- A disease complex characterized by persistent hyperglycemia caused by insufficient insulin production or resistance to the metabolic action of insulin. Diabetes mellitus (DM) is generally classified as insulin-dependent (IDDM, type I), non-insulin-dependent (NIDDM, type II), or secondary diabetes mellitus.

Causes and Incidence The precise causal mechanisms in DM are unknown, although genetics and a faulty autoimmune response are thought to play major roles in type I diabetes. Genetics and obesity are risk factors for type II diabetes. Secondary diabetes is caused by underlying primary pathologic abnormalities. DM affects approximately 6% of the U.S. population; it is the leading cause of irreversible blindness and chronic renal failure. Diabetes is found worldwide, and the incidence is increasing rapidly. Type I accounts for 10% to 15% of cases, and the age of onset is primarily childhood or adolescence. Type II accounts for 85% to 90% of cases, and onset generally occurs after age 40. A small number of cases are secondary DM, and the age of onset varies according to the cause of the underlying primary pathologic condition.

Disease Process Diabetes occurs if the body cannot produce insulin (type I), or if it is unable to use the insulin produced (type II); in either case, the ultimate result is hyperglycemia and impaired glucose transport. Type I diabetes is characterized by a genetic predisposition manifested in one of several human leukocyte antigens. Recent research suggests that the genetic predisposition, coupled with an unknown factor, triggers an ongoing autoimmune process that systematically destroys the beta-cells in the pancreas, thereby interfering with the body’s ability to produce insulin. Type II diabetes involves either a defect in the insulin release sites in the pancreas or a resistance to the action of insulin stemming from a decrease in the number of receptor sites in the peripheral tissues. This type of DM is often associated with obesity.
In both types of DM, the result is interference with glucose transport across cell membranes in peripheral muscle and adipose tissue, leading to faulty oxidation and energy production. Metabolism of fat, carbohydrate, and protein is impaired, as are storage of glycogen in the muscle and liver and storage of fatty acids and triglycerides in adipose tissue. Amino acid cell transport is disrupted. Unrestrained gluconeogenic and glycogenolytic processes in the liver cause overproduction of glucose. As the blood glucose level rises, renal tubules fail to reabsorb all the glucose; this produces glucosuria and osmotic diuresis, with water and electrolyte loss through the urine. Hyperglycemia also damages myelin nerve coverings, leading to neuropathy. Glycosylation (attaching of glucose to protein molecules) in the capillaries causes thickening of the capillary membrane and microangiopathy. Atherosclerotic processes are accelerated, and vessel elasticity diminishes.

Symptoms

Type I
Abrupt onset with polyuria, polydipsia, polyphagia, weight loss, weakness, fatigue, dehydration

Type II
Usually asymptomatic in early stages, with pruritus vulvae a common presenting symptom in women; later manifestations include skin infections, cold extremities, fatigue, blurred vision, delayed healing, and polyuria

Potential Complications Diabetic ketoacidosis is a common acute complication in type I diabetes. If left untreated, it leads to coma and death. Nonketotic hyperglycemic-hyperosmolar coma is an acute complication in type II diabetes. It is frequently accompanied by seizure activity and has a mortality rate of about 50%. Systemic chronic complications include cardiovascular and peripheral vascular disease, retinopathy, nephropathy, neuropathy, dermopathy, and impotence.

Diagnostic Tests

Fasting blood sugar
.140 mg/dl on two occasions

Glucose tolerance test
.200 mg/dl for 2-hour sample and one other sample after administration of 75 g of glucose

Blood insulin
Absent in type I; normal or elevated in type II

Plasma C-peptide
Absent in type I; normal or elevated in type II

Treatments

Surgery
Only for chronic complications such as coronary artery grafts, eye surgery.

Drugs
Insulin for type I; oral hypoglycemics for type II.

General
Dietary control aimed at maintaining stable body weight, distributing caloric intake into small, evenly spaced loads, avoiding highfat, high-sugar foods; weight reduction with obesity; regular monitoring of blood sugar; education about disease, complications, medications, diet; counseling, support for adaptation to long-term disease.

Medi-Info.COM finds at this phrases

• atherosclerosis histology
• myocardial+infarction+process
• what is the process of tyroid cancer
• hepatitis pathophysiology
• urinary incompetence
• raynaud's disease

- A change in bowel habits marked by frequent passage of loose, watery, unformed stool. Diarrhea may be an acute or a chronic condition.

Causes and Incidence Diarrhea can be caused by a wide range of factors, such as sugar intolerance, use of antacids that contain poorly absorbed salts, laxative abuse, ingestion of large amounts of certain sugar substitutes, bacterial toxins, viral infections, bile acids, drugs, fat or carbohydrate malabsorption syndromes, mucosal disease, and bowel surgery that alters intestinal transit and strictures. Diarrhea is a common symptom that may be transient or may indicate underlying disease.

Disease Process Diarrhea occurs when the amount of fluid absorbed by the body declines; when the amount of fluid produced increases, overwhelming the bowel’s absorptive capacities; when motor disturbances affect bowel motility and secretory capacities; or when injury to the bowel mucosa produces blood and mucus in the stool.

Symptoms The primary symptom is a change in normal bowel habits that results in frequent, loose, watery, unformed stools that are often accompanied by cramping, abdominal pain, and urgency.

Potential Complications Hypokalemia, dehydration, and vascular collapse are possible complications with severe or chronic diarrhea. Infants and small children are particularly prone to dehydration.

