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Vice Chair, University of Colorado School of Medicine

Although this result has not yet been replicated erectile dysfunction cleveland clinic buy discount kamagra 100mg online, the use of low doses of spironolactone merits consideration in patients with advanced heart failure erectile dysfunction and age cheap kamagra 100 mg with mastercard. Inhibition of this enzyme in the heart results in an increase in cardiac contractility; and for many decades erectile dysfunction shots buy kamagra 100mg visa, the benefits of digitalis in heart failure were ascribed to this positive inotropic action. These observations have led to the hypothesis that, in addition to increasing contractile force, digitalis may produce important vasodilatory effects by attenuating the activation of neurohormonal systems. Although a variety of digitalis glycosides have been used in the treatment of heart failure for the past 200 years, the most commonly used preparation in the United States is digoxin. Digoxin is the principal glycoside that has been evaluated in placebo-controlled trials. Controlled studies have shown that digoxin can improve symptoms, quality of life, and exercise tolerance in patients with mild-to-moderate heart failure. The addition of digoxin produces favorable effects on clinical status and ejection fraction, and the withdrawal of digoxin is followed by hemodynamic and clinical deterioration. However, in a long-term controlled clinical trial, digoxin did not reduce the risk of death and was associated with only a modest reduction in the combined risk of death and hospitalization. These results indicate that the primary benefit of digoxin in heart failure is to alleviate symptoms and improve clinical status. Digoxin provides a convenient, inexpensive, and well-tolerated means of improving the clinical status of patients with heart failure. However, the finding that the drug has little effect on the progression of heart failure has minimized any mandate for its early use; and, thus, it can be prescribed at any time if symptoms persist after the use of other drugs. Digoxin is a preferred agent in patients with heart failure who have atrial fibrillation and a rapid ventricular response (see Chapter 51). The drug is not recommended for use in patients who have no symptoms or for the stabilization of patients with acutely decompensated heart failure. Lower doses are indicated in patients who are elderly (> 70 years) or in those with impaired renal function (serum creatinine > 1. Higher doses may be needed to control the ventricular response in patients with atrial fibrillation. Although serum digoxin levels are commonly used to guide the administration of digoxin, there is little evidence to support this approach. There is no relation between drug levels and efficacy in patients in sinus rhythm, and patients with atrial fibrillation are better monitored by their heart rate response than by drug levels. These side effects are commonly associated with serum digoxin levels greater than 2 ng/mL, but digitalis toxicity may occur with lower digoxin levels, particularly if hypokalemia or hypomagnesemia coexist. The concomitant use of quinidine, verapamil, spironolactone, flecainide, propafenone, and amiodarone can increase serum digoxin levels and may increase the risk of adverse reactions. Patients with advanced heart block should not receive the drug unless a pacemaker is in place. Adverse effects occur primarily when the drug is administered in large doses, but large doses are generally not needed to produce clinical benefits. Nevertheless, there is persistent concern that digitalis may exert deleterious cardiovascular effects in the long term at doses that appear to be well tolerated in the short term. In a large-scale trial, the use of digoxin in doses that produced serum levels below the toxic range appeared to increase the 222 frequency of hospitalizations and deaths related to cardiovascular events other than heart failure. These observations raise the possibility that even low doses of digoxin can adversely affect the heart. Algorithm for the Management of Chronic Heart Failure the evidence summarized in this section can be synthesized into an algorithm that can guide the management of patients with symptoms of heart failure (Fig. Step 1: Establish the Diagnosis of Heart Failure Patients who are limited in their ability to exercise or perform activities of daily living because of dyspnea or fatigue should be evaluated for the presence of heart failure. During the initial evaluation, the clinician should obtain a two-dimensional echocardiogram, which can identify disorders of the valves, pericardium, or great vessels that may be corrected surgically and can quantify the type and magnitude of ventricular dysfunction. Patients with systolic dysfunction (ejection fraction 40%) should be distinguished from patients with preserved left ventricular function (> 40%). Patients who are in respiratory distress, have evidence for poor end-organ perfusion or fluid overload, or have a serious complicating illness should be hospitalized for treatment with intravenous agents.


