ECZEMA

Eczema is a general term for many types of skin inflammation, also known as dermatitis. The most common form of eczema is atopic dermatitis (some people use these two terms interchangeably). However, there are many different forms of eczema.

Eczema can affect people of any age, although the condition is most common in infants, and about 85% of people have an onset prior to 5 years of age. Eczema will permanently resolve by age 3 in about half of affected infants. In others, the condition tends to recur throughout life. People with eczema often have a family history of the condition or a family history of other allergic conditions, such as asthma or hay fever. Up to 20% of children and 1%-2% of adults are believed to have eczema. Eczema is slightly more common in girls than in boys. It occurs in people of all races.

Eczema is not contagious, but since it is believed to be at least partially inherited, it is not uncommon to find members of the same family affected.

Some forms of eczema can be triggered by substances that come in contact with the skin, such as soaps, cosmetics, clothing, detergents, jewelry, or sweat. Environmental allergens (substances that cause allergic reactions) may also cause outbreaks of eczema. Changes in temperature or humidity, or even psychological stress, can lead to outbreaks of eczema in some people.

Eczema most commonly causes dry, reddened skin that itches or burns, although the appearance of eczema varies from person to person and varies according to the specific type of eczema. Intense itching is generally the first symptom in most people with eczema. Sometimes, eczema may lead to blisters and oozing lesions, but eczema can also result in dry and scaly skin. Repeated scratching may lead to thickened, crusty skin.

While any region of the body may be affected by eczema, in children and adults, eczema typically occurs on the face, neck, and the insides of the elbows, knees, and ankles. In infants, eczema typically occurs on the forehead, cheeks, forearms, legs, scalp, and neck.

Eczema can sometimes occur as a brief reaction that only leads to symptoms for a few hours or days, but in other cases, the symptoms persist over a longer time and are referred to as chronic dermatitis.

Atopic dermatitis

Atopic dermatitis is a chronic skin disease characterized by itchy, inflamed skin and is the most common cause of eczema. The condition tends to come and go, depending upon exposures to triggers or causative factors. Factors that may cause atopic dermatitis (allergens) include environmental factors like molds, pollen, or pollutants; contact irritants like soaps, detergents, nickel (in jewelry), or perfumes; food allergies; or other allergies. Around two-thirds of those who develop the condition do so prior to 1 year of age. When the disease starts in infancy, it is sometimes termed infantile eczema. Atopic dermatitis tends to run in families, and people who develop the condition often have a family history of other allergic conditions such as asthma or hay fever.

Contact eczema

Contact eczema (contact dermatitis) is a localized reaction that includes redness, itching, and burning in areas where the skin has come into contact with an allergen (an allergy-causing substance to which an individual is sensitized) or with a general irritant such as an acid, a cleaning agent, or other chemical. Other examples of contact eczema include reactions to laundry detergents, soaps, nickel (present in jewelry), cosmetics, fabrics, clothing, and perfume. Due to the vast number of substances with which individuals have contact, it can be difficult to determine the trigger for contact dermatitis. The condition is sometimes referred to as allergic contact eczema (allergic contact dermatitis) if the trigger is an allergen and irritant contact eczema (irritant contact dermatitis) if the trigger is an irritant. Skin reactions to poison ivy and poison sumac are examples of allergic contact eczema. People who have a history of allergies have an increased risk for developing contact eczema.

Seborrheic eczema

Seborrheic eczema (seborrheic dermatitis) is a form of skin inflammation of unknown cause. The signs and symptoms of seborrheic eczema include yellowish, oily, scaly patches of skin on the scalp, face, and occasionally other parts of the body. Dandruff and "cradle cap" in infants are examples of seborrheic eczema. It is commonplace for seborrheic dermatitis to inflame the face at the creases of the cheeks and/or the nasal folds. Seborrheic dermatitis is not necessarily associated with itching. This condition tends to run in families. Emotional stress, oily skin, infrequent shampooing, and weather conditions may all increase a person's risk of developing seborrheic eczema. One type of seborrheic eczema is also common in people with AIDS.

Nummular eczema

Nummular eczema (nummular dermatitis) is characterized by coin-shaped patches of irritated skin -- most commonly located on the arms, back, buttocks, and lower legs -- that may be crusted, scaling, and extremely itchy. This form of eczema is relatively uncommon and occurs most frequently in elderly men. Nummular eczema is usually a chronic condition. Neurodermatitis

This form of eczema results in scaly patches of skin on the head, lower legs, wrists, or forearms. Over time, the skin can become thickened and leathery. Stress can exacerbate the symptoms of neurodermatitis.

Stasis dermatitis

Stasis dermatitis is a skin irritation on the lower legs, generally related to the circulatory problem known as venous insufficiency, in which the function of the valves within the veins has been compromised. Stasis dermatitis occurs almost exclusively in middle-aged and elderly people, with approximately 6%-7% of the population over 50 years of age being affected by the condition. The risk of developing stasis dermatitis increases with advancing age.

Dyshidrotic eczema

Dyshidrotic eczema (dyshidrotic dermatitis) is an irritation of the skin on the palms of hands and soles of the feet characterized by clear, deep blisters that itch and burn.

ERECTILE DYSFUNCTION

Erectile dysfunction (ED, "male impotence ") is a sexual dysfunction characterized by the inability to develop or maintain an erection of the penis sufficient for satisfactory sexual performance.

An erection occurs as a hydraulic effect due to blood entering and being retained in sponge-like bodies within the penis. The process is most often initiated as a result of sexual arousal, when signals are transmitted from the brain to nerves in the penis. Erectile dysfunction is indicated when an erection is consistently difficult or impossible to produce, despite arousal. There are various and often multiple underlying causes, some of which are treatable medical conditions. The most important organic causes are cardiovascular disease and diabetes, neurological problems (for example, trauma from prostatectomy surgery), hormonal insufficiencies (hypogonadism) and drug side effects. It is important to realize that erectile dysfunction can signal underlying risk for cardiovascular disease.

There is often a contributing and complicating and sometimes a primary psychological or relational problem. Psychological impotence is where erection or penetration fails due to thoughts or feelings (psychological reasons) rather than physical impossibility; this can often be helped. Notably in psychological impotence, there is a strong response to placebo treatment. Erectile dysfunction, tied closely as it is to cultural notions of potency, success and masculinity, can have severe psychological consequences. There is a strong culture of silence and inability to discuss the matter. In reality, it has been estimated that around 1 in 10 men will experience recurring impotence problems at some point in their lives.

Erectile dysfunction is characterized by the regular or repeated inability to obtain or maintain an erection. There are several ways that erectile dysfunction is analyzed:

• Obtaining full erections at some times, such as when asleep (when the mind and psychological issues, if any, are less present), tends to suggest the physical structures are functionally working.

• Obtaining erections which are neither rigid nor full (lazy erection), or are lost more rapidly than would be expected (often before or during penetration), can be a sign of a failure of the mechanism which keeps blood held in the penis, and may signify an underlying clinical condition, often cardiovascular in origin.[citation needed]

• Other factors leading to erectile dysfunction are diabetes mellitus (causing neuropathy) or hypogonadism (decreased testosterone levels due to disease affecting the testicles or the pituitary gland).[citation needed]

Erection problems are very common. The Sexual Dysfunction Association estimates that 1 in 10 men in the UK have recurring problems with their erections at some point in their life.[2][not in citation given]

[edit] Causes

• Drugs (anti-depressants (SSRIs) and nicotine are most common. A study entitled "Drug-induced male sexual dysfunction" concluded that of the 12 most commonly prescribed medications on the market today, 8 of those medications list impotence as a side-effect of the drug.[ Other drugs such as alcohol, cocaine, and heroin negatively impact male sexual libido.)[
• Neurogenic Disorders (spinal cord and brain injuries, nerve disorders such as Parkinson's disease, Alzheimer's disease, multiple sclerosis, and stroke.[4])
• Hormonal Disorders (pituitary gland tumor; low or abnormally high levels of the hormone testosterone).[

• Arterial Disorders (peripheral vascular disease, hypertension; reduced blood flow to the penis
• Venous leak[
• vernosal Disorders (Peyronie's disease.[5])
• Psychological causes: performance anxiety, stress, mental disorders (clinical depression, schizophrenia, substance abuse, panic disorder, generalized anxiety disorder, personality disorders or traits.[6]), psychological problems, negative feelings.[7][
• Surgery (radiation therapy, surgery of the colon, prostate, bladder, or rectum may damage the nerves and blood vessels involved in erection. Prostate and bladder cancer surgery often require removing tissue and nerves surrounding a tumor, which increases the risk for impotence.[8])
• Aging
• Lifestyle: alcohol and drugs, obesity, cigarette smoking (Incidence of impotence is approximately 85 percent higher in male smokers compared to non-smokers
• Smoking is a key cause of erectile dysfunction.
• Smoking causes impotence because it promotes arterial narrowing.[12] See also Tobacco and health. )

A few causes of impotence may be iatrogenic (medically caused). Various antihypertensives (medications intended to control high blood pressure) and some drugs that modify central nervous system response may inhibit erection by denying blood supply or by altering nerve activity.[citation needed]

Surgical intervention for a number of different conditions may remove anatomical structures necessary to erection, damage nerves, or impair blood supply. Complete removal of the prostate gland or external beam radiotherapy of the gland are common causes of impotence; both are treatments for prostate cancer. Some studies have shown that male circumcision may result in an increased risk of impotence, while others have found no such effect,] and another found the opposite.

Excessive alcohol use has long been recognised as one cause of impotence, leading to the euphemism "brewer's droop," or "whiskey dick] Shakespeare made light of this phenomenon in Macbeth.

A study in 2002 found that ED can also be associated with bicycling. The number of hours on a bike and/or the pressure on the penis from the saddle of an upright bicycle is directly related to erectile dysfunction.[

Penile erection is managed by two different mechanisms. The first one is the reflex erection, which is achieved by directly touching the penile shaft. The second is the psychogenic erection, which is achieved by erotic or emotional stimuli. The former uses the peripheral nerves and the lower parts of the spinal cord, whereas the latter uses the limbic system of the brain. In both conditions, an intact neural system is required for a successful and complete erection. Stimulation of penile shaft by the nervous system leads to the secretion of nitric oxide (NO), which causes the relaxation of smooth muscles of corpora cavernosa (the main erectile tissue of penis), and subsequently penile erection. Additionally, adequate levels of testosterone (produced by the testes) and an intact pituitary gland are required for the development of a healthy erectile system. As can be understood from the mechanisms of a normal erection, impotence may develop due to hormonal deficiency, disorders of the neural system, lack of adequate penile blood supply or psychological problems. Restriction of blood flow can arise from impaired endothelial function due to the usual causes associated with coronary artery disease, but can also be caused by prolonged exposure to bright light.

FILARIASIS

Filariasis (Philariasis) is a parasitic and infectious tropical disease, that is caused by thread-like filarial nematode worms in the superfamily Filarioidea, also known as "filariae". There are 9 known filarial nematodes which use humans as the definitive host. These are divided into 3 groups according to the niche within the body that they occupy: Lymphatic Filariasis, Subcutaneous Filariasis, and Serous Cavity Filariasis. Lymphatic Filariasis is caused by the worms Wuchereria bancrofti, Brugia malayi, and Brugia timori. These worms occupy the lymphatic system, including the lymph nodes, and in chronic cases these worms lead to the disease Elephantiasis. Subcutaneous Filariasis is caused by Loa loa (the African eye worm), Mansonella streptocerca, Onchocerca volvulus, and Dracunculus medinensis (the guinea worm). These worms occupy the subcutaneous layer of the skin, the fat layer. Serous Cavity Filariasis is caused by the worms Mansonella perstans and Mansonella ozzardi, which occupy the serous cavity of the abdomen. In all cases, the transmitting vectors are either blood sucking insects (fly or mosquito) or Copepod crustaceans in the case of Dracunculus medinensis.

Human filarial nematode worms have a complicated life cycle, which primarily consists of five stages. After the male and female worm mate, the female gives birth to live microfilariae by the thousands. The microfilariae are taken up by the vector insect (intermediate host) during a blood meal. In the intermediate host, the microfilariae molt and develop into 3rd stage (infective) larvae. Upon taking another blood meal the vector insect injects the infectious larvae into the dermis layer of our skin. After approximately one year the larvae molt through 2 more stages, maturing into the adult worm.

Individuals infected by filarial worms may be described as either "microfilaraemic" or "amicrofilaraemic," depending on whether or not microfilaria can be found in their peripheral blood. Filariasis is diagnosed in microfilaraemic cases primarily through direct observation of microfilaria in the peripheral blood. Occult filariasis is diagnosed in amicrofilaraemic cases based on clinical observations and, in some cases, by finding a circulating antigen in the blood.

The most spectacular symptom of lymphatic filariasis is elephantiasis-edema with thickening of the skin and underlying tissues-which was the first disease discovered to be transmitted by mosquito bites[ Elephantiasis results when the parasites lodge in the lymphatic system.

Elephantiasis affects mainly the lower extremities, while the ears, mucus membranes, and amputation stumps are affected less frequently. However, different species of filarial worms tend to affect different parts of the body: Wuchereria bancrofti can affect the legs, arms, vulva, breasts, and scrotum (causing hydrocele formation) while Brugia timori rarely affects the genitals[Interestingly, those who develop the chronic stages of elephantiasis are usually amicrofilaraemic, and often have adverse immunlogical reactions to the microfilaria as well as the adult worm[

The subcutaneous worms present with skin rashes, urticarial papules, and arthritis, as well as hyper- and hypopigmentation macules. Onchocerca volvulus manifests itself in the eyes causing "river blindness" (onchocerciasis), the 2nd leading cause of blindness in the world[Serous cavity filariasis presents with symptoms similar to subcutaneous filariasis, in addition to abdominal pain because these worms are also deep tissue dwellers.

