- A self-limiting, acute inflammation of the stomach and small intestine caused by ingestion of food, water, or feces contaminated with pathogenic agents, parasites, or toxins.

Causes and Incidence Causative agents include bacterial and viral pathogens, such as Campylobacter coli, Escherichia coli, Salmonella and Shigella organisms, Norwalk virus, and rotavirus; parasites, such as Ascaris, Enterobius, and Trichinella species; and toxins, such as poisonous plants or toadstools, arsenic, lead, and mercury. Inability to digest and absorb carbohydrates has also been implicated as a cause, although it is rare and the mechanism is poorly understood. Various forms of gastroenteritis are common manifestations worldwide and are often mistaken for food poisoning. Bacterial, parasitic, and viral types of gastroenteritis are infectious and can be transmitted directly or indirectly.

Disease Process The pathologic conditions depend on the causative agent. Toxigenic agents, such as some E. coli and Shigella strains, release an exotoxin that impairs intestinal absorption. Invasive pathogens, such as some Shigella and Salmonella species and E. coli, penetrate the mucosa of the small bowel, causing cellular destruction, necrosis, ulceration, bleeding, and exudation of protein-rich fluid. Pathogens such as rotaviruses attach to the mucosal wall and destroy cells in the intestinal villa, causing malabsorption of electrolytes. Parasites and toxins also interfere with intestinal functioning. The general result of all pathogenic agents is increased GI motility and increased secretion of fluids and electrolytes.

Symptoms The onset is often sudden, with abdominal pain and cramping, nausea and vomiting, diarrhea with or without blood and mucus, anorexia, general malaise, and muscle aches. Dehydration, hypokalemia, and hyponatremia occur with persistent vomiting and diarrhea.

Potential Complications Dehydration, shock, vascular collapse, and renal failure, in rare instances leading to death, are complications of gastroenteritis. Infants, small children, the elderly, and debilitated individuals are at greatest risk.

Diagnostic Tests Diagnosis relies on identification of the causative agent through stool and blood cultures, Gram’s stain, and direct swab rectal cultures.

Treatments

Surgery
None.

Drugs
Antidiarrheal agents for all types; antiemetics, except for viral or bacterial gastroenteritis, in which impairment of GI motility is avoided; antiinfective agents for bacterial gastroenteritis with systemic involvement (not generally recommended for simple gastroenteritis, because these drugs may prolong the carrier state and contribute to the emergence of drug-resistant organisms).

General
Rest; increased fluid intake; electrolyte replacement; bland diet.

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- A sexually transmitted disease of the genitalia andperianal regions characterized by multiple fleshy, painless growths.

Causes and Incidence Genital warts are caused by various strains of the human papilloma virus (HPV) and are transmitted by sexual contact. Worldwide the incidence has been increasing rapidly over the past decade.

Disease Process The virus invades superficial layers of the epidermis, infects cells in the stratum spinosum, and stimulates cell division, causing excessive cell proliferation and formation of the wartlike projections on the penis, vagina, cervix, vulva, perineum, rectum, and anus and in the perianal regions; they may also be seen on oral mucosa. Laryngeal warts have been seen in vaginally delivered infants born to infected mothers.

Symptoms Soft, moist, fleshy pink to brown projections that appear in clusters on genital, perianal, or oral mucosa.

Potential Complications Secondary infections, giant condylomata that destroy large segments of penile tissue, and malignant transformation are all possible complications.

Diagnostic Tests The diagnosis is made by clinical examination and confirmed by biopsy. Biopsy is also performed to rule out carcinoma and the condylomata seen in late-stage syphilis.

Treatments

Surgery
Removal by curette, cryotherapy, or electrosurgery.

Drugs
Topical application of trichloroacetic acid/ podophyllin/5-FU cream to warts.

General
Refraining from sexual activity until clear of disease; examination and treatment of all potentially exposed sex partners; instruction about sexually transmitted diseases, the importance of completing treatment regimens, and the importance of regular examinations for genital and cervical carcinoma.

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- A disorder in which increased intraocular pressure leads to eventual vision impairment and possibly to degeneration of the optic nerve. It may be primary or occur secondary to other ocular disease. Glaucoma is classified as open or closed angle.

Causes and Incidence The etiology of primary glaucoma is unknown, but predisposing factors include heredity, hyperopia, and vasomotor instability. It is estimated that 1.5% to 2% of Americans over 40 years of age have glaucoma, and more than 12% of newly diagnosed cases of blindness are attributable to glaucoma. Blacks and those with a family history are most susceptible. Ninety percent of primary glaucoma cases are the open-angle type, which occurs most often after age 65.

Disease Process Increased intraocular pressure (IOP) is related to an imbalance in the production, inflow, and outflow of aqueous humor. Inflow occurs through the pupil and outflow through the meshwork at the juncture of the iris and cornea. In secondary glaucoma the meshwork becomes clogged by blood, fibrin, or inflammatory cells produced by an underlying ocular disorder. Primary open-angle glaucoma is marked by degenerative changes to the meshwork that block outflow. In primary closed-angle glaucoma, the anterior chamber is shallow, the filtration angle is narrow, and the iris obstructs the meshwork at Schlemm’s canal. Sometimes dilation of the pupil or trauma pushes the iris forward, narrowing the angle and resulting in obstruction in an acute attack. Primary or secondary glaucoma may be congenital; the condition is hereditary (primary) or is caused by fetal defects in the ocular structure or underlying congenital systemic disorders (secondary).

