Barlow syndrome

Barlow syndrome is mitral valve prolapse (also known as “click murmur syndrome”), the most common heart valve abnormality, affecting 5-10% of the world population. Most patients have no symptoms and require no treatment. However, the condition can be associated with fatigue and/or palpitations. The mitral valve prolapse can often be detected by a doctor during examination of the heart and can be confirmed with an echocardiogram. Patients are usually given antibiotics prior to any procedure which might introduce bacteria into the bloodstream, including dental work and minor surgery.

Bacillary angiomatosis

A bacterial infection due to a cat scratch most often seen today in people with HIV. The disease characteristically presents with swollen lymph nodes (lymphadenitis), sore throat, fatigue, and fever, chills, sweats, vomiting, loss of appetite, and weight loss. There is usually a little bump (a papule) which may be pus-filled (a pustule) at the site of the scratch. Then more nodules appear on and under the skin. As the number of nodules increases, patients get sicker.

In normal people the disease is self-limited and usually goes away by itself in a few weeks. It can also be treated with antibiotics.

In persons with HIV/AIDS the disease can cause severe inflammation of the brain, bone marrow, lymph nodes, lungs, spleen and liver. The disease can be fatal in persons with HIV. It can be easily treated with antibiotics such as erythromycin and doxycycline. Treatment is given until the skin lesions resolve, usually in 3 to 4 weeks.

Bacillary angiomatosis is so characteristic today of AIDS that it is an AIDS defining disease, according to the CDC (Centers For Disease Control).

A cat carrying the microbe does not show symptoms. It is not necessary to get rid of the cat. If someone in the household is at high risk, a test to detect the infection can be done and the cat can be treated.

The disease is caused by a bacterium called Rochalimaea henselae, which was reclassified as Bartonella henselae, named for Diane Hensel, a microbiologist. Bacillary angiomatosis has also been called cat scratch disease, cat scratch fever, regional lymphadenitis, and benign lymphoreticulosis.

Jaundice

Jaundice, also known as icterus (attributive adjective: "icteric"), is yellowish discoloration of the skin, sclera (whites of the eyes) and mucous membranes caused by hyperbilirubinemia (increased levels of bilirubin in the blood). This hyperbilirubinemia subsequently causes increased levels of bilirubin in the extracellular fluids. Typically, the concentration of bilirubin in the plasma must exceed 1.5 mg/dL, three times the usual value of approximately 0.5mg/dL, for the coloration to be easily visible. Jaundice comes from the French word jaune, meaning yellow.


Normal Physiology

In order to understand how jaundice results, it is important to understand where the pathological processes that cause jaundice take their effect. It is also important to further recognize that jaundice itself is not a disease, but rather a symptom of an underlying pathological process that occurs at some point along the normal physiological pathway of the metabolism of bilirubin.

Pre-Hepatic events

When a red blood cell has completed its life span of approximately 120 days, their membranes become fragile and prone to rupture. As the cell traverses through the reticuloendothelial system, their cell membranes rupture and the contents of the red blood cell is released into the blood. The component of the red blood cell that is involved in jaundice is hemoglobin. The hemoglobin released into the blood is phagocytosed by macrophages, and split into its heme and globin portions. The globin portion, being protein, is degraded into amino acids and plays no further role in jaundice. Two reactions then take place to the heme molecule. The first reaction is the oxidation of heme to form biliverdin.This reaction is catalyzed by microsomal enzyme heme oxygenase and it results in biliverdin (green color pigment), iron and carbon monoxide. Next step is reduction of biliverdin to yellow color tetrapyrol pigment bilirubin by cytosolic enzyme biliverdin reductase. This bilirubin is known as "unconjugated", "free" or "indirect" bilirubin. Approximately 4 mg per kg of bilirubin is produced each day.The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described. However approximately 20 per cent comes from other heme sources, including ineffective erythropoiesis, breakdown of other heme protrins such as muscle myoglobin and cytochrome enzymes.

Hepatic events

The unconjugated bilirubin then travels to the liver through the bloodstream. Because this bilirubin is not soluble, however, it is transported through the blood bound to serum albumin. Once it arrives at the liver, it is conjugated with glucuronic acid (to form bilirubin diglucuronide, or just "conjugated bilirubin") to become more water soluble. The reaction is catalyzed by the enzyme UDP-glucuronide transferase.

