people of African ancestry but may also be found in those who can trace their roots to the Mediterranean area, South and Central America, the Middle East, India, and the Caribbean.

A screen for this condition may include several tests: a haemoglobin electrophoresis to identify the specific types of haemoglobin present, a sickle solubility test, a full blood count (FBC) to detect anaemia, and a reticulocyte count.

Complications of sickle cell disease may include pain, stroke, increased risk of infection, and leg ulcers. Signs of sickle cell crisis include fever, mild jaundice (yellowing of the skin and whites of the eyes), chest pain and shortness of breath. For a more complete list of both complications and signs of crisis, visit NHS Choices: Sickle cell anaemia - Symptoms  

There are different types of sickle cell ‘crisis’: eg. aplastic, haemolytic and painful.

Aplastic – This type is usually due to infection, specifically parvovirus, and results in a decrease in production of red blood cells. It may be self-limiting in 5-10 days but urgent red cell transfusion may sometimes be required.

Haemolytic – resulting from a sudden increase in the destruction of red blood cells. The bone marrow cannot produce cells fast enough to compensate for the loss, resulting in a critical decrease in haemoglobin and haematocrit.      Transfusions are frequently needed to replace the red blood cells. In      children, the spleen sometimes enlarges quickly and causes sudden severe anaemia (usually referred to as a ‘sequestration’ crisis)

Painful – This type is associated with severe pain due to the rigid sickle cells blocking the blood vessels, causing lack of oxygen and damage to cells and organs. It usually lasts 4-6 days, but may persist for weeks.


Newborns with sickle cell disease are often placed on penicillin to prevent pneumonia and other infections. Adults may be treated with hydroxyurea, which has been found to reduce the number of crises and lessen the severity of those that do occur. Intravenous fluids and oxygen are given in crises. Severe crises may be treated with blood transfusion or exchange transfusion to raise the red blood cell count and reduce the number of sickle cells.



                                        
                                        
    
        
            
                

                

                
                    <a title=``


info:
What is it?
Sjögren’s syndrome is an autoimmune disorder that can affect a wide range of organs in the body.  It particularly affects secretion production at the mucous membranes, causing dry mouth, decreased tear production, and dryness of other body membranes. Dry eyes and dry mouth is often referred to as `sicca syndrome` and Sjögren`s is a very important cause.

 Symptoms of Sjögren`s may include;

dry and gritty eyes

dry mouth with difficulty chewing and swallowing

decreased sense of taste and smell

swollen salivary glands, especially the parotid

dryness of the vagina, painful intercourse

swollen lymph nodes

joint pains

fatigue


More rarely the following may also occur

Raynaud’s (20%)

Kidney involvement

Neuropathy, causing numbness or tingling in hands or feet

Vasculitis, which can cause rashes especially on the legs


Sjögren’s syndrome is much more common in women than men (9:1), and usually occurs between 40-60 years. It is estimated that 0.5-3% of the adult population may be affected. In the UK, 500,000 people may be affected.

In Sjögren’s syndrome, the body’s immune system mistakenly reacts to the tissue in glands that produce secretions such as the salivary and tear glands. These glands typically have immune cells known as lymphcytes inside them which results in damage.  The presence of particular autoantibodies in the blood is used to help diagnosis.

Sjögren’s syndrome can occur alone (primary Sjögren’s syndrome) or from another well-defined autoimmune diseases such as rheumatoid arthritis (RA), progressive systemic sclerosis (PSS), polymyositis (PM), and Systemic Lupus Erythematosus (SLE).

There is an increased likelihood of lymphoma among patients with primary Sjogren’s syndrome. 



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests
Tests for Sjögren’s syndrome may include:

Positive Schirmer’s test. In this test, a piece of filter paper is hooked over the lower eyelid and left there for 5 minutes. It is used to assess dryness of the eyes, though is not specific for Sjogren’s.  Rose Bengal staining of the eyes can be used to look for scarring affecting the conjunctiva and cornea.

Antinuclear antibodies (ANA) (positive in most cases)  

Rheumatoid factor (RF) (often positive) 

Antibodies specific to Sjögren’s syndrome (SS): anti-SS-A and SS-B; SS-A is also called Ro, while SS-B is also called La. These tests form part of the ENA (extractable nuclear antigen) panel. 

Salivary gland antibodies

Full blood count - may show reductions in cell counts, especially white blood cells


ESR - often raised



Other tests:


In uncertain cases, salivary gland biopsy can be performed






                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatment
There is no cure, and treatment is based on the symptoms. Dry eyes are treated with artificial tears, a tear stimulant, or eye lubricant. Dry mouth may be helped by frequent small drinks of water or sugarless chewing gum to stimulate saliva production. Regular dental care is critical as the oral dryness predisposes to decay.