Diagnostic Tests The diagnosis is made by clinical evaluation, history, and examination of the stool macroscopically and microscopically. Stool measurements, cultures, microscopic examination, and flexible sigmoidoscopy can help determine the cause.

Treatments

Surgery
None.

Drugs
Antidiarrheal drugs that increase intestinal tone (i.e., paregoric), reduce peristalsis (anticholinergics), increase bulk (methylcellulose), and absorb fluid (pectin).

General
Treatment of underlying disorder; monitoring and replacement of fluid and electrolytes; perirectal skin care.

Medi-Info.COM finds at this phrases

• disease process of lupus
• Crohn\'s disease
• toxic+brain+syndrome
• post streptococcal GN
• diagnostic tests for parotitis
• atherosclerosis histology

Medi-Info.COM finds at this phrases

• disease process of measles
• diagnostic testing for diabetes insipidus
• hyena hernia
• difference between phlebitis and thrombophlebitis
• guillain barre syndrome
• late stages of muscular dystrophy

- Inflammation of acquired, saclike projections (diverticula) that have formed in the gastrointestinal wall and have pushed the mucosal lining through the surrounding muscle; they may become infected, bleed, or rupture.

Causes and Incidence Diverticula are thought to be caused by an increase in intraluminal pressure in the bowel, which forms a pouch in weakened areas of the wall. The mechanism that weakens the wall is unclear. However, a highly refined diet lacking in fiber is believed to be a contributing factor. Abnormal colonic motility patterns and spastic colon have also been implicated. The formation of diverticula is known as diverticulosis. An infection of the diverticula that causes inflammation is diverticulitis.
Diverticulosis and diverticulitis are most common in developed Western countries. The incidence of diverticulosis increases with age, and approximately one third of those over 60 years of age have the disease; of those, 10% to 20% will develop diverticulitis. Diverticulitis is more severe in those under 50 years of age, and men are three times more likely than women to be affected in that age group.

Disease Process Diverticulitis occurs when undigested food mixed with bacteria accumulates in a diverticulum, forming a hard mass called a fecalith. The fecalith diminishes the blood supply to the diverticulum and an infection ensues, followed by inflammation and a microperforation of the diverticular mucosa, submucosa, and adjacent serosa into the surrounding pericolic fat. A pericolic abscess forms, which may range from microscopic to a large mass. Repeated episodes of diverticulitis lead to scarring, fibrosis, and stricture of the bowel wall and continued narrowing of the lumen.

Symptoms Complaints of pain and localized tenderness in the lower left abdominal quadrant with a low-grade fever are the usual presenting symptoms. Nausea, vomiting, and abdominal distention are also seen.

Potential Complications Intestinal obstruction, fistula formation, and perforation of the bowel with peritonitis and hemorrhage are possible complications of recurrent bouts of diverticulitis.

Diagnostic Tests A history of diverticulosis, complaints of localized abdominal pain, and a possible palpable abdominal mass are highly suggestive. A water-soluble contrastenema or computed tomography scan is used to outline diverticula and display effacement of pericolic fat. Laboratory tests reveal a polymorphonuclear leukocytosis with an elevated sedimentation rate.

Treatments

Surgery
Bowel resection with or without colostomy to treat recurrent attacks or complications.

Drugs
Analgesics for pain; antibiotics for infection; stool softeners.

General
NPO with bed rest, nasogastric tube and IV hydration for acute attack; high-fiber diet after inflammation resolves; instruction about continuing diet with high-fiber content; colostomy care instructions.

Medi-Info.COM finds at this phrases

• diabetes disease process
• Kaposi’s sarcoma
• pictures of primary hyperparathyroidism
• bleeding varicosities
• dermoid eczema
• plasmodium ovale
• Medical Information

- Pain associated with menstruation.

Causes and Incidence The cause of primary dysmenorrhea is unknown, but the disorder is thought to be tied to uterine contractions and ischemia mediated by prosta-glandin. The most common cause of secondary dysmenorrhea is endometriosis. Dysmenorrhea is a common gynecologic complaint, occurring in 10% of adolescents and young adults. It declines in severity with age and childbirth.

Disease Process It is thought that increased sensitivity of the myometrium to prostaglandin causes uterine contractions and ischemia of the uterine muscle, resulting in a cramping pain. Secondary dysmenorrhea is tied to an underlying pelvic disorder that produces similar cramping conditions.

Symptoms An aching pain low in the abdomen may radiate to the lower back and legs. The pain begins with menses, peaks after 24 hours, and typically subsides within 2 days. Headache, nausea, diarrhea, and urinary frequency may also be present.

Potential Complications None

Diagnostic Tests With secondary dysmenorrhea, a pelvic examination or laparoscopy or both to rule out underlying disorders.

Treatments

Surgery
Laser ablation of endometriosis; dilatation and curettage (DoC), hysterectomy for underlying disorders; presacral neurectomy for primary dysmenorrhea that is unresponsive to medication.

Drugs
Prostaglandin synthetase inhibitors (e.g., ibuprofen, naproxen sodium) to relieve pain; low-dose oral contraceptives if pain continues.

General
Regular exercise; adequate rest; no tobacco use.

Medi-Info.COM finds at this phrases

• parkinsonism
• fibrocystic breast disease non proliferative change
• herpes type 2
• uremic frost on the oral mucosa
• hypertension disease process
• disease process of tuberculosis