- An infection and inflammation of the meninges of the brain and spinal cord resulting in altered neurologic function.

Causes and Incidence Bacterial meningitis can be caused by any number of bacteria, but 80% of cases are caused by one of three strains: Neisseria meningitidis, Haemophilus influenzae, and Streptococcus pneumoniae. The disease occurs worldwide and is both endemic and epidemic. Spread is through droplet contact, and the disease can be transmitted as long as the respiratory tract contains the causative bacteria. Children under 5 years of age are at greatest risk. Pneumococcal meningitis is the most common form of adult meningitis.

Disease Process The bacteria invade the respiratory passages and are disseminated by the bloodstream to the cerebrospinal fluid (CSF) space and the meninges of the brain and spinal cord. A growing exudate damages cranial nerves, obliterates CSF pathways, and induces vasculitis and thrombophlebitis. The exudate also generates metabolites and cytokines, which damage cell membranes, disrupt the blood-brain barrier, and cause cerebral edema and ischemic brain damage.

Symptoms A prodromal respiratory illness may precede symptoms of fever, severe headache, stiff neck, and vomiting. Changes in consciousness then occur, beginning with irritability, drowsiness, and confusion and followed by stupor and coma. Seizures are common.

Potential Complications Complications include hydrocephalus, blindness, deafness, arthritis, myocarditis, pericarditis, and cognitive deficit.

Diagnostic Tests Cultures of CSF, respiratory secretions, and blood are positive for the causative agent.

Treatments

Surgery
None.

Drugs
Antiinfective drugs specific for the causative agent; analgesics for muscle pain and headache; vaccine for prevention in at-risk populations; antiinfective drugs for those in close contact with an infected individual; corticosteroid use is under investigation.

General
Adequate hydration and balancing of electrolytes; monitoring and control of intracranial pressure; hemodynamic monitoring; ventilatory support if necessary; seizure precautions; secretion precautions to prevent spread; comfort measures for photophobia; monitoring of contacts with infected individuals.

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- An acute viral infectious disease characterized by fatigue, fever, pharyngitis, and lymphadenopathy.

Causes and Incidence Mononucleosis is caused by the Epstein-Barr virus (EBV) and transmitted via prolonged contact with infected saliva or through blood transfusion. After the primary infection the virus remains in the host for life and is periodically shed in nasal secretions. At any given time, 15% to 20% of the adult population are active carriers. Mononucleosis is common in the United States, Canada, and Europe, particularly among adolescents and young adults.

Disease Process EBV invades the host and incubates for 4 to 6 weeks. It then replicates in the nasopharynx and moves to the lymphatic system, where it infects B lymphocytes and stimulates the secretion of an antigen. T lymphocytes proliferate in response to the antigen, producing a generalized lymph node hyperplasia.

Symptoms Profound fatigue; a fever that peaks in the late afternoon at 38.3o to 40.6o C (101o to 105o F); severely painful and exudative pharyngitis; and symmetric lymphadenopathy are the hallmark signs. Splenomegaly is usually present in the second or third week. Mild hepatomegaly may also be present. A maculopapular rash, palatal petechiae, and periorbital edema are less common signs.

Potential Complications The prognosis is excellent; complications are rare but include splenic rupture, anemia, Guillain-Barre syndrome, meningitis, and encephalitis.

Diagnostic Tests The presence of clinical manifestations plus a differential WBC showing lymphocytes and monocytes over 50%; a heterophil agglutination antibody test with an antibody titer greater than 1:40; and an EBV-IgM test with antibodies over 1:80 are all suggestive of mononucleosis.

Treatments

Surgery
Removal of the spleen in cases of rupture.

Drugs
Nonaspirin analgesics and antipyretics; steroids for treating impending airway obstruction.

General
Bed rest during the acute phase; saline throat gargles; adequate hydration; avoidance of heavy lifting and contact sports for 2 months after recovery to prevent injury to spleen.

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- A chronic, progressive central nervous system disease with a disseminating demyelination of the nerve fibers of the brain and spinal cord characterized by exacerbation and remission of varied multiple neurologic symptoms.