GALL BLADDER STONES

Gallstones are small, pebble-like substances that develop in the gallbladder. The gallbladder is a small, pear-shaped sac located below your liver in the right upper abdomen. Gallstones form when liquid stored in the gallbladder hardens into pieces of stone-like material. The liquid-called bile-helps the body digest fats. Bile is made in the liver, then stored in the gallbladder until the body needs it. The gallbladder contracts and pushes the bile into a tube-called the common bile duct-that carries it to the small intestine, where it helps with digestion.

Bile contains water, cholesterol, fats, bile salts, proteins, and bilirubin-a waste product. Bile salts break up fat, and bilirubin gives bile and stool a yellowish-brown color. If the liquid bile contains too much cholesterol, bile salts, or bilirubin, it can harden into gallstones.

The two types of gallstones are cholesterol stones and pigment stones. Cholesterol stones are usually yellow-green and are made primarily of hardened cholesterol. They account for about 80 percent of gallstones. Pigment stones are small, dark stones made of bilirubin. Gallstones can be as small as a grain of sand or as large as a golf ball. The gallbladder can develop just one large stone, hundreds of tiny stones, or a combination of the two

Gallstones can block the normal flow of bile if they move from the gallbladder and lodge in any of the ducts that carry bile from the liver to the small intestine. The ducts include the

• hepatic ducts, which carry bile out of the liver
• cystic duct, which takes bile to and from the gallbladder
• common bile duct, which takes bile from the cystic and hepatic ducts to the small intestine

Bile trapped in these ducts can cause inflammation in the gallbladder, the ducts, or in rare cases, the liver. Other ducts open into the common bile duct, including the pancreatic duct, which carries digestive enzymes out of the pancreas. Sometimes gallstones passing through the common bile duct provoke inflammation in the pancreas-called gallstone pancreatitis-an extremely painful and potentially dangerous condition.

If any of the bile ducts remain blocked for a significant period of time, severe damage or infection can occur in the gallbladder, liver, or pancreas. Left untreated, the condition can be fatal. Warning signs of a serious problem are fever, jaundice, and persistent pain.

Scientists believe cholesterol stones form when bile contains too much cholesterol, too much bilirubin, or not enough bile salts, or when the gallbladder does not empty completely or often enough. The reason these imbalances occur is not known.

The cause of pigment stones is not fully understood. The stones tend to develop in people who have liver cirrhosis, biliary tract infections, or hereditary blood disorders-such as sickle cell anemia-in which the liver makes too much bilirubin.

The mere presence of gallstones may cause more gallstones to develop. Other factors that contribute to the formation of gallstones, particularly cholesterol stones, include

• Sex. Women are twice as likely as men to develop gallstones. Excess estrogen from pregnancy, hormone replacement therapy, and birth control pills appears to increase cholesterol levels in bile and decrease gallbladder movement, which can lead to gallstones.
• Family history. Gallstones often run in families, pointing to a possible genetic link.
• Weight. A large clinical study showed that being even moderately overweight increases the risk for developing gallstones. The most likely reason is that the amount of bile salts in bile is reduced, resulting in more cholesterol. Increased cholesterol reduces gallbladder emptying. Obesity is a major risk factor for gallstones, especially in women.
• Diet. Diets high in fat and cholesterol and low in fiber increase the risk of gallstones due to increased cholesterol in the bile and reduced gallbladder emptying.
• Rapid weight loss. As the body metabolizes fat during prolonged fasting and rapid weight loss-such as "crash diets"-the liver secretes extra cholesterol into bile, which can cause gallstones. In addition, the gallbladder does not empty properly.
• Age. People older than age 60 are more likely to develop gallstones than younger people. As people age, the body tends to secrete more cholesterol into bile.
• Ethnicity. American Indians have a genetic predisposition to secrete high levels of cholesterol in bile. In fact, they have the highest rate of gallstones in the United States. The majority of American Indian men have gallstones by age 60. Among the Pima Indians of Arizona, 70 percent of women have gallstones by age 30. Mexican American men and women of all ages also have high rates of gallstones.
• Cholesterol-lowering drugs. Drugs that lower cholesterol levels in the blood actually increase the amount of cholesterol secreted into bile. In turn, the risk of gallstones increases.
• Diabetes. People with diabetes generally have high levels of fatty acids called triglycerides. These fatty acids may increase the risk of gallstones.

As gallstones move into the bile ducts and create blockage, pressure increases in the gallbladder and one or more symptoms may occur. Symptoms of blocked bile ducts are often called a gallbladder "attack" because they occur suddenly. Gallbladder attacks often follow fatty meals, and they may occur during the night. A typical attack can cause

• steady pain in the right upper abdomen that increases rapidly and lasts from 30 minutes to several hours
• pain in the back between the shoulder blades
• pain under the right shoulder
• Notify your doctor if you think you have experienced a gallbladder attack. Although these attacks often pass as gallstones move, your gallbladder can become infected and rupture if a blockage remains.
• People with any of the following symptoms should see a doctor immediately:
• prolonged pain-more than 5 hours
• nausea and vomiting
• fever-even low-grade-or chills
• yellowish color of the skin or whites of the eyes
• clay-colored stools
• Many people with gallstones have no symptoms; these gallstones are called "silent stones." They do not interfere with gallbladder, liver, or pancreas function and do not need treatment.

GERD

Gerd may refer to Gastroesophageal Reflux Disease (GERD)

• Gastroesophageal reflux disease (GERD), gastro-oesophageal reflux disease (GORD), gastric reflux disease, or acid reflux disease is defined as chronic symptoms or mucosal damage produced by the abnormal reflux of stomach acid to the esophagus.[1] A typical symptom is heartburn.
• This is commonly due to transient or permanent changes in the barrier between the esophagus and the stomach. This can be due to incompetence of the lower esophageal sphincter, transient lower esophageal sphincter relaxation, impaired expulsion of gastric reflux from the esophagus, or a hiatal hernia.
• A different type of acid reflux which produces respiratory and laryngeal manifestations is laryngopharyngeal reflux (LPR), also called extraesophageal reflux disease (EERD). Unlike GERD, LPR is unlikely to produce heartburn, and is thus sometimes called silent reflux.

The most-common symptoms of GERD are:

• Heartburn
• Regurgitation
• Trouble swallowing (dysphagia)

Less-common symptoms include:

• Pain with swallowing (odynophagia)
• Excessive salivation (this is common during heartburn, as saliva is generally slightly basic[2] and is the body's natural response to heartburn, acting similarly to an antacid)
• Nausea[3]
• Chest pain

GERD sometimes causes injury of the esophagus. These injuries may include:

• Reflux esophagitis-necrosis of esophageal epithelium causing ulcers near the junction of the stomach and esophagus.
• Esophageal strictures-the persistent narrowing of the esophagus caused by reflux-induced inflammation.
• Barrett's esophagus-metaplasia (changes of the epithelial cells from squamous to columnar epithelium) of the distal esophagus.
• Esophageal adenocarcinoma-a rare form of cancer.[3]

Several other atypical symptoms are associated with GERD, but there is good evidence for causation only when they are accompanied by esophageal injury. These symptoms are:

• Chronic cough
• Laryngitis (hoarseness, throat clearing)
• Asthma
• Erosion of dental enamel
• Dentine hypersensitivity
• Sinusitis and damaged teeth[4]

Some people have proposed that symptoms such as pharyngitis, sinusitis, recurrent ear infections, and idiopathic pulmonary fibrosis are due to GERD; however, a causative role has not been established.[3]

GERD may be difficult to detect in infants and children. Symptoms may vary from typical adult symptoms. GERD in children may cause repeated vomiting, effortless spitting up, coughing, and other respiratory problems. Inconsolable crying, failure to gain adequate weight, refusing food, bad breath, and belching or burping are also common.

Common symptoms of Pediatric Reflux

• Irritability and pain, sometimes screaming suddenly when asleep. Constant or sudden crying or "colic" like symptoms. Babies can be inconsolable especially when laid down flat.
• Poor sleep habits typically with arching their necks and back during or after feeding
• Excessive possetting or vomiting
• Frequent burping or frequent hiccups
• Excessive dribbling or running nose
• Swallowing problems, gagging and choking
• Frequent ear infections or sinus congestion
• Babies are often very gassy and extremely difficult to "burp" after feeds
• Refusing feeds or frequent feeds for comfort
• Night time coughing, extreme cases of acid reflux can cause apnoea and respiratory problems such as asthma, bronchitis and pneumonia if stomach contents are inhaled.
• Bad breath - smelling acidy
• Rancid/acid smelling diapers with loose stool. Bowel movements can be very frequent or babies can be constipated.

HAEMORRHOIDS

The term hemorrhoids refers to a condition in which the veins around the anus or lower rectum are swollen and inflamed.

Hemorrhoids may result from straining to move stool. Other contributing factors include pregnancy, aging, chronic constipation or diarrhea, and anal intercourse.

Hemorrhoids are either inside the anus-internal-or under the skin around the anus-external.

Many anorectal problems, including fissures, fistulae, abscesses, or irritation and itching, also called pruritus ani, have similar symptoms and are incorrectly referred to as hemorrhoids.

Hemorrhoids usually are not dangerous or life threatening. In most cases, hemorrhoidal symptoms will go away within a few days.

Although many people have hemorrhoids, not all experience symptoms. The most common symptom of internal hemorrhoids is bright red blood covering the stool, on toilet paper, or in the toilet bowl. However, an internal hemorrhoid may protrude through the anus outside the body, becoming irritated and painful. This is known as a protruding hemorrhoid.

Symptoms of external hemorrhoids may include painful swelling or a hard lump around the anus that results when a blood clot forms. This condition is known as a thrombosed external hemorrhoid.

In addition, excessive straining, rubbing, or cleaning around the anus may cause irritation with bleeding and/or itching, which may produce a vicious cycle of symptoms. Draining mucus may also cause itching.

Hemorrhoids are common in both men and women. About half of the population has hemorrhoids by age 50. Hemorrhoids are also common among pregnant women. The pressure of the fetus on the abdomen, as well as hormonal changes, cause the hemorrhoidal vessels to enlarge. These vessels are also placed under severe pressure during childbirth. For most women, however, hemorrhoids caused by pregnancy are a temporary problem.

A thorough evaluation and proper diagnosis by the doctor is important any time bleeding from the rectum or blood in the stool occurs. Bleeding may also be a symptom of other digestive diseases, including colorectal cancer.

The doctor will examine the anus and rectum to look for swollen blood vessels that indicate hemorrhoids and will also perform a digital rectal exam with a gloved, lubricated finger to feel for abnormalities.

Closer evaluation of the rectum for hemorrhoids requires an exam with an anoscope, a hollow, lighted tube useful for viewing internal hemorrhoids, or a proctoscope, useful for more completely examining the entire rectum.

Medical treatment of hemorrhoids is aimed initially at relieving symptoms. Measures to reduce symptoms include

• tub baths several times a day in plain, warm water for about 10 minutes
• application of a hemorrhoidal cream or suppository to the affected area for a limited time

Preventing the recurrence of hemorrhoids will require relieving the pressure and straining of constipation. Doctors will often recommend increasing fiber and fluids in the diet. Eating the right amount of fiber and drinking six to eight glasses of fluid-not alcohol-result in softer, bulkier stools. A softer stool makes emptying the bowels easier and lessens the pressure on hemorrhoids caused by straining. Eliminating straining also helps prevent the hemorrhoids from protruding.

Good sources of fiber are fruits, vegetables, and whole grains. In addition, doctors may suggest a bulk stool softener or a fiber supplement such as psyllium (Metamucil) or methylcellulose (Citrucel).

The best way to prevent hemorrhoids is to keep stools soft so they pass easily, thus decreasing pressure and straining, and to empty bowels as soon as possible after the urge occurs. Exercise, including walking, and increased fiber in the diet help reduce constipation and straining by producing stools that are softer and easier to pass.

HEPATITIS

Hepatitis (plural hepatitides) implies inflammation of the liver characterized by the presence of inflammatory cells in the tissue of the organ. The name is from the Greek hepar the root being hepat- , meaning liver, and suffix -itis, meaning "inflammation" (The condition can be self-limiting (healing on its own) or can progress to fibrosis (scarring) and cirrhosis.

Hepatitis may occur with limited or no symptoms (subclinically), but often leads to jaundice, anorexia (poor appetite) and malaise. Hepatitis is acute when it lasts less than six months and chronic when it persists longer. A group of viruses known as the hepatitis viruses cause most cases of hepatitis worldwide, but it can also be due to toxins (notably alcohol, certain medications and plants), other infections and autoimmune diseases.

Acute

Initial features are of nonspecific flu-like symptoms, common to almost all acute viral infections and may include malaise, muscle and joint aches, fever, nausea or vomiting, diarrhea, and headache. More specific symptoms, which can be present in acute hepatitis from any cause, are: profound loss of appetite, aversion to smoking among smokers, dark urine, yellowing of the eyes and skin (i.e., jaundice) and abdominal discomfort. Physical findings are usually minimal, apart from jaundice in a third and tender hepatomegaly (swelling of the liver) in about 10%. Some exhibit lymphadenopathy (enlarged lymph nodes, in 5%) or splenomegaly (enlargement of the spleen, in 5%).[2]

Acute viral hepatitis is more likely to be asymptomatic in younger people. Symptomatic individuals may present after convalescent stage of 7 to 10 days, with the total illness lasting 2 to 6 weeks.[3]

A small proportion of people with acute hepatitis progress to acute liver failure, in which the liver is unable to clear harmful substances from the circulation (leading to confusion and coma due to hepatic encephalopathy) and produce blood proteins (leading to peripheral edema and bleeding). This may become life-threatening and occasionally requires a liver transplant.