Post Hepatic events

This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts as part of bile. Intestinal bacteria convert the bilirubin into urobilinogen. From here the urobilinogen can take two pathways. It can either be further converted into stercobilinogen, which is then oxidized to stercobilin and passed out in the faeces, or it can be reabsorbed by the intestinal cells, transported in the blood to the kidneys, and passed out in the urine as the oxidised product urobilin. Stercobilin and urobilin are the products responsible for the coloration of faeces and urine, respectively.

Causes

When a pathological process interferes with the normal functioning of the metabolism and excretion of bilirubin just described, jaundice may be the result. Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects. The three categories are:

* Pre-hepatic: The pathology is occurring prior the liver
* Hepatic: The pathology is located within the liver
* Post-Hepatic: The pathology is located after the conjugation of bilirubin in the liver

Pre-hepatic

Pre-hepatic jaundice is caused by anything which causes an increased rate of hemolysis (breakdown of red blood cells). In tropical countries, malaria can cause jaundice in this manner. Certain genetic diseases, such as sickle cell anemia, spherocytosis and glucose 6-phosphate dehydrogenase deficiency can lead to increased red cell lysis and therefore hemolytic jaundice. Commonly, diseases of the kidney, such as hemolytic uremic syndrome, can also lead to coloration. Defects in bilirubin metabolism also present as jaundice. Jaundice usually comes with high fevers.

Laboratory findings include:

* Urine: no bilirubin present, urobilirubin > 2 units (except in infants where gut flora has not developed).
* Serum: increased unconjugated bilirubin.

Hepatic

Hepatic jaundice causes include acute hepatitis, hepatotoxicity and alcoholic liver disease, whereby cell necrosis reduces the liver's ability to metabolise and excrete bilirubin leading to a buildup in the blood. Less common causes include primary biliary cirrhosis, Gilbert's syndrome (a genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population) and metastatic carcinoma. Jaundice seen in the newborn, known as neonatal jaundice, is common, occurring in almost every newborn as hepatic machinery for the conjugation and excretion of bilirubin does not fully mature until approximately two weeks of age.

Laboratory Findings include:

* Urine: bilirubin present, Urobilirubin > 2 units but variable (Except in children)

Post-hepatic

Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of bile in the biliary system. The most common causes are gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites known as "liver flukes" live in the common bile duct, causing obstructive jaundice. Other causes include strictures of the common bile duct, biliary atresia, ductal carcinoma, pancreatitis and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi's syndrome.

The presence of pale stools and dark urine suggests an obstructive or post-hepatic cause as normal feces get their color from bile pigments.

Patients also can present with elevated serum cholesterol, and often complain of severe itching or "pruritus".

Hepatitis

Hepatitis (plural hepatitides) implies injury to liver characterized by presence of inflammatory cells in the liver tissue. Etymologically from ancient Greek hepar (ηπαρ) or hepato- (ηπατο-), meaning 'liver,' and suffix -itis, denoting 'inflammation' (c. 1727). The condition can be self limiting, healing on its own, or can progress to scarring of the liver. Hepatitis is acute when it lasts less than 6 months and chronic when it persists longer. A group of viruses known as the hepatitis viruses cause most cases of liver damage worldwide. Hepatitis can also be due to toxins (notably alcohol), other infections or from autoimmune process. It may run a subclinical course when the affected person may not feel ill. The patient becomes unwell and symptomatic when the disease impairs liver functions that include, among other things, screening of harmful substances, regulation of blood composition, and production of bile to help digestion.

