- An acute infectious disease of the central nervous system characterized by intermittent tonic spasms of the voluntary muscles.

Causes and Incidence Tetanus is caused by the tetanospasmin exotoxin produced by the spore-forming Clostridium tetani bacillus. The organism enters the body through a wound contaminated with soil and feces containing viable spores. The incidence is sporadic, and the disease occurs worldwide. It is rare in developed countries, where immunization is common.

Disease Process The bacillus spores enter and multiply in a skin wound to produce the tetanospasmin toxin. The toxin travels to the central nervous system via the bloodstream and peripheral motor nerves and binds to ganglioside membranes, blocking release of an inhibitory transmitter. This induces a hyperexcitability in the motor neurons that results in tonic rigidity and spasms of the voluntary muscles. Once bound, the toxin cannot be neutralized by an antitoxin.

Symptoms The incubation period ranges from 2 to 50 days, with an average of 5 to 10 days before symptoms occur. The most common symptom is stiffness of the jaw. Others include irritability, restlessness, headache, fever, sore throat, stiff neck, and difficulty swallowing. As the disease progresses, the person has difficulty opening the mouth, facial spasms, and rigidity with a fixed grin; opisthotonos; painful, generalized tonic spasms; profuse sweating; cyanosis; and exaggerated reflexes.

Potential Complications The worldwide mortality rate is 50%, and prognosis is poor when the incubation period is short and the symptoms progress rapidly. Complications include cardiac and pulmonary failure and muscle rupture.

Diagnostic Tests The diagnosis is made by history and physical examination. Blood and wound cultures and tetanus antibody tests are commonly negative.

Treatments

Surgery
Debridement of deep penetrating wounds; tracheotomy if needed for prolonged respiratory management.

Drugs
Tetanus toxoid with subsequent booster shots for primary immunity; tetanus antitoxin or tetanus immune globulin may be given at time of penetrating injury with no history of recent vaccination; muscle relaxants to treat rigidity and spasm; antiinfective drugs for infection; analgesics for pain.

General
Prompt, thorough debridement of wound; intubation and mechanical ventilation if needed; tube feedings or hyperalimentation to manage nutrition; catheterization to manage urinary retention; coughing, turning, deep breathing to prevent pneumonia; cardiac and hemodynamic monitoring; adequate fluids and electrolytes; instruction in the importance of maintaining immunization with routine booster every 10 years.

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- A platelet disorder in which the platelet count falls below 200,000/mm3, leading to bleeding into the skin, mucous membranes, internal cavities, and organs.

Causes and Incidence Thrombocytopenia may be idiopathic, or it may occur secondary to another process that reduces the number of platelets or produces defective platelets. These processes include use of drugs that can cause platelet destruction (heparin, quinidine, sulfa, oral hypoglycemics, gold salts, rifampin); underlying disease (leukemia, aplastic anemia, cirrhosis, disseminated intravascular coagulation); severe infection; hypothermia; hypersplenism; and alcohol ingestion. Idiopathic thrombocytopenia purpura (ITP) may be either acute or chronic. The acute form usually follows a viral infection such as rubella or chicken pox and affects mostly children between 2 and 6 years of age. The chronic form is linked to immunologic disorders such as lupus and HIV and usually affects adults of all ages, particularly women.

Disease Process ITP is thought to be associated with an autoimmune process in which the platelets are prematurely destroyed by circulating antibodies. The pathophysiology in secondary forms of the disease is related to the causative agent.

Symptoms Common manifestations include petechiae and ecchymoses on the skin, particularly the lower extremities; easy bruising; bleeding from the nose and gums; melena in stools; hematemesis; heavy menses and breakthrough bleeding; and hematuria.

Potential Complications Complications include hemorrhage into organs such as the brain, gastrointestinal tract, or heart, which can be fatal without treatment.

Diagnostic Tests Other platelet disorders must be ruled out.

