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Other routine chemistry tests can help exclude renal or hepatic diseases arteries model labeled buy procardia with visa, and a complete blood cell count may help uncover a hematologic or myeloproliferative disorder blood vessels behind the eye buy procardia 30 mg with visa. Because multiple myeloma can mimic involutional osteoporosis coronary artery risk factors purchase genuine procardia line, it should be considered when evaluating patients with osteoporosis blood vessels keep popping in my hands 30mg procardia, particularly those with unexpectedly severe disease. Measuring serum parathyroid hormone and 25-hydroxyvitamin D levels is recommended to exclude hyperparathyroidism and vitamin D deficiency. A serum thyroid-stimulating hormone level should be checked when thyroid disease is suspected. In men with unexplained osteoporosis, a serum testosterone level should be measured. The clinical utility of measuring biochemical markers of bone turnover has not been established. Measurements of bone turnover markers may, however, be useful to evaluate patients with osteoporosis of unknown cause or of unexplained severity. Monitoring therapy in patients who cannot tolerate standard doses of antiresorptive agents 4. Monitoring therapy in patients with questionable absorption of antiresorptive agents 5. Predicting changes in bone density in patients receiving antiresorptive therapy 8. Finally, in selected patients, iliac crest bone biopsy after double tetracycline labeling may be useful, particularly for distinguishing osteoporosis from osteomalacia. Early intervention, however, can prevent osteoporosis in most people and later intervention can halt the progression of osteoporosis once it has developed. The choice of treatment for osteoporosis depends on its cause and the stage of the illness. If a secondary cause of osteoporosis is present, specific treatment should be aimed at correcting the underlying disorder. During the acute phase of vertebral compression, attention is directed toward relieving pain with analgesics, muscle relaxants, heat, massage, and/or rest. Many patients with discomfort related to osteoporotic fractures or deformity benefit from a well-designed program of physical therapy. Both weight-bearing and non-weight bearing exercises appear to have beneficial effects on bone mass. For most patients, exercises to strengthen the abdominal and back muscles are appropriate and referral to a physical therapist with expertise in treating osteoporotic patients is often helpful. Pharmacologic therapy is aimed at preventing further bone loss and decreasing the likelihood of future fracture. Both dietary calcium intake and fractional intestinal calcium absorption decrease with age. Most postmenopausal women consume less than 500 mg of calcium each day, far below the U. The effects of calcium supplementation on bone mass in early postmenopausal women have been examined in several prospective, randomized trials. In general, it appears that calcium can retard, but not arrest, cortical bone loss from the forearm in women who are within the first several years of the menopause. Most studies have failed to demonstrate a protective effect of calcium on spinal bone loss in early postmenopausal women. Calcium therapy appears to be more effective in arresting bone loss in late postmenopausal women, although some studies indicate that administering calcium does not halt their bone loss completely. Overall, it appears that calcium therapy is somewhat beneficial in both early and late postmenopausal women. Additional therapy, however, is needed if the goal of therapy is to prevent bone loss completely. In the United States, the recommended daily calcium intake for adolescents and young adults between the ages of 11 and 24 years is 1200 to 1500 mg.