Chronic

Chronic hepatitis often leads nonspecific symptoms such as malaise, tiredness and weakness, and often leads to no symptoms at all. It is commonly identified on blood tests performed either for screening or to evaluate nonspecific symptoms. The occurrence of jaundice indicates advanced liver damage. On physical examination there may be enlargement of the liver.[4]

Extensive damage and scarring of liver (i.e. cirrhosis) leads to weight loss, easy bruising and bleeding tendencies, peripheral edema (swelling of the legs) and accumulation of ascites (fluid in the abdominal cavity). Eventually, cirrhosis may lead to various complications: esophageal varices (enlarged veins in the wall of the esophagus that can cause life-threatening bleeding) hepatic encephalopathy (confusion and coma) and hepatorenal syndrome (kidney dysfunction).

Acne, abnormal menstruation, lung scarring, inflammation of the thyroid gland and kidneys may be present in women with autoimmune hepatitis.

Acute Causes

• Viral hepatitis:
  • Hepatitis A through E (more than 95% of viral cause)
  • Herpes simplex
  • Cytomegalovirus
  • Epstein-Barr
  • yellow fever virus
  • adenoviruses
• Non viral infection
  • toxoplasma
  • Leptospira
  • Q fever[5]
  • rocky mountain spotted fever[6]
• 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 Causes

• Viral hepatitis: Hepatitis B with or without hepatitis D, hepatitis C (neither hepatitis A nor hepatitis E causes chronic hepatitis)
• Autoimmune
  • Autoimmune hepatitis
• Alcohol
• Drugs
  • methyldopa
  • nitrofurantoin
  • isoniazid
  • ketoconazole
• Non-alcoholic steatohepatitis
• Heredity
  • Wilson's disease
  • alpha 1-antitrypsin deficiency
• Primary biliary cirrhosis and primary sclerosing cholangitis occasionally mimic chronic hepatitis[

HYPOTHYROIDISM

Hypothyroidism is a condition characterized by abnormally low thyroid hormone production. There are many disorders that result in hypothyroidism. These disorders may directly or indirectly involve the thyroid gland. Because thyroid hormone affects growth, development, and many cellular processes, inadequate thyroid hormone has widespread consequences for the body.

Thyroid hormones are produced by the thyroid gland. This gland is located in the lower part of the neck, below the Adam's apple. The gland wraps around the windpipe (trachea) and has a shape that is similar to a butterfly - formed by two wings (lobes) and attached by a middle part (isthmus).

The thyroid gland uses iodine (mostly available from the diet in foods such as seafood, bread, and salt) to produce thyroid hormones. The two most important thyroid hormones are thyroxine (T4) and triiodothyronine (T3), which account for 99% and 1% of thyroid hormones present in the blood respectively. However, the hormone with the most biological activity is T3. Once released from the thyroid gland into the blood, a large amount of T4 is converted into T3 - the active hormone that affects the metabolism of cells.

Hypothyroidism is a very common condition. It is estimated that 3% to 5% of the population has some form of hypothyroidism. The condition is more common in women than in men, and its incidence increases with age.

Below is a list of some of the common causes of hypothyroidism in adults followed by a discussion of these conditions.

• Hashimoto's thyroiditis
• Lymphocytic thyroiditis (which may occur after hyperthyroidism)
• Thyroid destruction (from radioactive iodine or surgery)
• Pituitary or hypothalamic disease
• Medications
• Severe iodine deficiency

Hashimoto's Thyroiditis

The most common cause of hypothyroidism in the United States is an inherited condition called Hashimoto's thyroiditis. This condition is named after Dr. Hakaru Hashimoto who first described it in 1912. In this condition, the thyroid gland is usually enlarged (goiter) and has a decreased ability to make thyroid hormones. Hashimoto's is an autoimmune disease in which the body's immune system inappropriately attacks the thyroid tissue. In part, this condition is believed to have a genetic basis. This means that the tendency toward developing Hashimoto's thyroiditis can run in families. Hashimoto's is 5 to 10 times more common in women than in men. Blood samples drawn from patients with this disease reveal an increased number of antibodies to the enzyme, thyroid peroxidase (anti-TPO antibodies). Since the basis for autoimmune diseases may have a common origin, it is not unusual to find that a patient with Hashimoto's thyroiditis has one or more other autoimmune diseases such as diabetes or pernicious anemia ( B12 deficiency). Hashimoto's can be identified by detecting anti-TPO antibodies in the blood and/or by performing a thyroid scan.

Lymphocytic thyroiditis following hyperthyroidism

Thyroiditis refers to inflammation of the thyroid gland. When the inflammation is caused by a particular type of white blood cell known as a lymphocyte, the condition is referred to as lymphocytic thyroiditis. This condition is particularly common after pregnancy and can actually affect up to 8% of women after they deliver. In these cases, there is usually a hyperthyroid phase (in which excessive amounts of thyroid hormone leak out of the inflamed gland), which is followed by a hypothyroid phase that can last for up to six months. The majority of affected women eventually return to a state of normal thyroid function, although there is a possibility of remaining hypothyroid.

Thyroid destruction secondary to radioactive iodine or surgery

Patients who have been treated for a hyperthyroid condition (such as Graves' disease) and received radioactive iodine may be left with little or no functioning thyroid tissue after treatment. The likelihood of this depends on a number of factors including the dose of iodine given, along with the size and the activity of the thyroid gland. If there is no significant activity of the thyroid gland six months after the radioactive iodine treatment, it is usually assumed that the thyroid will no longer function adequately. The result is hypothyroidism. Similarly, removal of the thyroid gland during surgery will be followed by hypothyroidism.

Pituitary or Hypothalamic disease

If for some reason the pituitary gland or the hypothalamus are unable to signal the thyroid and instruct it to produce thyroid hormones, a decreased level of circulating T4 and T3 may result, even if the thyroid gland itself is normal. If this defect is caused by pituitary disease, the condition is called "secondary hypothyroidism." If the defect is due to hypothalamic disease, it is called "tertiary hypothyroidism."

Severe iodine deficiency:

In areas of the world where there is an iodine deficiency in the diet, severe hypothyroidism can be seen in 5% to 15% of the population. Examples of these areas include Zaire, Ecuador, India, and Chile. Severe iodine deficiency is also seen in remote mountain areas such as the Andes and the Himalayas. Since the addition of iodine to table salt and to bread, iodine deficiency is rarely seen in the United States.

A diagnosis of hypothyroidism can be suspected in patients with fatigue, cold intolerance, constipation, and dry, flaky skin. A blood test is needed to confirm the diagnosis.

When hypothyroidism is present, the blood levels of thyroid hormones can be measured directly and are usually decreased. However, in early hypothyroidism, the level of thyroid hormones (T3 and T4) may be normal. Therefore, the main tool for the detection of hyperthyroidism is the measurement of the TSH, the thyroid stimulating hormone. As mentioned earlier, TSH is secreted by the pituitary gland. If a decrease of thyroid hormone occurs, the pituitary gland reacts by producing more TSH and the blood TSH level increases in an attempt to encourage thyroid hormone production. This increase in TSH can actually precede the fall in thyroid hormones by months or years (see the section on Subclinical Hypothyroidism below). Thus, the measurement of TSH should be elevated in cases of hypothyroidism

ICHTHYOSIS

Ichthyosis (plural ichthyoses) is a heterogeneous family of at least 28[1], generalized, mostly genetic skin disorders. All types of ichthyosis have dry, thickened, scaly or flaky skin.[1] In many types the skin is said to resemble the scales on a fish; the word ichthyosis comes from the Ancient Greek (ichthys), meaning "fish."[2] The severity of symptoms can vary enormously, from the mildest types such as ichthyosis vulgaris which may be mistaken for normal dry skin up to life-threatening conditions such as harlequin type ichthyosis. The most common type of ichthyosis is ichthyosis vulgaris, accounting for more than 95% of cases.

There are many types of ichthyosis and an exact diagnosis may be difficult. Types of ichthyosis are classified by their appearance and their genetic cause. Ichthyoses caused by the same gene can vary considerably in severity and symptoms. Some ichthyoses don't appear to fit exactly into any one type. Also different genes can produce ichthyosis with similar symptoms. The most common or well-known types are as follows:[4]

Genetic ichthyoses

• Ichthyosis vulgaris
• X-linked ichthyosis
• Congenital ichthyosiform erythroderma (nbCIE)
• Epidermolytic hyperkeratosis (bullous ichthyosis, bCIE)
• Harlequin type ichthyosis
• Ichthyosis bullosa of Siemens
• Ichthyosis hystrix
• Ichthyosis lamellaris (lamellar ichthyosis)

Ichthyoses with additional characteristics

• Carvajal syndrome
• CHILD Syndrome
• Conradi-Hünermann syndrome
• Darier's disease
• Erythrokeratodermia variabilis (Erythrokeratodermia figurata variabilis, Mendes da Costa type erythrokeratodermia)
• IFAP syndrome (Ichthyosis follicularis)
• Keratitis-ichthyosis-deafness syndrome
• Netherton syndrome
• Neutral lipid storage disease (Dorfman-Chanarin syndrome)
• Refsum's disease
• Rud syndrome
• Senter syndrome
• Sjögren-Larsson syndrome
• Tay syndrome (IBIDS syndrome, Trichothiodystrophy)

Non-genetic ichthyosis

• Ichthyosis acquisita

Treatment:

• Do not take hot baths or showers, they dry out the skin. Use warm to cool water. Soap should not be used on your skin because it irritates and dries the skin. You should use the soap substitute Cetaphil lotion which is available from the pharmacy without a prescription.
• Do not rub the skin dry after you bathe.  Blot your skin gently then apply an Alpha hydroxyacid lotions.  Neostrata 15 AHA Body/Face Lotion is a very effective treatment for ichthyosis when applied to moist skin after bathing.
• The doctor can prescribe an Alpha hydroxyacid lotion for your skin which will dissolve the scales and will increase the moisture content of your skin.
• There is no cure for ichthyosis. This is a life-long condition which can be managed or controlled.
• Living in a warm climate often improves ichthyosis.

IRREGULAR MENSES

Irregular menses, as measured from the start of one menses to the start of another, seem to occur in two patterns:

• Onset of menses varies irregularly from about 3 weeks to 6 weeks but not skipping a month altogether. It is called metrorrhagia if many of the menses are less than 4 weeks.
• Onset of menses varies from 4 weeks to 3-6 months having perhaps only 2-6 menses a year. This is called oligomenorrhea, infrequent menses.

Oligomenorrhea, the infrequent, irregular menses pattern is caused by lack of ovulation. However, it may further be subdivided into a low estrogen type in which there are no follicles being developed and a high estrogen type in which the follicles are developed but they are arrested so none of the eggs are released (ovulated) from the ovary.

To answer the question above, we really need to identify what type of irregular menses is involved as well as the goals of treatment. For example, is the goal just to have a more predictable menstrual flow or is it to try to time intercourse in order to improve the chances of conception? Is the goal to be more regular so that a rhythm method of contraception works or to plan work or leisure events so as to avoid interruption by a mense?

Causes of the metrorrhagia irregular menses pattern are unknown or are more likely related to stresses and ingested medications or substances that disrupt corpus luteum function or even act as anticoagulant blood thinners. Caffeine may act this way and disrupt corpus luteum function. Heavy caffeine consumers tend to have twice the risk of short cycle length (less than 24 days) (1). Their cycles are not heavier but they are often more frequent.

Cigarette smoking is another agent that can shorten menstrual cycles

(2). Cigarettes seem to shorten the follicular phase but heavier smoking also may shorten the luteal phase. Both heavy smoking and even smoking just 10 cigarettes or more a day may cause menstrual cycles to be shorter in length, as well as more variable in their lengths than nonsmokers.

Acute or excessive alcohol ingestion, getting drunk on occasion, is also known to alter menstrual patterns

(3). Sometimes it shortens cycles while at other times it can cause a delay of menses. The alcohol is thought to affect the liver's ability to properly metabolize estrogen and progesterone.

There are many things that can block ovulation in women. Stress is the most common cause. Eating disorders such as bulimia and anorexia also cause low estrogen and menstrual delay. If there are no menses at all, this is called hypothalamic amenorrhea. The mechanism for this is not totally known but probably has to do with alteration of brain proteins and hormones so that the normal ovulatory releasing factors do not work. When the brain releasing factors do not stimulate follicle development, there are few estrogens produced and a woman is then at risk for osteoporosis at a young age. This is why physicians prescribe estrogens in this condition, i.e., to prevent bone loss.

Recreational running does not seem to change menstrual cycle length , but strenuous endurance running can disturb cycle length and make a woman anovulatory. Long distance runners and other strenuous sports have been well known to cause anovulation of the low estrogen type. There has even been a suggestion that being a vegetarian may increase the risk of anovulation

While the most common cause of irregular delayed menses is due to stress type hypothalamic amenorrhea, the next most frequent type is due to polycystic ovarian syndrome. This is a complex condition of the ovaries in which follicles seem to grow and produce estrogen but the egg does not get released. This results in a high estrogen condition but infrequent menses. When the period does start, it often can be a very heavy one that persists for days or even weeks. The continuous, high estrogens cause the uterine lining to grow and proliferate and eventually it gets too thick and then sloughs off causing a menstrual like bleed. Because of the chronic and continuous estrogen stimulation, most doctors feel that a menstrual period should be induced with hormones (progesterone/progestin) so that a woman is not at risk for endometrial cancer.

