Medical Instructor, Keck School of Medicine of University of Southern California
Important clinical criteria include the duration of the illness prostate massagers for medical purposes purchase cheap casodex on line, signs or symptoms of associated disorders wikibooks prostate radiation oncology purchase line casodex, and the presence of features that suggest a hereditary abnormality prostate wellness proven casodex 50 mg. A nutritional history can be helpful in recognizing a low intake of vitamin D and calcium in the elderly mens health 15 minute workout casodex 50mg cheap, and a history of excessive alcohol intake may suggest magnesium deficiency. Neck surgery, even long past, however, can be associated with a delayed onset of postoperative hypoparathyroidism. Rickets and a variety of neuromuscular syndromes and deformities may indicate ineffective vitamin D action, either due to defects in vitamin D metabolism or to vitamin D deficiency. Most forms of hypomagnesemia are due to long-standing nutritional deficiency as seen in chronic alcoholics. Chronic renal failure is often associated with hypocalcemia and hyperphosphatemia, despite secondary hyperparathyroidism. Severe, Acute Hyperphosphatemia Severe hyperphosphatemia is associated with extensive tissue damage or cell destruction (Chap. The combination of increased release of phosphate from muscle and impaired ability to excrete phosphorus because of renal failure causes moderate to severe hyperphosphatemia, the latter causing calcium loss from the blood and mild to moderate hypocalcemia. Hypocalcemia is usually reversed with tissue repair and restoration of renal function as phosphorus and creatinine values return to normal. There may even be a mild hypercalcemic period in the oliguric phase of renal function recovery. Other causes of hyperphosphatemia include hypothermia, massive hepatic failure, and hematologic malignancies, either because of high cell turnover of malignancy or because of cell destruction by chemotherapy. Although calcium replacement may be necessary if hypocalcemia is severe and symptomatic, calcium administration during the hyperphosphatemic period tends 2488 ineffective due to associated abnormalities in vitamin D action. Recognition that mild hypocalcemia, rickets, and hypophosphatemia are due to anticonvulsant therapy is made by history. Vitamin D itself is the least expensive form of vitamin D replacement and is frequently used in the management of uncomplicated hypoparathyroidism and some disorders associated with ineffective vitamin D action. When vitamin D is used prophylactically, as in the elderly or in those with chronic anticonvulsant therapy, there is a wider margin of safety than with the more potent metabolites. In such situations, vitamin D is no safer than the active metabolite because intoxication can occur with high-dose therapy (because of storage in fat). Calcitriol is more rapid in onset of action and also has a short biologic half-life. The two agents, vitamin D or calcitriol and oral calcium, can be varied independently. If hypocalcemia alternates with episodes of hypercalcemia in high-brittleness patients with hypoparathyroidism, administration of calcitriol and use of thiazides, as discussed above, may make management easier. Although risk is lower in this group, more than 50% of fractures among postmenopausal women, including hip fractures, occur in this group with low bone density, because the number of individuals in this category is so much larger than that in the osteoporosis range. As a result, there are ongoing attempts to identify individuals within the low bone density range who are at high risk of fracture and might benefit from pharmacologic intervention. Furthermore, some have advocated using fracture risk as the "diagnostic" criterion for osteoporosis. Osteoporosis occurs more frequently with increasing age as bone tissue is lost progressively. As the population continues to age, the number of individuals with osteoporosis and fractures will also continue to increase, despite a recognized reduction in age-specific risk. It is estimated that about 2 million fractures occur each year in the United States as a consequence of osteoporosis, and that number is expected to increase as the population continues to age. The epidemiology of fractures follows the trend for loss of bone density, with exponential increases in both hip and vertebral fractures with age. Fractures of the distal radius have a somewhat different epidemiology, increasing in frequency before age 50 and plateauing by age 60, with only a modest age-related increase thereafter. In contrast, incidence rates for hip fractures double every 5 years after age 70. This distinct epidemiology may be related to the way the elderly fall as they age, with fewer falls on an outstretched hand and more falls directly on the hip. About 300,000 hip fractures occur each year in the United States, most of which require hospital admission and surgical intervention. The probability that a 50-year-old white individual will have a hip fracture during his or her lifetime is 14% for women and 5% for men; the risk for African Americans is lower (about one-half those rates), and the risk for Asians is roughly equal to that for whites. Its chief clinical manifestations are vertebral and hip fractures, although fractures can occur at almost any skeletal site. Osteoporosis affects almost 10 million individuals in the United States, but only a small proportion are diagnosed and treated. Loss of bone tissue is associated with deterioration in skeletal microarchitecture.
