- Skin cancers can be divided into two groups: melanomas and nonmelanomas. Three distinct types of nevi (moles) give rise to melanomas: common acquired, dysplastic, and congenital melanocytic; they produce four types of melanoma: superficial spreading (70%), nodular (15%), lentigomaligna (less than 10%), and acrolentiginous (less than 5%). Nonmelanomas are typically either basal cell or squamous cell in origin.

Causes and Incidence Environmental factors such as ultraviolet radiation and chronic sun exposure are strongly linked to the development of skin cancer. Long-term x-ray exposure and occupational exposure to radium, arsenic, coal tar, and creosote are also risk factors. Genetic risk factors such as a fair complexion, light hair, and difficulty tanning play a role, as does family history.
Skin cancer is the most common of all malignancies. An estimated 600,000 cases are diagnosed annually in the United States alone. Most are nonmelanomas, but more than 32,000 are melanomas, and the incidence of melanoma is increasing by 4% a year. Fair-skinned individuals over 40 years of age who live near the equator and have a history of long-term sun exposure are at highest risk.

Disease Process Basal cell carcinomas vary considerably in appearance but usually begin as a small, shiny, flesh-colored nodule on the skin. The carcinoma enlarges slowly and develops a pearly border with telangiectases on the surface. It often bleeds, crusts, and then rebleeds in a chronic cycle. It rarely metastasizes but does invade adjacent tissue structures. Squamous cell carcinomas are usually scaly and crusty or nodular, warty, and raised and often develop in keratotic tissue or old scars. They eventually ulcerate and invade the underlying tissue. They rarely metastasize, but when they do, the lungs are the most common site. Malignant melanomas arise from a mole that begins to show changes in size, color, shape, and consistency. They begin by growing on the epidermis and then invade the dermis and subcutaneous tissues. Once this occurs, the tumor metastasizes fairly rapidly through the vascular and lymphatic systems. Common metastatic sites include the bones, brain, liver, and lungs.

Symptoms A skin lesion that does not go away and that grows larger over time or a mole that changes appearance is a possible sign, as are itchiness, scaling, oozing, bleeding from a mole or lesion, and changes in sensation.

Potential Complications The prognosis is excellent with intervention, particularly with nonmelanoma carcinomas, because metastasis is rare. The long-term prognosis for melanomas is tied to the thickness of the tumor at the time of diagnosis. Tumors over 3 mm deep carry a survival rate of less than 50%. Metastasized disease reduces the survival rate dramatically. Common complications include scarring and disfigurement at the site of tumor removal.

Diagnostic Tests Tissue biopsy and a histologic examination form the base for definitive diagnosis.

Treatments

Surgery
Excision is the treatment of choice for melanoma; excision, cryosurgery, electrodesiccation and curettage, and Mohs chemosurgery are used for nonmelanomas.

Drugs
Topical chemotherapeutic agents to treat premalignant actinic keratosis; interferon to treat recurrent or advanced basal cell carcinoma; hyperthermic regional perfusions in combination with surgery to treat melanomas.

General
Radiation in combination with surgery for extensive nonmelanomas; radiation may be used instead of surgery in elderly patients or to treat nonmelanomatous lesions of the nose, eyelids, or lips (melanomas are radioresistant); prevention education about sun exposure and use of sun screens and protective clothing when in the sun.

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- A developmental malformation of the spine in which the posterior vertebral laminae fail to close, leaving the meninges and spinal cord exposed. There are three common types: spina bifida occulta, in which the only defect is vertebral and the meninges and spinal cord are normal; spina bifida with meningocele, in which the meninges protrude through the vertebral opening, forming a cyst filled with cerebrospinal fluid and covered with skin; and spina bifida with myelomeningocele, in which the protruding cyst also contains a portion of the spinal cord and spinal nerves and is covered by a thin membrane.

Causes and Incidence The etiology is unclear, but the most recent hypothesis suggests a genetic predisposition involving a polygenic interaction with environmental factors such as maternal malnutrition, alcohol, organic solvents, drugs, toxins, or potato blight. This interaction precipitates a faulty closure of the neural groove on day 28 of gestation. The geographic distribution and incidence of spina bifida vary widely, but it is the most common developmental defect of the central nervous system. It occurs in approximately 1 in every 1,000 live births in the United States, but the incidence has been steadily declining in recent decades. It is more common in individuals of European descent, females, and those in poverty.

Disease Process During the normal formative stages of the nervous system, a decided depression known as a neural groove appears on the dorsal ectoderm of the embryo at approximately 20 days of gestation. The groove deepens rapidly, spreads laterally, and then fuses dorsally to form the neural tube. Neural tube formation begins in the cervical region and advances caudally and cephalically until day 28 of gestation, when both ends of the tube seal themselves off. Spina bifida occurs when the neural tube fails to close or when a closed tube splits as a result of abnormal cerebrospinal fluid pressure.

