- Ischemic necrosis and ulceration of tissues that overlie a bony prominence and that have been subjected to prolonged external pressure from a supporting surface such as a bed or wheelchair.

Causes and Incidence Decubiti are caused by prolonged pressure on tissues compressed between an internal body structure, such as bone, and an external surface. The force and duration of the pressure directly determine the size of the ulcer. Contributing factors include immobilization, sensory and motor deficits, reduced circulation, malnutrition, anemia, edema, infection, friction, moisture, incontinence, shearing forces, decreased tissue integrity or viability, and aging.

Disease Process Pressure exerted over an area interferes with the blood supply to the tissue, producing ischemia and increasing capillary pressure. This leads to edema and multiple small-vessel thromboses and sets up an inflammatory reaction. If the pressure is not relieved, the ischemic tissue necroses and ulcerates.

Symptoms Decubitus formation has six definable stages with characteristic signs and symptoms.

Stage 1
Redness that blanches with pressure; skin is warm and soft to the touch

Stage 2
Redness, edema, and induration; skin often abraded or blistered

Stage 3
Breaks in the skin as it becomes necrotic; exposure of subcutaneous tissue; drainage from wound

Stage 4
Necrosis extends to subcutaneous tissue; drainage is foul smelling and yellow

Stage 5
Necrosis extends through fat to muscle; wound may develop a black, leathery eschar around the edges; drainage is greenish

Stage 6
Necrosis extends to bone; deep tunnels form in fat and muscle; body cavities (e.g., rectum or bladder) are eroded; bone is destroyed through periostitis and osteitis

Potential Complications Bacteremia and septicemia are common complications. Osteomyelitis, septic arthritis, and pathologic fractures also can occur.

Diagnostic Tests Clinical evaluation revealing the characteristic picture described under Clinical Manifestations; history of one or more predisposing and contributing factors.

Treatments

Surgery
Stages 4-6: debridement and closure; skin grafting, skin flaps, muscle flaps; joint disarticulation may be required with large stage 5 or stage 6 ulcers.

Drugs
Topical applications (e.g., enzymatic ointments) to debride necrotic tissue, hydrophilic gels for reepithelialization; topical antibiotics for debridement and to suppress infection; platelet-derived epidermal growth factors for tissue healing.

General
Elimination of pressure through frequent turning, special beds, mattress overlays, and wheelchair pads filled with gels, air, water, sand, or other pressurerelieving ingredients; use of lifting devices to prevent shearing; debridement with wetdry dressings; irrigation with whirlpool baths; electrical stimulation to promote antibacterial effect and stimulate muscle protein synthesis; balanced nutrition; control of incontinence and careful cleansing; instruction in ulcer prevention: frequent use of pressure relief measures (turning, raising off buttocks, weight shifts when seated); daily skin inspections; use of pressure relief mattress overlays and wheelchair cushions; clean, dry clothing and bed linens free of wrinkles and treated with fabric softener; lotion on all skin surfaces, especially over bony prominences, to reduce friction.

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- A superficial inflammation of the skin with redness, edema, vesicles, crusting, scaling, and sometimes itching. Common types include atopic, contact, nummular, or seborrheic dermatitis, all of which may be acute or chronic in nature.

Causes and Incidence The cause of atopic dermatitis is unknown, but the condition is often associated with other atopic diseases such as allergic rhinitis, asthma, or hay fever; these individuals have high serum levels of IgE antibodies. The response is thought to be hereditary, and it is seen in infants, children, and adults. Contact dermatitis, which can be irritant or allergic in nature, is caused by contact with various biologic or chemical irritants, such as acids, alkalis, dyes, detergents, latex, metals, plant oils, and solvents. The etiology of nummular dermatitis is unknown, but the condition is associated with increased stress and winter weather and is most commonly seen in middle age. The cause of seborrheic dermatitis is also unknown; this condition is associated with hereditary factors and underlying neurologic disease and can be seen in neonates and children, as well as adults.

Disease Process The histologic agent causes inflammatory changes in the skin, including vasodilation, edema, mononuclear cell infiltration into the dermis and epidermis, and breakdown of the epidermal cells. This leads to the visible changes on the skin’s surface (i.e., redness, swelling, oozing, crusting, scaling, and itching). If the process is repeated over a period of time, the epidermis thickens, producing hyperkeratosis and a chronic scaly appearance.