Patients who cannot be treated with enzyme men health tips generic 50mg casodex with mastercard, either because it is not effective or because they have an allergy or other hypersensitivities mens health report generic casodex 50mg mastercard, may be receive substrate reduction therapy with medications that decrease the production of the complex lipid molecules that are broken down by acid -glucosidase man health hu discount casodex 50 mg online. Visceral disease in type 3 is nearly identical to that in type 1 but is generally more severe prostate cancer oncologist buy generic casodex 50mg online. Type B has a later, more variable onset and is characterized by a progression of hepatosplenomegaly, with eventual development of cirrhosis and hepatic replacement by foam cells. Affected patients develop progressive pulmonary disease with dyspnea, hypoxemia, and a reticular infiltrative pattern on chest x-ray. Progressive hepatic or lung disease leads to death in adolescence or early adulthood. The efficacy of hepatic or bone marrow transplantation has not been clearly established. Wolman disease presents in early infancy with hepatosplenomegaly, diarrhea, vomiting, and abdominal distention, sometimes accompanied by adrenal calcification, anemia, and mixed hyperlipidemia. Death occurs before the age of 1 year and is often due to severe intestinal malabsorption. In addition, patients often develop very early-onset atherosclerotic vascular disease, which may be life-threatening in childhood. In the more severe forms, cardiac and respiratory diseases become life-threatening in childhood. Enzyme therapy effectively addresses hepatosplenomegaly and alleviates cardiac and respiratory disease. The classic severe infantile form presents with hypotonia, myocardiopathy, and hepatosplenomegaly. This variant is rapidly progressive and generally results in death in the first year of life. The late-onset variants may be as common as 1 in 40,000; patients typically present with a slowly progressive myopathy that may resemble limb-girdle muscular dystrophy. Respiratory insufficiency may be the presenting sign or may develop with advancing disease. In late stages of the disease, patients may require mechanical ventilation, report swallowing difficulties, and experience loss of bowel and bladder control. This treatment clearly prolongs life in the infantile form, consistently resulting in improved cardiac function. Some infants demonstrate marked improvement in motor functions, while others have minor changes in muscle tone or strength. Sucrose (fructose + glucose) is another dietary source of fructose and is a commonly used sweetener. Glycogen, the storage form of glucose in animal cells, is composed of glucose residues joined in straight chains by 1-4 linkages and Priya S. Glycogen forms a treelike molecule and can have a molecular weight of many millions. Glycogen may aggregate to form structures recognizable by Carbohydrate metabolism plays a vital role in cellular function by pro- electron microscopy. With the exception of type 0 disease, defects in viding the energy required for most metabolic processes. Glucose is the principal substrate the structure of stored glycogen can be normal or abnormal in the of energy metabolism in humans. The body obtains glucose through the ingestion of polysaccha- glycogen accumulation. Galactose and fructose are two other monosaccharides that metabolism differ markedly. The symptoms range from harmless serve as sources of fuel for cellular metabolism; however, their role as to lethal. Unlike disorders of lipid metabolism, mucopolysaccharifuel sources is much less significant than that of glucose. Galactose doses, or other storage diseases, many carbohydrate disorders have is derived from lactose (galactose + glucose), which is found in milk been effectively managed with dietary therapy. Advances in our understanding of the molecular G P aP basis of these diseases are being used Pb Pa to improve diagnosis and management. Complications in adulthood include hepatic adenomas, hepatic carcinoma, and renal failure. Some patients may have muscle weakness kinase deficiency phosphorylase kinase and atrophy. Congenital fetal form is rapidly fatal with hypertrophic cardiomyopathy and Wolff-Parkinson-White syndrome. The defects in both subtypes lead to inadequate conversion of glucose-6-phosphate to glucose in the liver and thus make affected individuals susceptible to fasting hypoglycemia. Hypoglycemia, hypoglycemic seizures, and lactic acidosis can develop after a short fast. These children usually have doll-like faces with fat cheeks, relatively thin extremities, short stature, and a protuberant abdomen that is due to massive hepatomegaly. The hepatocytes are distended by glycogen and fat, with large and prominent lipid vacuoles. Easy bruising and epistaxis are associated with a prolonged bleeding time as a result of impaired platelet aggregation/adhesion. Hyperlipidemia includes elevation of triglycerides, low-density lipoproteins, and phospholipids.