Symptoms Manifestations vary widely, depending on the degree and location of the spinal defect. Sensory and motor disturbances parallel one another.

Occulta
Typically asymptomatic; dimple or hair growth on the skin over the malformed vertebra; weakness in feet, bowel, or bladder sphincter possible as child grows if defect goes undetected and uncorrected

Meningocele
External cystic sac seen on spinal cord at birth; hydrocephalus possible; weakness in legs or bowel and bladder sphincters is rare if defect is surgically corrected

Myelomeningocele
At birth: round, raised, poorly epithelialized sac on spinal cord that may be bluish and may be leaking or ruptured; hydrocephalus; loss of partial or total motor and sensory control below the level of the lesion; poor anal sphincter and detrusor tone; possible rectal prolapse; constant urine dribbling or urinary retention; possible joint deformities and kyphosis formed in utero Developing in childhood: clubfeet, contractures in ankles, knees, and hips; hip dislocations; scoliosis; decreasing ability to ambulate; incontinence; urinary tract infections (UTIs); constipation; skin breakdown; obesity

Potential Complications An immediate complication often seen after birth with a leaking or ruptured sac is meningitis. Other immediate complications include hypoxia and hemorrhage. Other congenital abnormalities such as cardiac or gastrointestinal malformations may also be present. Long-term complications are associated with motor and sensory disability and include respiratory infection and failure, renal infection and failure, permanent skeletal deformities, and decubiti. In the 1950s most individuals with myelomeningocele died in infancy. Now, most have a normal life expectancy with careful and consistent health care.

Diagnostic Tests

Clinical evaluation
Pigmented spots, hairy patches, and spinal sinuses seen at birth may indicate spina bifida occulta; motor and sensory function tests determine level of injury in myelomeningocele; palpation of fontanelles and increasing head circumference indicate hydrocephalus

Ultrasound/computed tomography/magnetic resonance imaging
Abnormalities of head or spine or both

Myelography
Spinal defects

Intravenous pyelography
Abnormalities in renal system

Urodynamics
To assess detrusor and sphincter function

Fetal ultrasonography
May detect major myelomeningocele defects

Alpha-fetoprotein
Elevated at 16 to 18 weeks’ gestation

Treatments

Surgery
Repair and closure of defect within 24 to 72 hours after birth; ventriculoperitoneal shunt to treat hydrocephalus; shunt revisions as child ages or if shunt is not patent or functional; corrective orthopedic procedures for contractures, clubfeet, scoliosis (spinal instrumentation), hip dislocations; vesicostomy for vesicourethral reflux; augmentation enterocystoplasty to increase bladder capacity and reduce bladder pressure; placement of artificial urinary sphincter or ureteral sling to aid bladder emptying; urinary diversion to control chronic urine leakage and retention.

Drugs
Collagen injection in sphincter submucosa to control bladder incontinence; stool softeners and laxatives for constipation; antispasmodics to treat bladder spasms; antiinfective drugs for UTI.

General
Initial care: monitoring for associated defects and complications; measures to prevent infections; monitoring of patency and functioning of ventriculoperitoneal shunt; adequate hydration and nutrition; normal infant stimulation; meticulous skin care; proper positioning and body alignment; monitoring of intake and output; emotional support of family; teaching parents to hold, feed, and stimulate infant and any special techniques needed for care; physical therapy and range-of-motion (ROM) exercises; safety measures for decreased sensation Long term: consistent medical monitoring by neurologists/ neurosurgeons for shunt function and revision and spinal cord tethering; orthopedic surgeons for treatment of contractures, gait analysis, and bracing; urologists for bladder and kidney function; pediatricians for minor infections, bowel program and coordination; physical therapists for maintenance of ROM, prevention of contractures, gait training, strengthening, and endurance; occupational therapists for activities of daily living; intermittent catheterization for bladder control; weight-maintenance diet to prevent obesity and maintain ambulation; counseling for long-term adaptation; case management for long-term support and education of individual, family, and school and coordination of ongoing care.

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- An insult to the spinal cord that results in alteration of autonomic, motor, and sensory function below the level of injury. Paraplegia involves the lower extremities; quadriplegia involves all extremities. Injury to the cord may result in incomplete or total transection.

Causes and Incidence Spinal cord injury (SCI) may be caused by external trauma or internal disease or degeneration. Common traumatic causes of spinal cord injury include vehicle accidents (48%), falls (21%), acts of violence (15%), and sports injuries (14%). Metastatic carcinoma, spinal cord tumors, spondylosis, and vertebral disk degeneration are common nontraumatic causes of spinal cord injury. The worldwide incidence of SCI is about 55 million a year, and about 35 million people survive the acute injury. The worldwide number of SCI survivors is estimated to be 500 million to 900 million. About 10,000 cases occur in the United States annually, and at least 100,000 individuals are living with SCI in the United States today. About 55% of individuals are quadriplegic, and the remaining 45% are paraplegic. Traumatic injury occurs most often in young adult men, and nontraumatic injury is more common in individuals over 50 years of age.

