- An acute, sexually transmitted infection of the epithelium of the genitalia, perianus, and pharynx.

Causes and Incidence Gonorrhea is caused by Neisseria gonorrhoeae and is the most frequently reported bacterial infection in the United States. The peak incidence occurs between 20 and 24 years of age. Infants born to mothers infected with the disease can contract gonococcal ophthalmia during the passage through the vagina.

Disease Process After intimate contact, the gonococcus attaches to and penetrates the columnar epithelium, producing a patchy inflammatory response in the submucosa with resultant exudate. In men, affected areas include the urethra, prostate, Littre’s and Cowper’s glands, and seminal vesicles. In women, affected areas include the urethra and cervix and Bartholin’s and Skene’s glands. The rectum, pharynx, and conjunctivae are vulnerable in both sexes. Direct extension of the infection occurs through the lymphatics to the epididymis and fallopian tubes. The inflammatory exudate is replaced by fibroblasts, producing fibrous tissue and strictures of the lumen of the urethra, epididymis, or fallopian tubes.

Symptoms

Male genitalia
Urethral pain; dysuria, purulent discharge; urinary frequency and urgency

Female genitalia
Usually asymptomatic; urinary frequency

Pharynx
Sore throat; dry, red tongue

Perianal
Anal itching, burning, and bleeding; pain on defecation; diarrhea; rectal discharge

Conjunctivae
Purulent discharge

Potential Complications Complications arise with untreated disease and include pelvic inflammatory disease in women and epididymitis and urethral stricture in men. Both sexes may have disseminated disease, with pustular skin lesions, septicemia, endocarditis, meningitis, and arthritis.

Diagnostic Tests The primary diagnostic tools are the clinical examination, a history of exposure to an infected partner, and a culture of the exudate that is positive for the organism.

Treatments

Surgery
None.

Drugs
Antiinfective drugs sensitive to the organism, following treatment guidelines of the Centers for Disease Control and Prevention.

General
Instruction about sexually transmitted diseases and the importance of completing all treatment; refraining from sexual activity until free of disease; tracing all potentially exposed.

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- A primary or secondary recurrent, acute arthritis of the peripheral joints, particularly the great toe.

Causes and Incidence The precise causal mechanism in gout is unknown. However, a host of factors act as precursors to overproduction or undersecretion of uric acid, including genetic factors (hyperactivity of hypoxanthine guanine phosphoribosyl transferase, superactivity of phosphoribosyl pyrophosphate, fructose intolerance); environmental factors (ethanol abuse, diuretic use, severe muscle exertion); underlying disease processes (diabetes mellitus, polycythemia, hypertension, renal disease, leukemia, sickle cell anemia); and the evolutionary absence of the enzyme uri-case. Gout occurs most often in men. The incidence in the United States is about 14 per 1,000 in men and 6 per 1,000 in women. Gout is rare in women before menopause. The incidence of gout is increasing in developed countries.

Disease Process Some factor triggers an overproduction or undersecretion of uric acid. The plasma becomes supersaturated with uric acid, and a crystal urate precipitate is formed and deposited in avascular tissues (e.g., cartilage, tendons, and ligaments of peripheral joints) and in cooler tissues (e.g., the ears). Through some undefined mechanism, the crystals are released at various times, causing an acute inflammatory reaction in the joint with extension to the periarticular tissues. Repeated acute attacks lead to chronic arthritis and deformed joints.

Symptoms Acute pain, redness, swelling, tenderness, and heat at the affected joint are typical presenting features. Fever, chills, and malaise may also be present. Limited motion is present in the affected joint or joints.

Potential Complications Complications include infection of ruptured deposits, renal involvement with formation of renal calculi, and secondary degenerative arthritis.

Diagnostic Tests A tentative diagnosis is made by clinical examination and elevated serum uric acid levels and confirmed with needle aspiration of synovial fluid, which is positive for urate crystals.

Treatments Treatment is aimed at terminating the acute attack and preventing future attacks by lowering uric acid levels and resolving existing deposits.

Surgery
Removal of large crystal deposits (tophi).

Drugs
Colchicine for long-term prophylaxis and to reduce inflammation in acute attack; nonsteroidal antiinflammatory agents to reduce inflammation in established gout; antihyperuricemic drugs for those with frequent attacks or chronic disease to reduce uric acid levels or increase excretion of uric acid (lifelong treatment); sodium bicarbonate to alkalize urine in patients who form calculi.