Two distinct isoforms of 5alpha-reductase have been cloned: Type 1 is present in very low levels in the prostate and the sebaceous glands; type 2 is present in high levels in the prostate and in the Figure 246-2 Hormones involved in male differentiation of the reproductive tract cardiovascular specialists buy procardia 30 mg without prescription. Testosterone blood vessels enter and exit from the order line procardia, synthesized by Leydig cells arteries hardening in brain purchase genuine procardia on-line, maintains the wolffian ducts and virilizes the urogenital sinus and external genitalia after reduction to dihydrotestosterone cardiovascular urinary system cheap procardia 30 mg free shipping. Antimullerian hormone, produced by fetal Sertoli cells, inhibits development of the mullerian ducts, which would otherwise develop into the uterus and fallopian tubes. The gene coding for the androgen receptor is located on the long arm of the X chromosome. Genetic sex is established at fertilization by the nature of the sex chromosome donated by the spermatozoon. The presence or absence of sex-determining genes dictates gonadal sex, whereas the presence or absence of fetal testicular hormones determines somatic sex. Gender identity is established early in life by the sex of rearing but can be disrupted at puberty by hormonal factors. Disorders of Gonadal Sex Gonadal sex disorders may or may not be associated with sex chromosome abnormalities. The dysmorphism includes an increased carrying angle of the arms, sphinx-like neck, low hairline, shield chest, widely spaced Figure 246-4 Stages of sex differentiation. Genetic sex specified at fertilization determines gonadal sex, which in turn determines somatic and legal sex. The patients are infertile because the ovaries are dysgenetic and have become bilateral streaks without follicles. Because the internal genitalia include a normal uterus and fallopian tubes, patients may benefit from in vitro fertilization. In this condition, males have normal development of the penis and scrotum, but the testes are small and firm. At adolescence, gynecomastia is frequent and infertility is common as a result of azoospermia. Hormonal findings include elevated gonadotropin levels and a decreased serum testosterone concentration. True hermaphroditism, a rare and usually sporadic disorder, is defined as the coexistence of seminiferous tubules and ovarian follicles in the same subject. Most patients have an ovotestis with either an ovary or a testis on the opposite side; a testis is usually in the scrotum, an ovotestis more seldom. The genitalia are usually ambiguous; rare cases of completely masculine or feminine genitalia have been reported. The anatomy of the internal reproductive tract depends on the nature of the gonads. Most patients experience breast development, ovulation, and even menstruation at puberty; pregnancy and successful childbirth are possible if selective removal of testicular tissue is feasible. Unless gender has already been assigned, male orientation should be restricted to patients with no uterus and descended testicular tissue because testicular tissue is usually dysgenetic and prone to malignant degeneration. Testicular dysgenesis is characterized by seminiferous tubule degeneration and invasion by connective tissue arranged in whorls as in a streak gonad. Germ cells are rare or absent; the gonad is often maldescended and prone to malignant degeneration. The incidence of gonadal tumors may reach 30%, thus making castration and subsequent hormonal replacement the safest therapeutic option. Mixed gonadal dysgenesis, a frequent cause of sexual ambiguity, is characterized by the presence of a testis on one side and a fibrous streak on the other. Otherwise, Turner-like malformations may be present, the genitalia are ambiguous, and a gonad may or may not be palpable on one side. Patients with dysgenetic male pseudohermaphroditism have bilaterally differentiated dysgenetic testes. Their external genitalia are ambiguous, and mullerian derivatives are always present. The clinical, endocrine, and cytogenetic picture is similar to that of mixed gonadal dysgenesis. Patients with pure gonadal dysgenesis have a normal female phenotype, including uterus and fallopian tubes, but have fibrous streaks instead of gonads; they are free of Turner-like malformations and attain normal height. The implication that some testicular tissue was functional at least up to 10 weeks and subsequently regressed has led to the name "fetal testicular regression syndrome. Rarely, the female fetus is masculinized because of transplacental transfer of androgens from an ovarian or adrenocortical tumor in the mother or from exogenous steroids.

