Malignant melanoma

Incidence of malignant melanoma, a neoplasm that arises from melanocytes, has increased by 50% in the past 20 years. In particular, an increase in incidence of melanoma in situ suggests earlier detection. The disorder varies in different populations but is about 10 times more common in white than in nonwhite populations. The four types of melanomas are superficial spreading melanoma, nodular malignant melanoma, lentigo maligna melanoma, and acral-lentiginous melanoma.
Melanoma spreads through the lymphatic and vascular systems and metastasizes to the regional lymph nodes, skin, liver, lungs, and central nervous system (CNS). Its course is unpredictable, however, and recurrence and metastasis may occur more than 5 years after resection of the primary lesion. If it spreads to regional lymph nodes, the patient has a 50% chance of survival.
The prognosis varies with tumor thickness. Generally, superficial lesions are curable, whereas deeper lesions tend to metastasize. The Breslow Level Method measures tumor depth from the granular level of the epidermis to the deepest melanoma cell. Melanoma lesions less than 0.76 mm deep have an excellent prognosis, whereas deeper lesions (more than 0.76 mm deep) are at risk for metastasis. The prognosis is better for a tumor on an extremity (which is drained by one lymphatic network) than for one on the head, neck, or trunk (which is drained by several networks).
Causes
Several factors may influence the development of melanoma:
  • Excessive exposure to ultraviolet light. Melanoma is most common in sunny, warm areas and commonly develops on parts of the body that are exposed to the sun. A person who has a blistering sunburn before age 20 has twice the risk of developing melanoma.
  • Skin type. Most persons who develop melanoma have blond or red hair, fair skin, and blue eyes; are prone to sunburn; and are of Celtic or Scandinavian descent. Melanoma is rare among blacks; when it does develop, it usually arises in lightly pigmented areas (the palms, plantar surface of the feet, or mucous membranes).
  • Autoimmune factors. Genetic and autoimmune effects may be causes.
  • Hormonal factors. Pregnancy may increase risk and exacerbate growth.
  • Family history. A person with a family history of melanoma has eight times the risk of Continue reading “Malignant melanoma”

Carpal tunnel syndrome

The most common of the nerve entrapment syndromes, carpal tunnel syndrome results from compression of the median nerve at the wrist, within the carpal tunnel. This nerve passes through, along with blood vessels and flexor tendons, to the fingers and thumb. Compression neuropathy causes sensory and motor changes in the median distribution of the hand.
Carpal tunnel syndrome usually occurs in women between ages 30 and 60 and poses a serious occupational health problem. Assembly-line workers and packers, secretary-typists, and persons who repeatedly use poorly designed tools are most likely to develop this disorder. Any strenuous use of the hands—ustained grasping, twisting, or flexing—aggravates this condition.
Causes
The carpal tunnel is formed by the carpal bones and the transverse carpal ligament. Inflammation or fibrosis of the tendon sheaths that pass through the carpal tunnel can cause edema and compression of the median nerve.
Many conditions can cause the contents or structure of the carpal tunnel to swell and press the median nerve against the transverse carpal ligament. Such conditions include rheumatoid arthritis, flexor tenosynovitis (commonly associated with rheumatic disease), nerve compression, pregnancy, renal failure, menopause, diabetes mellitus, acromegaly, edema following Colles’ fracture, hypothyroidism, amyloidosis, myxedema, benign tumors, tuberculosis, and other granulomatous diseases. Another source of damage to the median nerve is dislocation or acute sprain of the wrist.
Signs and symptoms
The patient with carpal tunnel syndrome usually complains of weakness, pain, burning, numbness, or tingling in the involved hands. This paresthesia affects the thumb, forefinger, middle finger, and half of the fourth finger. The patient is unable to clench his hand into a fist. The nails may be Continue reading “Carpal tunnel syndrome”