Symptoms

Atopic type
Constant itching that sets up an itch-scratch-rash-itch cycle; red, scaly papules that coalesce into plaques that ooze and crust; common sites are hands, face, and flexural areas

Contact type
Transient redness to bulla formation; itching is common; weeping, crusting

Nummular type
Sharply circumscribed, moist, oozing discoid plaques that later become dry and scaly

Seborrheic type
Dry, diffuse scaling of scalp; oozing, crusted, red-yellow scalp lesions or scaly plaques that recur; may be found in external ear canals, eyebrows, and nasolabial folds and on sternum

Potential Complications Secondary infection is the most common complication. Chronic dermatitis, which appears on the hands or feet, can restrict function and become crippling.

Diagnostic Tests Clinical evaluation with characteristic manifestations; detailed history to locate possible source of contact rash; patch test may isolate allergens; immunofluorescence will show elevated IgE in atopic dermatitis.

Treatments

Surgery
None.

Drugs
Antipruritics for itching; topical/systemic corticosteroids to relieve inflammation; topical keratolytics to reduce scaling.

General
Oils on affected areas; removal of irritant in contact dermatitis; daily use of seborrheic shampoos; humidification; cool, wet cloths on open lesions.

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- A transient or permanent disturbance of water metabolism that results in excretion of excessive quantities of very dilute urine. It may be pituitary (central), renal (nephrogenic), or intake regulated (primary) in nature.

Causes and Incidence Central diabetes insipidus (DI) is the result of a lack of antidiuretic hormone (ADH), which can be caused by brain injury from head trauma, neurosurgery, irradiation of the pituitary, hypothalamic tumors, or infiltrative metastatic diseases. More than half of diagnosed cases are idiopathic. Nephrogenic DI results when the body is unable to respond normally to ADH. The condition is inherited as an X-linked recessive disorder or acquired in association with disorders such as renal disease, sickle cell disease, fibrosarcoma, granuloma, polynephritis, metabolic disease, polycystic disease, or pregnancy or with toxic agents that reduce glomerular filtration. Primary DI results from excessive water intake caused by psychogenic disorders (e.g., schizophrenia) or dipsogenic disorders (e.g., multiple sclerosis, meningitis, encephalitis, neurosarcoidosis, or tuberculosis).

Disease Process Central DI begins when some form of brain injury reduces the amount of ADH. This leads to a decrease in the hydroosmotic permeability of the distal collecting tubes in the kidney, allowing the dilute urine formed in the proximal nephrons to be excreted unchanged. The result is a slight dehydration effect, an increase in plasma osmolality, and stimulation of the thirst mechanism. The individual drinks more, and as a result input and output are balanced and osmotic pressure in the body stabilizes at an above-normal level. In nephrogenic DI the kidneys are rendered ADH resistant and hydroosmotic permeability is reduced, with the same end result as in central DI. Primary polydipsia is caused by excessive water intake, either because of a severe cognitive dysfunction or because the thirst regulator has been disrupted by disease or trauma. Plasma osmolality is reduced, which causes a decrease in the production of ADH and dilutes the urine, and excretion rises to meet intake. As intake and output are balanced, plasma osmolality stabilizes at below-normal levels.

Symptoms The most common presenting signs and symptoms are unquenchable thirst, polydipsia, frequency of urination, polyuria, nocturia, dry skin, slight dehydration, and constipation.

Potential Complications A prolonged increase in urine volume and flow can lead to hydroureter and hydronephrosis. An individual who has no thirst mechanism may experience severe dehydration and circulatory collapse.

Diagnostic Tests

Fluid deprivation test
Central and nephrogenic DI: urine osmolality remains low Primary DI: osmolality increases.

Vasopressin administration after fluid deprivation
Central DI: osmolality rises Nephrogenic and primary DI: osmolality is unchanged.

Treatments

Surgery
None unless related to underlying disease.

Drugs
Central DI: synthetic vasopressin or chlorpropamide to increase urine osmolality.

Nephrogenic DI: thiazide diuretics to reduce urine volume.

General
Identification and treatment of any underlying organic cause for DI; reduction of sodium and caffeine in diet for central DI and nephrogenic DI; monitoring for hypoglycemia if chlorpropamide is prescribed; information about long-term hormone replacement therapy.

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- 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.

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- 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.

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