Arthritis symptoms are treated with simple painkillers, or, non-steroidal anti-inflammatory medicines, such as ibuprofen and diclofenac. Corticosteroids and immunosuppressive medications are reserved for more severe cases.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
Overview
Stroke occurs when the blood supply to a part of the brain is suddenly blocked or diminished, altering the body function controlled by that area of the brain. If any part of the body - including the brain - is without a source of fresh blood and oxygen, the cells will be injured and may die. Although some cell injury is reversible, the death of brain cells is permanent, usually leaving lasting disability.

Each year about 110,000 people in the UK have a stroke. Most are over 65 but a stroke can occur at any age, even in childhood. The risk of stroke is increased in people with high blood pressure, heart disease, diabetes or raised blood cholesterol.  It is the third most common cause of death in the UK. More than 900,000 UK citizens live with disabilities caused by stroke, over half being dependent on others for help with everyday life.

There are three main types of stroke:

Thrombotic – the most common, caused by a clot that forms in an artery that may already be partially obstructed by the build-up of a plaque of atherosclerosis (fat) in its walls and blocks the flow of blood.

Embolic – caused by a circulating piece of a clot that lodges in a blood vessel in the brain. The clot forms elsewhere in the body, usually in the heart, and moves freely until it reaches the small vessels in the brain and cannot move further. Rarely, embolic stroke is caused by fat or air lodging in the brain after entering the blood stream following serious injury.

Haemorrhagic – may be caused by the rupture of a blood vessel within the brain or between the brain and the skull. The rupture may be of an aneurysm - a weak spot in the artery wall - or result from head injury. An aneurysm may be caused by a congenital defect, high blood pressure or atherosclerosis. Haemorrhagic strokes are the most severe and are often fatal. The chance of a full recovery is less than that for the other two types.


The most common symptoms of a stroke are:

sudden numbness, weakness, or paralysis of one side of the face

inability to move the arm and/or leg on one side of the body

loss of speech or trouble talking or understanding what is said

sudden blurred vision, dizziness, loss of balance

severe, unexplained headache


Click here for a complete list of stroke symptoms and signs.

Many strokes are preceded by one or more mini-strokes (called transient ischaemic attacks or TIA’s) in which symptoms are mild and disappear within 24 hours. A TIA should act as a warning to seek medical attention immediately.

There are no specific laboratory tests for stroke, but the laboratory may be requested to analyse blood glucose, urea and electrolytes immediately. The blood lipid profile and tests for the causes and consequences of hypertension (high blood pressure) may be requested in the longer term.

Treatment of stroke depends on the areas affected and the damage done. With strokes caused by blood clots, the use of “clot busting” drugs (as used in treating heart attacks) can be helpful in the early stages. Before giving such drugs the patient’s clotting system is usually tested with a full blood count, including platelets, a prothrombin time and an activated partial thromboplastin time. Sometimes anticonvulsant drugs are used in conjunction with other treatments.

Early treatment is essential to limit brain damage.  In July 2008 the UK National Institute for Health and Clinical Excellence (NICE) published Guidance about the diagnosis and management of acute stroke and transient ischaemic attacks. The guidance stated that because rapid treatment improves outcome after a stroke or TIA, all patients with a suspected stroke should be admitted immediately to a specialist stroke unit.  It is therefore critical that anyone with the sudden onset of symptoms suggestive of stroke or TIA should be brought to medical attention urgently by dialling 999.

Sym:
Overview
Stroke occurs when the blood supply to a part of the brain is suddenly blocked or diminished, altering the body function controlled by that area of the brain. If any part of the body - including the brain - is without a source of fresh blood and oxygen, the cells will be injured and may die. Although some cell injury is reversible, the death of brain cells is permanent, usually leaving lasting disability.

Each year about 110,000 people in the UK have a stroke. Most are over 65 but a stroke can occur at any age, even in childhood. The risk of stroke is increased in people with high blood pressure, heart disease, diabetes or raised blood cholesterol.  It is the third most common cause of death in the UK. More than 900,000 UK citizens live with disabilities caused by stroke, over half being dependent on others for help with everyday life.

There are three main types of stroke:

Thrombotic – the most common, caused by a clot that forms in an artery that may already be partially obstructed by the build-up of a plaque of atherosclerosis (fat) in its walls and blocks the flow of blood.

Embolic – caused by a circulating piece of a clot that lodges in a blood vessel in the brain. The clot forms elsewhere in the body, usually in the heart, and moves freely until it reaches the small vessels in the brain and cannot move further. Rarely, embolic stroke is caused by fat or air lodging in the brain after entering the blood stream following serious injury.