Symptoms

Open angle
Often asymptomatic; frequent changes in prescription for glasses; mild headaches, vague visual disturbances; halos around lights; difficulty adjusting to darkness

Closed angle
Severe pain in and around eye; tearing; colored rainbow halos around lights; recurring episodes of blurring and impaired vision; mild dilation of pupils; hazy cornea; possible nausea and vomiting

Potential Complications Untreated glaucoma leads to progressively diminishing vision, degeneration of the optic nerve, and blindness.

Diagnostic Tests

Tonometry
To measure elevation in IOP

Visual field studies
To detect impairment in central and peripheral visual fields

Gonioscopy
To detect cellular debris or adhesions and differentiate openangle from closed-angle type

Ophthalmoscopy
To visualize optic nerve

Treatments In secondary glaucoma, treatment focuses on the underlying disease process, in conjunction with mydriasis.

Surgery
Open angle: laser/external trabeculoplasty to improve drainage if medications fail; placement of filtering devices if trabeculoplasty fails.

Closed angle: laser iridotomy/peripheral iridectomy to push iris back and increase angle.

Ocular implants for some complex forms of glaucoma.

Drugs
Open angle: betaadrenergic blockers and diuretics to reduce production of aqueous humor, miotics to reduce pressure, and adrenergics to increase aqueous outflow.

Closed angle: hyperosmotic agents, carbonic anhydrase inhibitors, and miotics to reduce pressure or abort acute attack; narcotic analgesics for pain.

General
Open angle: avoidance of tobacco use, fatigue, emotional upset, and ingesting large quantities of fluid; instruction in instillation of eye drops, and long-term use of medications and their side effects.

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- A primary or secondary autoimmune renal disease involving the glomerulus in the kidney and classified as postinfectious, rapidly progressive (crescentic), or IgA neuropathy. (See also Nephrotic Syndrome.)

Causes and Incidence Postinfectious glomerulonephritis is caused by a bacterial, viral, or parasitic pathogen. Poststreptococcal glomerulonephritis (PSGN), the prototypic postinfectious disease, is caused by a streptococcal infection that occurs elsewhere in the body, such as in the respiratory tract or skin. The incidence of acute PSGN is dropping rapidly in developed countries. It is most common in boys 3 to 7 years of age but can occur at any age. It has a rapid onset and usually resolves spontaneously.
Rapidly progressive (crescentic) glomerulonephritis is either idiopathic, related to the production and deposition of the antiglomerular basement membrane antibody, or occurs as part of multisystem disease. This type of glomerulonephritis is rare and is most often seen in men. IgA neuropathy is idiopathic and is usually a primary disease, although it can be secondary. It is common in children and young adults and affects males six times as often as females. It is particularly prevalent in Asia.

Disease Process Acute glomerulonephritis (AGN) occurs when antigens from the etiologic agent provoke an antibody response, which results in antigen-antibody complexes that are deposited in the glomerular capillary walls. The deposits can be the continuous type or the more common discontinuous granular form. They cause a cascade of inflammatory changes in the glomeruli, resulting in vasoconstriction, a marked decrease in plasma flow, and a decrease in the filtering surface; this in turn reduces the glomerular filtration rate. A compensatory mechanism increases the synthesis of prostaglandins and the hydrostatic pressure in other glomeruli to increase flow and maintain the filtration rate. If the AGN is progressive, the compensatory mechanisms eventually induce glomerular damage through thickening and scarring of the filtration membrane.

Symptoms

PSGN
Onset of symptoms occurs 1 to 6 weeks after infection; symptoms include hypertension, headache, edema, oliguria, dark urine, reduced urine output, flank pain, weight gain, fever, chills, nausea, and

vomiting; about half of cases are asymptomatic

Crescentic type
Similar to PSGN, but the onset is more insidious and weakness, fatigue, and fever are the

predominant symptoms

IgA neuropathy
Similar to PSGN, but the onset usually occurs 1 to 2 days after upper respiratory infection or enteral illness and is often accompanied by hematuria

Potential Complications Complications include congestive heart failure, acute or chronic renal failure, and end-stage renal disease.

Diagnostic Tests

Urinalysis
Hematuria (microscopic or gross), proteinuria, sediment, RBC casts

Blood chemistry
Increased blood urea nitrogen, serum creatinine, and serum lipid; decreased serum albumin

Renal biopsy
Obstruction of glomerular capillaries

ASO titers
Positive in PSGN

IgA serum
Elevated in 50% of IgA nephropathy cases

IgA-fibronectin
Elevated aggregates with IgA nephropathy

Treatments Therapy focuses on treating symptoms and preventing complications.

Surgery
Renal transplantation for end-stage renal disease.

Drugs
Antihypertensives for hypertension; diuretics for edema; antiinfective drugs if infection is still present; Kayexalate for hyperkalemia; phosphatebinding agents; corticosteroids with crescentic glomerulonephritis.

General
Bed rest; fluid, potassium, and sodium restrictions; reduced protein intake if uremia is present; hemodialysis or peritoneal dialysis for renal failure.

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