Disease Process Injury may be direct or indirect. Direct injuries involve compression or transection of the cord by the causal agent (e.g., bone fragments, bullets, or other external debris in the cord; external severing of the cord; tumor growth on the cord, or bony overgrowth of the spine that squeezes the cord). Tissue necroses around the site of injury. Indirect injury involves compression, overstretching, rotation, wedging, or misalignment of the cord, which results in edema, swelling, and localized hemorrhage. This in turn reduces vascular perfusion, decreases oxygen tension, and increases the norepinephrine concentration, producing ischemia and tissue necrosis. Necrosed tissue is removed by bodily functions within a month of injury and is gradually replaced by connective scar tissue and glial fibers.

Symptoms Manifestations differ by level and completeness of injury.

Initial phase (spinal shock)
Partial or complete flaccid paralysis below injury level; partial or complete loss of proprioception, pain, touch, pressure, temperature, spinal reflexes, vasomotor tone, and visceral and somatic sensation below injury level; loss of ability to perspire below injury level; dysfunction of bowel and bladder; impaired or absent respiration if injury is above C5; bradycardia; hypotension

Autonomic hyperreflexia
Onset occurs after resolution of spinal shock and return of reflex activity; affects mostly those with an injury at T6 or above; paroxysmal hypertension, bradycardia, pounding headache, profuse sweating and flushing above injury level, nausea, nasal stuffiness

Long-term
Muscle spasms; exaggerated deep tendon reflexes; contractures; hyperesthesia immediately above injury level; paresthesias; neuropathic pain; impotence; trophic ulcers; dry skin; nail changes; skin breakdown

Potential Complications The immediate complications are generally life threatening and include respiratory failure, hemorrhage, and cardiac failure. Long-term complications include pneumonia and atelectasis, cardiovascular disease, orthostatic hypotension, severe bradycardia, hyperkalemia, deep vein thrombosis, pulmonary embolism, gastric atony, ileus, bladder and kidney infections, decubiti, pathologic fractures, heterotrophic ossification, degeneration of upper extremity joints, emotional debility, and suicide.

Diagnostic Tests

Clinical evaluation
Absence of reflexes, flaccidity, loss of sensation below injury level; examination of dermatomes and muscles to determine level of injury

Spinal xrays
Vertebral fractures, bony overgrowth

Computed tomography/ magnetic resonance imaging
Evidence of cord compression and edema or tumor formation

Lumbar puncture/ myelography
Spinal blockage

Treatments

Surgery
Initial: laminectomy or fusion for decompression and stabilization; wound debridement; placement of cervical tongs or halo traction for stabilization; tracheotomy for mechanical ventilation if needed Long term: myotomies, tenotomies, rhizotomies, and muscle transplantation to treat spasticity; contracture release; debridement of decubiti; spinal instrumentation to halt scoliosis; penile implant for impotence; colostomy for atonic colon; urinary diversion for incontinence or retention.

Drugs
Initial: massive corticosteroid therapy to improve outcome; prophylactic antiinfective drugs for open wounds; analgesics for pain; anticoagulants to prevent emboli and thrombus formation; antihypertensives for hyperreflexia; antianxiety agents to reduce emotional stress Long term: muscle relaxants for spasms; stool softeners and laxatives for constipation; anticholinergics for bladder spasticity.

General
Initial: spinal stabilization with backboard or cervical collar on initial transport; mechanical ventilation if necessary; cardiac monitoring; blood gases; monitoring of intake and output; vital signs and neurologic vital signs; maintenance of skeletal traction and body alignment; repositioning, turning every 2 hours; passive range-of-motion exercises; footboard; all activities of daily living (ADLs) performed for person; monitoring of bowel and bladder function; monitoring of skin integrity Long term: bowel training using digital stimulation, gravity, high-fiber diet, regularity, adequate hydration; bladder training using intermittent catheterization; physical therapy to diminish orthostatic hypotension, increase strength and endurance, decrease muscle spasticity, prevent contractures, teach functional mobility skills (e.g., transfer techniques, wheelchair manipulation); occupational therapy to aid adaptation of ADLs (e.g., feeding, bathing, hygiene, grooming, dressing) and to teach use of adaptive equipment; respiratory therapy to increase vital capacity and tidal volume; recreational therapy to enhance quality of life; speech therapy if injury is high enough to affect swallowing or when permanent ventilation requires alternative communication systems; long-term medical follow-up by physical medicine, urology, gastroenterology, and respiratory specialists to reduce complications; vocational training; counseling of individual and family for support and adaptation; instruction in bowel and bladder programs, skin inspection, pressure relief, decubitus prevention, prevention or early treatment of urinary tract and upper respiratory infections, and recognition of hyperreflexia.