Haemorrhagic – may be caused by the rupture of a blood vessel within the brain or between the brain and the skull. The rupture may be of an aneurysm - a weak spot in the artery wall - or result from head injury. An aneurysm may be caused by a congenital defect, high blood pressure or atherosclerosis. Haemorrhagic strokes are the most severe and are often fatal. The chance of a full recovery is less than that for the other two types.


The most common symptoms of a stroke are:

sudden numbness, weakness, or paralysis of one side of the face

inability to move the arm and/or leg on one side of the body

loss of speech or trouble talking or understanding what is said

sudden blurred vision, dizziness, loss of balance

severe, unexplained headache


Click here for a complete list of stroke symptoms and signs.

Many strokes are preceded by one or more mini-strokes (called transient ischaemic attacks or TIA’s) in which symptoms are mild and disappear within 24 hours. A TIA should act as a warning to seek medical attention immediately.

There are no specific laboratory tests for stroke, but the laboratory may be requested to analyse blood glucose, urea and electrolytes immediately. The blood lipid profile and tests for the causes and consequences of hypertension (high blood pressure) may be requested in the longer term.

Treatment of stroke depends on the areas affected and the damage done. With strokes caused by blood clots, the use of “clot busting” drugs (as used in treating heart attacks) can be helpful in the early stages. Before giving such drugs the patient’s clotting system is usually tested with a full blood count, including platelets, a prothrombin time and an activated partial thromboplastin time. Sometimes anticonvulsant drugs are used in conjunction with other treatments.

Early treatment is essential to limit brain damage.  In July 2008 the UK National Institute for Health and Clinical Excellence (NICE) published Guidance about the diagnosis and management of acute stroke and transient ischaemic attacks. The guidance stated that because rapid treatment improves outcome after a stroke or TIA, all patients with a suspected stroke should be admitted immediately to a specialist stroke unit.  It is therefore critical that anyone with the sudden onset of symptoms suggestive of stroke or TIA should be brought to medical attention urgently by dialling 999.


info:
Also known as: Scoline Apnoea 


                                                
                                            

What is it?
Suxamethonium (succinylcholine) apnoea is rare and occurs when a patient has been given this muscle relaxant prior to surgery but is incapable of metabolising the drug sufficiently rapidly. They remain paralysed and unable to breathe after the surgery is complete because they cannot regain their muscle function quickly enough.

Uses
Suxamethonium is a fast acting muscle relaxant and its main use in anaesthesia is to allow the rapid intubation of the trachea. It is also used to modify fits after ECT (electroconvulsive therapy). 
Suxamethonium is useful in these situations because it acts and subsides quickly for the vast majority of patients lasting just long enough to meet the needs of the surgical procedure.

How it works 
Suxamethonium depolarises skeletal muscle and is the fastest acting of all the available muscle relaxants and lasts for between 2 and 10 minutes. Further doses can be given as required. Part of the structure is similar to the neurotransmitter acetylcholine and as such it is able to prevent acetylcholine from binding at the neuromuscular junction. It binds non-competitively at the synaptic junction, which means that it cannot be reversed by other drugs, and as a result it wears off very slowly until the drug is eliminated by other routes.

Causes of Suxamethonium Apnoea 
The majority of suxamethonium is metabolised by an enzyme called cholinesterase and about 10% of the drug is excreted by the kidneys. Suxamethonium apnoea is rare and can be either inherited or acquired. In the case of inherited suxamethonium apnoea the degree of sensitivity to this drug varies with the phenotype of the patient (see section on cholinesterase). The phenotypes (which express a particular form of the enzyme cholinesterase) that are most susceptible to apnoea are the atypical, silent  fluoride resistant phenotypes and to a variable degree the UA phenotype. The action of suxamethonium can be increased from 30 minutes to over two hours in these cases.
 In the acquired form situations such as pregnancy, liver disease, kidney disease, hypothyroidism and if taking drugs such as methotrexate or monoamine oxidase inhibitors, the action of suxamethonium can be increased by minutes as opposed to hours.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Tests
The total activity for the cholinesterase enzyme in blood is measured, also known as butyrylcholinesterase.

A cholinesterase phenotype for the patient is also reported as this will enable the doctor to predict the likelihood of suxamethonium apnoea. The phenotype is a study of the characteristics of the enzyme activity and is determined by the effect of a range of compounds that inhibit the cholinesterase enzyme

If a phenotype is difficult to confirm or there is an atypical type in the immediate family, genotype studies which identify the inherited genes should be considered.




