Disease Process The severity varies by exposure and cause. The etiologic agent comes in contact with and irritates the conjunctiva, setting up an inflammatory response. Recurrent inflammation leads to thickening of the conjunctival layer and lid margins.

Symptoms

Bacterial type
Purulent drainage, lid swelling, moderate discomfort, redness of conjunctiva

Viral type
Clear discharge, swollen preauricular node, tearing, redness, moderate discomfort, light sensitivity

Allergen or irritant
Clear discharge, profuse tearing, feeling of something in the eye, intense itching (allergen), severe swelling of the lid, generalized redness of the eye, moderate burning feeling

Potential Complications If left untreated, infection may spread from conjunctiva to cornea and cause ulceration, perforation, and blindness.

Diagnostic Tests Smears and cultures of discharge are done to determine if viral or bacterial agent is present. Conjunctival scrapings are used to rule out inclusion conjunctivitis, trachoma, and vernal conjunctivitis. Vision, intraocular pressure, cornea, iris, pupil, and pupillary response are all normal.

Treatments

Surgery
None.

Drugs
Topical antiinfective drugs for bacterial cause; topical antivirals for viral cause; topical corticosteroids for allergens.

General
Saline irrigation for discharge and comfort; warm compresses for inflammation, cool compresses for itching.

Disease Process When the heart is unable to pump a sufficient supply of blood to meet the body’s demands, three primary compensatory mechanisms attempt to maintain cardiac function: (1) the sympathetic nervous system response increases, with increased catecholamine discharge, in an effort to increase myocardial contractility, which in turn causes vasoconstriction that increases peripheral resistance and cardiac workload; (2) cardiac fluid volume increases in an effort to stretch the fibers in the ventricles and increase the force of the contraction; and (3) the myocardium hypertrophies in an attempt to increase the amount of contractile tissue available and thus increase contractility.
When these compensatory mechanisms are insufficient or when they are active over extended periods, they become ineffective and eventually contribute to failure of the pump. Pump failure usually begins with the left ventricle and progresses to the right ventricle. It may be either acute or chronic, depending on the cause.

Symptoms

Left ventricle failure
Tachycardia, fatigue and dyspnea on exertion, intolerance to cold, cough, bloodtinged sputum, restlessness, paroxysmal nocturnal dyspnea, insomnia, crackles and wheezes in the lungs, ventricular and atrial gallops

Right ventricle failure
Fatigue, fullness in the neck and abdomen, ankle swelling, distention of neck veins, weakness, anorexia, nausea, liver enlargement, nocturia, ascites, tricuspid murmur

Potential Complications Acute pulmonary edema occurs with acute heart failure and is manifested as extreme dyspnea, cyanosis, hyperpnea, and plunging oxygen saturation. Death occurs if the condition is not treated immediately. Myocardial infarction and renal failure are other complications of CHF.

Diagnostic Tests

Blood chemistry
Elevated blood urea nitrogen, creatinine, glucose; decreased potassium, sodium; elevated aspartate aminotransferase, bilirubin; prolonged partial thromboplastin time

Arterial blood gases
Decreased oxygen saturation

Complete blood count
Decreased hemoglobin and hematocrit with anemia

Chest x-ray
Cardiomegaly; engorged pulmonary vasculature

Echocardiography
To visualize increased or decreased chamber dimensions, decreased wall motion

Cardiac catheterization
Definitive diagnosis of cause and extent of damage

Treatments

Surgery
Heart transplantation for end-stage failure; intraaortic balloon pump to provide circulatory assistance; left ventricular assistive device for those awaiting transplantation.

Drugs
Diuretics to reduce edema and ventricular filling volume; vasodilators, antihypertensives, or alpha-adrenergic blocking agents to dilate vessels and reduce venous filling pressure and peripheral resistance; inotropics (digitalis) to increase contractility; angiotensinconverting enzyme inhibitors to reduce angiotensin II in individuals with advanced CHF.

General
Bed rest with head elevated; oxygenation; low-salt diet; fluid restriction; monitoring and support of vital functions; prevention of thrombosis, pneumonia, and skin breakdown; stress reduction.

Disease Process Over a period of 5 years or longer, the adenomatous polyps degenerate into malignant tumors, which are most often located in the rectum or lower colon. The tumor spreads by direct extension through the bowel wall and by intraluminal, hematogenous, and regional lymph node metastases. The liver and lungs are common sites of distant metastasis.

