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Atherosclerosis and Hypertension Atherosclerosis involving the arteries of the heart medicine doctor dexamethasone 0.5 mg low price, lower extremities medications contraindicated in pregnancy purchase 4mg dexamethasone fast delivery, and brain is the major cause of death from diabetes symptoms checklist discount 0.5mg dexamethasone overnight delivery. The atherosclerotic process is indistinguishable from that affecting the non-diabetic population but begins earlier and may be more severe treatment plan for ptsd generic dexamethasone 0.5mg with mastercard. The predilection to atherosclerosis is observed over the entire spectrum of diabetes-from difficult-to-control insulin-dependent patients to patients with mild hyperglycemia not necessitating insulin. For unclear reasons, the disparity between diabetic and normal subjects is more pronounced in women. Diabetes is an independent risk factor for accelerated atherosclerosis and not solely attributable to an increased frequency of the other recognized risk factors. Clinical studies indirectly support the hypothesis that hyperinsulinemia per se may contribute to macrovascular disease in diabetes, perhaps by stimulatory effects on smooth muscle proliferation. Diabetes may be accompanied by other risk factors for atherosclerosis that markedly increase the incidence of macrovascular complications. The prevalence of hypertension is increased at least 2-fold in patients with type 2 diabetes, partly because of the clustering of both disorders in patients with obesity and insulin resistance. Hypertension is not associated with type 1 diabetes in the absence of renal disease but develops in most patients with nephropathy. The presence of dyslipidemia is associated with the severity of macrovascular disease. Thus the major cardiovascular risk factors-hypertension, hypercholesterolemia, and smoking-interact with diabetes to further promote atherosclerosis. As a result, the risk of myocardial infarction is 2- to 3-fold greater in diabetes but increases to about 8-fold in the presence of hypertension and to nearly 20-fold if hypercholesterolemia coexists. The diagnosis of diabetes should prompt a careful search for other risk factors for atherosclerotic vascular disease and initiation of aggressive preventive measures. Because hypertension accelerates not only atherosclerosis but also nephropathy and retinopathy, even minimal elevations in blood pressure should be treated that in non-diabetics might be dismissed. It should be noted that the normal nocturnal fall in blood pressure may be lost in diabetic patients, thus leading to more sustained hypertension throughout the day. Initially, non-pharmacologic treatment measures such as weight loss, exercise training, and sodium restriction may be tried. The selection of drugs should be individualized, with other coexisting medical problems taken into consideration. Moreover, beta-blockers are known to be cardioprotective for patients who have had a myocardial infarction. Diuretics may be helpful as adjuncts if a volume component is associated with the hypertension. If thiazides are used, they should be given in small doses to minimize their adverse effects on glucose and lipid control. Recent data suggest that hypertensive treatment with calcium channel blockers, although effective in lowering Figure 242a-12 the key elements of a comprehensive management plan for patients with diabetes. Because women with diabetes have a cardiovascular risk similar to that of men, all diabetic patients should be viewed as "high risk," regardless of gender. If this measure fails, hepatic hydroxymethylglutaryl coenzyme A reductase inhibitors (or, alternatively, bile sequestrants) are recommended. Nicotinic acid is less useful because it increases insulin resistance and hyperglycemia. These variables often respond to weight reduction, diet modification, regular exercise, and other measures aimed at improving glycemic control. Low-dose aspirin therapy should be routinely recommended because it reduces cardiovascular events in diabetic patients much like its effect in non-diabetic individuals. Large vessel disease in diabetics is as well treated surgically as it is in non-diabetic illness. Similarly, the frequency of multiple coronary vessel disease and the outcome of coronary vascular surgery differ only slightly between diabetic and non-diabetic persons. In contrast, the benefits of angioplasty for the treatment of multiple coronary artery occlusions are significantly reduced in diabetic patients. The association of diabetes with premature atherosclerosis may only represent the "tip of the iceberg. Although this state of chronic hyperinsulinemia may successfully defend against the development of diabetes, it has been suggested that a price may be paid.