Platelets
Count decreased; size and morphologic appearance may be abnormal in ITP

Platelet survival
To help distinguish between ineffective and inappropriate platelet production

Bone marrow
Abundance of megakaryocytes

Bleeding time
Prolonged

Coagulation time
Normal

Capillary fragility
Increased

Treatments

Surgery
Splenectomy for severe thrombocytopenia related to hypersplenism or splenomegaly.

Drugs
Corticosteroids to enhance platelet production and promote capillary integrity; immunosuppressants when disease does not respond to steroids; immune globulin to prepare severely thrombocytic individuals for surgery; discontinuing any drug that may be causing the disorder.

General
Platelet transfusions for severe bleeding; safety precautions to prevent bruising; balance of rest and activity; monitoring for bleeding episodes; instruction in infection precautions for those taking immunosuppressants.

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- An abnormal vascular condition in which a thrombus develops in a vein. Thrombophlebitis refers to a thrombus accompanied by inflammation of the vein (phlebitis). Phlebothrombosis refers to a thrombus with minimal inflammation. Dislodgment and migration of a thrombus are known as thromboembolism.

Causes and Incidence A number of factors acting in concert contribute to thrombus formation, including intimal damage to the vein from indwelling catheters, injection of irritating substances or septic phlebitis; hypercoagulability related to underlying disorders (idiopathic thrombocytopenia purpura, malignancies, blood dyscrasias) and use of oral contraceptives; and stasis from prolonged immobilization or postpartum or postoperative states. Venous thrombosis is the most commonly seen venous disorder except for varicose veins. Individuals at greatest risk are postoperative patients and those receiving IV therapy.

Disease Process Most thrombi begin forming in the valve cusps of deep calf veins. Tissue thromboplastin is released and forms thrombin and fibrin that trap RBCs to form a clot. The clot continues to enlarge until it eventually occludes the lumen of the vessel. It may break off and migrate to the systemic circulation.

Symptoms

Deep veins
Calf pain and tenderness; positive Homans’ sign (calf pain on foot dorsiflexion); dilated superficial veins; edema, increased size of involved extremity; redness and warmth over vein site

Superficial veins
Redness, warmth, and tenderness over affected vein, which is visible and palpable

Potential Complications Chronic venous insufficiency and pulmonary embolus are the most common complications of thrombosis.

Diagnostic Tests A physical examination is the primary diagnostic tool in detecting venous thrombosis and in distinguishing arterial from venous obstructions. Noninvasive tests include ultrasonography and plethysmography, which show reduced blood flow. Contrast venography is the most accurate and the confirmatory diagnostic tool.

Treatments

Surgery
Ligation, clipping, plication, and thrombectomy when thrombosis fails to respond to conservative therapy; extravascular vena cava interruption with possible placement of intracaval filter when emboli are probable.

Drugs
Superficial: nonsteroidal antiinflammatory drugs for pain and inflammation Deep vein: fibrinolytics to lyse clots; anticoagulants (heparin for acute treatment, warfarin for maintenance) to augment thrombolysis; antiplatelets to prevent thrombus formation; analgesics (aspirin is contraindicated because it interferes with platelet function).

General
Superficial: moist compresses to treat discomfort Deep vein: bed rest with elevation of affected extremity above the level of the heart; warm, moist packs; antiembolism hose when ambulatory; monitoring of prothrombin time and partial thromboplastin time during anticoagulant therapy; monitoring for signs of pulmonary embolus; instruction about bleeding precautions while undergoing anticoagulants.

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- Papillary carcinomas are the most common type of thyroid cancer (60% to 70%). Follicular carcinomas account for 15% to 20% of diagnosed cases, anaplastic carcinomas for 10%, and medullary carcinomas for less than 5%.

Causes and Incidence There is a strong link between radiation therapy to the neck region (a popular childhood treatment to shrink tonsils, adenoids, and thymus glands in the 1950s) and papillary cancer. Other suspected precursors of thyroid cancer include prolonged secretion of thyroid-stimulating hormone (TSH), iodine deficiencies, and chronic goiter. Familial predisposition (autosomal dominant trait) is strongly suspected in medullary cancer. About 10,000 cases of thyroid cancer are diagnosed in the United States each year. It can occur at any age, although anaplastic carcinoma is seen almost exclusively in the elderly. Thyroid cancer is two to three times more common in women than in men.