Symptoms Cancer of the bowel is largely asymptomatic during the early stages. The most common presenting sign is rectal bleeding on defecation. Changes in bowel patterns, excessive gas, bloating, and cramping may also occur. Pain is unlikely until advanced stages of the disease.

Potential Complications The chance of survival falls below 50% with regional node involvement, and more than half of these individuals have node involvement at the time of diagnosis. Bowel obstruction or perforation, paralytic ileus, hemorrhage, and liver failure occur with advancing disease.

Diagnostic Tests A history of risk factors, positive result on occult fecal blood test, or palpable lesion on rectal examination indicates a need for follow-up. Visualization of a lesion by colonoscopy or barium enema examination or an elevated carcinoembryonic antigen level indicates the need for tissue biopsy, which is the only definitive mode of diagnosis.

Treatments

Surgery
Excision of welldifferentiated rectal tumors; resection of the colon around the tumor with removal of the associated lymphatic drainage system; colostomy; laser or bypass surgery for inoperable obstructing tumors.

Drugs
Adjunct systemic chemotherapy of 5-fluorouracil (5-FU) and levamisole for colon tumors; 5-FU and metronidazole for rectal tumors.

General
Radiation plus chemotherapy when four or more positive nodes are found and for palliation; instruction in ostomy care, ostomy support groups; counseling for altered body image.

Disease Process Cirrhosis is the end-stage disease that begins with one of the many etiologic factors. The development and progression of cirrhosis are tied to the severity of the injury and the liver’s response. A severe, acute injury may be involved, as in hepatitis, or a moderate chronic injury may be the cause, as in alcohol abuse. When an injury causes destruction of parenchymal cells, the initial response is fibrosis, as the liver attempts to repair itself. Fat-storing cells proliferate and are transformed into myofibroblasts, which alter the secretion, synthesis, and degradation of collagen. This results in deposition of excessive connective tissue, which alters normal lobular structures, interferes with cellular nutrition, obstructs hepatic blood flow, and forms anastomotic channels that shunt arterial blood away to efferent hepatic veins. The regenerative attempts continue as long as an injury is present. The resulting changes in the intrahepatic circulatory pathways make the system less efficient and eventually lead to an increase in portal vein pressure. The change in or destruction of lobular architecture interferes with various liver functions, such as metabolism, detoxification, storage, and blood and bile formation.

Symptoms

Early
Often asymptomatic; otherwise, abdominal pain, diarrhea, nausea, vomiting, fatigue, fever

Mid-course
Chronic dyspepsia, constipation, anorexia, weight loss, pruritus, easy bruising, bleeding gums, nose bleeds, upper gastrointestinal bleeding, enlarged liver

Late
Telangiectasis, spider angiomas, enlarged breasts, testicular atrophy, jaundice, impotence, enlarged spleen, depression, abdominal vein distention, ascites, encephalopathy, peripheral neuropathy

Potential Complications Complications include bleeding esophageal varices, which can lead to massive hemorrhage; hepatorenal syndrome, which leads to renal failure; and hepatic encephalopathy, which leads to coma and death.

Diagnostic Tests

Liver biopsy
Definitive histologic changes

Serum albumin
Decreased

Prothrombin time
Prolonged

Complete blood count
Evidence of anemia, leukopenia, thrombocytopenia

Blood glucose
Decreased

Ultrasonography
Hepatosplenomegaly, enlarged portal veins

Liver scans
Reduced liver uptake

Treatments

Surgery
Liver transplantation for advanced disease; portal systemic shunt to treat resistant esophageal varices; peritoneovenous shunt for ascites.

Drugs
Diuretics to reduce edema; digestants to promote fat digestion; supplemental vitamins; stool softeners.

General
Elimination of toxic agents such as alcohol or drugs; diet high in protein, carbohydrates, and calories and low in sodium; blood and blood products, gastric lavage, esophageal balloon for bleeding varices; abdominal paracentesis for ascites; renal dialysis for renal failure.

- An umbrella term encompassing a cluster of diseases in which recurrent obstruction of airflow is a prominent feature.

Causes and Incidence Causes are discussed under the specific disease processes; however, smoking, air pollution, and industrial exposure are major risk factors. Fifteen million people in the United States are estimated to have some type of chronic obstructive pulmonary disease (COPD). This disease constellation is the fifth leading cause of death in the United States, and the incidence and death rate are increasing.

Pathophysiology, Clinical Manifestations, Diagnostic Tests, Therapeutic Management: See specific disease.