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Biopsies of vascular lesions obtained during endoscopy usually are non-specific impotence libido discount kamagra online amex, and the risk of biopsy is not justified erectile dysfunction surgery cost order kamagra amex. Colonic vascular ectasias may not be evident in patients with severely reduced blood volumes or those who are in shock erectile dysfunction venous leak purchase 50 mg kamagra otc, so accurate evaluation may not be possible until red blood cell and volume deficits are corrected. Angiography can determine the site and nature of lesions during active bleeding and can identify colonic vascular ectasias even when bleeding has ceased if a slowly emptying and tortuous vein, a vascular tuft, or an early filling vein is present. It has been estimated that less than 10% of patients with such lesions eventually bleed, data that further support the recommendation not to treat incidental colonic vascular ectasias. Although some colonoscopists remain eager to treat colonic vascular ectasias, almost half the patients may not bleed again after the initial episode. Laser therapy, sclerosis, electrocoagulation, and the argon plasma coagulator heater probe all have been used to ablate colonic vascular ectasias. None has been established as superior, but the heater probe and bipolar coagulation are most commonly used. Moreover, no data prove that endoscopic ablation of colonic vascular ectasias changes their natural history. Right hemicolectomy is performed if the bleeding continues and an experienced endoscopist is not available or endoscopic ablation has been unsuccessful. The extent of colonic resection is not altered by the presence or absence of diverticulosis in the left colon; only the right half of the colon is removed. Because up to 80% of bleeding diverticula are located in the right side of the colon, the risks of leaving a left colon containing diverticula are far outweighed by the increased morbidity and mortality of the larger procedure, a subtotal colectomy. Subtotal colectomy should be performed only as a last resort: that is, in the patient in whom active colonic bleeding persists, the angiogram is completely normal, and colonoscopy either yields negative findings or is not helpful. This autosomal dominant familial disorder is characterized by telangiectasias of the skin and mucous membranes and recurrent gastrointestinal bleeding. Lesions are frequently noticed in the first few years of life, and recurrent epistaxis in childhood is characteristic. By age 10, about one half of patients have some gastrointestinal bleeding, but severe hemorrhage is unusual before the fourth decade and has a peak incidence in the sixth decade. In most patients, bleeding presents as melena; hematochezia and hematemesis are less frequent. Lesions are usually present on the lips, oral and nasopharyngeal membranes, tongue, or periungual regions. Telangiectasias occur in the colon but are more common in the stomach and small bowel, where they are also more likely to cause significant bleeding. Telangiectasias are easily seen on endoscopy as millet seed-sized cherry-red hillocks, although, in the presence of severe anemia and blood loss, they may transiently become invisible or subtle. Angiography may be normal or may demonstrate arteriovenous communications, conglomerate masses of abnormal vessels, phlebectasias, and aneurysms. Pathologically, the major changes involve the capillaries and venules, but arterioles also may be affected. Lesions consist of irregular ectatic tortuous blood spaces lined by a single layer of endothelial cells and supported by a fine layer of fibrous connective tissue. No elastic lamina or muscular tissue is present in these vessels, so they cannot contract, perhaps explaining why they tend to bleed. Many forms of treatment have been recommended for bleeding telangiectasias, including estrogens, endoscopic ablation, and resection of involved bowel. These lesions may be the source of occult or clinically significant bleeding and are best treated, if possible, by endoscopic ablation. This term describes an unusual vascular lesion of the gastric antrum consisting of tortuous dilated vessels radiating outward from the pylorus like spokes from a wheel and resembling the dark stripes on the surface of a watermelon. It produces both acute and chronic occult bleeding, but its cause is unknown; gastric peristalsis may cause prolapse of the loose antral mucosa with consequent elongation and ectasia of the mucosal vessels. The lesion is seen particularly in middle-aged or older women and is associated with achlorhydria, atrophic gastritis, and cirrhosis. The cirrhosis and portal hypertension found in almost half of the reported cases of watermelon stomach suggest an association with portal gastropathy. Microscopic features include dilated capillaries with focal thrombosis, dilated tortuous submucosal venous channels, and fibromuscular hyperplasia. Corticosteroid treatment is unsuccessful, and antrectomy or preferably transendoscopic therapy are more likely to be successful.