                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatment
Suxamethonium apnoea is often only apparent at the end of an operation. These patients may remain paralysed for up to several hours after a standard dose of suxamethonium. They are kept anesthetised and ventilated in a high dependency unit until this muscle relaxant is cleared by other slower means and the patient begins breathing spontaneously. The length of support will depend on the defect in the cholinesterase phenotype/genotype.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis. TB may affect many body organs, but it primarily affects the lungs. It is spread through the air from person to person through lung secretions such as sputum (spit or phlegm) or aerosols released by coughing, sneezing, laughing, or breathing. Most of those who become infected with M. tuberculosis manage to confine the mycobacteria to a few cells in their body, where they stay alive in an inactive form. This inactive or latent TB infection does not make the patient sick or infectious and, in most cases, it does not progress to cause active tuberculosis.

However, some patients - especially those with damaged or compromised immune systems - may proceed directly from initial TB infection to active tuberculosis. And in another 10% of those with latent TB infection, the mycobacteria will later be reactivated and begin to multiply - leading to active progressive tuberculosis disease.

TB has been a leading cause of death for thousands of years. In the days before the discovery of antibiotics it was called consumption, and those who contracted it were put into long-term hospitals called sanatoriums for the rest of their lives. TB first became a statutorily notifiable disease in the UK in 1913; with almost 120,000 cases in that year. The number of new cases fell progressively until the mid 1980s. However, the number started to rise again in the early 1990s and there has been a 25% increase to the current figure in the past 10 years. This is now slightly more than 9000 cases, including contributing to 334 deaths, in the UK in 2009. Worldwide, TB is still the leading cause of death due to infection - killing more than 3 million people a year.

In developed countries such as the USA or the UK, the majority of these cases were among those living in overcrowded or confined conditions such as prisons, nursing homes, and schools. The most vulnerable were those who had poor health care or had diseases and conditions that weakened their immune systems, such as: the homeless, alcoholics, intravenous drug users, those with HIV or AIDS, and those with chronic kidney or liver diseases. Often these new cases were multi-drug resistant (MDR), making them more difficult to treat. The revised UK immunisation programme on TB is to target infants in areas where the incidence of TB is greater than 40 cases / 100000, or have parents or grandparents who were born in countries with such an incidence.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Signs and Symptoms
Inactive or latent TB infection does not cause any symptoms. Someone may have latent TB infection for years without knowing it. It is usually diagnosed when a patient has a positive TB skin test.

The symptoms of active tuberculosis depend on what part(s) of the body are involved. The classic symptoms tend to be pulmonary (TB in the lungs) and include:

Chronic cough, sometimes with bloody sputum

Fever

Chills

Weight loss

Weakness


If the TB is extrapulmonary (outside of the lungs), it may cause few noticeable symptoms or a wide range including:

Back pain and paralysis (spinal TB)

Weakness due to anaemia (TB in the bone marrow)

Joint pain

Pain associated with reproductive system or urinary tract, and possibly, resulting in infertility

Abdominal pain

Fever and shortness of breath (TB in the lining around the heart, affecting the pericardium, or miliary TB, a large number in the bloodstream)

Altered mental state, headache and coma (TB in the brain and/or central nervous system)


All of these symptoms may also be seen in a variety of other conditions. A diagnosis of active tuberculosis depends on the positive identification of Mycobacterium tuberculosis in the body fluids or tissues.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
Laboratory Tests

Latent TB infection
Testing for Mycobacterium tuberculosis begins with a TB skin test for latent TB infection. This is not used as a general screen, but is targeted at those who are at a high risk for contracting the disease and at those who work or live with high-risk patients. The TB skin test may also be done as part of a physical examination prior to starting school or a new job. Positive results may indicate a latent TB infection, this may be confirmed by a further blood test, and should be followed by other investigations such as chest X-rays to look for signs of active disease. 

Active Tuberculosis
To diagnose TB of the respiratory tract, 3 - 5 sputum specimens are collected first thing in the morning when they are most likely to contain the most TB bacteria. If extrapulmonary TB is suspected, samples are collected based upon where in the body the infection is likely to be. Multiple samples of gastric washings/aspirates or urine may be collected and submitted to the laboratory. Sometimes cerebral spinal fluid (CSF), biopsied tissue, or other body fluids are also collected.

A presumptive diagnosis of TB can be made by examining a smear of the patient`s specimen under the microscope after it has been stained with a special stain to detect acid fast bacteria. Positive ABF smears are likely to indicate a TB infection, since M. tuberculosis is the most common acid-fast bacillus, but the smears cannot distinguish between the different species of ``acid-fast`` bacilli.

A genetic probe or molecular TB test can add additional information. It amplifies/replicates genetic components of TB and can narrow the identification to a group of mycobacteria (of which M. tuberculosis is the most common). While AFB smears and genetic tests may be available the same day that the samples are submitted, both positive and negative results must be confirmed with AFB cultures.