General
Rest of joint; avoidance of alcohol and purinerich foods; weight reduction if necessary to reduce wear and tear on joints; increased fluid intake; instruction in long-term use of medications and their side effects.

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- A rapidly progressive, acute inflammatory demyelinating polyneuropathy characterized by muscle weakness and paralysis of the extremities and possible respiratory paralysis with abnormal sensation and loss of reflexes.

Causes and Incidence The cause is unknown, but Guillain-Barre syndrome (GBS) is hypothesized to be an autoimmune disorder involving sensitization of peripheral nerve myelin. It is thought to be connected to a previous nonspecific infection and has been associated with inoculation for the swine flu. The incidence of GBS in the United States is 1.7 per 100,000 individuals, and the disorder occurs across age and gender lines.

Disease Process Mononuclear cells infiltrate the peripheral nervous system and set up an inflammatory response in the blood vessels of the cranial and spinal nerves. Demyelination of the peripheral nerves results, causing muscle weakness that begins in the lower extremities and ascends through the body in a symmetric fashion. Respiratory paralysis and facial weakness occur in 30% to 40% of cases. In some cases axonal destruction can cause atrophy in distal muscles and permanent neurologic impairment.

Symptoms The first sign is symmetric muscle weakness in the distal extremities accompanied by paresthesia. This weakness spreads upward to the arms and trunk and then to the face. This ascension usually peaks about 2 weeks after onset. Deep tendon reflexes are absent. Difficulty chewing, swallowing, and speaking may occur, and respiratory paralysis may develop. Bladder atony, postural hypotension, tachycardia, and heart block may be seen. Deep, aching muscle pain is also common.

Potential Complications About 5% of affected individuals die of respiratory failure. Another 10% have permanent residual neurologic deficits. About 90% of survivors make a full recovery, but the recovery time may be as long as 3 years.

Diagnostic Tests The diagnosis is based on the clinical presentation and cerebrospinal fluid samples, which show an increase in protein without an increase in lymphocyte count. Electromyography produces abnormal nerve conductionresults.

Treatments

Surgery
Tracheostomy to provide ventilation in the event of respiratory failure.

Drugs
Immunoglobulin given IV to counteract neurologic defect; narcotic analgesics for pain; prophylactic antiinfectives

Corticosteroids are contraindicated because they worsen the ultimate outcome.

General
Plasma exchange to speed recovery of neurologic deficit; respiratory monitoring and mechanical ventilation for respiratory paralysis; cardiac monitoring for sinus tachycardia, bradyarrhythmia; communication systems if ventilator is used or with facial paralysis; passive range-of-motion exercises; turning to prevent contracture and skin breakdown; rehabilitation to aid neurologic recovery; counseling and support of individual and family for long-term adaptation.

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- Pain or aching of the head associated with various intracranial or extracranial factors; headaches may be categorized as tension, vascular (cluster, migraine), or traction inflammatory.

Causes and Incidence Although tension headaches are the most common type, their precise etiology is not well defined. However, most are related to muscle tension, minor trauma, increased stress or anxiety, food and environmental allergens, infection or lesions of the oral or nasal cavity, ear infections, or eye strain. Traction inflammatory headaches are either intracranial or cranial. Intracranial headaches may be caused by increased intracranial pressure stemming from an underlying process such as a brain tumor, abscess, or hematoma; meningitis; syphilis; tuberculosis; cancer; or subarachnoid hemorrhage. Cranial changes in the skull caused by neoplasms, temporal arteritis, or involvement of the sensory nerves of the scalp with a disease such as herpes zoster also can cause headaches. Vascular disturbances caused by exposure to toxic substances (e.g., alcohol, lead, arsenic, and carbon monoxide) are causes of headache. Some vascular headaches, such as migraines and cluster headaches, are idiopathic.
Each year approximately 30 million Americans seek medical treatment for recurrent headache. Tension headaches are most common and occur in adults across age and gender lines. Migraines affect about 5% of the general U.S. population, and women in their early childbearing years are the most susceptible, particularly just before or during menstrual periods. Cluster headaches are most common in men in their 30s and 40s.

Disease Process Headache pain occurs when afferent pain fibers on the cranial nerves (V, VII, IX, or X) carry sensory stimuli to central nervous system tissue. The location and diffusion of the pain are dictated by the cause, the extent of tissue affected, and the cranial nerve or nerves involved. Pain can be highly localized and specific or diffuse and generalized. Involvement of the deep brain structure often causes referred pain.