If combined management with alpha- plus beta-adrenergic antagonists is not fully effective medicine glossary buy cheap dexamethasone 4mg, the tyrosine hydroxylase inhibitor alpha-methylparatyrosine is added at an oral dose of 0 medicine buddha dexamethasone 4 mg with amex. Its use may be complicated by sedation medicine ball slams order 0.5 mg dexamethasone otc, fatigue symptoms 8 dpo buy dexamethasone 4mg line, anxiety, diarrhea, or extrapyramidal reactions. For acute management of severe hypertensive crises, intravenous nitroprusside is effective. Intravenous non-selective alpha1 /alpha2 -blockade with phentolamine (1-mg bolus, then by continuous infusion) is also useful. Calcium channel blockade with sublingual nifedipine (10 mg broken under the tongue) has also been used. Opiates (narcotic analgesics), narcotic antagonists (such as naloxone), histamine, adrenocorticotropic hormone, saralasin, glucagon, or indirect sympathomimetic amines (such as phenylpropanolamine or tyramine) should be avoided. All of these agents may provoke hypertensive surges by releasing catecholamines from the tumor. Dopaminergic antagonists (such as metoclopramide or sulpiride) may result in hypertension. Autopsy series of pheochromocytoma indicate that even clinically unsuspected cases can be lethal. At least 90% of pheochromocytomas are benign, and surgical resection provides a cure, although up to 25% of patients may retain some lesser degree of hypertension. Residual tumor may be diagnosed by urinary catecholamine measurement 1 to 2 weeks postoperatively. In malignant pheochromocytoma, the individual course is highly variable, but long-term 50% survival is less than 5 years. Several surgical approaches are feasible, depending on the particular characteristics of the pheochromocytoma; the experience of the surgeon is crucial. Intravenous glucose replacement (5% dextrose in water or saline) should be given to prevent hypoglycemia, a frequent occurrence after tumor removal. Times at which hypertensive surges are likely to occur include anesthetic induction, intubation, tumor palpation, and ligation of tumor veins. If intraoperative hypotension occurs, the initial treatment should be saline infusion to expand intravascular volume. Only after plasma volume expansion to euvolemia is norepinephrine infusion appropriate. For intraoperative blood pressure surges, intravenous nitroprusside is often used. Alternatively, alpha-blockade can be accomplished with intravenous phentolamine (an alpha1 - and alpha2 -antagonist), starting with a 1-mg dose and proceeding to infusion. Most commonly, hypotension results from hypovolemia and responds to saline infusion; several liters may be required, often with the guidance of central pressure measurements. Plasma catecholamine levels remain elevated for several days after complete pheochromocytoma resection. Even 2 weeks postoperatively, up to one fourth of patients still have hypertension. At this time the differential diagnosis includes residual unresected tumor, essential hypertension, or hypertension secondary to renal damage caused by prior hypertension. A urine collection for catecholamines, obtained at least 1 to 2 weeks after tumor resection, will clarify matters. After correction of catecholamine excess, insulin release may be increased and end-organ responsiveness to insulin augmented, resulting in hypoglycemia. Infusion of glucose (5% dextrose in water or saline) during the intraoperative and immediate postoperative period is useful. Although most pheochromocytomas are well-encapsulated, localized growths, approximately 5 to 10% are malignant. Malignancy is diagnosed by the biologic behavior of the tumor in the form of adjacent tissue invasion or distant metastatic spread. Extra-adrenal tumors are more likely to metastasize than are primary adrenal ones. In patients with malignant pheochromocytoma, alpha- and beta-adrenergic blockade with phenoxybenzamine and propranolol remains the mainstay of management of the symptoms and signs of catecholamine excess.