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Much to the chagrin of health care planners impotence at 30 kamagra 50mg fast delivery, no plateau in the number of patients is in sight erectile dysfunction best medication order kamagra online from canada. Many of these patients have survived without natural kidney function for more than 20 years hypothyroidism causes erectile dysfunction purchase kamagra with amex. In 1972, the Congress of the United States was approached with a trial of dialysis. Physicians performed hemodialysis on a renal failure patient in front of the legislators. The performance won Medicare financial coverage for end-stage renal failure patients in the United States. Nephrology is the only medical subspecialty that has dealt with a "single-payer" reimbursement system since 1973. It is impossible to separate the clinical aspects of dialysis from its unique (in the United States) form of financing. The dialysis procedure is based on two scientific principles-diffusion and ultrafiltration. Diffusion is not how the normal kidney works, yet it plays a critical role in dialysis. Ultrafiltration (which is more akin to normal kidney function) plays a less crucial role in dialysis. Small particles of differing concentrations in two different solutions will, with time, equalize their concentration when separated by a thin, semipermeable membrane. The smaller the particle, the more brownian movement there is, and the more quickly it will move across the semipermeable membrane. The direction of net movement the particle (or solute) takes is from the solution of higher concentration to the solution of lower concentration. The cellophane membranes were replaced by cuprophan or cuprophane, which, like cellophane, is derived from cellulose. This device allows blood and solution (dialysate) to be separated by a large surface area of semipermeable membrane. Important, then, in dialysis by diffusion are the membrane (its pore number and size), the time that solutions are exposed to the membrane, and the concentration of the particles in the solutions. The difference in concentration gradient between blood and the dialysate is important, and thus the flow rate of blood and dialysate consequentially influences clearance of small molecules. The normal kidney does not employ diffusion and is quite effective in removing both small molecules such as urea and larger molecules. If larger molecules are responsible for uremia, this may be a problem in assessing how well artificial kidneys function. Ultrafiltration, on the other hand, depends on pressure to move particles or water across a membrane. This forced fluid moves (drags) small and relatively large molecules (up to a point) equally well. In dialysis, pressure from the heart and specially designed extracorporeal blood pumps (Fig. Large particles that move slowly or not at all across the semipermeable membrane attract water to move in their direction. Some use of parallel-plate dialyzers continues, but coil dialyzers have almost disappeared from clinical use. It reclaims from the ultrafiltrate exactly those solutes that are needed and excretes (and secretes) those that are toxic and not needed. Without the tubular function of reclamation, we would all quickly die of ultrafiltration. Just how the kidney "knows" what to keep and what to discard is the question that has created the entire branch of medicine called "nephrology. It is not known for certain, however, what substances are responsible for the uremic syndrome and uremic death when the kidneys fail (see Chapter 104). Without this knowledge, it might seem that an artificial kidney would be impossible to develop-even with an understanding of diffusion and ultrafiltration and their ability to remove and replace solutes and water. The genius of the early pioneers of dialysis was their ability to put aside (for the moment) the unknown but to continue the thought process. Dialysis of this solution against a solution with unknown toxic substances should result in moving these unknown toxic substances into the normal solution. This assumes that the toxic substances are small enough to pass the membrane pores, not tightly bound to huge proteins, and located in the blood.

