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Other Symptoms Non-productive cough is often an early manifestation of elevated pulmonary venous pressure and otherwise unsuspected heart failure medications parkinsons disease order 200ml liv 52. Fatigue and weakness are common accompaniments of advanced cardiac disease and reflect an inability to perform normal activities symptoms xanax cheap liv 52 60ml with amex. Hemoptysis is a classic presenting finding in patients with pulmonary embolism symptoms throat cancer liv 52 100 ml on line, but it is also common in patients with mitral stenosis symptoms nausea dizziness buy 200ml liv 52 visa, pulmonary edema, bronchiectasis, and bronchitis. Claudication, which is pain in the extremities with exertion, should alert the physician to possible peripheral arterial disease (see Chapters 67 and 68). The Complete Medical History the complete medical history should include a thorough review of systems, family history, social history, and past medical history. The review of systems may reveal other symptoms that suggest a systemic disease as the cause of any cardiovascular problems. The social history should include specific questioning about cigarette smoking, alcohol intake, and use of illicit drugs. The past medical history may reveal prior conditions or medications that suggest systemic diseases, ranging from chronic obstructive pulmonary disease, which may explain a complaint of dyspnea, to hemochromatosis, which may be a cause of restrictive cardiomyopathy. A careful history to inquire about recent dental work or other procedures is critical if bacterial endocarditis is part of the differential diagnosis. The cardiovascular physical examination begins with careful measurement of the pulse and blood pressure. If aortic dissection (see Chapter 66) is a consideration, blood pressure should be measured in both arms and, preferably, in at least one leg. When coarctation of the aorta is suspected (see Chapter 57), blood pressure must be measured in the leg as well as in the arms. Discrepancies in blood pressure between the two arms can also be caused by atherosclerotic disease of the great vessels. Pulsus paradoxus, which is a decrease in the systolic blood pressure of more than the usual 10 mm Hg drop in inspiration, is typical of pericardial tamponade (see Chapter 65). General Appearance the respiratory rate may be increased in patients with heart failure. Patients with pulmonary edema are usually markedly tachypneic and may have labored breathing. Angina with strenuous or rapid or activity does not cause undue fatigue, palpitation, prolonged exertion at work or recreation. Patients can perform to completion any activity requiring 7 metabolic equivalents. Ordinary physical activity results in fatigue, palpitations, dyspnea, or anginal pain. Walking more than 2 blocks on the level and climbing more than one flight of ordinary stairs at a normal pace and in normal conditions. Patient can perform to completion any activity requiring 5 metabolic equivalents but cannot and does not perform to completion activities requiring 7 metabolic equivalents. Patient can perform to completion any activity requiring 2 metabolic equivalents but cannot and does not perform to completion any activities requiring 5 metabolic equivalents. Patient cannot or does not perform to completion activities requiring 2 metabolic equivalents. They are comfortable blocks on the level and climbing more than one flight in normal at rest. Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at rest. From Goldman L, et al: Comparative reproducibility and validity of systems for assessing cardiovascular functional class: Advantages of a new specific activity scale. Osteogenesis imperfecta, which is associated with blue sclerae, is also associated with aortic dilatation and mitral valve prolapse. Retinal artery occlusion may be caused by an embolus from clot in the left atrium or left ventricle, a left atrial myxoma, or atherosclerotic debris from the great vessels. Hyperthyroidism may present with exophthalmos and typical stare, whereas myotonic dystrophy, which is associated with atrioventricular block and arrhythmia, is often associated with ptosis and an expressionless face. Jugular Veins the external jugular veins help in assessment of mean right atrial pressure, which normally varies between 5 and 10 cm H2 O; the height (in centimeters) of the central venous pressure is measured by adding 5 cm to the height of the observed jugular venous distension above the sternal angle of Louis. The normal jugular venous pulse, best seen in the internal jugular vein (and not seen in the external jugular vein unless insufficiency of the jugular venous valves is present), includes an a wave, caused by right atrial contraction; a c wave, reflecting carotid artery pulsation; an x-descent; a v wave, which corresponds to isovolumetric right ventricular contraction and is more marked in the presence of tricuspid insufficiency; and a y descent, which occurs as the tricuspid valve opens and ventricular filling begins.