Causes

Acute hepatitis

* Viral Hepatitis: Hepatitis A to E (more than 95% of viral cause), Herpes simplex, Cytomegalovirus, Epstein-Barr, yellow fever virus, adenoviruses.
* Non viral infection: toxoplasma, Leptospira, Q fever,[2] rocky mountain spotted fever[3]
* Alcohol
* Toxins: Amanita toxin in mushrooms, carbon tetrachloride, asafetida
* Drugs: Paracetamol, amoxycillin, antituberculosis medicines, minocycline and many others (see longer list below).
* Ischemic hepatitis (circulatory insufficiency)
* Pregnancy
* Auto immune conditions, e.g. Systemic Lupus Erythematosus (SLE)
* Metabolic diseases, e.g. Wilson's disease

Chronic hepatitis

* Viral hepatitis: Hepatitis B with or without hepatitis D, hepatitis C (Hepatitis A and E do not lead to chronic disease)
* Autoimmune: Autoimmune hepatitis
* Alcohol
* Drugs: methyl-dopa, nitrofurantoin, isoniazide, ketoconazole
* Non-alcoholic steatohepatitis
* Heredity: Wilson's disease, alpha 1-antitrypsin deficiency
* Primary biliary cirrhosis and primary sclerosing cholangitis occasionally mimic chronic hepatitis

Sickle-cell disease

Sickle-cell disease or sickle-cell anaemia (or anemia) is a blood disorder characterized by red blood cells that assume an abnormal, rigid, sickle shape. Sickling decreases the cells' flexibility and results in their restricted movement through blood vessels, depriving downstream tissues of oxygen. The disease is chronic and lifelong: individuals are most often well, but their lives are punctuated by periodic painful attacks and a risk of various other complications. Life expectancy is shortened, with older studies reporting an average life expectancy of 42 and 48 years for males and females, respectively.

Sickle-cell disease occurs more commonly in people (or their descendants) from parts of the world such as sub-Saharan Africa, where malaria is or was common, but it also occurs in people of other ethnicities. This is because those with one or two alleles of the sickle-cell disease are resistant to malaria since the sickle red blood cells are not conducive to the parasites - in areas where malaria is common there is a survival value in carrying the sickle-cell genes.

Alzheimer's disease

Alzheimer's disease (AD), also called Alzheimer disease or simply Alzheimer's, is the most common cause of dementia, afflicting 24 million people worldwide. Alzheimer's is a degenerative and terminal disease for which there is currently no known cure. In its most common form, it occurs in people over 65 years old although a less-prevalent early-onset form also exists. The disease can begin many years before it is eventually diagnosed. In its early stages, short-term memory loss is the most common symptom, often initially thought to be caused by aging or stress by the sufferer. Later symptoms include confusion, anger, mood swings, language breakdown, long-term memory loss, and the general withdrawal of the sufferer as his or her senses decline. Gradually the sufferer loses minor, and then major bodily functions, until death occurs. Although the symptoms are common, each individual experiences the symptoms in unique ways. The duration of the disease is estimated as being between 5 and 20 years.

The symptoms of Alzheimer's disease are generally reported to a physician when memory-loss causes concern, and on suspecting Alzheimer’s disease, the physician or healthcare specialists will confirm the diagnosis with a behavioral assessment and cognitive tests, often followed by a brain scan.

The cause and progression of Alzheimer's disease is not well understood, but is associated with plaques and tangles in the brain.Possible causes and potential cures of the disease have been conjectured, with varying evidence supporting each claim. No treatment has been found to stop or reverse the disease, and it is not known whether current treatments slow the progression, or simply manage the symptoms. Many preventative measures have been suggested for Alzheimer's disease, but their value is unproven in reducing the course and severity of the disease. Mental stimulation, exercise and a balanced diet are often recommended, both as a possible prevention and as a sensible way of managing the disease.

Due to the incurable and degenerative nature of the disease, care-management of Alzheimer's is essential. The role of the main caregiver is often taken by the spouse or a close relative.[11] Caregivers may themselves suffer from stress, over-work, depression, and being physically hit or struck.


Causes

Most cases of Alzheimer's disease do not exhibit familial inheritance. At least 80% of sporadic AD cases involve genetic risk factors. Inheritance of the ε4 allele of the apolipoprotein E (ApoE) gene is regarded as a risk factor for development of up to 50% of late-onset sporadic Alzheimer's. The presence of this gene allele along with infection by Herpes simplex virus type 1 (HSV-1) further increases the risk of Alzheimer's disease. Several viral-host interactions are postulated, most relating to HSV-1’s targeting of Alzheimer’s susceptibility genes.[42][43] Genetic experts agree that there are other risk and protective factor genes that influence the development of late onset Alzheimer's disease. Over 400 genes have been tested for association with late-onset sporadic AD.