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The episodic airway narrowing that constitutes an asthma attack results from obstruction of the airway lumen to airflow erectile dysfunction medications generic generic kamagra 100mg free shipping. Although it is now well established that infiltration of the airway with inflammatory cells-especially eosinophils-and mast cells occurs in asthma erectile dysfunction evaluation generic 100 mg kamagra otc, the links between these cells and the pathobiologic processes that account for asthmatic airway obstruction have not been clearly delineated erectile dysfunction 5x5 discount kamagra 50 mg on-line. Three possible, but not mutually exclusive, links have been postulated: (1) constriction of airway smooth muscle, (2) thickening of the airway epithelium, and (3) the presence of liquids within the confines of the airway lumen. Among these mechanisms, the constriction of airway smooth muscle due to the local release of bioactive mediators or neurotransmitters is the most widely accepted explanation for the acute reversible airway obstruction in asthma attacks. Several bronchoactive mediators are thought to be the agents causing airway obstruction in the asthmatic. Acetylcholine released from intrapulmonary motor nerves causes constriction of airway smooth muscle through direct stimulation of muscarinic receptors of the M3 subtype. The potential role for acetylcholine in the bronchoconstriction of asthma primarily derives from the observation that atropine and its congeners have proven therapeutic efficacy in asthma. Histamine, or beta-imidazolylethylamine, was identified as a potent endogenous bronchoactive agent more than 90 years ago. Mast cells, which are prominent in airway tissues obtained from patients with asthma, constitute the major pulmonary source of histamine. Clinical trials with novel potent antihistamines 388 Figure 74-1 Schematic renderings of airway anatomy from a normal subject (top) and a mildly allergic asthmatic subject (bottom). The airway in the asthmatic patient exhibits subepithelial fibrosis, edema, and inflammatory cell infiltration. Bradykinin and related molecules are cleaved from plasma precursors by the actions of enzymes known as kallikreins; at least one type of kallikrein is released from activated mast cells. It is also unique among asthmatic mediators in that the sensation of dyspnea evoked by exogenous administration of bradykinin has been shown to mimic the subjective sensations reported by patients during spontaneously occurring asthmatic episodes. Clinical trials with leukotriene receptor antagonists or synthesis inhibitors have shown significant clinical efficacy in the treatment of chronic persistent asthma, leading to the conclusion that the leukotrienes are important mediators of the asthmatic response. Two prophlogistic peptides, substance P and neurokinin A (substance K), are found in the terminal axon dendrites of certain sensory nerves. When these nerves are stimulated by appropriate sensory stimuli, their peptides are released into the airway microenvironment. In contrast to these contractile peptides, vasoactive intestinal peptide, a bronchodilator peptide also found in pulmonary nerves, is believed to play a homeostatic role in the airways. The contractile/inhibitory action of substance P, neurokinin A, and vasoactive intestinal peptide is regulated by specific peptidases located at or near the site of their action or release. As a consequence, inhibition of the function of these peptidases enhances the biologic effects of these peptides. The availability, as experimental tools, of nonpeptide antagonists at neuropeptide receptors may lead to elucidation of the role of these peptides in the asthmatic response; for the present, their role in asthma is speculative. Physiologic Changes in Asthma the consequence of the airway obstruction induced by smooth muscle constriction, thickening of the airway epithelium, or free liquid within the airway lumen is an increased resistance to airflow, which is manifested by increased airway resistance (Raw) and decreased flow rates throughout the vital capacity. At the onset of an asthma attack, obstruction occurs at all airway levels; as the attack resolves, these changes reverse-first in the large airways. This anatomic sequence of onset and reversal is reflected in the physiologic changes observed during resolution of an asthmatic episode (Fig. Specifically, as an asthma attack resolves, flow rates first normalize at a high point in the vital capacity, and only later at a low point in the vital capacity. Because asthma is an airway disease, no primary changes occur in the static pressure-volume curve of the lungs. However, during an acute attack of asthma, airway narrowing may be so severe as to result in airway closure, with individual lung units closing at a volume that is near their maximal volume. This closure results in a change of the pressure-volume curve such that, for a given contained gas volume within the thorax, elastic recoil is decreased, which in turn further depresses expiratory flow rates. Additional factors influence the mechanical behavior of the lungs during an acute attack of asthma. During inspiration in an asthma attack, the pleural pressure drops far below the 4 to 6 cm H2 O subatmospheric pressure usually required for tidal airflow. The expiratory phase of respiration also becomes active as the patient tries to force air from the lungs.

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