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A secondary effect of serotonin overproduction occurs when a large fraction of dietary tryptophan is shunted into the hydroxylation pathway cardiovascular system song proven 30 mg procardia, leaving less tryptophan available for the formation of nicotinic acid and protein arteries for pulse buy 30mg procardia amex. The diagnosis also must be considered when any one of its clinical manifestations is present cardiovascular institute of the south purchase generic procardia. Elevation in the range of 9 to 25 mg may be seen with carcinoid syndrome heart disease kills more women than cancer discount procardia 30 mg on-line, nontropical sprue, or acute intestinal obstruction. Measurement of serotonin in blood or platelets is of interest but has less diagnostic value than assay of the major metabolite of serotonin in the urine. Assessment of the extent and localization of both primary and metastatic tumor is aided by computed tomographic scans of the abdomen and chest and by imaging with radionuclide-labeled somatostatin receptor ligands. The origin of the tumor influences the biologically active substances produced and their storage and release. The typical carcinoid syndrome usually results from tumors of midgut origin, which almost invariably secrete serotonin. Tumor serotonin content is likely to be high, and the tumor usually contains dense nests of argentaffin-positive cells. Patients with gastric carcinoids frequently exhibit unique flushing, which begins as a bright, patchy erythema with sharply delineated serpentine borders; these patches tend to coalesce as the blush heightens. With carcinoid tumors arising from the bronchus, attacks of flushing tend to be prolonged and severe and may be associated with periorbital edema, excessive lacrimation and salivation, hypotension, tachycardia and tachyarrhythmias, anxiety, and tremulousness. Nausea, vomiting, explosive diarrhea, and bronchoconstriction may progress to a severe degree. This group is therapeutically unique in that severe flushes often can be prevented by corticosteroids. The discovery that somatostatin can prevent the flushing and other endocrine manifestations of the carcinoid syndrome has provided the basis for a major advance in the treatment of these patients. The development of analogues of somatostatin, with longer biologic half-lives than the native hormone, has made subcutaneous administration a feasible route of therapy. One of the somatostatin analogues, octreotide, has been found to markedly improve the flushing and other endocrine manifestations of most patients with carcinoid syndrome. With the improvement of these endocrine symptoms, including fatigue, a considerable improvement in quality of life may be 1297 achieved. Octreotide is administered subcutaneously at intervals of approximately 8 hours, usually beginning with 75 to 150 mug and titrating upward until maximum inhibition of flushing and other symptoms is achieved, which usually occurs at single doses of 750 mug or less. An uncommon but severe adverse effect of octreotide is hypoglycemia, probably as a result of the inhibition of glucagon and growth hormone secretion. The suppression of pancreatic exocrine function by octreotide can cause steatorrhea, and inhibition of the release of cholecystokinin can cause cholelithiasis. In patients receiving octreotide, about 5% achieve tumor regression, and in the group as a whole, less tumor progression and a longer median survival are seen in comparison with historical controls. Octreotide can prevent or treat carcinoid crises that accompany the massive release of mediators that sometimes occurs during operative procedures and tumor necrosis. In patients with histamine-secreting gastric carcinoids, blockade of both H1 - and H2 -histamine receptors markedly ameliorates flushing. Early diagnosis of the carcinoid syndrome has led to complete surgical cure of a few patients with tumors arising in ovarian or testicular teratomas or in the bronchus. By releasing their humoral mediators directly into the systemic circulation, these tumors can produce the syndrome before metastatic disease occurs. In contrast, tumors that release humoral substances into the portal circulation to be largely metabolized by the liver usually produce the syndrome only after liver metastases occur. Given the slow progression of this neoplasm, however, effective reduction in tumor mass can ameliorate morbidity and improve the quality of life even after metastases have occurred. In selected patients, this can be achieved by surgical debulking of tumor, including hemihepatectomy for unilobar metastases, excision of large superficial hepatic metastases, and removal of the primary tumor together with regional lymph nodes containing metastases. Elective cholecystectomy during the surgical intervention will prevent the complications of cholelithiasis that may result from octreotide treatment.