AFB cultures are set up using decontaminated, digested, and concentrated body samples. Nutrients and incubation provide a supportive environment for the slow growing mycobacteria. The results of cultures are definitive: They can tell your doctor what organisms are present and what drugs are likely to kill them but they take time - days to several weeks for positive samples, up to six to eight weeks to confirm negative results.

Once M. tuberculosis has been identified and treatment has begun, AFB smears and cultures are used to monitor the effectiveness of treatment.

Non-Laboratory Tests

X-rays are often used as a follow-up to positive TB skin tests to look for signs of mycobacteria growth and to help determine whether someone has active tuberculosis or a latent TB infection. Infection with TB can cause a number of characteristic findings on x-rays, including cavities (holes) and calcification in organs such as the lungs and kidneys. More information on radiological tests can be found at The Royal College of Radiologists.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What is it?
Testicular cancer is an abnormal, uncontrolled growth of cells that forms a tumour in one or both testicles. Men have two testicles (testes, gonads) that are located in the scrotum, the pouch of loose skin below the base of the penis. The testicles are responsible for producing sperm and male hormones (mainly testosterone) that regulate reproductive organ development. 

Testicular cancer is the most common cancer in males between 20 and 40 years of age. About 2,000 men are diagnosed with the condition in the UK each year.  It is several times more common in white males than in men of African, Hispanic, or Asian descent, although the cause for this additional risk is not known. Other factors that can increase risk include undescended testicles (cryptorchidism) if not corrected before the age of 11, abnormal development of the testes (gonadal dysgenesis), inflammation of the testes (orchitis) which can rarely occur after mumps, genetic disorder called Klinefelter’s syndrome, and a family history of testicular cancer.  Individuals who handle pesticides, leather workers, miners, oil well workers, and HIV positive persons also appear to be at higher risk.

Germ cells, which normally develop into sperm, account for about 94% of testicular tumours.  These tumours are devided into two groups, seminomas (40%) and non-seminomas (60%). Seminomas occur most ofter in men in their thirties.  They tend to grow very slowly and usually do not spread (metastasize). Non-seminomas mainly affect men in their twenties and tend to grow and spread more quickly. 

About 4-5% of all testicular tumours (20% children) form in the cells that produce hormones. These tumours may secrete oestradiol, a female sex hormone which can then cause breast growth (gynaecomastia).

 



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Symptoms
Testicular cancer is usually first detected as a painless lump or swelling about the size of a pea on the front or side of one testicle. It is most often found by the patient, but may also be found during a routine physical examination or during a medical examination done for other purposes such as the investigation of infertility. The cancer may give no warning signs or it may be due to symptoms such as a heaviness or collection of fluid in the scrotum, a dull ache in the abdomen or groin, pain in the testicle and an enlargement or tenderness in the breasts. If you have these symptoms you should discuss them with your GP, but you should keep in mind that they may not be due to cancer. 

If testicular cancers are found early they can be easily treated, and so young men should examine themselves once a month or so after a warm bath or shower when the skin of the scrotum is relaxed.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Tests
The reasons for testing are to detect and help diagnose testicular cancer, to distinguish between different types, to determine how far it has spread, to follow the effectiveness of treatment and to monitor for recurrence.

Non-laboratory tests
 The diagnosis of testicular cancer begins with a physical examination by your GP after you have explained your symptoms. If your GP suspects that the lump in your testicle may be cancer, you will be referred to a hospital for further tests. 

 A scrotal ultrasound scan is a painless procedure that uses high-frequency sound waves to produce an image of your testicle. It will help the radiologist decide whether the lump is solid or filled with fluid. A lump filled with fluid is known as a cyst and is usually harmless. A more solid lump may be a sign of cancer.

 If laboratory tests (below) suggest testicular cancer, you may have a chest  X-ray to check for signs that the tumour has spread. You may also need a scan of your entire body, such as magnetic resonance imaging (MRI) or computerised tomography (CT).

Laboratory tests
 Testicular cancer often produces substances that can be measured in your blood. The tumour markers that are usually measured to help confirm the diagnosis are

AFP (alpha-fetoprotein)

hCG (human chorionic gonadotropin)

LDH (lactate dehydrogenase)


AFP is almost always elevated in non-seminomas while hCG may be elevated in both seminomas and non-seminomas. As well as helping the diagnosis of testicular cancer, if the initial levels are raised they can be used to follow response to treatment and monitor for recurrence. LDH is elevated in most testicular cancers. It is an enzyme found in many body tissues that is released into the bloodstream when cellular damage occurs. It is not specific for testicular cancer but can help the doctor decide the stage and risk for both tumour types. There is still a small chance that you have testicular cancer even if all your blood test results are normal.