Women who have polycystic ovarian syndrome (PCOS) will frequently have abnormal carbohydrate metabolism called insulin resistance or even develop diabetes. Additionally, excess hair growth due to extra testosterone occurs in many women with PCOS.

For a metrorrhagia type of irregular menstrual pattern, it is important to give up tobacco, alcohol and cut caffeine servings down to 2 or less per day. Try to minimize any medications that you do not have to take. If menses are mildly irregular and you are trying to time conception, taking a phytoestrogen supplement on a daily basis may help stabilize the menstrual cycle length.

For a low estrogen, irregular menstrual problem, the key treatments are:

• stress reduction and/or relaxation techniques
• elimination of overly strenuous physical exercise
• eliminate any eating disorders such as purging, bulimia, or anorexia
• take supplemental, measured estrogens such as phytoestrogens in soy or clover products

For a high estrogen irregular menses pattern such as that found in PCOS, weight reduction using a low carbohydrate diet is essential. Even a 10% weight loss will help restore normal menstrual patterns in obese women who are anovulatory

KIDNEY STONES

Kidney stones, one of the most painful of the urologic disorders, have beset humans for centuries. Scientists have found evidence of kidney stones in a 7,000-year-old Egyptian mummy. Unfortunately, kidney stones are one of the most common disorders of the urinary tract. Each year, people make almost 3 million visits to health care providers and more than half a million people go to emergency rooms for kidney stone problems.

Most kidney stones pass out of the body without any intervention by a physician. Stones that cause lasting symptoms or other complications may be treated by various techniques, most of which do not involve major surgery. Also, research advances have led to a better understanding of the many factors that promote stone formation and thus better treatments for preventing stones.

A kidney stone is a hard mass developed from crystals that separate from the urine within the urinary tract. Normally, urine contains chemicals that prevent or inhibit the crystals from forming. These inhibitors do not seem to work for everyone, however, so some people form stones. If the crystals remain tiny enough, they will travel through the urinary tract and pass out of the body in the urine without being noticed.

Kidney stones may contain various combinations of chemicals. The most common type of stone contains calcium in combination with either oxalate or phosphate. These chemicals are part of a person's normal diet and make up important parts of the body, such as bones and muscles.

A less common type of stone is caused by infection in the urinary tract. This type of stone is called a struvite or infection stone. Another type of stone, uric acid stones, are a bit less common, and cystine stones are rare.

Urolithiasis is the medical term used to describe stones occurring in the urinary tract. Other frequently used terms are urinary tract stone disease and nephrolithiasis. Doctors also use terms that describe the location of the stone in the urinary tract. For example, a ureteral stone-or ureterolithiasis-is a kidney stone found in the ureter. To keep things simple, the general term kidney stones is used throughout this fact sheet.

Cystinuria and hyperoxaluria are two other rare, inherited metabolic disorders that often cause kidney stones. In cystinuria, too much of the amino acid cystine, which does not dissolve in urine, is voided, leading to the formation of stones made of cystine. In patients with hyperoxaluria, the body produces too much oxalate, a salt. When the urine contains more oxalate than can be dissolved, the crystals settle out and form stones.

Hypercalciuria is inherited, and it may be the cause of stones in more than half of patients. Calcium is absorbed from food in excess and is lost into the urine. This high level of calcium in the urine causes crystals of calcium oxalate or calcium phosphate to form in the kidneys or elsewhere in the urinary tract.

Other causes of kidney stones are hyperuricosuria, which is a disorder of uric acid metabolism; gout; excess intake of vitamin D; urinary tract infections; and blockage of the urinary tract. Certain diuretics, commonly called water pills, and calcium-based antacids may increase the risk of forming kidney stones by increasing the amount of calcium in the urine.

Calcium oxalate stones may also form in people who have chronic inflammation of the bowel or who have had an intestinal bypass operation, or ostomy surgery. As mentioned earlier, struvite stones can form in people who have had a urinary tract infection. People who take the protease inhibitor indinavir, a medicine used to treat HIV infection, may also be at increased risk of developing kidney stones.

Foods and Drinks Containing Oxalate

People prone to forming calcium oxalate stones may be asked by their doctor to limit or avoid certain foods if their urine contains an excess of oxalate.

High-oxalate foods-higher to lower

• rhubarb
• spinach
• beets
• swiss chard
• wheat germ
• soybean crackers
• peanuts
• okra
• chocolate
• black Indian tea
• sweet potatoes

Foods that have medium amounts of oxalate may be eaten in limited amounts.

Medium-oxalate foods-higher to lower

• grits
• grapes
• celery
• green pepper
• red raspberries
• fruit cake
• strawberries
• marmalade
• liver

Kidney stones often do not cause any symptoms. Usually, the first symptom of a kidney stone is extreme pain, which begins suddenly when a stone moves in the urinary tract and blocks the flow of urine. Typically, a person feels a sharp, cramping pain in the back and side in the area of the kidney or in the lower abdomen. Sometimes nausea and vomiting occur. Later, pain may spread to the groin.

If the stone is too large to pass easily, pain continues as the muscles in the wall of the narrow ureter try to squeeze the stone into the bladder. As the stone moves and the body tries to push it out, blood may appear in the urine, making the urine pink. As the stone moves down the ureter, closer to the bladder, a person may feel the need to urinate more often or feel a burning sensation during urination.

If fever and chills accompany any of these symptoms, an infection may be present. In this case, a person should contact a doctor immediately.

LEUCODERMA

Leucoderma, also known as vitiligo, is a distressing skin condition. The word literally means white skin. There is a gradual loss of the pigment melanin from the skin layers which results in white patches The condition does not cause any organic harm. This disease is caused neither by any germs, nor is it due to bad blood. It is considered to be neither infectious nor contagious.

Vitiligo is a pigmentation disorder in which melanocytes (the cells that make pigment) in the skin are destroyed. As a result, white patches appear on the skin in different parts of the body. Similar patches also appear on both the mucous membranes (tissues that line the inside of the mouth and nose), and the retina (inner layer of the eyeball). The hair that grows on areas affected by vitiligo sometimes turns white.

The cause of vitiligo is not known, but doctors and researchers have several different theories. There is strong evidence that people with vitiligo inherit a group of three genes that make them susceptible to depigmentation. The most widely accepted view is that the depigmentation occurs because vitiligo is an autoimmune disease -- a disease in which a person's immune system reacts against the body's own organs or tissues.

About 0.5 to 1 percent of the world's population, or as many as 65 million people, have vitiligo. In the United States, 1 to 2 million people have the disorder. Half the people who have vitiligo develop it before age 20; most develop it before their 40th birthday. The disorder affects both sexes and all races equally; however, it is more noticeable in people with dark skin.

Scientists do not know the reason for the association between vitiligo and these autoimmune diseases. However, most people with vitiligo have no other autoimmune disease.

Vitiligo may also be hereditary; that is, it can run in families. Children whose parents have the disorder are more likely to develop vitiligo. In fact, 30 percent of people with vitiligo have a family member with the disease. However, only 5 to 7 percent of children will get vitiligo even if a parent has it, and most people with vitiligo do not have a family history of the disorder.

People who develop vitiligo usually first notice white patches (depigmentation) on their skin. These patches are more commonly found on sun-exposed areas of the body, including the hands, feet, arms, face, and lips. Other common areas for white patches to appear are the armpits and groin, and around the mouth, eyes, nostrils, navel, genitals, and rectum.

Vitiligo generally appears in one of three patterns:

1. focal pattern -- the depigmentation is limited to one or only a few areas

2. segmental pattern -- depigmented patches develop on only one side of the body

3. generalized pattern -- the most common pattern. Depigmentation occurs symmetrically on both sides of the body.

In addition to white patches on the skin, people with vitiligo may have premature graying of the scalp hair, eyelashes, eyebrows, and beard. People with dark skin may notice a loss of color inside their mouths.

Focal pattern vitiligo and segmental vitiligo remain localized to one part of the body and do not spread. There is no way to predict if generalized vitiligo will spread. For some people, the depigmented patches do not spread. The disorder is usually progressive, however, and over time the white patches will spread to other areas of the body. For some people, vitiligo spreads slowly, over many years. For other people, spreading occurs rapidly. Some people have reported additional depigmentation following periods of physical or emotional stress.

The diagnosis of vitiligo is made based on a physical examination, medical history, and laboratory tests.

A doctor will likely suspect vitiligo if you report (or the physical examination reveals) white patches of skin on the body-particularly on sun-exposed areas, including the hands, feet, arms, face, and lips. If vitiligo is suspected, the doctor will ask about your medical history. Important factors in the diagnosis include a family history of vitiligo; a rash, sunburn, or other skin trauma at the site of vitiligo 2 to 3 months before depigmentation started; stress or physical illness; and premature (before age 35) graying of the hair.

To help confirm the diagnosis, the doctor may take a small sample (biopsy) of the affected skin to examine under a microscope. In vitiligo, the skin sample will usually show a complete absence of pigment-producing melanocytes. On the other hand, the presence of inflamed cells in the sample may suggest that another condition is responsible for the loss of pigmentation.

LOW BACK PAIN

Low back pain (or lumbago) is a common musculoskeletal disorder affecting 80% of people at some point in their lives. It accounts for more sick leave and disability than any other medical condition.[1] It can be either acute, subacute or chronic in duration. Most often, the symptoms of low back pain show significant improvement within a few weeks from onset with conservative measures.

Most cases of lower back pain are due to benign musculoskeletal problems and are referred to as non specific low back pain. They are generally believed to be due to a sprain or strain in the muscles of the back and the soft tissues,[2] especially if the pain arose suddenly during physical load to the back, and the pain is lateral to the spine. The rate of serious causes is less than 1%.[3] The full differential diagnosis includes many other less common conditions.

• Mechanical:
  • Apophyseal osteoarthritis
  • Diffuse idiopathic skeletal hyperostosis
  • Degenerative discs
  • Scheuermann's kyphosis
  • Spinal disc herniation (slipped disc)
  • Spinal stenosis
  • Spondylolisthesis and other congenital abnormalities
  • Fractures
  • Leg length difference
  • Restricted hip motion
  • Misaligned pelvis - pelvic obliquity, anteversion or retroversion
  • Abnormal Foot Pronation

• Inflammatory:
  • Seronegative spondylarthritides (e.g. ankylosing spondylitis)
  • Rheumatoid arthritis
  • Infection - epidural abscess or osteomyelitis

• Neoplastic:
  • Bone tumors (primary or metastatic)
  • Intradural spinal tumors

• Metabolic:
  • Osteoporotic fractures
  • Osteomalacia
  • Ochronosis
  • Chondrocalcinosis

• Psychosomatic
  • Tension myositis syndrome

• Paget's disease

• Referred pain:
  • Pelvic/abdominal disease
  • Prostate Cancer
  • Posture

• Depression
• Oxygen deprivation

Low back pain is more likely to be persistent among people who previously required time off from work because of low back pain, those who expect passive treatments to help, those who believe that back pain is harmful or disabling or fear that any movement whatever will increase their pain, and people who have depression or anxiety.[6] A systematic review (2010) published as part of the Rational Clinical Examination Series in the Journal of the American Medical Association reviews the factors that predict disability from back pain.[44] The data quantified that patients with back pain who have poor coping behaviors or those fear activity are about 2.5 times as likely to have poor outcomes at 1 year.

• Exercise appears to be slightly effective for chronic low back pain.[35] The Schroth method, a specialized physical exercise therapy for scoliosis, kyphosis, spondylolisthesis, and related spinal disorders, has been shown to reduce severity and frequency of back pain in adults with scoliosis.[

MENIERE’S DISEASE

Meniere's disease is a disorder of the inner ear which causes episodes of vertigo, ringing in the ears (tinnitus), a feeling of fullness or pressure in the ear, and fluctuating hearing loss. The area of the ear affected is the entire labyrinth, which includes both the semicircular canals and the cochlea.

A typical attack of Meniere's disease is preceded by fullness in one ear. Hearing fluctuation or changes in tinnitus may also precede an attack. A Meniere's episode generally involves severe vertigo (spinning), imbalance, nausea and vomiting. The average attack lasts two to four hours. Following a severe attack, most people find that they are exhausted and must sleep for several hours. There is a large amount of variability in the duration of symptoms. Some people experience brief "shocks", and others have constant unsteadiness. High sensitivity to visual stimuli (visual dependence) is common. During the attack the eyes jump (this is called "nystagmus").

A particularly disabling symptom is a sudden fall. These typically occur without warning. These falls are called "otolithic crisis of Tumarkin", from the original description of Tumarkin (1936). They are attributed to sudden mechanical deformation of the otolith organs (utricle and saccule), causing a sudden activation of vestibular reflexes. Patients suddenly feel that they are tilted or falling (although they may be straight), and bring about much of the rapid repositioning themselves. This is a very disabling symptom as it occurs without warning and can result in severe injury. Often destructive treatment (e.g. labyrinthectomy or vestibular nerve section) is the only way to manage this problem. Other otologic conditions also occasionally are associated with Tumarkin type falls (Black et al, 1982; Ishiyama et al, 2003). See here for more information about drop attacks.