Disease Process Papillary and follicular carcinomas begin in the epithelial cells of the thyroid, growing slowly and forming nodules in the gland. Papillary tumors are usually nonencapsulated, extend to adjacent tissue beyond the thyroid, and metastasize to local cervical lymph nodes. Distant metastasis is rare. Follicular tumors are encapsulated, invade local tissue and cervical nodes, and metastasize to distant sites (e.g., lungs, bone) through the bloodstream.
Anaplastic carcinomas arise from the epithelium of the thyroid and are characterized by rapid, painful invasive growth to the trachea and major blood vessels, with metastasis to the bones and liver. Medullary carcinoma arises from the parafollicular cells of the thyroid and causes excessive secretion of calcitonin, lowering serum calcium and phosphate levels. Amyloid and calcium deposits are common. The tumor grows rapidly and metastasizes through lymphatics to cervical and mediastinal nodes and to the liver, lungs, and bone, leaving dense calcifications in its wake.

Symptoms The most common presenting sign is a palpable, symptomless lump in the neck.

Potential Complications The prognosis is excellent for papillary and follicular cancers if they are treated before distant metastasis occurs. Medullary and anaplastic cancers have a much higher death rate. Medullary tumors are treated successfully only if detected very early, before any tissue invasion is evident; anaplastic tumors are resistant to treatment and spread so rapidly they often cause death within 6 months of diagnosis. Complications include dysphagia, stridor, and tracheal obstruction.

Diagnostic Tests X-ray examination, thyroid scans, ultrasound and computed tomography scans, and magnetic resonance imaging are used to visualize the size and extent of the tumor and calcifications. A calcitonin assay for elevated levels of calcitonin is a reliable indicator for medullary carcinoma. The definitive diagnosis is made through fine needle aspiration biopsy.

Treatments

Surgery
Thyroidectomy with or without lymph node dissection as primary treatment; modified radical neck resection for recurrence or metastasis.

Drugs
Palliative treatment in widespread disease; thyroid hormone as replacement therapy and to suppress TSH production.

General
Radioactive iodine ablation as adjuvant to surgery or alone for palliation; instruction about lifelong use of thyroid replacement hormones.

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- The perception of sound in the absence of an acoustic stimulus, which may be intermittent, continuous, or pulsatile.

Causes and Incidence The etiology is unknown, but tinnitus occurs as a symptom in nearly every disorder of the ear. Contributory factors include obstruction of the external ear canal; infection and inflammation; use of certain drugs (sali-cylates, quinine, aminoglycoside antibiotics, thiazide diuretics); exposure to certain toxins (carbon monoxide, heavy metals, alcohol); damage to cranial nerve VIII; underlying cardiovascular disease, anemia, or hypothyroidism; and acoustic or head trauma. An estimated 30 million individuals in the United States are thought to suffer from tinnitus.

Disease Process The pathophysiologic mechanisms of tinnitus remain obscure.

Symptoms The primary manifestation is a sound variously described as ringing, roaring, sizzling, whistling, humming, buzzing, hissing, or clicking. It may be intermittent, continuous, or pulsatile and may be accompanied by a hearing loss.

Potential Complications Tinnitus that is loud, high pitched, and continuous has been known to drive some individuals to attempt suicide if treatment fails.

Diagnostic Tests An audiologic examination is done to rule out underlying systemic disease or disease of the ear known to produce tinnitus. The examination will also reveal any hearing loss. Measurements of tone masking also are done. Pulsatile tinnitus calls for a workup of the vascular system for aneurysm, obstruction, and neoplasm.

Treatments

Surgery – None.

Drugs
Antianxiety agents and anticonvulsants (e.g., Tegretol) combined with Mysoline or Dilantin at night for sedative effect.

General
Correction of any associated hearing loss; treatment of underlying disease; use of background noise to mask tinnitus; use of a tinnitus masker worn in the ear to produce a more pleasant sound; avoidance of causative drugs or toxins.

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