Hypoparathyroidism now usually occurs after surgery for hyperparathyroidism when the surgeon prostate cancer 12 tumors buy casodex online now, facing the dilemma of removing too little tissue and thus not curing the hyperparathyroidism androgen hormone queen discount casodex 50 mg line, removes too much androgen hormone oxytocin casodex 50 mg mastercard. Parathyroid function may not be totally absent in all patients with postoperative hypoparathyroidism androgen hormone order casodex 50 mg otc. Rare causes of acquired chronic hypoparathyroidism include radiation-induced damage subsequent to radioiodine therapy of hyperthyroidism and glandular damage in patients with hemochromatosis or hemosiderosis after repeated blood transfusions. Infection may involve one or more of the parathyroids but usually does not cause hypoparathyroidism because all four glands are rarely involved. Transient hypoparathyroidism is frequent following surgery for hyperparathyroidism. After a variable period of hypoparathyroidism, normal parathyroid function may return due to hyperplasia or recovery of remaining tissue. In most patients, blood calcium and phosphate levels are satisfactorily regulated, but some patients show resistance and a brittleness, with a tendency to alternate between hypocalcemia and hypercalcemia. The wide dosage range reflects the variation encountered from patient to patient; precise regulation of each patient is required. Because of its storage in fat, when vitamin D is withdrawn, weeks are required for the disappearance of the biologic effects, compared with a few days for calcitriol, which has a rapid turnover. Oral calcium and vitamin D restore the overall calcium-phosphate balance but do not reverse the lowered urinary calcium reabsorption typical of hypoparathyroidism. Thiazide diuretics lower urine calcium by as much as 100 mg/d in hypoparathyroid patients on vitamin D, provided they are maintained on a lowsodium diet. Use of thiazides seems to be of benefit in mitigating hypercalciuria and easing the daily management of these patients. Restoration of the totalbody magnesium deficit leads to rapid reversal of hypocalcemia. Greater change in magnesium than in calcium is needed to influence hormone secretion. The mechanism of the cellular abnormalities caused by hypomagnesemia is unknown, although effects on adenylate cyclase (for which magnesium is a cofactor) have been proposed. Serum phosphate levels are often not elevated, in contrast to the situation with acquired or idiopathic hypoparathyroidism, probably because phosphate deficiency is often seen in hypomagnesmia (Chap. Attention must be given to restoring the intracellular deficit, which may be considerable. If the cause of the hypomagnesemia is renal magnesium wasting, magnesium may have to be given long-term to prevent recurrence (Chap. The uremic state also causes impairment of intestinal absorption by mechanisms other than defects in vitamin D metabolism. Nonetheless, treatment with supraphysiologic amounts of vitamin D or calcitriol can correct the impaired calcium absorption. Severe hypocalcemia rarely occurs in moderately severe vitamin D deficiency of the elderly, but vitamin D deficiency must be considered in the differential diagnosis of mild hypocalcemia. Mild hypocalcemia, secondary hyperparathyroidism, severe hypophosphatemia, and a variety of nutritional deficiencies occur with gastrointestinal diseases. Hypocalcemia itself can lead to steatorrhea, due to deficient production of pancreatic enzymes and bile salts. Depending on the disorder, vitamin D or its metabolites can be given parenterally, guaranteeing adequate blood levels of active metabolites. The more marginal the vitamin D intake in the diet, the more likely that anticonvulsant therapy will lead to abnormal mineral and bone metabolism. Both alleles are inactivated in affected patients, and compound heterozygotes, harboring distinct mutations, are common. Clinical features include hypocalcemia, often with tetany or convulsions, hypophosphatemia, secondary hyperparathyroidism, and osteomalacia, often associated with skeletal deformities and increased alkaline phosphatase. The clinical features resemble those of the type I disorder and include hypocalcemia, hypophosphatemia, secondary hyperparathyroidism, and rickets but also partial or total alopecia. This disorder is caused by mutations in the gene encoding the vitamin D receptor; treatment is difficult and requires regular, usually nocturnal calcium infusions, which dramatically improve growth but do not restore hair growth (Chap. Studies, both clinical and basic, have clarified some aspects of these disorders, including the variable clinical spectrum, the pathophysiology, the genetic defects, and their mode of inheritance. Reduction of hyperphosphatemia and restoration of normal intestinal calcium absorption by calcitriol can improve blood calcium levels and reduce the manifestations of secondary hyperparathyroidism. Quantitative histomorphometric analysis of bone biopsy specimens from such individuals reveals widened osteoid seams consistent with osteomalacia (Chap. Patients have low calcium and high phosphate levels, as with true hypoparathyroidism. Amorphous deposits of calcium and phosphate are found in the basal ganglia in about one-half of patients. The defects in metacarpal and metatarsal bones are sometimes accompanied by short phalanges as well, possibly reflecting premature closing of the epiphyses. The former two entities, often traced through multiple generations, have an inheritance pattern consistent with genetic imprinting. The phenomenon of gene imprinting, involving methylation of genetic loci, independent of any mutation, impairs transcription from either the maternal or the paternal allele (Chap. The Gs transcript is biallelically expressed in most tissues; expression from paternal allele is silenced through as-of-yet unknown mechanisms in some tissues including the proximal renal tubules and the thyroid; consequently, inheritance of a defective paternal allele has no implications with regard to hormonal function.