Meniere's episodes may occur in clusters; that is, several attacks may occur within a short period of time. However, years may pass between episodes. Between the acute attacks, most people are free of symptoms or note mild imbalance and tinnitus.

Meniere's affects roughly 0.2% of the population (click here for more details about the epidemiology). Meniere's disease usually starts confined to one ear but it often extends to involve both ears over time so that after 30 years, 50% of patients with Meniere's have bilateral disease (Stahle et al, 1991). There is some controversy about this statistic however -- some authors, for example Silverstein, suggest that the prevalence of bilaterality is as low as 17% (Silverstein, 1992). We suspect that this lower statistic is due to a lower duration of follow up and that the 50% figure is more likely to be correct. Other possibilities, however, are selection bias and different patterns of the disease in different countries. Silverstein suggested that 75% of persons destined to become bilateral do so within 5 years.

In most cases, a progressive hearing loss occurs in the affected ear(s). A low-frequency sensorineural pattern is commonly found initially, but as time goes on, it usually changes into either a flat loss or a peaked pattern

Hair cell death: Conventional thought is that repeated attacks of Meniere's kills hair cells in the inner ear. This is a gradual process over years, but frequently resulting in unilateral  functional deafness. Cochlear (hearing) hair cells are the most sensitive. Vestibular hair cells seem more resilient but there is also a slow decline in the caloric response in the diseased ear over roughly 15 years (Stahle et al, 1991).

2. Mechanical changes to the ear. Mechanical disruption of the inner ear is also likely with dilation of the utricle and saccule of the ear being a well known pathological finding. The saccule may dilate so that in later stages, it is adherent to the underside of the stapes footplate. This mechanical disruption and distortion of normal inner ear structures may result in the gradual onset of a chronic unsteadiness, even when patients are not having attacks. The periodic dilation and shrinkage of the utricle is also a reasonable explanation for periodic attacks of another inner ear disorder, BPPV. Finally, it also seems likely that there may be rupture of the suspensory system for the membranous labyrinth. This might create some mechanical instability of the utricle and saccule and consequently some chronic unsteadiness.

There is presently no evidence that Meniere's disease kills the cochleovestibular nerve (see Kitamura et al, 1997). Thus the term "nerve deafness" is inappropriate.

NEPHROLITHIASIS (KIDNEY STONES)

Nephrolithiasis specifically refers to calculi in the kidneys, but this article discusses both renal calculi, shown below, and ureteral calculi (ureterolithiasis). Ureteral calculi almost always originate in the kidneys, although they may continue to grow once they lodge in the ureter.

• Patients with urinary calculi may report pain, infection, or hematuria. Small nonobstructing stones in the kidneys only occasionally cause symptoms. If present, symptoms are usually moderate and easily controlled.
• The passage of stones into the ureter with subsequent acute obstruction, proximal urinary tract dilation, and spasm is associated with classic renal colic.
  • Renal colic is characterized by undulating cramps and severe pain and is often associated with nausea and vomiting.
  • As the stone travels through the ureter, the pain moves from the flank to the lower abdomen, down to the groin, and eventually to the scrotal or labial areas.
  • Associated irritative bladder symptoms are common when the stone is located in the distal or intramural ureter.
• • Staghorn refers to the presence of a branched kidney stone occupying the renal pelvis and at least one calyceal system. Such calculi usually manifest as infection and hematuria rather than as acute pain.
  • Asymptomatic bilateral obstruction, which is uncommon, manifests as symptoms of renal failure.
• Important historical features are as follows:
  • Duration, characteristics, and location of pain
  • History of urinary calculi
  • Prior complications related to stone manipulation
  • Urinary tract infections
  • Loss of renal function
  • Family history of calculi
  • Solitary or transplanted kidney
  • Chemical composition of previously passed stones

Physical

• Dramatic costovertebral angle tenderness is common; this pain can move to the upper or lower abdominal quadrant as a ureteral stone migrates distally.
• Peritoneal signs are usually absent-an important consideration in distinguishing renal colic from other sources of flank or abdominal pain.
• Findings should correlate with the reports of pain, so that complicating factors (eg, urinary extravasation, abscess formation) can be detected.
• Beyond this, the specific location of tenderness does not always correlate with the exact location of the stone, although the calculus is often in the general area of maximum discomfort.

Causes

• Most research on the etiology and prevention of urinary tract stone disease has been directed toward the role of elevated urinary levels of calcium, oxalate, and uric acid in stone formation, as well as reduced urinary citrate levels.
• Hypercalciuria is the most common metabolic abnormality. Some cases of hypercalciuria are related to increased intestinal absorption of calcium (associated with excess dietary calcium and/or overactive calcium absorption mechanisms), some are related to excess resorption of calcium from bone (ie, hyperparathyroidism), and some are related to an inability of the renal tubules to properly reclaim calcium in the glomerular filtrate (renal-leak hypercalciuria).
• Magnesium and especially citrate are important inhibitors of stone formation in the urinary tract. Decreased levels of these in the urine predispose to stone formation.
• A low fluid intake, with a subsequent low volume of urine production, produces high concentrations of stone-forming solutes in the urine. This is an important, if not the most important, environmental factor in kidney stone formation.
• The exact nature of the tubular damage or dysfunction that leads to stone formation has not been characterized.
• The most common findings on 24-hour urine studies include hypercalciuria, hyperoxaluria, hyperuricosuria, hypocitraturia, and low urinary volume. Other factors, such as high urinary sodium and low urinary magnesium concentrations, may also play a role. To identify these risk factors, a 24-hour urine profile, including appropriate serum tests of renal function, uric acid, and calcium, is needed. Such testing is available from various commercial laboratories. A finding of hypercalcemia should prompt follow-up with an intact parathyroid hormone study to evaluate for primary and secondary hyperparathyroidism.

OBESITY

Obesity is a chronic condition defined by an excess amount body fat. A certain amount of body fat is necessary for storing energy, heat insulation, shock absorption, and other functions. The normal amount of body fat (expressed as percentage of body fat) is between 25%-30% in women and 18%-23% in men. Women with over 30% body fat and men with over 25% body fat are considered obese.

The calculation of body mass index (BMI) has also been used in the definition of obesity. The body mass index (BMI) equals a person's weight in kilograms (kg) divided by their height in meters (m) squared. Since BMI describes body weight relative to height, it is strongly correlated with total body fat content in adults. "Obesity" is defined as a BMI of 30 and above.

Obesity is not just a cosmetic consideration; it is a dire health dilemma directly harmful to one's health. In the United States, roughly 300,000 deaths per year are directly related to obesity, and more than 80% of these deaths are in patients with a BMI (body mass index, which will be discussed later in this article) over 30. For patients with a BMI over 40, life expectancy is reduces significantly (as much as 20 years for men and 5 years for women ). Obesity also increases the risk of developing a number of chronic diseases including:

• Insulin Resistance. Insulin is necessary for the transport of blood glucose (sugar) into the cells of muscle and fat (which is then used for energy). By transporting glucose into cells, insulin keeps the blood glucose levels in the normal range. Insulin resistance (IR) is the condition whereby the effectiveness of insulin in transporting glucose (sugar) into cells is diminished. Fat cells are more insulin resistant than muscle cells; therefore, one important cause of insulin resistance is obesity. The pancreas initially responds to insulin resistance by producing more insulin. As long as the pancreas can produce enough insulin to overcome this resistance, blood glucose levels remain normal. This insulin resistance state (characterized by normal blood glucose levels and high insulin levels) can last for years. Once the pancreas can no longer keep up with producing high levels of insulin, blood glucose levels begin to rise, resulting in type 2 diabetes, thus insulin resistance is a pre-diabetes condition. In fact scientists now believe that the atherosclerosis (hardening of the arteries) associated with diabetes likely develops during this insulin resistance period.

• Type 2 (adult-onset) diabetes. The risk of type 2 diabetes increases with the degree and duration of obesity. Type 2 diabetes is associated with central obesity; a person with central obesity has excess fat around his/her waist, so that the body is shaped like an apple.

• High blood pressure (hypertension). Hypertension is common among obese adults. A Norwegian study showed that weight gain tended to increase blood pressure in women more significantly than in men. The risk of developing high blood pressure is also higher in obese people who are apple shaped (central obesity) than in people who are pear shaped (fat distribution mainly in hips and thighs).

• High cholesterol (hypercholesterolemia)

• Stroke (cerebrovascular accident or CVA)

• Heart attack. A prospective study found that the risk of developing coronary artery disease increased three to four times in women who had a BMI greater than 29. A Finnish study showed that for every one kilogram (2.2 pounds) increase in body weight, the risk of death from coronary artery disease increased by one percent. In patients who have already had a heart attack, obesity is associated with an increased likelihood of a second heart attack.

• Congestive heart failure

• Cancer. While not conclusively proven, some observational studies have linked obesity to cancer of the colon in men and women, cancer of the rectum and prostate in men, and cancer of the gallbladder and uterus in women. Obesity may also be associated with breast cancer, particularly in postmenopausal women. Fat tissue is important in the production of estrogen, and prolonged exposure to high levels of estrogen increases the risk of breast cancer.

• Gallstones

• Gout and gouty arthritis

• Osteoarthritis (degenerative arthritis) of the knees, hips, and the lower back

• Sleep apnea

Causes : The balance between calorie intake and energy expenditure determines a person's weight. If a person eats more calories than he or she burns (metabolizes), the person gains weight (the body will store the excess energy as fat). If a person eats fewer calories than he or she metabolizes, he or she will lose weight. Therefore the most common causes of obesity are overeating and physical inactivity. At present, we know that there are many factors that contribute to obesity, some of which have a genetic component:

• Genetics. A person is more likely to develop obesity if one or both parents are obese. Genetics also affect hormones involved in fat regulation. For example, one genetic cause of obesity is leptin deficiency. Leptin is a hormone produced in fat cells, and also in the placenta. Leptin controls weight by signaling the brain to eat less when body fat stores are too high. If, for some reason the body cannot produce enough leptin, or leptin cannot signal the brain to eat less, this control is lost, and obesity occurs. The role of leptin replacement as a treatment for obesity is currently being explored.

• Overeating. Overeating leads to weight gain, especially if the diet is high in fat. Foods high in fat or sugar (for example, fast food, fried food, and sweets) have high energy density (foods that have a lot of calories in a small amount of food). Epidemiologic studies have shown that diets high in fat contribute to weight gain.

• A diet high in simple carbohydrates. The role of carbohydrates in weight gain is not clear. Carbohydrates increase blood glucose levels, which in turn stimulate insulin release by the pancreas, and insulin promotes the growth of fat tissue and can cause weight gain. Some scientists believe that simple carbohydrates (sugars, fructose, desserts, soft drinks, beer, wine, etc.) contribute to weight gain because they are more rapidly absorbed into the blood-stream than complex carbohydrates (pasta, brown rice, grains, vegetables, raw fruits, etc.) and thus cause a more pronounced insulin release after meals than complex carbohydrates. This higher insulin release, some scientists believe, contributes to weight gain.

• Frequency of eating. The relationship between frequency of eating (how often you eat) and weight is somewhat controversial. There are many reports of overweight people eating less often than people with normal weight. Scientists have observed that people who eat small meals four or five times daily, have lower cholesterol levels and lower and/or more stable blood sugar levels than people who eat less frequently (two or three large meals daily). One possible explanation is that small frequent meals produce stable insulin levels, whereas large meals cause large spikes of insulin after meals.

• Slow metabolism. Women have less muscle than men. Muscle burns (metabolizes) more calories than other tissue (which includes fat). As a result, women have a slower metabolism than men, and hence, have a tendency to put on more weight than men, and weight loss is more difficult for women. As we age, we tend to lose muscle and our metabolism slows; therefore, we tend to gain weight as we get older particularly if we do not reduce our daily caloric intake.

• Physical inactivity. Sedentary people burn fewer calories than people who are active. The National Health and Nutrition Examination Survey (NHANES) showed that physical inactivity was strongly correlated with weight gain in both sexes.

• Medications. Medications associated with weight gain include certain antidepressants (medications used in treating depression), anti-convulsants [medications used in controlling seizures such as carbamazepine (Tegretol, Tegretol XR , Equetro, Carbatrol) and valproate], diabetes medications (medications used in lowering blood sugar such as insulin, sulfonylureas and thiazolidinediones), certain hormones such as oral contraceptives and most corticosteroids such as Prednisone. Weight gain may also be seen with some high blood pressure medications and antihistamines.

• Psychological factors. For some people, emotions influence eating habits. Many people eat excessively in response to emotions such as boredom, sadness, stress or anger. While most overweight people have no more psychological disturbances than normal weight people, about 30 percent of the people who seek treatment for serious weight problems have difficulties with binge eating.

• Diseases such as hypothyroidism, insulin resistance, polycystic ovary syndrome and Cushing's syndrome, are also contributors to obesity.

OTITIS MEDIA

Otitis media is an infection or inflammation of the middle ear. This inflammation often begins when infections that cause sore throats, colds, or other respiratory or breathing problems spread to the middle ear. These can be viral or bacterial infections. Seventy-five percent of children experience at least one episode of otitis media by their third birthday. Almost half of these children will have three or more ear infections during their first 3 years. Although otitis media is primarily a disease of infants and young children, it can also affect adults.

There are many reasons why children are more likely to suffer from otitis media than adults. First, children have more trouble fighting infections. This is because their immune systems are still developing. Another reason has to do with the child's eustachian tube. The eustachian tube is a small passageway that connects the upper part of the throat to the middle ear. It is shorter and straighter in the child than in the adult. It can contribute to otitis media in several ways.