Introduction to Alcoholism

A chronic disorder, alcoholism is usually described as an uncontrolled intake of alcoholic beverages that interferes with physical and mental health, social and family relationships, and occupational responsibilities. Alcoholism cuts across all social and economic groups, involves both sexes, and occurs at all stages of the life cycle, beginning as early as elementary school age. About 20% of patients, even in affluent areas, have alcoholism. Lifetime risk for dependence is 10% to 15% for men and 5% for women.
Causes
Numerous biological, psychological, and sociocultural factors appear to be involved in alcohol addiction. An offspring of one alcoholic parent is seven to eight times more likely to become an alcoholic than is a peer without an alcoholic parent. Biological factors include genetic and biochemical abnormalities, nutritional deficiencies, endocrine imbalances, and allergic responses.
Psychological factors include the urge to drink alcohol to reduce anxiety or symptoms of mental illness; the desire to avoid responsibility in family, social, and work relationships; and the need to bolster self-esteem.
Sociocultural factors include the availability of alcoholic beverages, peer pressure, an excessively stressful lifestyle, and social attitudes that approve of frequent drinking.
Signs and symptoms
Because people with alcohol dependence may hide or deny their addiction and may temporarily manage to maintain a functional life, assessing a patient for alcoholism can be difficult. However, there are various physical and psychosocial symptoms that can facilitate assessment.
The patient’s history may suggest a need for daily or episodic alcohol use to maintain adequate functioning, an inability to discontinue or reduce alcohol intake, episodes of anesthesia or amnesia (blackouts) during intoxication, episodes of violence during intoxication, or interference with social and familial relationships and occupational responsibilities.
Many minor complaints that the patient may have may also be alcohol related. He may mention malaise, dyspepsia, mood swings, depression, or more infections. Note any evidence of an unusually high tolerance for sedatives and narcotics.
Secretive behavior is another indication. When confronted, the patient may deny or rationalize his problem with alcohol. Alternatively, he may be guarded or hostile in his response. He also may project his anger or feelings of guilt or inadequacy onto others to avoid confronting his illness.
With chronic alcohol abuse, the patient may experience malnutrition, cirrhosis of the liver, peripheral neuropathy, brain damage, or cardiomyopathy. Continue reading “Introduction to Alcoholism”

Brief Summary on Electric shock

electric shockWhen an electric current passes through the body, the damage it does depends on the intensity of the current (amperes, milliamperes, or microamperes), the resistance of the tissues it passes through, the kind of current (alternating current, direct current, or mixed), and the frequency and duration of current flow.
Electric shock may cause ventricular fibrillation, respiratory paralysis, burns, and death. The prognosis depends on the site and extent of damage, the patient’s state of health, and the speed and adequacy of treatment.
Causes
Electric shock usually follows accidental contact with exposed parts of electrical appliances or wiring, but it may also result from lightning or the flash of electric arcs from high-voltage power lines or machines.
The increased use of electrical medical devices in the hospital, many of which are connected directly to the patient, has raised serious concern for electrical safety and has led to the development of electrical safety standards. However, even well-designed equipment with reliable safety features can cause electric shock if it’s mishandled.
Signs and symptoms
Severe electric shock usually causes muscle contraction, followed by unconsciousness and loss of reflex control, sometimes with respiratory paralysis (by way of prolonged contraction of respiratory muscles or a direct effect on the respiratory nerve center).
After momentary shock, hyperventilation may follow muscle contraction. Passage of even the smallest electric current—if it passes through the heart— may induce ventricular fibrillation or another arrhythmia that progresses to fibrillation or myocardial infarction.
Electric shock from a high-frequency current (which generates more heat in tissues than a low-frequency current) usually causes burns as well as local tissue coagulation and necrosis. Low-frequency currents can also cause serious burns if contact with the current is concentrated in a small area—for example, when a toddler bites into an electrical cord.
Contusions, fractures, and other injuries can result from violent muscle contractions or falls during the shock; later, the patient may develop renal shutdown. Residual hearing impairment, Continue reading “Brief Summary on Electric shock”

