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While this convention has the potential for confusion erectile dysfunction pump price buy kamagra gold overnight, the meaning is usually clear from the context. Metastases to the pericardium, however, may involve both the parietal and visceral layers. Pericardial innervation is derived from the phrenic nerve anteriorly and the esophageal plexus posteriorly, both supplied by the vagus nerve. Myocardial innervation is supplied by the same nerves, which helps explain the similarities of anginal pain and pericardial pain when prominent pleuritic features are absent. Lymphatic drainage is to the anterior and posterior mediastinal lymph nodes, and retrograde spread through these vessels is an important source of metastatic tumor spread, especially for cases of breast and lung cancers. The pericardial space normally contains up to 50 ml of fluid, which is continuously secreted by the mesothelial cells of the visceral pericardium. Three major sinuses within the pericardial space (superior, transverse, and oblique) serve to store accumulated fluid without affecting cardiac function or causing symptoms. When preclinical but nevertheless pathologic pericardial effusions are present, these sinuses can be seen to be enlarged with various imaging modalities. The pericardium serves many other physiologic functions in addition to lubrication of the heart. The relatively fixed volume and inherent elasticity combine to keep the pericardial sac under tension, which contributes to diastolic pressures within the heart and helps maintain the classic pressurevolume relationships of cardiac physiology. For instance, under conditions that increase left ventricular volume, a condition commonly encountered in the cancer patient (anthracycline cardiomyopathy, renal dysfunction, etc. Within the pericardial space, there is a small negative pressure (~3 mmHg) that serves to augment diastolic filling. When cancer results in a diseased pericardium, any of these functions can be disrupted, often leading to complex pathophysiology. Primary Tumors of the Pericardium Primary pericardial tumors (both benign and malignant) are extraordinarily rare. Five tumor types make up the vast majority of primary pericardial tumors, accompanied by a longer list of very rare entities. Benign pericardial tumors are more common than primary malignancies, and present more commonly in the pediatric population. The bulk of epidemiologic data regarding primary cardiac tumors comes from a series of 533 such cases by the Armed Forces Institute of Pathology,6 and has been summarized and updated more recently. They consist of a lining of mesothelial cells surrounded by fibrous connective tissue and contain a clear, straw-colored fluid, which may communicate with the pericardial space. Pericardial cysts are usually small (less than 3 cm) but have the capacity to expand considerably, and may achieve dimensions of up to 15 cm. Only 1/3 of patients present with symptoms, which can include chest pain, dyspnea, and arrhythmias. Treatment, when necessary, consists of surgical excision, percutaneous drainage, or thorascopic drainage. Teratoma Teratomas are tumors derived from all 3 germ layers, and though usually benign, can carry malignant potential. Pericardial teratomas arise from the base of the pulmonary artery or aorta, which often complicates their surgical removal. Approximately 80% occur in the pediatric population,5 typically in infancy or in utero. Clinical presentation can be dramatic, with compression of the right atrium or right ventricle, or tamponade from an associated pericardial effusion. Presentation includes hydrops fetalis, fetal pericardial effusion, and dyspnea, cyanosis, cardiomegaly, cardiac murmurs, and sudden cardiac death in the neonatal or pediatric patient. In rare cases of malignant transformation, teratomas can invade adjacent structures such as myocardium. In these unfortunate cases surgical excision is not feasible and the prognosis is poor. Mesothelioma Mesothelioma is the most common primary malignancy of the pericardium. Further confounding the debate is the fact that some mesotheliomas thought to be of pericardial origin are actually derived from the pleura with local invasion in to the pericardium. Some evidence implicates Simian Virus 40 as well as asbestos in the pathogenesis of mesothelioma; this virus has been found in up to 80% of patients with mesothelioma, and has been found to cause mesothelioma in animal models. Local invasion can occur to the pleura, mediastinum, mediastinal lymph nodes, and occasionally through the diaphragm to the peritoneum. Invasion to the deep myocardium is rare, in contrast with other pericardial malignancies. Diagnosis of mesothelioma is confirmed by pathologic evaluation of the fluid or pericardial biopsy. Distinction between mesothelioma and reactive mesothelial hyperplasia (seen in response to inflammation) can present a challenge. Given the behavior patterns of this malignancy, surgical resection is very difficult, and operative mortality high. Prognosis is poor with or without surgery, with one series reporting a 60% 6-month mortality. Unlike mesothelioma, angiosarcoma commonly invades the myocardium, and can present with intracardiac masses or valvular obstruction. Distant metastases are possible and occur in approximately 1/4 of all cases,5 with a predilection for the central nervous system. Symptoms and clinical findings include those of acute pericarditis, pericardial effusion, congestive heart failure, arrhythmias, and constitutional symptoms. Surgical resection may be possible in selected patients but treatment is generally palliative, and includes chemotherapy and radiation. Other Primary Pericardial Tumors Pericardial lipomas resemble those found elsewhere in the body.