Symptoms

Tension
Bilateral, dull, nonpulsatile ache, typically bifrontal or nuchal-occipital; transient or chronic

Migraine
Paroxysmal, throbbing, unilateral pain that lasts hours to days; cyclic pattern; possible nausea and vomiting; aversion to light and noise; may be preceded by an aura (shimmering visual manifestation) or prodromal behavioral alterations ranging from depression to euphoria or triggering food cravings

Cluster
Deep, agonizing, nonthrobbing pain often beginning during sleep and involving an eye, temple, cheek, and forehead on one side; lasts from 30 minutes to 3 hours, with several headaches occurring each day for several weeks; tearing and redness of affected eye

Traction
Deep, dull, steady ache that is worse in the morning and aggravated by coughing or straining

Arteritis
Soreness of one or both temples that becomes a chronic, burning, well-localized pain; the affected scalp artery is prominent, tender, incompressible, and pulseless

Potential Complications Complications are usually associated with an underlying disease process rather than the headache itself. However, headaches associated with temporal arteritis, if left untreated, may cause blindness.

Diagnostic Tests Diagnosis centers on classification of the head pain and identifying the potential cause. A neurologic history and a physical examination, with identification of precipitating or underlying disease, are paramount. Computed tomography and magnetic resonance imaging are useful in detecting intracranial lesions. Cerebral angiography may help detect vascular abnormality.

Treatments

Surgery
None

Drugs
Tension: analgesics

Migraine: analgesics, ergot preparations, sumatriptan for acute attacks; betablockers, serotonin agonists for prophylaxis in chronic retractable syndromes.

Cluster: prophylaxis with drugs such as valproic acid, verapamil, or lithium carbonate is more effective than administration of drugs during acute attacks.

General
Treatment of any identified underlying disease; application of cold or heat compresses; elimination of food or environmental allergens; counseling, stress management, biofeedback.

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- Acquired or congenital diminished auditory capacity that may be classified as sensorineural, conductive, or central. Loss with no organic basis has been labeled psychogenic or functional. Hearing loss ranges from partial to complete.

Causes and Incidence Causes of sensorineural impairment include trauma, noise, infection, aging, exposure to certain toxins, and drugs. Conductive loss results from disorders of the middle and external ear, such as otitis media, otosclerosis, or perforation of the eardrum. Central hearing loss is induced when the brain’s auditory pathways are damaged by such underlying disorders as cerebrovascular accident or a brain tumor. Congenital losses may result from fetal or neonatal anoxia; delivery trauma; fetal exposure to toxins, rubella, or syphilis; Rh incompatibilities; and bilirubin toxicity. Psychogenic loss has no traceable organic basis and is thus thought to be psychologic in origin.

Disease Process In sensorineural impairment, damage to the cochlea or cranial nerve VIII results in interference with bone conduction of sound waves from the inner ear. Conductive loss occurs when injury to the middle or external ear results in interference with air conduction of sound waves to the inner ear. Some individuals have both conductive and sensorineural impairment. Central impairments interfere with auditory brainstem pathways. There is no organic pathologic condition in functional hearing loss.

Symptoms The overriding manifestation is a reduced ability to distinguish sound. It is frequently progressive and may range from a mild loss to total deafness.

Potential Complications Permanent, nontreatable deafness is the central complication.

Diagnostic Tests

Weber tuning fork
Lateralization of sound to deaf ear in conductive loss and to better ear in sensorineural loss

Rinne tuning fork
Bone conduction heard longer than or as long as air conduction in conductive loss; air conduction heard longer in sensorineural loss

Schwabach test
Examiner hears longer than examinee in sensorineural loss and vice versa for conductive loss

Audiometry
To distinguish types and identify degree of impairment

Treatments

Surgery
Stapedectomy for loss caused by otosclerosis; cochlear implants in some cases to treat profound deafness.

Drugs
None.

General
Hearing aids for conductive loss; instruction in sign language, speech, and lip reading for the profoundly deaf; use of specialized assistive devices (e.g., amplified or typed-message telephones, low-frequency or flashing doorbells, closed-caption TV decoders, flashing alarm clocks, alarm bed vibrators, flashing smoke detectors); counseling and support groups for adaptation.

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