Disseminated intravascular coagulation

Also called consumption coagulopathy and defibrination syndrome, disseminated intravascular coagulation (DIC) occurs as a complication of diseases and conditions that accelerate clotting. This accelerated clotting process causes small blood vessel occlusion, organ necrosis, depletion of circulating clotting factors and platelets, and activation of the fibrinolytic system—which, in turn, can provoke severe hemorrhage.
Clotting in the microcirculation usually affects the kidneys and extremities but may occur in the brain, lungs, pituitary and adrenal glands, and GI mucosa. Other conditions, such as vitamin K deficiency, hepatic disease, and anticoagulant therapy, may cause a similar hemorrhage.
DIC is generally an acute condition but may be chronic in cancer patients. The prognosis depends on early detection and treatment, the severity of the hemorrhage, and treatment of the underlying disease or condition.
Causes
DIC may result from:
  • infection (the most common cause of DIC), including gram-negative or gram-positive septicemia; viral, fungal, or rickettsial infection; and protozoal infection (falciparum malaria)
  • obstetric complications, such as abruptio placentae, amniotic fluid embolism, and retained dead fetus
  • neoplastic disease, including acute leukemia and metastatic carcinoma
  • disorders that produce necrosis, such as extensive burns and trauma, brain tissue destruction, transplant rejection, and hepatic necrosis.
Other causes include heatstroke, shock, poisonous snakebite, cirrhosis, fat embolism, incompatible blood transfusion, cardiac arrest, surgery necessitating cardiopulmonary bypass, giant hemangioma, severe venous thrombosis, and purpura fulminans.
It isn’t clear why such disorders lead to DIC; nor is it certain that they lead to it through a common mechanism. In many patients, the triggering mechanisms may be the entrance of foreign protein into the circulation and vascular endothelial injury.
Results of accelerated clotting
Regardless of how DIC begins, the typical accelerated clotting results in generalized activation of prothrombin and a consequent excess of thrombin. Excess thrombin converts fibrinogen to fibrin, producing fibrin clots in the microcirculation.
This process consumes exorbitant amounts of coagulation factors (especially fibrinogen, prothrombin, platelets, and factor V and factor VIII), causing hypofibrinogenemia, hypoprothrombinemia, thrombocytopenia, and deficiencies in factor V and factor VIII. Circulating thrombin activates the fibrinolytic system, which lyses fibrin clots into fibrin Continue reading “Disseminated intravascular coagulation”

Juvenile rheumatoid arthritis

Affecting children younger than age 16, juvenile rheumatoid arthritis (JRA), also known as juvenile chronic arthritis, is an immune-mediated inflammatory disorder of the connective tissues characterized by joint swelling and pain or tenderness. It may also involve such organs as the skin, heart, lungs, liver, spleen, and eyes, producing extra-articular signs and symptoms.
JRA has three major types: systemic (Still’s disease or acute febrile type), polyarticular, and pauciarticular. Depending on the type, this disease can occur as early as age 6 weeks—although rarely before 6 months—with peaks of onset between ages 1 and 3 and 8 and 12. It’s considered the major chronic rheumatic disorder of childhood; overall incidence is twice as high in girls, with variation among the types.
Causes
JRA is thought to be an autoimmune disorder. Research has linked causation to genetic and immune factors. Viral or bacterial (particularly streptococcal) infection, trauma, and emotional stress have been identified as precipitating factors.
Signs and symptoms
Signs and symptoms vary with the type of JRA.

Systemic JRA
Affecting boys and girls almost equally, systemic JRA accounts for 20% to 30% of cases. Affected children may have mild, transient arthritis or frank poly-arthritis associated with fever and rash.
Fever in systemic JRA occurs suddenly and spikes to 103° F (39.4° C) or higher once or twice daily, usually in the late afternoon, then rapidly returns to normal or subnormal. (This sawtooth, or intermittent spiking, fever pattern helps differentiate JRA from other inflammatory disorders.) When fever spikes, an evanescent rheumatoid rash typically appears, consisting of small, pale or salmon pink macules, most commonly on the trunk and proximal extremities and occasionally on the face, palms, and soles.
Massaging or applying heat intensifies this rash, which is usually most conspicuous where the skin has been rubbed or subjected to pressure, such as that from underclothing.
Other signs and symptoms of systemic JRA include hepatosplenomegaly, lymphadenopathy, pleuritis, pericarditis, myocarditis, and nonspecific abdominal pain.
Polyarticular JRA
Polyarticular JRA is four to nine times more common in girls than in boys and may be seronegative or seropositive for rheumatoid factor (RF). It involves five or more joints and usually develops insidiously. The joints most commonly involved are the wrists, elbows, knees, ankles, and small joints of the hands and feet.
Polyarticular JRA can also affect larger joints, including the temporomandibular joints and those of the cervical spine, hips, and shoulders. These joints become swollen, tender, and stiff.
Usually, the arthritis is symmetrical; it may be remittent or indolent. The patient may run a low-grade fever with daily peaks. Listlessness and weight loss can occur, possibly with lymphaden-opathy and hepatosplenomegaly. Other signs of polyarticular JRA include subcutaneous nodules on the elbows or heels and noticeable developmental retardation.
Seropositive polyarticular JRA, the more severe type, usually occurs late in childhood and can cause destructive arthritis that mimics adult RA.
Pauciarticular JRA
Involving few joints (usually no more than four), pauciarticular JRA usually affects the knees and other large joints. It accounts for 45% of cases. Three major subtypes exist: Continue reading “Juvenile rheumatoid arthritis”

