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Myasthenia Gravis

Posted by: admin in Diseases

- A progressive neuromuscular disease of the lower motor neurons characterized by muscle weakness andfatigue.

Causes and Incidence The cause of myasthenia gravis (MG) is unknown. More than 80% of individuals with MG also have thymic abnormalities, but the link is unclear. The incidence is 3 to 6 per 100,000 individuals in the United States. The age of onset is either 20 to 30 years (primarily in women) or 50 to 60 years (primarily in men).

Disease Process An antigen attack on the acetylcholine receptor of the postsynaptic neuromuscular junction results in dysfunction of the receptor, which fails to act on the acetylcholine. Because of this, nerve impulses do not pass on to the skeletal muscle at the myoneural junction.

Symptoms The most common manifestations are ptosis, diplopia, and muscle fatigue after exercise. Dysarthria, dysphagia, ocular palsy, head bobbing, and facial and proximal limb weakness are also reported. Symptoms are milder on awakening and become worse as the day progresses. Rest temporarily improves symptoms. Respiratory involvement leads to breathlessness and reduced tidal volume and vital capacity. Manifestations can be remitting, static, or progressive. Factors such as stress, menses, heat, and illness can exacerbate symptoms.

Potential Complications Myasthenic crisis is an acute exacerbation of symptoms; it usually involves respiratory distress and can lead to respiratory failure or aspiration and cardiopulmonary arrest.

Diagnostic Tests A characteristic pattern of fatigue and weakness on exertion that improves with rest, and a positive Tensilon test, are indicators. A computed tomography scan may indicate the presence of thymoma; electromyography may show muscle fiber contraction with progressive decremental response.
Treatments

Surgery
Thymectomy for treatment of thymoma and remission of adultonset MG.

Drugs
Anticholinesterases and corticosteroids to counteract muscle weakness and fatigue; immunosuppressants with autoimmune pathogenesis; flu shots to prevent respiratory infection.

General
Plasmapheresis to treat weakness and fatigue; ventilatory support in respiratory crisis; physical therapy to prevent disuse problems, occupational therapy to aid in activities of daily living; balance of exercise and rest; instruction about cholinergic crisis caused by excessive anticholinesterase medication; counseling for long-term adaptation to disease; information about the importance of preventing respiratory infection or recognizing and treating symptoms early.

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Myeloma (Multiple)

Posted by: admin in Diseases

- A progressive, hematologic neoplastic disease of the plasma cells.

Causes and Incidence The etiologic factors are not clearly understood, but chromosomal abnormalities, genetic factors, viruses, and chronic antigen stimulation have been implicated as probable contributors. An important risk factor is occupational exposure to petroleum products, asbestos, or radiation. Multiple myeloma is a relatively rare disease that occurs primarily in those over 40 years of age and peaks around age 60. Men and women are equally affected, but the disease rate for blacks is 14 times that of whites. More than 13,000 cases are diagnosed in the United States each year, with 9,400 deaths.

Disease Process Multiple myeloma involves an abnormal growth and proliferation of plasma cells and the development of single or multiple plasma cell tumors in the bone marrow. This leads to mass destruction of bone marrow and bone throughout the body. Plasma cells also produce an M protein immunoglobulin that coats the RBCs and inhibits the production of effective antibodies; this can lead to anemia. Metastasis is via the lymph nodes to the liver, kidneys, and spleen.

Symptoms Early symptoms are nonspecific and include fatigue, weakness, anorexia, and weight loss. These are followed by complaints of bone pain, particularly in the back and thorax, and frequent bacterial infections, particularly pneumonia and anemia. Later manifestations include thrombocytopenia and leukopenia; urinary changes; changes in cognitive, sensory, and motor functions; pathologic fractures and vertebral collapse; spinal cord compression; and paraplegia.

Potential Complications The disease is progressive, and currently there is no cure. Life expectancy is tied to the extent of disease at time of diagnosis; the median survival rate is 2 to 3 years. Complications include infection, hyperuricemia, hypercalcemia, pyelonephritis, renal failure, and GI bleeding.

Diagnostic Tests The diagnosis is made based on one or more of the following criteria: plasma cell infiltration above 10% in bone marrow; a monoclonal spike on serum electrophoresis; radiographic visualization of osteoporosis and osteolytic lesions; soft-tissue plasma cell tumors.

Treatments

Surgery
None.

Drugs
Chemotherapy is the primary treatment; antiinfective drugs for bacterial infections; allopurinol for hyperuricemia; corticosteroids for hypercalcemia.

General
Radiation in chemotherapyresistant disease and for palliation of bone pain; bone marrow transplantation has been used with limited success; ambulation maintained as long as possible; physical therapy to maintain function; fracture precautions; adequate hydration to prevent dehydration associated with proteinuria; transfusions for anemia; monitoring for bleeding episodes; precautions against exposure to infections; emotional support for adaptation to chronic, terminal disease.

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Myocardial Infarction (Heart Attack)

Posted by: admin in Diseases

- Ischemic necrosis of the myocardium resulting from inadequate coronary artery blood flow. (See also Coronary Artery Disease and Angina.)