The eustachian tube is usually closed but opens regularly to ventilate or replenish the air in the middle ear. This tube also equalizes middle ear air pressure in response to air pressure changes in the environment. However, a eustachian tube that is blocked by swelling of its lining or plugged with mucus from a cold or for some other reason cannot open to ventilate the middle ear. The lack of ventilation may allow fluid from the tissue that lines the middle ear to accumulate. If the eustachian tube remains plugged, the fluid cannot drain and begins to collect in the normally air-filled middle ear.

One more factor that makes children more susceptible to otitis media is that adenoids in children are larger than they are in adults. Adenoids are composed largely of cells (lymphocytes) that help fight infections. They are positioned in the back of the upper part of the throat near the eustachian tubes. Enlarged adenoids can, because of their size, interfere with the eustachian tube opening. In addition, adenoids may themselves become infected, and the infection may spread into the eustachian tubes.

Bacteria reach the middle ear through the lining or the passageway of the eustachian tube and can then produce infection, which causes swelling of the lining of the middle ear, blocking of the eustachian tube, and migration of white cells from the bloodstream to help fight the infection. In this process the white cells accumulate, often killing bacteria and dying themselves, leading to the formation of pus, a thick yellowish-white fluid in the middle ear. As the fluid increases, the child may have trouble hearing because the eardrum and middle ear bones are unable to move as freely as they should. As the infection worsens, many children also experience severe ear pain. Too much fluid in the ear can put pressure on the eardrum and eventually tear it.

Otitis media not only causes severe pain but may result in serious complications if it is not treated. An untreated infection can travel from the middle ear to the nearby parts of the head, including the brain. Although the hearing loss caused by otitis media is usually temporary, untreated otitis media may lead to permanent hearing impairment. Persistent fluid in the middle ear and chronic otitis media can reduce a child's hearing at a time that is critical for speech and language development. Children who have early hearing impairment from frequent ear infections are likely to have speech and language disabilities.

Otitis media is often difficult to detect because most children affected by this disorder do not yet have sufficient speech and language skills to tell someone what is bothering them. Common signs to look for are

• unusual irritability
• difficulty sleeping
• tugging or pulling at one or both ears
• fever
• fluid draining from the ear
• loss of balance
• unresponsiveness to quiet sounds or other signs of hearing difficulty such as sitting too close to the television or being inattentive

Specific prevention strategies applicable to all infants and children such as immunization against viral respiratory infections or specifically against the bacteria that cause otitis media are not currently available. Nevertheless, it is known that children who are cared for in group settings, as well as children who live with adults who smoke cigarettes, have more ear infections. Therefore, a child who is prone to otitis media should avoid contact with sick playmates and environmental tobacco smoke. Infants who nurse from a bottle while lying down also appear to develop otitis media more frequently. Children who have been breast-fed often have fewer episodes of otitis media. Research has shown that cold and allergy medications such as antihistamines and decongestants are not helpful in preventing ear infections. The best hope for avoiding ear infections is the development of vaccines against the bacteria that most often cause otitis media. Scientists are currently developing vaccines that show promise in preventing otitis media. Additional clinical research must be completed to ensure their effectiveness and safety.

PARALYSIS

Paralysis is also called: Hemiplegia, Palsy, Paraplegia, Quadriplegia

Paralysis is the loss of muscle function in part of your body. It happens when something goes wrong with the way messages pass between your brain and muscles. Paralysis can be complete or partial. It can occur on one or both sides of your body. It can also occur in just one area, or it can be widespread. Paralysis of the lower half of your body, including both legs, is called paraplegia. Paralysis of the arms and legs is quadriplegia.

Most paralysis is due to strokes or injuries such as spinal cord injury or a broken neck. Other causes of paralysis include

• Nerve diseases such as amyotrophic lateral sclerosis
• Autoimmune diseases such as Guillain-Barre syndrome
• Bell's palsy, which affects muscles in the face

Polio used to be a cause of paralysis, but polio no longer occurs

There are many potential causes of paralysis. The two most common causes of paralysis in the United States are stroke and trauma, particularly to the nervous system or the brain. Certain diseases or afflictions, such as poliomyelitis, peroneal dystrophy, spina bifida, amyotrophic lateral sclerosis, Bell’s palsy, Guillain-Barre Syndrome, and multiple sclerosis may also cause paralysis to occur. Botulism, paralytic shellfish poisoning, and certain types of poisons, particularly those that directly affect the nervous system, may also lead to paralysis.

The precise type of paralysis a person experiences depends on the underlying cause. With Bell’s palsy, for example, the paralysis is usually localized, which means it only affects a small area of the person’s body. Typically, only one side of the person’s face becomes paralyzed as the facial nerve on that side becomes inflamed. When only one side of a person’s body is affected, paralysis is considered unilateral. When it affects both sides, it is bilateral.

A person who has experienced a stroke, on the other hand, may experience weakness throughout his or her body. This is referred to as global paralysis. Conversely, the person may only experience weakness on one side of his or her body. Medically, this is known as hemiplegia.

Generally, the most severe form of paralysis is caused by damage to the spinal cord. A person who experiences trauma in his or her upper spinal cord may develop quadriplegia as a result. A person who is quadriplegic is unable to move his or her arms and legs. Injury to the lower spinal cord may cause paraplegia, which results in either the legs or the arms becoming paralyzed.

In severe cases of paralysis, it may be necessary for the individual to be fed through feeding tubes. Occupational therapy, physical therapy, and speech therapy may also be necessary to help treat paralysis.

PILES (HAEMORRHOIDS)

Pityriasis is one of any of a number of skin diseases that have in common lesions that resemble dandruff-like scales without obvious signs of inflammation.

Types of pityriasis include: pityriasis alba (also called pityriasis streptogenes, pityriasis simplex, erythema streptogenes); pityriasis rosea; pityriasis rubra pilaris; and pityriasis versicolor (tinea versicolor).

Description of Pityriasis

Pityriasis alba

This is characterized by hypopigmented, round to oval, scaling patches on the face, upper arms, neck, or shoulders. The patches vary in size, usually being a few centimeters in diameter. The color is white or light pink. The scales are fine and adherent.

Usually, the patches are sharply demarcated; the edges may be erythematous and slightly elevated. As a rule, pityriasis is asymptomatic. However, there may be mild pruritis. The disease occurs chiefly in children and teenagers.

The cause is unknown. Excessively dry skin following exposure to strong sunlight appears to be contributory. Efforts to find an infectious agent - either bacterial, viral, or fungal - have been unsuccessful.

Pityriasis rosea

This is a mild, inflammatory exanthem of unknown origin, characterized by salmon-colored papular and macular lesions that are at first discrete but may become confluent. The individual patches are oval or circinate and covered with finely crinkled, dry epidermis, which often desquamates, leaving collaterate scaling.

The disease usually begins with a single herald or mother patch, usually larger than succeeding lesions, which may persist a week or more before others appear. By that time involution of the herald patch has begun. The efflorescence of new lesions spreads rapidly, and after three to eight weeks they usually disappear spontaneously.

The incidence is highest between the ages of 15 and 40 years, and the disease is most prevalent in the spring and autumn. Women are more frequently affected.

The eruption is usually generalized, affecting chiefly the trunk, and sparing sun-exposed surfaces. At times it is localized to a certain area, such as the neck, thighs, groins, or axillae.

Moderate pruritis may be present, particularly during the outbreak, and there may be mild constitutional symptoms prior to the onset. The cause is unknown.

Pityriasis rubra pilaris

This is a chronic skin disease characterized by small follicular papules, disseminated yellowish pink scaling patches, and often, solid confluent palmoplantar hyperkeratosis.

The papules are the most important diagnostic feature, being more or less acuminate, reddish brown, about pinhead size, and topped by a central horny plug. In the horn center a hair, or part of one, is usually embedded. The disease generally manifests itself first by scaliness and erythema of the scalp.

The eruption is limited in the beginning, having a predilection for the sides of the neck and trunk and the extensor surfaces of the extremities. Then, as new lesions occur, extensive areas are converted into sharply marginated patches of various sizes, which look like exaggerated goose-flesh and feel like a nutmeg grater. The involvement is generally symmetric and diffuse with, however, characteristic small islands of normal skin within the affected areas.

Pityriasis Versicolor (tinea versicolor)

On the upper trunk and extending onto the upper arms, finely scaling, guttate or nummular patches appear, particularly on young adults who perspire freely. The individual patches are yellowish or brownish macules in pale skin, or hypopigmented macules in dark skin, with delicate scaling. Mild itching and inflammation about the patches may be present.

This common fungal disease is most prevalent in the tropics where there are high humidity and high temperatures and frequent exposure to sunlight.

POTT’S DISEASE

Pott's disease, is a presentation of extrapulmonary tuberculosis that affects the spine, a kind of tuberculous arthritis of the intervertebral joints.

Pott's disease is often experienced as a local phenomenon that begins in the thoracic section of the spinal column. Early signs of the presence of Pott's disease generally begin with back pain that may seem to be due to simple muscle strain. However, in short order, the symptoms will begin to multiply. Night sweats may become common, along with a running a fever during the day. As the condition worsens, it is not unusual to experience a loss of appetite, resulting in an anorexic state and the resulting weight loss. There is also often periods in which there is a tingling or numb sensation in the legs, accompanied with a sense of not having much strength in the legs.

Fortunately, there are several ways to determine if Pott's disease is the root cause of the symptoms. Blood tests can help determine if there is an elevation in the rate of erythrocyte sedimentation. A bone scan will determine if there is some indication of problems, which may lead to the scheduling of a bone biopsy. Conducting a CT scan as well as a radiograph of the spine is also likely to provide valuable information about the presence and current status of Pott's disease.

Once the presence of Pott's disease is confirmed, there are several treatment options available. The first line of defense will involve the use of analgesics and various antituberculous drugs, which can help to arrest the progress of the disease, as well as begin to alleviate symptoms. In some cases, it may be necessary to insert a rod into the area of the spine, providing needed stability. This is often the case if some degree of spinal cord compression has been noted. Finally, more ambitious surgery may be required, especially in situations where there is a need to drain fluid from pockets or abscesses that have formed, or if conditions indicate impending collapse of the vertebrae in the spinal column.

Signs and symptoms

• back pain
• fever
• night sweating
• anorexia
• weight loss
• Spinal mass, sometimes associated with numbness, paraesthesia, or muscle weakness of the legs

Diagnosis

• blood tests - elevated erythrocyte sedimentation rate
• tuberculin skin test
• radiographs of the spine
• bone scan
• CT of the spine
• bone biopsy
• MRI

Late complications

• Vertebral collapse resulting in kyphosis
• Spinal cord compression
• sinus formation
• paraplegia (so called Pott's paraplegia)

PSORIASIS

Psoriasis is a noncontagious common skin condition that causes rapid skin cell reproduction resulting in red, dry patches of thickened skin. The dry flakes and skin scales are thought to result from the rapid buildup of skin cells. Psoriasis commonly affects the skin of the elbows, knees, and scalp.

Some people have such mild psoriasis (small, faint dry skin patches) that they may not even suspect that they have a medical skin condition. Others have very severe psoriasis where virtually their entire body is fully covered with thick, red, scaly skin.

Psoriasis is considered a non-curable, long-term (chronic) skin condition. It has a variable course, periodically improving and worsening. Sometimes psoriasis may clear for years and stay in remission. Some people have worsening of their symptoms in the colder winter months. Many people report improvement in warmer months, climates, or with increased sunlight exposure.

Psoriasis is seen worldwide, in all races, and both sexes. Although psoriasis can be seen in people of any age, from babies to seniors, most commonly patients are first diagnosed in their early adult years.

Patients with more severe psoriasis may have social embarrassment, job stress, emotional distress, and other personal issues because of the appearance of their skin.

The exact cause remains unknown. There may be a combination of factors, including genetic predisposition and environmental factors. It is common for psoriasis to be found in members of the same family. The immune system is thought to play a major role. Despite research over the past 30 years looking at many triggers, the "master switch" that turns on psoriasis is still a mystery.

Psoriasis typically looks like red or pink areas of thickened, raised, and dry skin. It classically affects areas over the elbows, knees, and scalp. Essentially any body area may be involved. It tends to be more common in areas of trauma, repeat rubbing, use, or abrasions.

Psoriasis has many different appearances. It may be small flattened bumps, large thick plaques of raised skin, red patches, and pink mildly dry skin to big flakes of dry skin that flake off.

There are several different types of psoriasis including psoriasis vulgaris (common type), guttate psoriasis (small, drop like spots), inverse psoriasis (in the folds like of the underarms, navel, and buttocks), and pustular psoriasis (liquid-filled yellowish small blisters). Additionally, a separate entity affecting primarily the palms and the soles is known as palmoplantar psoriasis.

Sometimes pulling of one of these small dry white flakes of skin causes a tiny blood spot on the skin. This is medically referred to as a special diagnostic sign in psoriasis called the Auspitz sign.

Genital lesions, especially on the head of the penis, are common. Psoriasis in moist areas like the navel or area between the buttocks (intergluteal folds) may look like flat red patches. These atypical appearances may be confused with other skin conditions like fungal infections, yeast infections, skin irritation, or bacterial Staph infections.

On the nails, it can look like very small pits (pinpoint depressions or white spots on the nail) or as larger yellowish-brown separations of the nail bed called "oil spots." Nail psoriasis may be confused with and incorrectly diagnosed as a fungal nail infection.

