- Adenocarcinomas account for most endometrial cancer; other tumor types include adenoacanthoma and clear cell and squamous cell tumors.

Causes and Incidence The cause of endometrial cancer has not yet been firmly established although a long-established link exists to hormone-related disorders. However, approximately 40% of endometrial tumors appear to be autonomous with no known etiology. Associated risk factors include adenomatous hyperplasia of the endometrium, menstrual irregularities, delayed menopause, infertility, diabetes or hypertension, and a history of breast or ovarian cancer.
Endometrial cancer is the most common of the gynecologic malignancies, with more than 31,000 new cases a year in the United States. This cancer is found primarily in postmenopausal women between 55 and 60 years of age. The women tend to be from highly industrialized countries, and the prevalence has increased sharply.

Disease Process Cells begin as endometrial hyperplasia and change to cancer cells, beginning in the fundus of the uterus and spreading to the entire endometrium. The tumor may then extend down the endocervical canal and involve the cervix and vagina. It also spreads through the uterine wall to the abdominal cavity and adjacent structures and metastasizes to the pelvic and paraaortic lymph nodes, lungs, bone, and brain.

Symptoms The only significant clinical sign of endometrial cancer is inappropriate uterine bleeding. Approximately one third of postmenopausal women who experience such bleeding have endometrial cancer.

Potential Complications Advanced disease leads to complications such as bowel obstruction, ascites, and respiratory distress, and the prognosis is poor.

Diagnostic Tests A Papanicolaou smear is helpful but undependable, because 30% to 40% of smears yield false-negative results. Malignant cells on endometrial biopsy and fractional curettage yield a definitive diagnosis.

Treatments

Surgery
Hysterectomy

Drugs
Chemotherapy for recurrent lesions and metastasis; hormones (e.g., progestin) to treat metastasis or precancerous lesions.

General
Radiation as adjunct to surgery and palliation; counseling for body image and sexual functioning alterations.

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- Well-circumscribed, nonencapsulated, benign tumors of the uterus.

Causes and Incidence The etiology is unclear, but the tumors tend to grow in response to excess estrogen levels and shrink after menopause. Fibroids are the most common pelvic neoplasm and occur in about 30% of women over age 35. In the United States, the incidence is higher in black women.

Disease Process Fibroids arise from the smooth muscle within the myometrium of the uterus. They may be seen on the intramural, submucosal, or subserous surface of the uterus or in the musculature of the cervix or broad ligaments. Tumor growth often outstrips blood supply, causing the tumor to hyalinize. The hyaline tissue may then liquefy and calcify.

Symptoms Most fibroids are asymptomatic. Symptoms, when present, include prolonged or excessive menstrual bleeding with no change in the cycle interval. Pain, heaviness, or tenderness in the lower abdomen may also be present.

Potential Complications Complications include hemorrhage, torsion and infection, adhesions, and infertility.

Diagnostic Tests The diagnosis is made on abdominal and bimanual palpation of the uterus. Ultrasound scanning may be used to distinguish endometriosis from leiomyomas. Cytologic tests and cervical biopsy may be done to rule out cancer.

Treatments

Surgery
Hysteroscopic or laparoscopic myomectomy to preserve uterus for childbearing; hysterectomy to control heavy bleeding.

Drugs – None.

General
Ongoing gynecologic examinations to monitor fibroids.

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- Infection and inflammation of the vaginal mucosa, often extending secondarily to the vulva.

Causes and Incidence Most vaginitis is caused by bacteria (Gardnerella vaginalis), protozoa (Trichomonas vaginalis), fungi (Candida sp.), and viruses (human papilloma virus). Other causes include mechanical forces (foreign objects, vigorous wiping or cleansing); irritating chemicals found in douches, deodorant sprays, laundry soaps, and bathwater additives; and sensitivity to spermicides, latex condoms, or latex diaphragms. Tight, nonporous, nonabsorbent underclothing or poor hygiene may foster growth of pathogens. Women exposed to diethylstilbestrol have vaginal adenosis, which can produce a vaginal discharge. Older, postmenopausal women have vaginal and mucosal atrophy, which predisposes them to infection. Vaginitis is a common disorder, and most women can expect to have at least one vaginal infection in their lifetime. All age groups are at risk. In the reproductive years, vaginitis is usually caused by infection. Premenopausal and postmenopausal causes are more often mechanical or chemical.

Disease Process The causative agent sets up an infective or inflammatory process. Infective agents invade and grow in the warm, moist environment of the vagina, often aided by a decrease in acidity and an increase in the sugar level in the vaginal environment. Infective agents are often introduced by sexual activity (Trichomonas and Gardnerella spp., papilloma virus) or are part of the normal vaginal flora (Candida albicans) that overgrow when vaginal conditions are ripe, such as before menstruation and during pregnancy. Inflammation occurs with mechanical, chemical, or other sensitivity, often with an inadequately lubricated or a thinning vaginal mucosa.

Symptoms The most common presenting sign is vaginal discharge with or without itching, odor, or pain.