Introduction to Nephrotic syndrome

Nephrotic syndromeNephrotic syndrome (or nephrosis) is characterized by marked proteinuria, hypoalbuminemia, hyperlipemia, and edema. Although nephrotic syndrome isn’t a disease itself, it results from a specific glomerular defect and indicates renal damage. The prognosis is highly variable, depending on the underlying cause. Some forms may progress to end-stage renal failure.
Causes
About 75% of nephrotic syndrome cases result from primary (idiopathic) glomerulonephritis. Classifications include the following:
  • With minimal change disease (lipid nephrosis or nil disease)—the main cause of nephrotic syndrome in children—the glomeruli appear normal by light microscopy. Some tubules may contain increased lipid deposits.
  • Membraneous glomerulonephritis—the most common lesion in patients with adult idiopathic nephrotic syndrome—is characterized by uniform thickening of the glomerular basement membrane containing dense deposits. It can eventually progress to renal failure.
  • Focal glomerulosclerosis can develop spontaneously at any age, follow kidney transplantation, or result from heroin abuse. Lesions initially affect the deeper glomeruli, causing hyaline sclerosis, with later involvement of the superficial glomeruli. These lesions generally cause slowly progressive deterioration in renal function. Remissions occur occasionally.
  • With membranoproliferative glomerulonephritis, slowly progressive lesions develop in the subendothelial region of the basement membrane. These lesions may follow infection, particularly streptococcal infection. This disease occurs primarily in children and young adults.
Other causes of nephrotic syndrome include metabolic diseases such as diabetes mellitus; collagen-vascular disorders, such as systemic lupus erythematosus and polyarteritis nodosa; Continue reading “Introduction to Nephrotic syndrome”

APlastic and Hypoplastic Anemias

Aplastic and hypoplastic anemias result from injury to or destruction of stem cells in bone marrow or the bone marrow matrix, causing pancytopenia (anemia, granulocytopenia, thrombocytopenia) and bone marrow hypoplasia. Although often used interchangeably with other terms for bone marrow failure, aplastic anemias properly refer to pancytopenia resulting from the decreased functional capacity of a hypoplastic, fatty bone marrow.
These disorders generally produce fatal bleeding or infection, particularly when they’re idiopathic or stem from the use of chloramphenicol or from infectious hepatitis. Mortality for patients who have aplastic anemia with severe pancytopenia is 80% to 90%.
Causes
Aplastic anemias usually develop when damaged or destroyed stem cells inhibit red blood cell (RBC) production. Less commonly, they develop when damaged bone marrow microvasculature creates an unfavorable environment for cell growth and maturation. About half of such anemias result from drugs (antibiotics, anticonvulsants), toxic agents (such as benzene and chloramphenicol), or radiation. The rest may result from immunologic factors (unconfirmed), severe disease (especially hepatitis), or preleukemic and neoplastic infiltration of bone marrow.
Idiopathic anemias may be congenital and account for about 50% of all confirmed occurrences. Two such forms of aplastic anemia have been identified: congenital hypoplastic anemia (Blackfan-Diamond anemia), which develops between ages 2 months and 3 months, and Fanconi’s syndrome, which develops between birth and age 10.
With Fanconi’s syndrome, chromosomal abnormalities are typically associated with multiple congenital anomalies—such as dwarfism and hypoplasia of the kidneys and spleen. In the absence of a consistent familial or genetic history of aplastic anemia, researchers suspect that these congenital abnormalities result from an induced change in the development of the fetus.
Signs and symptoms
Signs and symptoms of aplastic anemias vary with the severity of pancytopenia but usually Continue reading “APlastic and Hypoplastic Anemias”