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- Most malignant lesions of the stomach are adenocarcinomas (95%). The rest are lymphomas and leiomyosarcomas.

Causes and Incidence The cause of stomach cancer is unknown but is thought to be related to dietary factors connected to food preservation and preparation. Gastritis, gastric atrophy, and genetic factors are believed to be predisposing factors. The incidence varies worldwide. Stomach cancer is the most common malignancy in Japan, and the incidence is extremely high in Iceland and Chile. The number of cases has declined significantly in western Europe and the United States. About 23,000 new cases are seen in the United States each year. The incidence is higher in men (2:1 ratio), in individuals 50 to 70 years of age, and in people of lower socioeconomic status.

Disease Process Cancer cells usually begin to grow in the distal end of the stomach in the lesser curvature. The cells form a tumor that spreads along the mucosa, eventually invading and moving through the stomach wall. The tumor then spreads directly to surrounding structures such as the spleen, esophagus, pancreas, colon, duodenum, and peritoneum. The cancer is also spread via the lymphatics to regional nodes and via the bloodstream to the liver.

Symptoms No specific symptoms appear in the early stages. Most people have generalized gastrointestinal (GI) complaints such as indigestion, burping, and fullness after eating. Later signs may include vomiting, dysphagia, anorexia, weight loss, and back pain.

Potential Complications The prognosis for long-term survival is poor (16%), primarily because most cases are diagnosed after metastasis has occurred. Complications include malnutrition and GI obstruction.

Diagnostic Tests Double-contrast x-ray studies of the stomach can delineate suspicious lesions. The definitive diagnosis is made by endoscopy with brush biopsy.

Treatments

Surgery
Excision of the tumor and regional lymph nodes; subtotal or total gastric resection or gastrectomy for resection for cure, depending on tumor location; gastroenterostomy for palliation.

Drugs
Systemic chemotherapy to treat advanced metastatic disease.

General
Radiation for palliation of GI obstruction.

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- An inflammation or ulceration of the mouth that may be locally or systemically induced.

Causes and Incidence Causes of stomatitis include viral or bacterial infection; drugs or toxic agents (barbiturates, antibiotics, chemotherapy, radiation, lead, mercury, acids, heavy metals); trauma from cheek biting, mouth breathing, or ill-fitting orthodontia; overuse of tobacco or alcohol; sensitivity to toothpastes, mouthwash, food dyes, or preservatives and spices; poor nutrition; and poor oral hygiene. Thrush, a common form of stomatitis, is seen in more than 80% of individuals with HIV or AIDS. Canker sores are also common and are seen frequently in adolescence or young adulthood. Herpetic stomatitis, the most common virally induced stomatitis, is seen in infants and small children. Mechanically induced stomatitis is often seen in older individuals with dentures that are difficult to fit because of continuing deterioration of gum and bone. Necrotizing ulceration is often seen in individuals using certain antibiotics and in people who have depressed immune systems.

Disease Process The pathophysiology depends on the cause, but it involves a process that creates tissue inflammation in the oral mucosa or gums. These inflammatory changes lead to redness, ulceration, and fissures in the mouth.

Symptoms Manifestations vary by type of stomatitis.

Allergic
Shiny erythema with slight edema, itching, drying, burning

Thrush
White, raised, milk curd patches; bleeding; dryness of the mouth; diminished taste; pain; fever; lymphadenopathy

Gingivitis
Redness, swelling, bleeding of gums; gum retraction from teeth

Herpetic
Ulcers 34 cm in diameter scattered over mucous membranes; swollen, inflamed gums; enlarged lymph nodes

Canker sores
Small, yellowish, hardened, painful sores with red, raised margins that often appear singly or in groups on the lips or in the corner of mouth

Necrotizing
Necrotic ulceration of mucous membranes with severe pain, increased salivation, and inability to eat; fetid breath; bleeding gums; difficulty talking and swallowing; pseudomembrane on ulcers
Complications: Tissue sloughing from necrosis may create craters and other altered tissue topography.

Diagnostic Tests The diagnosis is made on the clinical history and a physical examination. Cultures or smears may aid in identification of the causative organism in cases arising from infection.

Treatments

Surgery
None.

Drugs
Topical anesthetics for pain; antiinfective drugs (topical, systemic) for bacterial or fungally induced stomatitis.

General
Meticulous oral hygiene; mild mouthwashes for comfort; treatment of underlying etiology (stopping drugs, avoiding toxins, refitting orthodontics, eliminating allergens); bland, soft, pureed, or liquid diet if eating is a problem; avoidance of alcohol and tobacco product.

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