Mechanical/chemical
Increase in clear, viscous discharge; burning; redness; itching

Bacterial (Gardnerella)
Malodorous (fishy) white or grayish yellow discharge; itching, burning

Protozoan (Trichomonas)
Copious frothy, bubbly, greenish gray, malodorous discharge; itching, dyspareunia; vulvar edema, hyperemia

Viral (papilloma virus)
Vaginal or vulvar warts, discharge, odor; spotty bleeding

Fungi (C. albicans)
Thick, cheesy white or yellow discharge; intense itching, redness

Atrophic
Itching, dryness, redness, irritation, burning, spotty bleeding

Potential Complications Chronic vulvitis and vulvar dystrophies can occur and are most often seen after menopause.

Diagnostic Tests The diagnosis is made by the history, a pelvic examination, and a wet smear or culture to identify the causative organisms. Pap smears and biopsies may be done to rule out cancer.

Treatments

Surgery
Laser therapy, cautery, or cryotherapy to remove warts.

Drugs
Topical or systemic antiinfective drugs to treat specific causative pathogen; treatment of sex partner for pathogens; estrogen supplements with atrophic vaginitis.

General
Removal of chemical, mechanical, or other sources of irritation; instruction about vaginal hygiene; use of loose underwear that breathes (i.e., cotton).

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- Elongated, dilated, and tortuous superficial veins usually seen in the lower extremities.

Causes and Incidence Varicose veins occur because of incompetency in the valves of the vein, which permits a backflow of blood in the dependent position. The cause of valvular incompetence is unclear, but predisposing factors include familial tendency, inherent weakness in the vein walls, congenital arteriovenous fistulas, pregnancy, ascites, occupations requiring prolonged standing, and vein trauma or occlusion. Varicosities increase with age and are more common in women than in men.

Disease Process The pathophysiology is unclear. The prevailing hypothesis for pathogenesis is that valve failure occurs at the perforator veins in the lower leg, resulting in high-pressure flow and increased volume in the superficial veins during muscular contraction. Over time the superficial veins become dilated, separating the valve cusps and reversing blood flow in the affected veins.

Symptoms Initially the vein may be palpated but invisible, and the individual may have a feeling of heaviness in the legs that gets worse at night and in hot weather. Aching also occurs after prolonged standing or walking, during menses, or when fatigued. Over time, the veins can be seen as dilated, purplish, and ropelike.

Potential Complications Venous insufficiency and venous stasis ulcers are the two most common complications.

Diagnostic Tests The initial diagnosis is made on inspection and palpation and is checked by a manual compression test that reveals a palpable impulse. A Trendelenburg test can help pinpoint the location of incompetent valves. Plethysmography and ultrasound scans can be used to detect venous backflow.

Treatments

Surgery
Stripping and ligation of severely affected veins.

Drugs
Sclerotherapy (injection of chemicals designed to sclerose the affected veins is sometimes used instead of surgery).

General
Lightweight compression hosiery and avoidance of prolonged standing for mild varicosities; customfitted, surgical weight antiembolism stockings with graduated pressure (high at ankle, lower at top) with prescribed exercise program to promote circulation and prevent stasis with moderate varicosities.

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- A syndrome marked by hypergastrinemia, gastric acid hypersecretion, and recurrent peptic ulcerations.

Causes and Incidence The cause of Zollinger-Ellison syndrome (ZES) is excessive gastrin secretion produced by a non-beta islet cell tumor in the pancreas. Most individuals have several tumors, and about 50% of the tumors are malignant. ZES often occurs in conjunction with other endocrine abnormalities, particularly of the parathyroids. About 60% of cases are seen in men. The peak incidence occurs between 30 and 50 years of age.

Disease Process The high serum gastrin levels continuously stimulate HCl hypersecretion from parietal cells. This constant production of HCl overcomes the duodenum’s ability to neutralize the acid, and peptic ulcers result. The gastrin stimulates intestinal motility and increases secretion of water and electrolytes, and the HCl increases peristalsis. Intestinal pH and fat breakdown are diminished, which inactivates pancreatic lipase and interferes with absorption of a variety of substances in the intestine. Gastrin also stimulates intrinsic factor secretion and interferes with vitamin B12 absorption.

Symptoms The major manifestations stem from peptic ulcer formation and include burning epigastric pain that is relieved by food and coffee ground or bloody emesis. Diarrhea, steatorrhea, foul-smelling stools, anorexia, and weight loss may also be present.

Potential Complications The mortality rate is high because of malignant metastasis to the liver, spleen, bone, skin, and peritoneum and perforation and hemorrhage of the peptic ulcers.

Diagnostic Tests

Serum gastrin
Elevated to 500 pg/ml or higher

Endoscopy/x-ray
To detect ulcers

Provocative tests
Serum gastrin rises within 30 minutes of injection of secretin and calcium

Arteriography
To locate pancreatic tumors

Treatments

Surgery
Resection of tumor possible in 20% of cases; total gastrectomy when ulcers are not responding to medication.

Drugs
Histamine-receptor antagonists to reduce gastric acid output; antacids to relieve pain; anticholinergics in refractory cases; omeprazole or octreotide to reduce gastric acid when resistance to histaminereceptor antagonists develops; chemotherapy to treat malignant tumors; vitamin B12 injections, iron and calcium supplements.

General
Fluid replacement with diarrhea; monitoring for dehydration and electrolyte imbalance; support to aid in adaptation.

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