Sympathomimetic agents could thus benefit the acutely failing heart: b1-stimulation by an inotropic effect erectile dysfunction age factor 100 mg kamagra gold order free shipping, b2-stimulation by afterload reduction (peripheral arterial vasodilation), and a-stimulation by restoring pressure in hypotensive states (see Table 6-2). Although b2-activation achieves beneficial vasodilation and also mediates some inotropic effect, such stimulation also causes hypokalemia with enhanced risk of arrhythmias. A further and serious problem is that prolonged or vigorous b1-stimulation may lead to or increase receptor downgrading with a diminished inotropic response. These are the reasons why sympathomimetics are used only in short-term treatment of acute heart failure. In severe acutely decompensated chronic heart failure patients, those admitted on b-blockers, and also at discharge, had a decreased 180-day mortality. Although the latter aim can be achieved by pure a-stimulants, such as phenylephrine (5 to 20 mg in 500 mL slow infusion) or methoxamine (5 to 10 mg at 1 mg/min), this option is not logical, because heart failure automatically invokes reflex adrenergic vasoconstriction. Combined inotropic and vasoconstrictor effects are occasionally required, as may be achieved by high-dose dopamine. If inotropic stimulation plus peripheral vasodilation is required, then dobutamine and a vasodilator, low-dose dopamine, or milrinone is appropriate. Dobutamine Dobutamine, a synthetic analog of dopamine, is a competitive b-adrenergic stimulating agent (b1. However, its b2 stimulatory effect may lead to hypotension and sometimes to a fall in diastolic pressure with reflex tachycardia. Furthermore, long-term mortality may be increased,19 as well as increasing cardiac sympathetic activity in heart failure patients Pharmacokinetics, dose, and indications. A precaution is to dilute in sterile water or dextrose or saline, not in alkaline solutions. Dopamine Dopamine is a catecholamine-like agent used for therapy of severe heart failure and cardiogenic shock. Physiologically, it is both the precursor of norepinephrine and releases norepinephrine from the stores in the nerve-endings in the heart. However, in the periphery this effect is overridden by the activity of the prejunctional dopaminergic-2 receptors, inhibiting norepinephrine release and thereby helping to vasodilate. Therefore overall dopamine stimulates the heart by both b- and a-adrenergic responses and causes vasodilation through dopamine receptors. Dopamine, a "flexible molecule," also fits in to many receptors to cause direct b1- and b2-receptor stimulation, as well as a-stimulation. The latter explains why in high doses dopamine causes significant vasoconstriction. Dopamine can only be given intravenously, which restricts its use to short-term treatment. Worsening renal function and hypokalemia related to diuretic use for acute decompensated heart failure are common and associated with poor prognosis. In acute heart failure patients, the combination of low-dose furosemide (5 mg/h) and low-dose dopamine (5 mcg/kg/min) as a continuous infusion for 8 hours was equally 6 - Heart Failure 179 effective as high-dose furosemide but associated with improved renal function profile and potassium homeostasis. Dopamine is sometimes given for renal protection or for diuresis in critically ill patients at a typical dose of 0. This dose did not work in an intensive care setting, arguing against the renoprotective concept. In critically ill hypoxic patients, dopamine may have undesirable side effects such as depression of ventilation and increased pulmonary shunting, which may require supplemental oxygen. Extravasation can cause sloughing, prevented by infusing the drug in to a large vein through a plastic catheter, and treated by local infiltration with phentolamine. Dopamine is the preferred inotrope in the patient who requires both a pressor effect (high-dose a-effect) and increase in cardiac output, and who does not have marked tachycardia or ventricular irritability. In cardiogenic shock, infusion of equal concentrations of dopamine and dobutamine may afford more advantages than either drug singly. The key to the effective use of these (and all intravenous inotropes) is careful monitoring of the clinical and hemodynamic response in the individual patient. Epinephrine (Adrenaline) Epinephrine gives mixed b1- and b2-stimulation with some added a-mediated effects at a high dose (see Table 6-2). It is used chiefly when combined inotropic-chronotropic stimulation is urgently needed, as in cardiac arrest. Side effects include tachycardia, arrhythmias, anxiety, headaches, cold extremities, cerebral hemorrhage and pulmonary edema. Contraindications include late pregnancy because of risk of inducing uterine contractions. Norepinephrine (Noradrenaline) Norepinephrine is given in an intravenous dose of 8 to 12 mcg/min with a terminal half-life of 3 minutes. Norepinephrine chiefly stimulates a-receptors in the periphery (with more marked a-effects than epinephrine) and b-receptors in the heart. Logically, norepinephrine should be of most use when a shocklike state is accompanied by peripheral vasodilation ("warm shock"). Side effects of norepinephrine include headache, tachycardia, bradycardia, and hypertension. As with all of the catecholamines and vasodilators, note the risk of necrosis with extravasation. Contraindications include late pregnancy (see "Epinephrine" earlier in chapter) and preexisting excess vasoconstriction. Its cardiovascular effects closely resemble those of exercise, including a positive inotropic and vasodilatory effect.