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A disproportionate elevation of the blood urea nitrogen:creatinine ratio may indicate bleeding from a proximal gastrointestinal site medicine 100 years ago purchase 0.5 mg dexamethasone free shipping. In addition medicine dropper discount dexamethasone 4 mg overnight delivery, gross abnormalities of liver function tests may suggest varices as the cause of hemorrhage treatment effect definition cheap dexamethasone 0.5mg fast delivery. Upper Gastrointestinal Tract Bleeding Ulcer disease medications 2355 dexamethasone 4mg mastercard, the most common cause of upper gastrointestinal tract bleeding, is responsible for 50% of moderately severe and 35% of severe bleeding episodes (see Table 123-1). Bleeding from peptic ulcers may not always be associated with heartburn or epigastric burning pain, especially in older patients. Hemorrhage from esophageal or gastric varices (responsible for nearly one third of the episodes of massive upper gastrointestinal hemorrhage) is usually associated with known or suspected chronic liver disease. Most patients with variceal hemorrhage due to alcohol abuse have physical stigmata of liver disease such as a large, firm liver or enlarged spleen, gross ascites, scleral icterus, palmar erythema, and evidence of peripheral muscle wasting. However, patients with cirrhosis due to hepatitis B or C often lack overt peripheral stigmata of chronic liver disease. Variceal hemorrhage usually involves brisk bleeding, with regurgitation of large amounts of dark, clotted blood without emesis. However, variceal hemorrhage may occasionally be accompanied by only "coffee grounds" emesis and melena. Mallory-Weiss tears of the gastroesophageal junction (causing 5% of minor and 20% of severe upper gastrointestinal hemorrhage) are usually associated with antecedent, forceful retching, but they may occur after forceful sneezing, coughing, or singultus. Nearly half the patients with Mallory-Weiss tears abuse alcohol and report "dry heaves" followed by small and then progressively larger amounts of bloody emesis. The signs and symptoms of gastritis-associated bleeding may be identical to those of gastric ulcer disease. Esophagitis, particularly in the patient with long-standing reflux or regurgitation, is suggested by substernal burning pain occasionally relieved by ingestion of food or antacids (see Chapter 124). Alcohol abusers or patients with prolonged recumbency may sometimes have brisk bleeding from esophagitis or esophageal ulcers without any antecedent substernal burning. Gastrointestinal tract malignancies, such as esophageal and gastric cancer or carcinoma of the ampulla of Vater, rarely cause hemodynamically significant upper gastrointestinal tract bleeding. Rare causes of upper gastrointestinal tract bleeding include aortoduodenal fistulas in patients with atherosclerotic aneurysms of the abdominal aorta, usually after prosthetic grafting; chronic renal disease and acquired vascular ectasias; and ectasias associated with other systemic conditions, such as hereditary hemorrhagic telangiectasias (Osler-Weber-Rendu syndrome). Patients with trauma to the liver or with pancreatic pseudocysts may have signs and symptoms that suggest upper gastrointestinal tract bleeding but are actually bleeding from adjacent organs. For patients with hemodynamically significant upper gastrointestinal tract bleeding (bleeding associated with shock, postural vital sign changes, or transfusion requirements of multiple units), endoscopy is the diagnostic procedure of choice because of its high accuracy and immediate therapeutic potential. Endoscopy, however, must be performed only after adequate resuscitation and clinical assessment of the patient. If bleeding is severe, the patient should be transferred to an intensive care unit where adequate monitoring and resuscitation can be maintained. In patients with significant cardiopulmonary disease, however, endoscopy is not without risk, because it does require sedation and analgesia. An endoscopic evaluation of a vigorously bleeding, unstable patient should be performed only by an expert endoscopist because it requires careful sedation, lavage, and selection of instruments and the use of accessory therapeutic procedures. Although endoscopy is used in virtually all patients with manifestations of acute gastrointestinal tract hemorrhage, it is urgently indicated primarily for patients with any of the following: postural vital sign changes or shock, multiple transfusions, a hematocrit below 30%, a high index of suspicion of variceal hemorrhage, recurrent hemorrhage from unknown sources, and high risk for surgery (before a surgical procedure is undertaken). Relative contraindications to endoscopy include acute myocardial infarction, severe chronic lung disease (S O2 90%), hemodynamic instability, and patient agitation, but emergency endoscopy is commonly performed in these situations when diagnosis is critical and/or therapeutic interventions guided by the endoscopy are needed. In addition to documenting the site and probable cause of hemorrhage, endoscopy offers definitive therapy for most active bleeding. Acute variceal bleeding, for example, can be controlled with endoscopic sclerotherapy or varix band ligation in nearly 90% of patients, with a decrease in the likelihood of recurrent bleeding (Color Plate 2 A). These techniques, essentially comparable to one another in effectiveness, not only control acute hemorrhage but also decrease transfusion requirements, the necessity for surgery, and the duration and cost of hospitalization. Barium radiography is noninvasive, costs less than endoscopy, and is readily available but has significant disadvantages, particularly in patients who are bleeding briskly.