On the scalp, it may look like severe dandruff with dry flakes and red areas of skin. It may be difficult to tell the difference between scalp psoriasis and seborrhea (dandruff). However, the treatment is often very similar for both conditions

The joint disease associated with psoriasis is referred to as psoriatic arthritis. Patients may have inflammation of any joints (arthritis), although the joints of the hands, knees, and ankles tend to be most commonly affected. Psoriatic arthritis is an inflammatory, destructive form of arthritis and is treated with medications to stop the disease progression.

The average age for onset of psoriatic arthritis is 30-40 years of age. In most cases, the skin symptoms occur before the onset of the arthritis.

The diagnosis of psoriatic arthritis is typically made by a physician examination, medical history, and relevant family history. Sometimes, lab tests and X-rays may be used to determine the severity of the disease and to exclude other diagnoses like rheumatoid arthritis and osteoarthritis.

Psoriasis may involve solely the nails in a limited number of patients. Usually, the nail symptoms accompany the skin and arthritis symptoms. Nails may have small pinpoint pits or large yellowish separations of the nail plate called "oil spots." Nail psoriasis is typically very difficult to treat. Treatment option are somewhat limited and include potent topical steroids applied at the nail-base cuticle, injection of steroids at the nail-base cuticle, and oral or systemic medications as described below for the treatment of psoriasis.

RENAL FAILURE

RENAL CALCULUS

Renal stone or calculus or lithiasis is one of the most common diseases of the urinary tract. It occurs more frequently in men than in women and in whites than in blacks. It is rare in children. It shows a familial predisposition.

                       Urinary calculus is a stone-like body composed of urinary salts bound together by a colloid matrix of organic materials. It consists of a nucleus around which concentric layers of urinary salts are deposited.

 Aetiology

(1)         Hyperexcretion of relatively insoluble urinary constituents such as oxalates, calcium, uric acid, cystine and certain drugs (such as magnesium trisilicate in the treatment of peptic ulcer).

(2)         Physiological changes in urine such as Urinary pH (which is influenced by diet and medicines), Colloid content, Decreased concentration of crystalloids, Urinary magnesium/calcium ratio.

(3)         ALTERED URINARY CRYSTALLOIDS AND COLLOIDS

·        Either there is an increase in the crystalloid level or a fall in the colloid level, urinary stones may be formed.

·        If there is any modification of the colloids e. g. they lose their solvent action or adhesive property, urinary stones may develop.

(4)         DECREASED URINARY OUTPUT OF CITRATE

(5)         VITAMIN A DEFICIENCY

·        The desquamated cells form nidus for stone formation. This is more applicable to bladder stones.

(6)         URINARY INFECTION

·        Infection disturbs the colloid content of the urine, also causes abnormality in the colloids (which may cause the crystalloid to be precipitated).

·        Infection also changes urinary pH and also causes increase in concentration of crystalloids.

(7)         URINARY STASIS

·        It causes a shift of the pH of the urine to the alkaline side, predisposes urinary infection, and allows the crystalloids to precipitate.

(8)         HYPERPARATHYROIDISM

·        Due to overproduction of parathormone the bones become decalcified and calcium concentration in the urine is increased. This extra calcium may be deposited in the renal tubules or in the pelvis to form renal calculus.

(9)         Prolonged immobilisation

 (10)    NIDUS OF STONE FORMATION

ENVIRONMENTAL AND DIETARY FACTORS

(a)         Low urine volumes

(b)        High ambient temperatures

(c)         Low fluid intake

(d)        Diet

(e)         High protein intake

(f)           High sodium

(g)        Low calcium

(h)        High sodium excretion

(i)           High oxalate excretion

(j)           High urate excretion

(B) OTHER MEDICAL CONDITIONS

(a)         Hypercalcemia of any cause

(b)        Ileal disease or resection (leading to increased oxalate absorption and urinary excretion)

(c)         Renal tubular acidosis type I

 

(C) CONGENITAL AND INHERITED CONDITIONS

(a)         Familial hypercalciuria

(b)        Medullary sponge kidney

(c)         Cystinuria

(d)        Renal tubular acidosis type I

Types of renal calculi

      Basically the renal stones can be divided into two major groups

I. Primary stones

II. Secondary stones.

(I) PRIMARY STONES

            They appear in apparently healthy urinary tract without any antecedent inflammation.

(a)   Calcium oxalate

(b)  Uric acid calculi

(c)   Cystine calculi

(d)  Xanthine calculi

(e)   Indigo calculi

(II) SECONDARY STONES

            They are usually formed as the result of inflammation.

(a)   Triple phosphate calculus

(b)  Mixed stones

SYMPTOMS

(a)   Quiescent calculus

(b)  Pain

·        Fixed renal pain

·        Ureteric colic

·        Referred pain

(c)   Hydronephrosis (a lump in the loin and a dull ache)

(d)  Haematuria

(e)   Pyuria

RHEUMATOID ARTHRITIS

Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic inflammation of the joints. Rheumatoid arthritis can also cause inflammation of the tissue around the joints, as well as in other organs in the body. Autoimmune diseases are illnesses that occur when the body's tissues are mistakenly attacked by their own immune system. The immune system contains a complex organization of cells and antibodies designed normally to "seek and destroy" invaders of the body, particularly infections. Patients with autoimmune diseases have antibodies in their blood that target their own body tissues, where they can be associated with inflammation. Because it can affect multiple other organs of the body, rheumatoid arthritis is referred to as a systemic illness and is sometimes called rheumatoid disease.

While rheumatoid arthritis is a chronic illness, meaning it can last for years, patients may experience long periods without symptoms. However, rheumatoid arthritis is typically a progressive illness that has the potential to cause joint destruction and functional disability.

Rheumatoid arthritis is a common rheumatic disease, affecting approximately 1.3 million people in the United States, according to current census data. The disease is three times more common in women as in men. It afflicts people of all races equally. The disease can begin at any age, but it most often starts after 40 years of age and before 60 years of age. In some families, multiple members can be affected, suggesting a genetic basis for the disorder.

The cause of rheumatoid arthritis is unknown. Even though infectious agents such as viruses, bacteria, and fungi have long been suspected, none has been proven as the cause. The cause of rheumatoid arthritis is a very active area of worldwide research. It is believed that the tendency to develop rheumatoid arthritis may be genetically inherited. It is also suspected that certain infections or factors in the environment might trigger the activation of the immune system in susceptible individuals. This misdirected immune system then attacks the body's own tissues. This leads to inflammation in the joints and sometimes in various organs of the body, such as the lungs or eyes.

The symptoms of rheumatoid arthritis come and go, depending on the degree of tissue inflammation. When body tissues are inflamed, the disease is active. When tissue inflammation subsides, the disease is inactive (in remission). Remissions can occur spontaneously or with treatment and can last weeks, months, or years. During remissions, symptoms of the disease disappear, and people generally feel well. When the disease becomes active again (relapse), symptoms return. The return of disease activity and symptoms is called a flare. The course of rheumatoid arthritis varies among affected individuals, and periods of flares and remissions are typical.

When the disease is active, symptoms can include fatigue, loss of energy, lack of appetite, low-grade fever, muscle and joint aches, and stiffness. Muscle and joint stiffness are usually most notable in the morning and after periods of inactivity. Arthritis is common during disease flares. Also during flares, joints frequently become red, swollen, painful, and tender. This occurs because the lining tissue of the joint (synovium) becomes inflamed, resulting in the production of excessive joint fluid (synovial fluid). The synovium also thickens with inflammation (synovitis).

In rheumatoid arthritis, multiple joints are usually inflamed in a symmetrical pattern (both sides of the body affected). The small joints of both the hands and wrists are often involved. Simple tasks of daily living, such as turning door knobs and opening jars, can become difficult during flares. The small joints of the feet are also commonly involved. Occasionally, only one joint is inflamed. When only one joint is involved, the arthritis can mimic the joint inflammation caused by other forms of arthritis, such as gout or joint infection. Chronic inflammation can cause damage to body tissues, including cartilage and bone. This leads to a loss of cartilage and erosion and weakness of the bones as well as the muscles, resulting in joint deformity, destruction, and loss of function. Rarely, rheumatoid arthritis can even affect the joint that is responsible for the tightening of our vocal cords to change the tone of our voice, the cricoarytenoid joint. When this joint is inflamed, it can cause hoarseness of the voice.

SARCOIDOSIS

Sarcoidosis is a disease of unknown cause that leads to inflammation. It can affect various organs in the body.

Normally, your immune system defends your body against foreign or harmful substances. For example, it sends special cells to protect organs that are in danger.

These cells release chemicals that recruit other cells to isolate and destroy the harmful substance. Inflammation occurs during this process. Once the harmful substance is destroyed, the cells and the inflammation go away.

In people who have sarcoidosis, the inflammation doesn't go away. Instead, some of the immune system cells cluster to form lumps called granulomas in various organs in your body.

Sarcoidosis can affect any organ in your body. However, it's more likely to occur in some organs than in others. The disease usually starts in the lungs, skin, and/or lymph nodes (especially the lymph nodes in your chest).

The disease also often affects the eyes and the liver. Although less common, sarcoidosis can affect the heart and brain, leading to serious complications.

If many granulomas form in an organ, they can affect how the organ works. This can cause signs and symptoms. Signs and symptoms vary depending on which organs are affected. Many people who have sarcoidosis have no symptoms or mild symptoms.

Lofgren's syndrome is a classic set of signs and symptoms that is typical in some people who have sarcoidosis. Lofgren's syndrome may cause fever, enlarged lymph nodes, arthritis (usually in the ankles), and/or erythema nodosum (er-i-THE-ma no-DO-sum).

Erythema nodosum is a rash of red or reddish-purple bumps on your ankles and shins. The rash may be warm and tender to the touch.

Treatment for sarcoidosis also varies depending on which organs are affected. Your doctor may prescribe topical treatments and/or medicines to treat the disease. Not everyone who has sarcoidosis needs treatment.

The outcome of sarcoidosis varies. Many people recover from the disease with few or no long-term problems.

More than half of the people who have sarcoidosis have remission within 3 years of diagnosis. "Remission" means the disease isn't active, but it can return.

Two-thirds of people who have the disease have remission within 10 years of diagnosis. People who have Lofgren's syndrome usually have remission. Relapse (return of the disease) 1 or more years after remission occurs in less than 5 percent of patients.

Sarcoidosis leads to organ damage in about one-third of the people diagnosed with the disease. Damage may occur over many years and involve more than one organ. Rarely, sarcoidosis can be fatal. Death usually is the result of complications with the lungs, heart, or brain.

Poor outcomes are more likely in people who have advanced disease and show little improvement from treatment.

Certain people are at higher risk for poor outcomes from chronic (long-term) sarcoidosis. This includes people who have lung scarring, heart or brain complications, or lupus pernio (LU-pus PAR-ne-o). Lupus pernio is a serious skin condition that sarcoidosis may cause.

Research is ongoing for new and better treatments for sarcoidosis.

SEBORRHOEA

Seborrhoea , a medical term applied to describe an accumulation on the skin of the normal sebaceous secretion mixed with dirt and forming scales or a distinct incrustation. On the head, where it is commonly seen, it may interfere with the nutrition of the hair and cause partial baldness.

A form of this disease occurs in young infants. The main treatment consists in thoroughly cleansing the parts. The crusts may be softened with oil and the affected skin regularly washed with soft soap and rectified spirit. The sebum frequently accumulates in the sebaceous ducts, giving rise to the minute black points often noticed on the face, back and chest in young adults, to which the term comedones is applied.

A form of this disorder, of larger size and white appearance, is termed milium. These affections may to a large extent be prevented by strict attention to ablution and brisk friction of the skin, which will also often remove them when they begin to appear. The retained secretion may be squeezed out or evacuated by incision and the skin treated with some simple sulfur application.

Seborrhoeic dermatitis is a common, harmless, scaling rash affecting the face, scalp and other areas. It is most likely to occur where the skin is oily. The American spelling is 'seborrheic', and 'dermatitis' is sometimes called 'eczema'.

Dandruff (also called 'pityriasis capitis') is an uninflamed form of seborrhoeic dermatitis. Dandruff presents as scaly patches scattered within hair-bearing areas of the scalp.

Seborrhoeic dermatitis may appear at any age after puberty. It fluctuates in severity and may persist for years. It may predispose to psoriasis. However, the plaques of psoriasis are more persistent, thicker, and a deeper red colour, with large flakes of white scale. Psoriasis is very likely to affect elbows and knees as well as the scalp. However, sometimes it is difficult to tell psoriasis from seborrhoeic dermatitis on the face, scalp and chest and your doctor may diagnose an overlap condition, known as 'sebopsoriasis'.

Within the scalp, seborrhoeic dermatitis causes ill-defined dry pink or skin coloured patches with yellowish or white bran-like scale. It may spread to affect the entire scalp.

Seborrhoeic dermatitis is common within the eyebrows, on the edges of the eyelids (blepharitis), inside and behind the ears and in the creases beside the nose. It can result in pale pink round or ring shaped patches on the hairline.

Sometimes it affects the skin-folds of the armpits and groin, the middle of the chest or upper back. It causes salmon-pink flat patches with a loose bran-like scale, sometimes in a ring shape (annular). It may or may not be itchy and can be quite variable from day to day.

STROKE

A stroke, or cerebrovascular accident (CVA), occurs when blood supply to part of the brain is disrupted, causing brain cells to die. When blood flow to the brain is impaired, oxygen and glucose cannot be delivered to the brain. Blood flow can be compromised by a variety of mechanisms.