 The only way to be sure whether a testicular mass is cancerous is to do a biopsy. If cancer is suspected, the testicle is usually removed and looked at by a pathologist. A cut is made in the groin and the testicle and spermatic cord (which contains the vas deferens) are taken out of the scrotum.

If the lump is cancerous, a pathologist will report the type of testicular cancer and the risk that cancer has spread. The preferred treatment will depend on the type and stage of cancer.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
 

Thalassaemia is a group of inherited disorders that affect the amount of haemoglobin a person produces. Haemoglobin refers to a family of compounds all made up of haem (an iron-containing complex), and various globins (protein chains that surround the haem complex). Haemoglobin (Hb) molecules are found in all red blood cells, and are the reason for their red colour. They bind oxygen in the lungs, carry it through the bloodstream, and release it to the body’s tissues. 

Normal adult haemoglobins include:

Haemoglobin A (about 95% - 98%).  HbA contains two alpha (α) chains and two beta (ß) chains.

HbA2 (about 2% - 3.5%), has two alpha (α) and two delta (δ) chains

HbF (up to 2%).  This is the primary haemoglobin produced by the fetus during gestation.  Its production usually falls to a low level within a year after birth.  HbF has two alpha (α) and two gamma (γ) chains.


Mutations in the genes coding for the globin chains can cause disorders in haemoglobin production. There are 4 genes coding for alpha globin chains and 2 genes coding for the beta globin chains.

Inherited disorders of haemoglobin production fall into two categories:

Thalassaemia: decreased production of normal haemoglobins

Haemoglobinopathy: production of an abnormal haemoglobin molecule


Thalassaemias are a group of disorders in which mutations in one or more of the alpha or beta globin genes cause a reduction in the amount of the HbA produced. This leads to a reduction in HbA, the relative increase in the amount of minor haemoglobins HbA2 and HbF, and perhaps detection of unusual haemoglobin types.

The thalassaemias are usually classified by the type of globin chain whose synthesis is reduced.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Alpha thalassaemia is due to a deletion or mutation in one or more of the 4 alpha globin gene copies. The more genes affected, the less alpha globin produced. The four different types of alpha thalassaemia include:

•   Silent Carrier State (1 affected gene). The silent carrier will have normal haemoglobin levels red cell indices which are normal or show a slightly decreased MCH (hypochromia). Carriers can pass on the affected gene to their offspring. Often these individuals are identified only after having a child with HbH disease or alpha thalassaemia trait. 

•   Alpha Thalassaemia Trait (2 affected genes). Patients who have alpha thalassaemia trait have smaller (microcytic), paler (hypochromic) red blood cells and a mild chronic Anaemia but do not generally experience any symptoms. This is an Anaemia that does not respond to iron supplements. Diagnosis of alpha thalassaemia trait is usually by exclusion of other causes of microcytic Anaemia. Confirmatory testing by DNA analysis is available but is not routinely done.

•   Haemoglobin H Disease (3 affected genes). With this condition, the large decrease in the amount of alpha globin chains produced causes an excess of beta chains which then aggregate into beta4 tetramers (groups of 4 beta chains), known as Haemoglobin H. HbH disease can cause moderate to severe Anaemia and splenomegaly (enlarged spleen). The clinical picture associated with HbH disease is extremely variable, however. Some individuals are asymptomatic while others have severe Anaemia. Haemoglobin H disease is found most often in individuals of Southeast Asian or Eastern Mediterranean descent.

•   Alpha Thalassaemia Major (also called hydrops fetalis, 4 affected genes). This is the most severe form of alpha thalassaemia. In this condition, no alpha globin is produced, therefore, no HbA or HbF are produced. Fetuses affected by alpha thalassaemia major become anemic early in pregnancy. They become hydropic (retain fluids), and frequently have enlarged hearts and livers. This diagnosis is frequently made in the last months of pregnancy when a fetal ultrasound indicates a hydropic fetus. About 80% of the time the mother will have toxaemia and can develop severe postpartum hemorrhage. Fetuses with alpha thalassaemia major are usually miscarried, stillborn, or die shortly after birth.

Individuals with alpha thalassaemia may be misdiagnosed as iron deficient by unwary doctors, as iron deficiency also leads to small pale (microcytic hypochromic) red cells. It is important that iron therapy in thalassaemic patients is only given when specific iron tests (FERRITIN, SERUM IRON, TIBC & TRANSFERRIN) have confirmed iron deficiency. This is especially important in alpha thalassaemia, where there is a small potential for dangerous iron overload to develop.

Alpha thalassaemia is found most commonly in individuals with an ethnic background of Southeast Asia, Southern China, the Middle East, India, Africa and the Mediterranean.