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Two syndromes exist: simple pneumoconiosis and an advanced form how erectile dysfunction pills work generic kamagra gold 100 mg buy on-line, progressive massive fibrosis. The Coal Workers Pneumoconiosis Scheme has been set up specifically for this purpose. Although not all claims are successful, many patients are able to get some compensation for the disease that they have subsequently developed. These patients should be managed in the same way as all other patients in acute respiratory failure (see Ch. Worsening or first presentation of severe pulmonary fibrosis can be treated initially with intravenous corticosteroids, with cyclophosphamide as second-line therapy. Assessment by an intensive care physician should also be made and decisions about ceiling of care discussed with the patient. One must also consider other diagnoses associated with the underlying cause of the pulmonary fibrosis. This is particularly important in those with asbestosis, as they are at risk of mesothelioma. Simple pneumoconiosis Simple pneumoconiosis is the commonest type of pneumoconiosis, reflecting coal dust deposition within the lung. It is asymptomatic and diagnosis is made on the basis of small round opacities in the upper zone on chest X-rays. Progressive massive fibrosis In progressive massive fibrosis, large, round fibrotic nodules measuring more than 10 mm in diameter are seen, usually in the upper lobes. Symptoms include dyspnoea, cough and sputum production (which may be black as cavitating lesions rupture). Lymphocytes and macrophages then infiltrate, leading to the development of noncaseating granulomas, which may resolve or organize, leading to pulmonary fibrosis. Asbestosis Asbestosis is diffuse pulmonary fibrosis caused by the inhalation of asbestos, a mixture of silicates of iron, nickel, magnesium, aluminium and cadmium mined from the ground. Therefore those with occupations such as plumbers, electricians and builders are at high risk of exposure. Several types of asbestos exist: serpentine fibres, which do not cause pulmonary disease, and amphibole fibres, which do. The most important type of amphibole asbestos is crocidolite (blue asbestos), a straight fibre 50 mm long and 12 mm wide that cannot be cleared by the immune system. Fibres remain in the lung indefinitely and become coated in iron (haemosiderin) to form the classic drumstick-shaped asbestos bodies. Histology shows asbestos bodies and features of pulmonary fibrosis, affecting the lower lobes more commonly. A considerable time lag, sometimes as long as 2040 years, exists between exposure and disease development. Bilateral endinspiratory crackles indicate significant diffuse pulmonary fibrosis. Clinical features these consist of cough, shortness of breath, fever and malaise that occur acutely several hours after exposure to antigen. Investigations There are many different ways to investigate extrinsic allergic alveolitis. These include polymorphonuclear leucocyte count, precipitating antibodies (evidence of exposure, not disease), nodular shadowing on chest X-ray, lung function tests showing a restrictive pattern and bronchoalveolar lavage. Treatment Most diseases will regress once the patient is prevented from further exposure to the antigen. Corticosteroids may speed recovery but do not alter the ultimate level of lung function and are thought to be mostly of benefit in severe disease. Also known as fibrosing alveolitis or cryptogenic fibrosing alveolitis, idiopathic pulmonary fibrosis is a rare, progressive chronic pulmonary fibrosis of unknown aetiology. Pathology the alveolar walls are thickened because of fibrosis, predominantly in the subpleural regions of the lower lobes. An increased number of chronic inflammatory cells are in the alveoli and interstitium. Pathogenesis Antigens that can cause allergic lung disease include: · · · · Mouldy hay. Clinical features Clinical features of idiopathic pulmonary fibrosis include progressive breathlessness and a dry cough. There is progression to cyanosis, respiratory failure, pulmonary hypertension and cor pulmonale over time. Clubbing occurs in two-thirds of patients; chest expansion is reduced and bilateral, fine, end-inspiratory crackles are heard on auscultation. Investigations Several investigations are made: · Transbronchial or open-lung biopsy to confirm histological diagnosis. Alveolar proteinosis is associated with a high incidence of concomitant fungal infections and may complicate other interstitial disease. The course of the disease is variable, but the majority of patients enjoy spontaneous remission. A proliferation of macrophages in the alveolar air spaces occurs, along with interstitial thickening by mononuclear inflammatory cells. Desquamative interstitial pneumonitis has a distinctly uniform histological pattern. Typically, patients are aged 4070 years at presentation; only 23% occur in younger patients. Tumours may occur as discrete or mixed histological patterns; the development from the initial malignant change to presentation is variable: · Squamous cell carcinoma: 8 years. Cigarette smoking is the largest contributory factor: · It is related to the amount smoked, duration and tar content: 20% of smokers will develop lung cancer.