Blockage of an artery

• Narrowing of the small arteries within the brain can cause a so-called lacunar stroke, (lacune=empty space). Blockage of a single arteriole can affect a tiny area of brain causing that tissue to die (infarct).
• Hardening of the arteries (atherosclerosis) leading to the brain. There are four major blood vessels that supply the brain with blood. The anterior circulation of the brain that controls most motor, activity, sensation, thought, speech, and emotion is supplied by the carotid arteries. The posterior circulation, which supplies the brainstem and the cerebellum, controlling the automatic parts of brain function and coordination, is supplied by the vertebrobasilar arteries.

If these arteries become narrow as a result of atherosclerosis, plaque or cholesterol, debris can break off and float downstream, clogging the blood supply to a part of the brain. As opposed to lacunar strokes, larger parts of the brain can lose blood supply, and this may produce more symptoms than a lacunar stroke.

• Embolism to the brain from the heart. In situations in which blood clots form within the heart, the potential exists for small clots to break off and travel (embolize) to the arteries in the brain and cause a stroke.

Rupture of an artery (hemorrhage)

• Cerebral hemorrhage (bleeding within the brain substance). The most common reason to have bleeding within the brain is uncontrolled high blood pressure. Other situations include aneurysms that leak or rupture or arteriovenous malformations (AVM) in which there is an abnormal collection of blood vessels that are fragile and can bleed.

Blockage of an artery

The blockage of an artery in the brain by a clot (thrombosis) is the most common cause of a stroke. The part of the brain that is supplied by the clotted blood vessel is then deprived of blood and oxygen. As a result of the deprived blood and oxygen, the cells of that part of the brain die. Typically, a clot forms in a small blood vessel within the brain that has been previously narrowed due to a variety of risk factors including:

• high blood pressure (hypertension),
• high cholesterol,
• diabetes, and
• smoking.

Embolic stroke

Another type of stroke may occur when a blood clot or a piece of atherosclerotic plaque (cholesterol and calcium deposits on the wall of the inside of the heart or artery) breaks loose, travels through open arteries, and lodges in an artery of the brain. When this happens, the flow of oxygen-rich blood to the brain is blocked and a stroke occurs. This type of stroke is referred to as an embolic stroke. For example, a blood clot might originally form in the heart chamber as a result of an irregular heart rhythm, such as occurs in atrial fibrillation. Usually, these clots remain attached to the inner lining of the heart, but occasionally they can break off, travel through the blood stream, form a plug (embolism) in a brain artery, and cause a stroke. An embolism can also originate in a large artery (for example, the carotid artery, a major artery in the neck that supplies blood to the brain) and then travel downstream to clog a small artery within the brain.

Cerebral hemorrhage

A cerebral hemorrhage occurs when a blood vessel in the brain ruptures and bleeds into the surrounding brain tissue. A cerebral hemorrhage (bleeding in the brain) can cause a stroke by depriving blood and oxygen to parts of the brain. Blood is also very irritating to the brain and can cause swelling of brain tissue (cerebral edema). Edema and the accumulation of blood from a cerebral hemorrhage increases pressure within the skull and causes further damage by squeezing the brain against the bony skull.

Subarachnoid hemorrhage

In a subarachnoid hemorrhage, blood accumulates in the space beneath the arachnoid membrane that lines the brain. The blood originates from an abnormal blood vessel that leaks or ruptures. Often this is from an aneurysm (an abnormal ballooning out of the wall of the vessel). Subarachnoid hemorrhages usually cause a sudden, severe headache and stiff neck. If not recognized and treated, major neurological consequences, such as coma, and brain death will occur.

Vasculitis

Another rare cause of stroke is vasculitis, a condition in which the blood vessels become inflamed.

THYROID DISEASES

Thyroid problems are among the most common medical conditions but, because their symptoms often appear gradually, they are commonly misdiagnosed.

The three most common thyroid problems are the underactive thyroid, the overactive thyroid , and thyroid nodules.

HYPOTHYROIDISM (Underactive thyroid)

The most common cause of hypothyroidism is Hashimoto's thyroiditis. In this condition, the body's immune system mistakenly attacks the thyroid gland.

Common symptoms of hypothyroidism are:

• Fatigue or lack of energy
• Weight gain
• Feeling cold
• Dry skin and hair
• Heavy menstrual periods
• Constipation
• Slowed thinking

The most common cause of hyperthyroidism is Graves' disease. This occurs when the body's immune system overstimulates the thyroid.

Common symptoms of hyperthyroidism are:

• Jitteriness, shaking, increased nervousness, irritability
• Rapid heart beat or palpitations
• Feeling hot
• Weight loss
• Fatigue, feeling exhausted
• More frequent bowel movements
• Shorter or lighter menstrual periods

In addition to symptoms of hyperthyroidism, some patients with Graves' disease develop eye symptoms such as a stare, eye irritation, bulging of the eyes and, occasionally, double vision or loss of vision. Involvement of the eyes is called Graves' Ophthalmopathy.

THYROID NODULES(Lumps)

Thyroid nodules are fairly common and usually harmless. However, about 4% of nodules are cancerous, so further testing needs to be done. This is usually best accomplished by fine needle aspiration biopsy. This is a quick and simple test that takes just a few minutes to perform in the doctor's office. If the biopsy does not raise any suspicion of cancer, the nodule is usually observed. Some thyroid specialists recommend treatment with thyroid hormone to try to decrease the size of the nodule. A second biopsy is usually recommended 6-12 months later, to make sure there continues to be no evidence of cancer. If a nodule is cancerous, suspicious for cancer, or grows large enough to interfere with swallowing or breathing, surgical removal is advised.

TUBERCULOSIS

Tuberculosis (TB) is an infectious disease caused by bacteria whose scientific name is Mycobacterium tuberculosis. It was first isolated in 1882 by a German physician named Robert Koch who received the Nobel Prize for this discovery. TB most commonly affects the lungs but also can involve almost any organ of the body. Many years ago, this disease was referred to as "consumption" because without effective treatment, these patients often would waste away. Today, of course, tuberculosis usually can be treated successfully with antibiotics.

There is also a group of organisms referred to as atypical tuberculosis. These involve other types of bacteria that are in the Mycobacterium family. Often, these organisms do not cause disease and are referred to as "colonizers" because they simply live alongside other bacteria in our bodies without causing damage. At times, these bacteria can cause an infection that is sometimes clinically like typical tuberculosis. When these atypical mycobacteria cause infection, they are often very difficult to cure. Often, drug therapy for these organisms must be administered for one and a half to two years and requires multiple medications.

A person can become infected with tuberculosis bacteria when he or she inhales minute particles of infected sputum from the air. The bacteria get into the air when someone who has a tuberculosis lung infection coughs, sneezes, shouts, or spits (which is common in some cultures). People who are nearby can then possibly breathe the bacteria into their lungs. You don't get TB by just touching the clothes or shaking the hands of someone who is infected. Tuberculosis is spread (transmitted) primarily from person to person by breathing infected air during close contact.

There is a form of atypical tuberculosis, however, that is transmitted by drinking unpasteurized milk. Related bacteria, called Mycobacterium bovis, cause this form of TB. Previously, this type of bacteria was a major cause of TB in children, but it rarely causes TB now since most milk is pasteurized (undergoes a heating process that kills the bacteria).

Anyone can get TB, but certain people are at higher risk, including

• people who live with individuals who have an active TB infection,
• poor or homeless people,
• foreign-born people from countries that have a high prevalence of TB,
• nursing-home residents and prison inmates,
• alcoholics and intravenous drug users,
• people with diabetes, certain cancers, and HIV infection (the AIDS virus),
• health-care workers.

There is no strong evidence for a genetically determined (inherited) susceptibility for TB.

As previously mentioned, TB infection usually occurs initially in the upper part (lobe) of the lungs. The body's immune system, however, can stop the bacteria from continuing to reproduce. Thus, the immune system can make the lung infection inactive (dormant). On the other hand, if the body's immune system cannot contain the TB bacteria, the bacteria will reproduce (become active or reactivate) in the lungs and spread elsewhere in the body.

It may take many months from the time the infection initially gets into the lungs until symptoms develop. The usual symptoms that occur with an active TB infection are a generalized tiredness or weakness, weight loss, fever, and night sweats. If the infection in the lung worsens, then further symptoms can include coughing, chest pain, coughing up of sputum (material from the lungs) and/or blood, and shortness of breath. If the infection spreads beyond the lungs, the symptoms will depend upon the organs involved.

Symptoms of TB depend on where in the body the TB bacteria are growing. TB bacteria usually grow in the lungs. TB in the lungs may cause symptoms such as

•  a bad cough that lasts 3 weeks or longer
•  pain in the chest
•  coughing up blood or sputum (phlegm from deep inside the lungs)

Other symptoms of active TB disease are

•  weakness or fatigue
•  weight loss
•  no appetite
•  chills
•  fever
•  sweating at night

ULCERS

• Ulcer (dermatology), a discontinuity of the skin
• Oral ulcer, an open sore inside the mouth
  • Aphthous ulcer, a specific type of oral ulcer also known as a canker sore
• Peptic ulcer, a discontinuity of the gastrointestinal mucosa (stomach ulcer)
• Corneal ulcer, an inflammatory or infective condition of the cornea
• Venous ulcer, a wound thought to occur due to improper functioning of valves in the veins
• Genital ulcer, an ulcer located on the genital area
• A peptic ulcer, also known as ulcus pepticum, PUD or peptic ulcer disease,[1] is an ulcer (defined as mucosal erosions equal to or greater than 0.5 cm) of an area of the gastrointestinal tract that is usually acidic and thus extremely painful. As many as 70-90% of ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach, however only 40% of those cases go to a doctor. Ulcers can also be caused or worsened by drugs such as aspirin and other NSAIDs.
• Contrary to general belief, more peptic ulcers arise in the duodenum (first part of the small intestine, just after the stomach) rather than in the stomach. About 4% of stomach ulcers are caused by a malignant tumor, so multiple biopsies are needed to exclude cancer. Duodenal ulcers are generally benign.

• Stomach (called gastric ulcer)
• Duodenum (called duodenal ulcer)
• Oesophagus (called Oesophageal ulcer)
• Meckel's Diverticulum (called Meckel's Diverticulum ulcer)

Signs and symptoms

• abdominal pain, classically epigastric with severity relating to mealtimes, after around 3 hours of taking a meal (duodenal ulcers are classically relieved by food, while gastric ulcers are exacerbated by it);
• bloating and abdominal fullness;
• waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus);
• nausea, and copious vomiting;
• loss of appetite and weight loss;
• hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.
• melena (tarry, foul-smelling feces due to oxidized iron from hemoglobin);
• rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis. This is extremely painful and requires immediate surgery.

A history of heartburn, gastroesophageal reflux disease (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer include NSAID (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase, and most glucocorticoids (e.g. dexamethasone and prednisolone).

In patients over 45 with more than two weeks of the above symptoms, the odds for peptic ulceration are high enough to warrant rapid investigation by EGD (see below).

The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers: A gastric ulcer would give epigastric pain during the meal, as gastric acid is secreted, or after the meal, as the alkaline duodenal contents reflux into the stomach. Symptoms of duodenal ulcers would manifest mostly before the meal-when acid (production stimulated by hunger) is passed into the duodenum. However, this is not a reliable sign in clinical practice.

Complications

• Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening.[2] It occurs when the ulcer erodes one of the blood vessels.
• Perforation (a hole in the wall) often leads to catastrophic consequences. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain. Posterior wall perforation leads to pancreatitis; pain in this situation often radiates to the back.
• Penetration is when the ulcer continues into adjacent organs such as the liver and pancreas.[3]
• Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet obstruction. Patient often presents with severe vomiting.
• Cancer is included in the differential diagnosis (elucidated by biopsy), Helicobacter pylori as the etiological factor making it 3 to 6 times more likely to develop stomach cancer from the ulcer.[4]

Cause

A major causative factor (60% of gastric and up to 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonizes the antral mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastritis), resulting in a defect in the regulation of gastrin production by that part of the stomach, and gastrin secretion can either be decreased (most cases) resulting in hypo- or achlorhydria or increased. Gastrin stimulates the production of gastric acid by parietal cells and, in H. pylori colonization responses that increase gastrin, the increase in acid can contribute to the erosion of the mucosa and therefore ulcer formation.

Another major cause is the use of NSAIDs (see above). The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins. COX-2 selective anti-inflammatories (such as celecoxib or the since withdrawn rofecoxib) preferentially inhibit cox-2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration. As the prevalence of H. pylori-caused ulceration declines in the Western world due to increased medical treatment, a greater proportion of ulcers will be due to increasing NSAID use among individuals with pain syndromes as well as the growth of aging populations that develop arthritis.

Stress

Researchers also continue to look at stress as a possible cause, or at least complication, in the development of ulcers. There is debate as to whether psychological stress can influence the development of peptic ulcers. Burns and head trauma, however, can lead to physiologic stress ulcers, which are reported in many patients who are on mechanical ventilation.

An expert panel convened by the Academy of Behavioral Medicine Research concluded that ulcers are not purely an infectious disease and that psychological factors do play a significant role.[1] Researchers are examining how stress might promote H. pylori infection. For example, Helicobacter pylori thrives in an acidic environment, and stress has been demonstrated to cause the production of excess stomach acid. This was supported by a study on mice showing that both long-term water-immersion-restraint stress and H. pylori infection were independently associated with the development of peptic ulcers.[12]