Beta thalassaemia is due to mutations, in one or both of the beta globin genes. There are 100 to 200 mutations that have been identified but only about 20 are common. The severity of the Anaemia caused by beta thalassaemia depends on which mutations are present and on whether they decrease beta globin production (called beta+ thalassaemia) or completely eliminate it (called beta0 thalassaemia). The different types of beta thalassaemia include:

•   Beta Thalassaemia Trait. A person with this condition has one normal gene and one with a mutation. They will usually experience no health problems other than microcytosis (small red blood cells) and a possible mild Anaemia that will not respond to iron supplements. This gene mutation can be passed on to an individual’s children.

•   Thalassaemia Intermedia. In this condition, an affected person has two abnormal genes but is still producing some beta globin. The severity of the Anaemia and health problems experienced depends on the mutations present. The dividing line between thalassaemia intermedia and thalassaemia major is the degree of Anaemia and the number and frequency of blood transfusions required to treat it. Those with thalassaemia intermedia may need occasional transfusions but do not require them on a regular basis.

•   Thalassaemia Major (also called Cooley`s Anaemia). This is the most severe form of beta thalassaemia. The patient has two abnormal genes that cause either a severe decrease or complete lack of beta globin production, preventing the production of significant amounts of HbA. This condition usually appears in an infant after 3 months of age and causes life-threatening Anaemia. This Anaemia requires lifelong regular blood transfusions and considerable ongoing medical care. Over time these frequent transfusions lead to excessive amounts of iron in the body. Left untreated, this excess iron can deposit into the liver, heart and other organs, and can lead to a premature death from organ failure.

Other forms of thalassaemia occur when a gene for beta thalassaemia is inherited in combination with a gene for a haemoglobin variant. (link to Hb Variant page) The most important of these are:

•   HbE – beta thalassaemia. HbE is one of the most common haemoglobin variants, found predominantly in people of Southeast Asian descent. If a person inherits one HbE gene and one beta thalassaemia gene, the combination produces HbE-beta thalassaemia which causes a moderately severe Anaemia similar to beta thalassaemia intermedia.

 •   HbS – beta thalassaemia or sickle cell – beta thalassaemia. HbS is one of the most well known of the haemoglobin variants. Inheritance of one HbS gene and one beta thalassaemia gene results in HbS-beta thalassaemia. The severity of the condition depends on the amount of beta globin produced by the beta gene. If no beta globin is produced, the clinical picture is almost identical to sickle cell disease.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


info:
What are they?
“Travellers` diseases” is a broad term for bacterial, viral, fungal, and parasitic infections that may be caught when someone travels away from home, especially when travelling from a developed or industrialized area to a less developed area. (Some of the conditions discussed in this article, however, can be acquired while at home, not just while travelling, such as HIV and hepatitis). Every travel destination and every area has its hazards, including when travelling in the UK. Those who live in a place, however, are generally aware of their own diseases and dangers and do their best to make accommodations for them. The British for instance, would be able to identify stinging nettles with ease but not venomous spiders!

While spiders and nettles are outside the scope of an article on microorganisms, it shows the need for travellers to understand the risks that they may come across. Staying in an city hotel in a developed country for a few days can be very different from a two-week outdoor adventure in Thailand or Malaysia . Travellers should educate themselves and discuss their destinations, expected lengths of stay, and planned activities with their GP or practice nurse. With the proper care, many travellers’ diseases are preventable, by avoiding particular environments, risky activities, careful choice food and source of water, and the appropriate use of medicines and vaccines.

Traveller’s diseases can be acquired through contaminated food or water, from animal droppings, and from soil. Close exposure to infected animals and contact with animal skin can put someone at risk. People will usually not be able to see, smell, or taste the contamination. Diseases are also carried by biting mosquitoes, flies, and ticks. Some can be picked up from swimming in freshwater and by walking on the beach with bare feet, while others are passed from person to person – through close contact, needle sharing, blood, and unprotected sex. The symptoms of some diseases may be so mild and self-limited that they go unnoticed; many may be a miserable annoyance for a few days, and a few may cause an acute medical emergency. There are diseases that may not become apparent until the traveller has returned home with symptoms that may resolve, cycle, grow gradually worse, or stay for a long time. Left untreated, a few of the diseases can lead to blindness, organ failure, coma, and death.

The most frequently seen traveller’s illnesses are diarrhoea, nausea, being sick, fever, and skin manifestations (rashes, sores, swelling, etc). Also seen are hepatitis (liver inflammation) and accompanying jaundice, headaches, meningitis and/or encephalitis. Some diseases will also cause breathing problems and coughing.