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The diagnosis of acute liver failure is based on clinical findings (rapid onset of jaundice cardiovascular technologist bls discount procardia 30mg mastercard, decreased liver size cardiovascular disease complications generic 30mg procardia with mastercard, evidence of hepatic encephalopathy) and biochemical abnormalities (elevated aminotransferase levels coronary heart with wings buy procardia 30mg mastercard, hyperbilirubinemia cardiovascular system labeling quiz order discount procardia on line, hyperammonemia, hypoglycemia, coagulopathy) in a patient without prior history of chronic liver disease. Imaging studies (abdominal ultrasonography, computed tomography) can help in the evaluation of liver size and in detecting stigmata of portal hypertension (presence of ascites, varices, splenomegaly), which more often accompany chronic liver disease. Imaging studies may also detect space-occupying lesions or occlusion of major blood vessels. Blood serology and toxicologic screens are helpful in identifying patients with suspected viral hepatitis or poisoning. Liver biopsy may be necessary to document the characteristic histologic patterns in patients with vaso-occlusive diseases, graft-versus-host disease, and other less common causes of acute liver failure. However, biopsy is very risky in patients with acute liver failure because they generally have a serious coagulopathy. Patients with acute liver failure usually require care in an intensive-care unit, especially when they develop stage 2 to 3 hepatic encephalopathy, serious bleeding, sepsis, or recurrent bouts of hypoglycemia; most such patients require a central venous pressure monitor, arterial line, urinary catheter, and nasogastric tube. It is excreted in the urine, so urine output and plasma osmolality must be monitored carefully. Regular determination of peripheral blood glucose (every 4-6 hours) is recommended. Coagulopathy is common in patients with acute liver failure due to decreased platelet count and inadequate synthesis of clotting factors. Patients with clinically significant bleeding and those who need invasive procedures. Orthotopic liver transplantation (see Chapter 155) offers a definitive treatment for acute liver failure. However, this surgery is an option only for highly selected patients with hepatic failure (Table 154-2). Despite advances in medical therapy and intensive care, the survival rate of patients whose acute liver failure progresses to stages 3 to 4 of hepatic encephalopathy is still poor (10-40%). Survival depends on the age, time between the onset of hepatic failure and development of hepatic encephalopathy, the prothrombin time, and, most importantly, the cause of acute liver failure. With the introduction of orthotopic liver transplantation, survival rates have increased to 60 to 80%. Chronic liver failure, which is a progressive decline of multiple liver functions in patients with established chronic liver disease, is frequently associated with intermittent episodes of hepatic encephalopathy. Hepatic encephalopathy can occur in cirrhosis of any cause and typically signifies significant portal hypertension and end stage of chronic liver disease. It is important to distinguish reversible precipitating factors from the inexorable progression of chronic liver disease. The exact prevalence of chronic liver failure is unknown, but chronic liver failure is much more common than acute liver failure and probably accounts for most liver-related deaths. Loss of more than 70% of functioning liver cells results in the covert redistribution of splanchnic blood flow, an energy-deficient state, and the failure of multiple secondary organs. Chronic liver injury eventually results in the death of hepatocytes followed by the accumulation of fibrous tissue. The fibrous tissue distorts the architecture of the organ, causing portal hypertension and the development of portosystemic shunting. Clinical manifestations of chronic liver failure evolve over many months to years and eventually include recurrent episodes of hepatic encephalopathy, progressive metabolic derangements (hypoalbuminemia, osteodystrophy, hyponatremia, acidosis, hyperbilirubinemia, glucose intolerance, and hypoglycemia), worsening of portal hypertension and its life-threatening complications (variceal bleeding, ascites, spontaneous bacterial peritonitis), severe pruritus, hematologic abnormalities (coagulopathy, leukopenia, thrombocytopenia, anemia, folate deficiency, hemoptysis), altered metabolism of endogenous hormones and drugs, and the development of functional renal failure. The Child-Pugh classification, which was developed to assess the severity of chronic liver failure, is based on five equally weighted clinical-laboratory parameters (encephalopathy, ascites, serum albumin, serum bilirubin, nutritional status) with a maximal possible score of 15 (Table 154-3). Patients with compensated chronic liver failure are Child-Pugh A (score 1-5), whereas those with advanced cirrhosis are Child-Pugh C (score 11-15). Treatment of chronic liver failure includes identification and correction of potentially reversible factors that may precipitate liver failure in patients with chronic liver disease, such as sepsis, gastrointestinal bleeding, heavy loads of dietary protein, and un-necessary medications. Hepatic encephalopathy (see earlier) and other complications of portal hypertension (see Chapter 153) must be treated appropriately, and orthotopic liver transplantation should be considered (see Chapter 155). Patients with recurrent hepatic encephalopathy, refractory ascites, hepatorenal syndrome, and/or recurrent variceal bleeding should be considered for possible liver transplantation (see Chapter 155). Currently, absolute contraindications for orthotopic liver transplantation include extrahepatic hepatobiliary malignancy, active sepsis outside the hepatobiliary system, and cardiopulmonary failure.

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