Delayed findings include nail deformities prostate cancer young investigator award cheap casodex 50mg amex, cutaneous carcinomas anti androgen hormone pills buy casodex 50mg cheap, and epiphyseal damage in children man health yoga cheap generic casodex canada. With refractory perniosis prostate cancer 3b cheap casodex 50 mg overnight delivery, alternatives include nifedipine, steroids, and limaprost, a prostaglandin E1 analogue. Danzl Heat-related illnesses include a spectrum of disorders ranging from heat syncope, muscle cramps, and heat exhaustion to medical emergencies such as heatstroke. In contrast to severe hyperthermia, the far more common sign of fever reflects intact thermoregulation. The heat load from metabolic heat production and environmental heat absorption is balanced by a variety of heat dissipation mechanisms. These dissipation pathways are orchestrated by the central thermostat, which is located in the preoptic nucleus of the anterior hypothalamus. Efferent signals sent via the autonomic nervous system trigger cutaneous vasodilation and diaphoresis to facilitate heat loss. The evaporation of skin moisture is the single most efficient mechanism of heat loss but becomes progressively ineffective as the relative humidity rises to >70%. The radiation of infrared electromagnetic energy directly into the surrounding environment occurs continuously. Factors that interfere with the evaporation of diaphoresis significantly increase the risk of heat illness. Examples include dripping of sweat off the skin, constrictive or occlusive clothing, dehydration, and excessive humidity. While air is an effective insulator, the thermal conductivity of water is 25 times greater than that of air at the same temperature. The wet-bulb globe temperature is a commonly used index to assess the environmental heat load. This calculation considers the ambient air temperature, the relative humidity, and the degree of radiant heat. The central thermostat activates the effectors that produce peripheral vasodilation and sweating. This dramatic increase in skin blood flow, coupled with the maintenance of peripheral vasodilation, efficiently radiates heat. At the same time, there is a compensatory vasoconstriction of the splanchnic and renal beds. Acclimatization to heat reflects a constellation of physiologic adaptations that permit the body to lose heat more efficiently. This process often requires one to several weeks of exposure and work in a hot environment. During acclimatization, the thermoregulatory set point is altered, and this alteration affects the onset, volume, and content of diaphoresis. The threshold for the initiation of sweating is lowered, and the amount of sweat increases, with a lowered salt concentration. After the individual leaves the hot environment, improved tolerance to heat stress dissipates rapidly, the plasma volume decreases, and de-acclimatization occurs within weeks. Heat waves exacerbate the mortality rate, particularly among the elderly and poor and among persons lacking adequate nutrition and access to air-conditioned environments. Secondary vascular events, including cerebrovascular accidents and myocardial infarctions, occur at least 10 times more often in conditions of extreme heat. Exertional heat illness continues to occur when laborers, military personnel, or athletes exercise strenuously in the heat. In addition to the very young and very old, preadolescents and teenagers are at risk since they may use poor judgment when vigorously exercising in high humidity and heat. Other risk factors include obesity, poor conditioning and lack of acclimatization, and mild dehydration. Any physiologic or pharmacologic impediment to cutaneous perfusion will impair heat loss. Anticholinergic agents impair sweating and blunt the normal cardiovascular response to heat. Phenothiazines also have anticholinergic properties that interfere with the function of the preoptic nucleus of the anterior hypothalamus due to central depletion of dopamine. Calcium channel blockers, beta blockers, and various stimulants also inhibit sweating by reducing peripheral blood flow. To maintain the mean arterial blood pressure, increased cardiac output must be capable of compensating for progressive dehydration. A variety of stimulants and substances of abuse also increase muscle activity and heat production. Careful consideration of the differential diagnosis is important in the evaluation of a patient for a potential heat-related illness. The clinical setting may suggest other etiologies, such as malignant hyperthermia after general anesthesia or neuroleptic malignant syndrome in a patient taking certain antipsychotic medications. The principal mechanism involves cutaneous vasodilation and pooling of interstitial fluid in response to heat stress. Systemic causes of edema, including cirrhosis, nephrotic syndrome, and congestive heart failure, can usually be excluded by the history and physical examination.
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