These endocrine cells in the fundic gland mucosa contain histamine and are distinguished by characteristic granules and silver staining properties medicine hunter purchase 4mg dexamethasone with mastercard. Enterochromaffin-like cells do not contain serotonin medicine clipart order 4mg dexamethasone visa, and thus these tumors do not produce the classic carcinoid syndrome found with tumors composed of serotonin-containing enterochromaffin cells (see Chapter 245) medicine x protein powder order dexamethasone 0.5 mg. Enterochromaffin-like carcinoids associated with hypergastrinemia can be metastatic symptoms 6 days before period due order dexamethasone 4mg without a prescription, but they are usually indolent, multifocal tumors that may respond to antrectomy and local excision. In contrast, gastric carcinoids found without hypergastrinemia are solitary, aggressive tumors. Other than replacing vitamin B12, no specific therapy exists for pernicious anemia. It is reasonable to evaluate family members for gastritis and vitamin B12 deficiency. Gastric adenocarcinomas (see Chapter 138) have been reported to occur with increased frequency with pernicious anemia, but the assessment of increased risk is variable, ranging from none to threefold in different series. At the time of an initial diagnosis, endoscopic biopsy is usually recommended to obtain sufficient antral and fundic gland tissue to assess the severity of intestinal metaplasia and epithelial dysplasia; although imperfect, these features are the best indicators of the cancer risk. Using this approach, only those patients with dysplasia warrant close follow-up and/or surgical intervention. Characteristic subepithelial (intramucosal) hemorrhages, with the endoscopic appearance of "blood under a plastic wrap," are commonly found in individuals who abuse alcohol. Termed hemorrhagic gastritis, these lesions are 670 composed of hemorrhage and edema in the interstitial space under the surface epithelium, without inflammation. If more severe bleeding is found, associated lesions, such as portal hypertension, peptic ulcer, or a Mallory-Weiss tear, should be sought (see Chapter 123). This rarely encountered, purulent process involves the gastric submucosa and wall. The course is usually fulminant, and medical management is generally ineffective; surgery is usually unavoidable. Herpes simplex virus type I has been implicated as a cause of ulcer disease in normal hosts (see Chapter 126). The Ascaris-like larva, Anisakis (see Chapter 433), present in raw fish, may infect the normal gastric mucosa, producing pain and dyspepsia. Strongyloides stercoralis (see Chapter 433) usually involves the small intestine but can also involve the stomach. Mycelia may occur at the ulcer margin, but ulcer healing does not appear to be impaired, and antifungal therapy does not accelerate healing, suggesting colonization rather than an initial infectious etiology. In this condition, lesions are multiple and consist of gastric erosions on top of small nodules, usually involving the body and fundus more than the antrum. The multiplicity and chronicity distinguish this entity from occasional isolated antral erosions found without symptoms. Symptoms are non-specific and include abdominal pain, nausea, vomiting, anorexia, weight loss, and sometimes bleeding. Macroscopic gastropathy with a dramatic red color may develop rapidly after gastric resection or pyloroplasty, but this endoscopic appearance does not correlate with symptoms, bile reflux, or histologic inflammation. The characteristic histologic picture is reactive gastropathy, with elongation of the glands in the pit region resulting in a corkscrew appearance (foveolar hyperplasia). The occurrence of this difficult-to-treat complication of surgery for peptic ulcer (see Chapter 128) is another rationale for avoiding surgery or doing the least physiologically disruptive operation. Ischemic gastric injury is rarely recognized, although erosive changes have been reported with vasculitis and atheromatous embolization. Hypochlorhydria is generally present, but a hypersecretory variant (which may be an unrelated entity) has been described. Symptoms are variable and may include abdominal pain, nausea, vomiting, weight loss, and edema. The disease is more common in men than in women and generally presents after age 50, although a childhood form exists. Typically, biopsies confirm the diagnosis, but variant patterns warrant the less specific diagnosis of idiopathic hypertrophic gastropathy.
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