Causes and Incidence More than 90% of all myocardial infarctions (MIs) are caused by obstruction of a plaque-lined coronary artery by an acute thrombus. MI also may be caused by arterial embolization from valvular stenosis or endocarditis and by arterial spasm after cocaine ingestion. Each year more than 1 million people in the United States suffer an MI; one in four dies, and more than half of the deaths occur within 1 hour of onset.

Disease Process Occlusion of a coronary artery causes a persistent cellular ischemia that interferes with myocardial tissue metabolism, causing rapid, permanent cell damage and necrosis. The extent of necrosis is dictated by the size of the infarct, the vessel occluded, and the length of time it remains occluded. Damage initially occurs to the left ventricle but often extends to other cardiac chambers. Infarcts may be classified by the thickness of the myocardial tissue involved. Transmural infarcts (Q wave) involve the full thickness of the myocardium from the epicardium to endocardium and cause abnormal Q waves on the ECG. Nontransmural infarcts (non–Q wave) do not extend through the ventricular wall and cause ST segment or T wave ECG abnormalities.

Symptoms Most individuals have prodromal symptoms such as fatigue, shortness of breath, and crescendo angina days or weeks before the acute attack. The first symptom of the attack is usually a deep, substernal, visceral pain that may be described as aching, squeezing, or crushing, or as a heavy weight on the chest. The pain may radiate to the back, neck, jaw, teeth, or left arm, and it is not relieved by rest, nitroglycerin, or antacids. Other signs and symptoms include anxiety; restlessness; sweating; nausea; vomiting; cold, clammy skin; low-grade fever; and dyspnea.

Potential Complications Complications include arrhythmia, cardiogenic shock, heart failure, pulmonary edema, cerebral or pulmonary emboli, myocardial rupture, pericarditis, postmyocardial infarction syndrome, and sudden death.

Diagnostic Tests The diagnosis is made using a clinical history; electrocardiography, which illustrates an elevation in the ST segment, T wave inversion, and deep Q waves; laboratory tests of cardiac enzymes (aspartate aminotransferase, creatine phosphokinase, lactate dehydrogenase), which are elevated for days after the event; a complete blood count, which reveals an elevated white count and erythrocyte sedimentation rate; a thallium perfusion scan, to determine the size and location of the infarct and resulting ischemia; and an echocardiogram, to detect contraction abnormalities of ventricles.

Treatments

Surgery
Angioplasty post thrombolysis is contraindicated; recent clinical trials have shown no benefit and possible harm from angioplasty performed within the first few days after an attack; angioplasty may have a rescue role in cardiogenic shock that is unresponsive to other treatment.

Drugs
Thrombolytic drugs are given within 6 hours of onset to interrupt MI evolution; aspirin and anticoagulants for antiplatelet, anticoagulant effects; beta-adrenergic blockers to reduce reinfarction and infarct size; vasodilators and narcotic analgesics for pain; stool softeners to avoid straining at stool; sedatives and tranquilizers to increase rest.

General
Cardiovascular monitoring; oxygen therapy; bed rest; decreased environmental stimuli; monitoring for and treatment of depression, particularly about the third day; quitting smoking; restriction of caffeine and cholesterol; antiembolism hose; rehabilitation with stepped exercise program; sexual counseling; regular medical follow-up.

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Organic Mental Syndromes (Organic Brain Syndrome)

Posted by: admin in Syndromes

- A constellation of behavioral signs and symptoms associated with transient or permanent dysfunction of the brain and characterized by impaired intellectual functioning, confusion, and agitation. The most common categories and the ones discussed here are delirium and dementia. Delirium is a reversible, self-limiting condition characterized by a reduced ability to maintain attention to or appropriately shift attention among external stimuli. Dementia is a structurally caused, permanent decline in memory, abstract thinking, and judgment.

Causes and Incidence Delirium most often occurs as a result of withdrawal from intoxication in chronic alcohol and barbiturate abusers and in acute inflammatory disorders such as meningitis and encephalitis. The most common cause of dementia is Alzheimer’s disease; other causes include vascular disease, HIV infection, central nervous system infection, severe head injury, toxic metabolic disturbances, normal pressure hydrocephalus, underlying neurologic disease (parkinsonism, Huntington’s chorea, multiple sclerosis, Pick’s disease), and drug, alcohol, or nutritional abuse. More than 1 million individuals in the United States have dementia, and the elderly are at greatest risk. As the incidence of AIDS increases, the incidence of dementia is expected to increase (an estimated 50% of individuals with end-stage AIDS develop dementia).

Disease Process The pathophysiology of organic mental syndromes is not yet understood. Pathologic changes vary by causation, and in Alzheimer’s-related dementia include atrophy of brain tissue with wide sulci and dilated ventricles, senile plaque formation, and neurofibrillary tangles. Vascular disease–induced dementia is characterized by multiple cerebral infarcts. In AIDS-related dementia, the neurons are infected with HIV, and in hydrocephalus, cerebrospinal fluid circulation and absorption are impeded.