Some diseases are global in nature - they are found throughout the world and, unless prevented through vaccination, frequently cause childhood illnesses. In some cases, these illnesses can lead to lifelong complications. Many nations have vaccination programs to decrease the number of people who get conditions such as measles, rubella (German measles), mumps, and polio. In areas that are unable to vaccinate all of their population, these conditions may be very common. Travellers who are not protected through previous vaccinations, young children who have not been fully immunized, and patients who are immunocompromised may be at an increased risk of getting one of these infections. Travellers from foreign countries may also have diseases not normally seen in the UK.

Travellers` diarrhoea can be caused by a variety of bacteria, viruses, and parasites throughout the world. These microorganisms may be found in water and food wherever sanitation and food handling practices are poor. People are often get used to their own local bacteria and viruses but are affected by those present in other places. Parasites can affect both local inhabitants and those who travel.

Some viral and bacterial diarrhoeas tend to occur within a few hours of infection and may be self-limiting and get better. Some, such as Salmonella and Shigella, have a 48-72 hour incubation period. Parasitic diarrhoeas tend to have a longer incubation time and, without treatment, may become chronic illnesses in some individuals.

Hepatitis A virus, which can cause liver inflammation and jaundice, can also be picked up from contaminated food and water. Infection with hepatitis B virus (HBV) and/or hepatitis C virus (HCV) may cause symptoms similar to hepatitis A, but they are picked up through exposure to blood and body fluids, sexual contact, or perinatally (mother to infant). Risky behaviours, such as unprotected sex, may also expose travellers to HIV and other sexually transmitted diseases.

The most common infections which produce fever are malaria, dengue fever, and yellow fever. All of these diseases are carried by mosquitoes, and they are very common in tropical areas of the world. A vaccine is available for yellow fever, and proof of vaccination may be required for entry into some countries. Regular medication is available to prevent malaria. Dengue fever is a rapidly growing disease, found in an increasing number of countries, and is causing progressively larger epidemics. There is no preventative treatment for dengue but can be avoided by taking measures to avoid mosquito bites.

Travellers can also catch colds and the flu while in airplanes and other modes of transport while travelling to or from their travel destination.



                                        
                                        
    
        
            
                

                

                
                    <a title=``

Sym:
Laboratory Testing
It is important to identify the cause of the disease in travellers, not only to treat the individual but also to prevent and document the spread of the disease, both in returning travellers and in the countries they visited.

Causes of bacterial diarrhoea may be identified with a stool culture and may be treated with antimicrobial agents when symptoms appear and/or may get better without the need for further tests to identify the pathogen. Parasitic causes of diarrhoea can be identified through the OCP (ova and parasite) stool test. This test is used to identify parasites and their eggs in a fresh or specially preserved stool sample. For some parasites, such as Giardia intestinalis (lamblia), antigen tests have been developed. These tests identify proteins associated with the parasite and can be useful when parasites are present in low numbers. Because identifying the cause of viral diarrhoea is complex, viral causes of diarrhoea may not be identified by specific cultures or tests unless the virus causes a large number of people to become ill, such as an outbreak of norovirus on a cruise ship.

The parasite that causes malaria (Plasmodium spp.) infects red blood cells. It can be identified by collecting a blood sample and examining specially stained “thick and thin” blood smears on slides under the microscope. Many of the other travellers’ diseases can be identified either by growing the microorganism, looking at it under the microscope, and/or testing for antibodies or antigens. Patients who return from travelling with a a short or longer lasting disease should see their doctor, who may occasionally suggest a consultation with an infectious disease and/or tropical medicine specialist.

Non-Laboratory Tests
Sometimes x-rays or CT scans may be used to look at body organs, such as the lungs or liver, for evidence of infection or damage.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``

Tests:
Treatments
Advance planning can help prevent many travellers’ diseases. Prior to a trip, people should consult with their doctor and check that they have been vaccinated for diseases such as mumps, measles, rubella, polio, and tetanus and check whether any boosters are needed to maintain a protective level of antibodies. They should discuss their travel plans and get additional vaccinations as recommended for diseases such as hepatitis A, typhoid and yellow fever. If they are going to go to areas where malaria is common, they will usually be given medicines, such as mefloquine or chloroquine, to begin taking prior to their trip. These will need to be taken regularly during the trip and for a specified time period after the traveller’s return.

The NHS in Scotland has up to date information on travellers health and preventative strategies (see Related Pages).

In spite of taking every precaution, travellers may still become ill, either during their trip or several months after they have returned home. In general, the earlier that travellers’ diseases are detected and diagnosed, the easier they are to treat. Travellers should know which symptoms signal the need to seek prompt medical care in the country they are visiting and which may be safely self-treated. For several months after their return home, they should note any symptoms that occur and bring them to their doctor’s attention.



                                        
                                        
    
        
            
                
                    « Prev
                

                  
                
                        |
                
                

                
                    <a title=``