Causes and Incidence The exact etiology of multiple sclerosis (MS) is unknown, but an immunologic abnormality, allergic response, or slow-acting virus is suspected. MS is the most prevalent demyelinating disease and the third leading cause of disability in young and middle adulthood. More than 8,000 cases are diagnosed in the United States each year.

Disease Process Multifocal plaques of demyelination form continuously and are distributed randomly throughout the white matter of the central nervous system, with accompanying destruction of oligodendroglia and perivascular inflammation. As myelin breakdown continues, lipid byproducts undergo phagocytosis, and the myelin sheath is destroyed. This leads to a decrease in velocity and blockage of nerve conduction, and interference with or failure of impulse transmissions. Cell bodies and axons are preserved early in the disease, but eventually the axons are stripped bare. Discrete lesions extend and coalesce into larger lesions. Astrocytic processes proliferate, transforming older lesions into glial scars. The scars stop the inflammation and edema of the lesion, leading to remission early in the disease process. However, as the disease progresses, symptoms become permanent.

Symptoms Signs and symptoms depend on the size, age, activity, and location of the lesions. Remissions may last months or years early in the disease. Later remission intervals are shorter, and eventually permanent, progressive disablement occurs.

Early
The onset is generally insidious and symptoms are transient, beginning with paresthesias in extremities, trunk, or face; clumsiness and muscle weakness; transient visual disturbances and optic pain; ataxia; bladder incontinence; and vertigo

Midcourse
Emotional lability, apathy, shortened attention span; seizures; diplopia; dysarthria; static tremor; spasticity, gait disturbances; transient bowel incontinence

Late
Dementia; scanning speech; nystagmus; intention tremor; hemiplegia; generalized muscular weakness and atrophy; inability to stand and walk; loss of bowel and bladder control

Potential Complications Some individuals have frequent attacks, leading to rapid incapacitation with an unremitting, progressive course that ends in death within 1 to 2 years. Others are prone to complications related to progressive disease and disuse syndrome, such as pressure sores, contractures, pathologic fractures, pneumonia, renal infection, and septicemia. Death usually is caused by complications rather than the primary disease.

Diagnostic Tests Diagnosis is elusive and indirect and is deduced from clinical features and laboratory tests, which include elevated cerebrospinal fluid (CSF) IgG coupled with normal serum IgG; normal CSF protein; slowed nerve conduction in evoked potential studies; and computed tomography and magnetic resonance imaging scans of lesions.

Treatments

Surgery
Rhizotomy for unresponsive spasms; contracture releases.

Drugs
Muscle relaxants for spasticity; corticosteroids for acute attacks; immunosuppresive use is in clinical trials.

General
Balance of rest and activity; long-term rehabilitation (occupational, physical, and speech therapy) to maintain activities of daily living, adapt to progressive loss of function, prevent disuse syndrome, and promote bowel and bladder control; assistive devices (canes, walkers, bracing, casting, wheelchairs); counseling and psychologic support of individual and family; respite home care; ventilatory assistance and communication devices in end-stage disease; care in feeding if dysphagia is present; evaluation for cognitive dysfunction; plasmapheresis and total lymphoid irradiation are under investigation.

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- An acute, contagious viral disease characterized by unilateral or bilateral edema and enlargement of the salivary glands.

Causes and Incidence The causative agent is the paramyxovirus, and the disease is spread by droplet or direct contact with infected saliva. It is most communicable immediately before and during the glandular swelling. Mumps is most often seen in children 5 to 15 years of age, although it may occur at any age. Adults are more likely to have a severe course of the disease. Permanent immunity occurs after infection. About 25% to 30% of cases are subclinical.

Disease Process After a 2- to 3-week incubation period, the virus invades one or more salivary glands, causing tissue edema and infiltration of lymphocytes. Cells in the glandular ducts degenerate and produce necrotic debris, which plugs the ducts.

Symptoms Onset begins with fever, headache, and malaise about 24 hours before swelling of the gland or glands (usually the parotid glands), either unilaterally or bilaterally. Pain is noted on chewing and swallowing. The glands remain swollen about 72 hours before receding.