Five to ten percent of AD cases involve a clear familial pattern of inheritance in which the patient has at least two first-degree relatives with a history of AD. These cases often have an early age of onset (usually younger than sixty years). Nearly 200 different mutations in the presenilin-1 or presenilin-2 genes have been documented in over 500 families. Mutations of presenilin 1 (PS1) lead to the most aggressive form of familial Alzheimer's disease. Over twenty different mutations in the amyloid precursor protein (APP) gene on chromosome 21 can also cause early onset of the disease. The presenilins have been identified as essential components of the proteolytic processing machinery that produces beta amyloid peptides through cleavage of APP. Most mutations in the APP and presenilin genes increase the production of a small protein (peptide) called Abeta42, the main component of senile plaques in brains of AD patients.
Prevention
At present contradictory results in global studies, incapacity to prove causal relationships between risk factors and the disease, and possible secondary effects indicate a lack of specific measures to prevent or delay the onset of AD.[93] Different epidemiological studies have proposed relationships between certain modifiable factors, such as diet, cardiovascular risk, pharmaceutical products, or intellectual activities among others, and a population's likelihood of developing AD. Only further research, including clinical trials, will reveal whether, in fact, these factors can help to prevent AD.

The components of a Mediterranean diet, which include fruit and vegetables, bread, wheat and other cereals, olive oil, fish, and red wine, may all individually or together reduce the risk and course of Alzheimer's disease. Vitamins E, B, and C, or folic acid have appeared to be related to a reduced risk of AD, but other studies indicate that they do not have any significant effect on the onset or course of the disease, while at the same time may have important secondary effects in conjunction with other therapies. Curcumin in curry has shown some effectiveness in preventing brain damage in mouse models.

Although cardiovascular risk factors, such as hypercholesterolemia, hypertension, diabetes, and smoking, are associated with a higher risk of onset and course of AD, statins, which are cholesterol lowering drugs, have not been effective in preventing or improving the course of the disease. However long-term usage of non-steroidal anti-inflammatory drug (NSAIDs), is associated with a reduced likelihood of developing AD in some individuals. Other pharmaceutical therapies such as female hormone replacement therapy are no longer thought to prevent dementia, while a 2007 systematic review concluded that there was inconsistent and unconvincing evidence that ginkgo has any positive effect on dementia or cognitive impairment.

Intellectual activities such as playing chess, completing crossword puzzles or regular social interaction, may also delay the onset or reduce the severity of Alzheimer's disease. Bilingualism is also related to a later onset of Alzheimer.

Are u a fitness fanatic??

100 Smartest Diet Tips Ever

1. Add just one fruit or veggie serving daily. Get comfortable with that, then add an extra serving until you reach 8 to 10 a day.

2. Eat at least two servings of a fruit or veggie at every meal.

3. Resolve never to supersize your food portions—unless you want to supersize your clothes.

4. Make eating purposeful, not mindless. Whenever you put food in your mouth, peel it, unwrap it, plate it, and sit. Engage all of the senses in the pleasure of nourishing your body.

5. Start eating a big breakfast. It helps you eat fewer total calories throughout the day.

6. Make sure your plate is half veggies and/or fruit at both lunch and dinner.

Are there Any Easy Tricks to Help Me Cut Calories?
7. Eating out? Halve it, and bag the rest. A typical restaurant entree has 1,000 to 2,000 calories, not even counting the bread, appetizer, beverage, and dessert.

8. When dining out, make it automatic: Order one dessert to share.

9. Use a salad plate instead of a dinner plate.

10. See what you eat. Plate your food instead of eating out of the jar or bag.

11. Eat the low-cal items on your plate first, then graduate. Start with salads, veggies, and broth soups, and eat meats and starches last. By the time you get to them, you'll be full enough to be content with smaller portions of the high-calorie choices.

12. Instead of whole milk, switch to 1 percent. If you drink one 8-oz glass a day, you'll lose 5 lb in a year.

13. Juice has as many calories, ounce for ounce, as soda. Set a limit of one 8-oz glass of fruit juice a day.

14. Get calories from foods you chew, not beverages. Have fresh fruit instead of fruit juice.

and much more....
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