Symptoms

Delirium
Rapid onset; disorientation, including loss of self-recognition in some instances; impaired memory; inability to maintain or shift attention; irritability, agitation, restlessness, hyperactivity; perceptual disturbance, hallucinations, delusions; rambling, fragmented speech; impaired

sleep-wake cycle; lucid intervals, symptoms worse at night; duration about 1 week on average

Dementia
Symptoms vary widely, but the overall picture is a slow, insidious disintegration of personality and intellect with impaired insight and judgment and loss of affect; memory impairment is often the most prominent initial symptom, and others include increasing rigidity of thought; restricted interests; easy distractibility; lack of initiation; speech disturbances; loss of impulse control; change of former traits or exaggeration of those traits (e.g., a neat person becomes slovenly or becomes obsessively preoccupied with orderliness); depression

Potential Complications Delirium may lead to dementia. Dementia (except that caused by trauma) is progressive; the individual eventually becomes totally oblivious to his or her surroundings and ultimately dies. Individuals with dementia are more susceptible to accidents and infection.

Diagnostic Tests The diagnosis of delirium is based on the clinical presentation, particularly the fluctuation of symptoms with periods of lucidity, and a history of one or more etiologic agents. Electroencephalography shows a generalized slowing of background activity. A diagnosis of dementia is warranted with demonstrable impairment of long- and short-term memory and demonstrable disturbances in abstract thinking, judgment, personality, or other higher cortical functions that interfere with social activities and relationships. Attention and arousal tend to be normal in dementia, and manifestations are relatively stable, worsening over time. A definitive diagnosis is available only on autopsy.

Treatments

Surgery
None.

Drugs
Delirium: withdrawal of toxic agents (alcohol, barbiturates) and IV sedation with antianxiety agents for agitation, seizure activity, and tremors Dementia: treatment of underlying disorders; antianxiety agents as disease progresses to relieve anxiety and frustration.

General
Delirium: adequate fluid and electrolytes; seizure precautions; safety precautions (e.g., to prevent wandering, climbing over bedrails); long-term treatment for substance abuse when it is the etiologic agent Dementia: kept in familiar surroundings with minimal environmental changes; use of frequent orientation devices (clocks, calendars, schedules, memory books, name tags); encouragement to do familiar, repetitive routines; safety precautions to prevent wandering; use of adult day care, respite care, or home care to relieve caregiver; family support groups and counseling; prevention of disuse syndrome in end-stage disease.

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Osteomyelitis

Posted by: admin in Diseases

- An infection of the bone and bone marrow.

Causes and Incidence Osteomyelitis is caused by a pathogen that is introduced directly through an open fracture, penetrating trauma, or surgical procedure, or indirectly from another infection that spreads through the bloodstream or from adjacent tissues. The most common pathogens are Staphylococcus aureus, Streptococcus pneumoniae, Escherichia coli, Pseudomonas aeruginosa, and Haemophilus influenzae. The incidence is highest in childhood and early adolescence, and the disorder occurs more often in boys. Those undergoing hemodialysis, drug abusers, diabetics, and individuals with peripheral arterial insufficiency are also at risk.

Disease Process The long bones are most often involved. The invading pathogen travels to the metaphysis, located between the shaft and the epiphysis. The pathogen grows and multiplies in the metaphysis, producing pus, which eventually interferes with the blood supply in the bone, causing necrosis. An inflammatory response is set up, and macrophages are produced to combat the pathogens; necrosis continues, and the enlarging mass spreads through the bone cortex to contiguous tissues. New bone trabeculae are formed in an effort to keep the infection localized. The infection can spread to the bone marrow and to the skin through sinus tracts. Periodic drainage occurs until all dead bone is destroyed or excised. In adults the spine is oftenaffected.

Symptoms Pain, tenderness, edema, and warmth at the site are the most common manifestations. Bone pain on use or on palpation may be evident, as well as systemic symptoms such as fever, chills, sweats, malaise, weakness, headache, and nausea. Later signs include drainage from sinus tracts to the skin and fractures.

Potential Complications Osteomyelitis can lead to chronic infection, joint and skeletal deformities, and (in children) disturbed bone growth and limb shortening.

Diagnostic Tests The diagnosis is made from the clinical presentation; a history of antecedent infection or open trauma in the preceding 2 to 4 weeks; an elevated WBC count and erythrocyte sedimentation rate; and a positive radionucleotide scan with technetium phosphate. X-ray examination may reveal bone destruction, but only after 3 weeks or longer. Cultures of any identified mass are positive for the pathogen. If spread is via the bloodstream, serum cultures should be positive for the pathogen.

Treatments

Surgery
Surgical excision (saucerization) of infected and dead bone, sterilization of the abscess, bone grafts to affected site; amputation in some cases related to underlying diabetes.

Drugs
Antiinfective drugs specific for pathogen.

General
Splints to reduce joint pain; external fixation or casting for weakened bones to prevent fractures; initially bed rest, followed by progressive ambulation; dressing changes for draining wounds; hyperbaric oxygen therapy to increase circulating WBCs.

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