Potential Complications Occasionally, particularly in adults, other glands in the testes, ovaries, breasts, and thyroid are involved, and the disease course is often more severe. Complications include meningoencephalitis, pericarditis, deafness, arthritis, nephritis, and in rare cases sterility in men.

Diagnostic Tests Characteristic swelling plus positive cell cultures from saliva or urine.

Treatments

Surgery
None.

Drugs
Analgesics, antipyretics; live mumps virus vaccine for active immunity.

General
Bed rest; hydration; isolation during communicability; compresses on swelling; support of scrotum with orchitis.

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- A group of inherited, progressive, degenerative muscle disorders characterized by an insidious loss of muscle strength in a variety of muscle groups. Duchenne’s muscular dystrophy (DMD) is the most common of the disorders.

Causes and Incidence DMD and Becker’s muscular dystrophy (BMD; a clinical variant of DMD) are X-linked recessive disorders involving the gene that encodes dystrophin. Males are exclusively affected, and the incidence in the United States is 1 in every 3,000 live male births. These disorders typically manifest in boys 3 to 7 years of age. Females are carriers. Other dystrophies (Landouzy-Dejerine dystrophy [LDMD], Leyden-Mobius dystrophy [LMMD], Erb’s dystrophy, and mitochondrial and congenital myopathies) are also inherited, but the specific genetic link is less clear. These disorders are seen in children and adults, affect males and females, and are milder.

Disease Process Dystrophin, a protein product in skeletal muscle, is absent in individuals with DMD and reduced in those with BMD. The resulting pathogenesis is not clear, but lack of dystrophin is thought to impair fast muscle fiber function and to induce a number of biochemical anomalies, including intracellular accumulation of calcium. A number of systemic sequelae have also been noted. Serotonin in the platelets is reduced, and nonmuscle cells have reduced adhesiveness and generalized membrane abnormalities. Central nervous system neuropathology is noted, as is reduced gastrointestinal motility. Platelet function and the vascularity of endothelial cells are abnormal.

Symptoms

DMD
Delays in gross motor development; difficulty walking, running, climbing stairs, and riding a tricycle appears about 3 to 5 years of age; progressive weakness with waddling gait, lordosis, difficulty rising from

a sitting or supine position; calf muscle hypertrophy; scoliosis; contractures and joint deformities; inability to ambulate by about age 12; mild mental retardation; respiratory and accessory muscles involved in end stage with cardiomegaly

BMD
Onset occurs at 5 to 25 years of age; symptoms are similar to but milder than DMD; ambulation is lost about 20 years after onset; contractures, scoliosis, and ventilatory failure are rare, and the life span usually is normal

LDMD
Onset from 7 to 20 years of age; weakness of facial and shoulder girdle muscles; difficulty whistling, closing eyes, and raising arms; footdrop develops late; life span is normal

LMMD/Erb’s
Adult onset with weakness of pelvic girdle (LMMD) and shoulder girdle (Erb’s)

Potential Complications The major complications of DMD are disuse atrophy, contractures, and cardiopulmonary problems, resulting in respiratory infections. Death is usually a result of complications rather than the primary disease.

Diagnostic Tests DMD and BMD are diagnosed through clinical evaluation and the characteristic manifestations; electromyography reveals rapidly recruited myopathic motor units without spontaneous activity; muscle biopsy shows necrosis and varied muscle fiber size; dystrophin immunoblotting is done in which dystrophin is absent (DMD) or abnormal (BMD). Other types are distinguished primarily on clinical grounds.

Treatments

Surgery
Contracture release; spinal instrumentation to correct scoliosis; tracheostomy in end-stage DMD.

Drugs
Random clinical trials are being conducted with steroids; antiinfective drugs for bacterial infections in end-stage DMD.

General
Long-term rehabilitation (occupational and physical therapy) to maintain activities of daily living and help adapt to progressive loss of function, prevent disuse syndrome, and promote bowel and bladder control; assistive devices (canes, walkers, bracing, casting, wheelchairs); counseling and psychologic support of individual and family; respite home care; ventilatory assistance and communication devices in end-stage DMD; family genetic counseling, identification of carriers.

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