Introduction to Diverticular disease

Diverticular disease is an outpouching of the colon, usually the sigmoid. It develops from the musculature in the colon working against increased intraluminal pressures to move hard stools through. Other typical sites are the duodenum, near the pancreatic border or the ampulla of Vater, and the jejunum. Diverticular disease of the stomach is rare and commonly a precursor of peptic or neoplastic disease. Diverticular disease of the ileum (Meckel’s diverticulum) is the most common congenital anomaly of the GI tract.
Diverticular disease has two clinical forms. In diverticulosis, diverticula are present but usually the patient is asymptomatic or the symptoms (abdominal pain, fluctuating bowel habits, constipation) are questionable because they may be related to underlying irritable bowel syndrome. In diverticulitis, diverticula are inflamed and may cause potentially fatal obstruction, infection, or hemorrhage.
Causes
Diverticular disease is most prevalent in men older than age 40 and is rarely found in cultures whose diets are high in residue. Diverticula probably result from high intraluminal pressure on areas of weakness in the GI wall, where blood vessels enter. Herniation of mucosa occurs through weak areas of the GI tract.
Diet may also be a contributing factor because lack of roughage reduces fecal residue, narrows the bowel lumen, and leads to higher intra-abdominal pressure during defecation. The fact that diverticulosis is most prevalent in Western industrialized nations, where processing removes much of the roughage from foods, supports this theory. Diverticulosis is less common in nations where the diet contains more natural bulk and fiber.
In diverticulitis, retained undigested food mixed with bacteria accumulates in the diverticular sac, forming a hard mass (fecalith). This substance cuts off the blood supply to the thin walls of the sac, making them more susceptible to attack by colonic bacteria.
Inflammation follows, possibly leading to perforation, abscess, peritonitis, obstruction, or hemorrhage. Occasionally, the inflamed colon segment may produce a fistula by adhering to the bladder or other organs.
Signs and symptoms
The two forms of diverticular disease produce different signs and symptoms. Continue reading “Introduction to Diverticular disease”

Brief Summary of Gastroesophageal reflux

The backflow or reflux of gastric and duodenal contents into the esophagus and past the lower esophageal sphincter (LES), without associated belching or vomiting, is called gastroesophageal reflux. Reflux may or may not cause symptoms or pathologic changes. Persistent reflux may cause reflux esophagitis (inflammation of the esophageal mucosa). The prognosis varies with the underlying cause.

Causes
The function of the LES—a high-pressure area in the lower esophagus, just above the stomach—is to prevent gastric contents from backing up into the esophagus. Normally, the LES creates pressure, closing the lower end of the esophagus, but relaxes after each swallow to allow food into the stomach.
Reflux occurs when LES pressure is deficient or when pressure within the stomach exceeds LES pressure.
The amount of time the reflux is in contact with the esophagus as well as the potency of the reflux relates to esophageal damage. Gastroesophageal reflux can also be related to delayed gastric emptying resulting from partial gastric outlet obstruction or gastroparesis. It may also be attributed to an abnormal esophageal clearance. In this instance, acid isn’t cleared and neutralized by esophageal peristalsis and salivary bicarbonates, as it is normally.
Predisposing factors include the following:
  • pyloric surgery (alteration or removal of the pylorus), which allows reflux of bile or pancreatic juice
  • long-term nasogastric (NG) intubation (more than 5 days)
  • any agent that lowers LES pressure, such as food, alcohol, cigarettes, anticholinergics (atropine, belladonna, and propantheline), and other drugs (morphine, diazepam, and Continue reading “Brief Summary of Gastroesophageal reflux”