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Although B lymphocytes do not appear to play a primary role in the disease treatment locator generic liv 52 100ml mastercard, their function is altered secondarily by mediators released from activated T lymphocytes symptoms 1 week after conception buy 200ml liv 52 visa. Polyclonal hyperglobulinemia results symptoms your having a boy order liv 52 now, with formation of antibodies reactive against a variety of microbial agents and self-antigens symptoms upper respiratory infection purchase liv 52 100 ml free shipping. Not only can almost any organ system be affected, but the clinical presentation and natural history of disease affecting a particular organ system are also quite variable. The respiratory system is most commonly affected, with approximately 90% of patients demonstrating intrathoracic involvement on a chest radiograph. Patients can develop extrathoracic disease either with or without concomitant intrathoracic involvement. Extrathoracic disease can be the predominant component of the clinical picture or alternatively can be either subclinical or less problematic than intrathoracic disease. Thirty to 60 per cent of patients have no symptoms at the time of presentation, and the disease is identified because of abnormalities on a chest radiograph. Alternatively, patients commonly present with respiratory symptoms, such as dyspnea and cough, which may or may not be accompanied by constitutional symptoms, such as fever and malaise. Presentations related primarily to extrathoracic involvement are less common; specific signs and symptoms depend on the particular organ system(s) involved. Intrathoracic nodal involvement and parenchymal lung disease are the two most common ways in which sarcoidosis affects the respiratory system. Both hilar and mediastinal lymph nodes may be affected; involvement of the hilar nodes is usually bilateral and relatively symmetrical. The pulmonary parenchyma demonstrates well-defined, non-caseating granulomas within the pulmonary interstitium, typically in a pattern that preferentially follows bronchovascular bundles. The granulomatous inflammation is often accompanied by non-specific mononuclear cell infiltration; in severe disease, parenchymal involvement may progress to irreversible fibrosis and honeycombing. Cystic lesions may be complicated by colonization with Aspergillus and the development of intracavitary aspergillomas. The upper respiratory tract may be affected by sarcoidosis, with involvement taking the form of nasal mucosal, nasal bone, or laryngeal disease. Pleural disease is relatively infrequent, with effusions occurring in fewer than 5% of patients. Dyspnea and cough, typically non-productive, are the primary symptoms that accompany either pulmonary parenchymal or endobronchial sarcoidosis. Examination of the chest can reveal crackles resulting from parenchymal lung involvement, although the examination is often notable for the paucity or even absence of findings despite the extent of radiographic changes. Wheezing may be present in a small proportion of cases, resulting either from endobronchial involvement or airway distortion as a consequence of end-stage fibrotic disease. Pulmonary function tests in the presence of parenchymal lung disease often demonstrate a pattern of restrictive disease, with a relatively symmetric decrease in lung volumes, although they can remain normal despite parenchymal changes on chest radiograph. The diffusing capacity of the lung for carbon monoxide may be either normal or abnormal and does not necessarily follow the presence or absence of abnormal lung volumes. Cutaneous manifestations of sarcoidosis resulting from granulomatous involvement of the skin affect 15 to 20% of patients. A variety of lesions can be seen, including papules, plaques, nodules, infiltration of old scars, and lupus pernio. Old scars or tattoos often become infiltrated with granulomas, so that previously atrophic scars develop an appearance of keloid formation. Lupus pernio is a chronic, violaceous, often disfiguring lesion primarily affecting the nose, cheeks, and ears. It tends to affect women older than 40 years of age, especially those from the West Indies. These raised, red, tender, nodular lesions, generally but not exclusively on the anterior surface of the lower leg, do not represent granulomatous involvement of the skin. Rather, the histopathology is primarily that of a panniculitis, with cellular inflammation and edema of the deep dermis and subcutaneous tissue, especially involving connective tissue septa of adipose tissue. Ocular sarcoidosis can take a number of forms, including anterior or posterior uveitis, conjunctival involvement, and papilledema. Anterior uveitis, the most common form of ocular sarcoidosis, is often associated with the relatively acute onset of a red eye, photophobia, and ocular discomfort. Posterior uveitis, which may be obscured on examination by anterior chamber involvement, can present with vitreous infiltrates, choroidal nodules, periphlebitis, retinal hemorrhage, and papilledema.

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Similarly medications gerd cheap liv 52 200 ml amex, cardiac drugs such as beta-adrenergic blockers and calcium channel blockers medications you can buy in mexico order liv 52 amex, when co-administered medicine search 200ml liv 52 for sale, have additive negative inotropic effects medicine logo buy generic liv 52, resulting in an increased risk of cardiac failure. To recognize the presence of a drug interaction, the index of suspicion must be high whenever multiple drugs are used together. Because of the ever-increasing list of known and suspected drug interactions, it is impossible for a clinician to remember all or even a significant number of the possible interactions. Several clinical settings should raise concern about the possibility of drug interactions: (1) the use of any drug with a low therapeutic index (Table 26-3) should be suspect. This risk may be even higher for patients with the acquired immunodeficiency syndrome, who have an immunocompromised state as well as being on a great number of drugs. Several steps can be taken to prevent drug interactions: (1) In taking the medical history, it is important to document all the drugs the patient is taking, including prescription, over-the-counter, and other addictive drugs. The actual incidence of adverse drug responses is somewhat difficult to quantify, because many cases are not recognized. Several large studies have demonstrated that the incidence may approach 20% for outpatients (even higher for patients on more than 15 drugs) and 2 to 7% for inpatients. Recent meta-analyses of several prospective studies indicate that adverse drug reactions may be the fourth to sixth leading cause of death in hospitalized patients. It is clear from recent surveys that a relatively small group of drugs (see Table 26-3) continues to be implicated in most of the reported adverse drug responses. Current trends suggest that the incidence of adverse drug responses is likely to increase as a result of an increase in the number of both prescribed and over-the-counter medications. Most adverse drug responses are caused by either (1) exaggerated (but predictable) pharmacologic effect of the drug or (2) toxic or immunologic effect of drug or metabolite (not typically expected). Exaggerated drug responses that cause adverse drug effects may be due to any condition that causes either altered pharmacokinetics or pharmacodynamics (discussed earlier). Recently there has been interest in the role of genetic factors as a cause of increased susceptibility to adverse drug responses, primarily through an effect on drug metabolism. Genetic polymorphism of drug metabolizing enzymes can account for variability in pharmacokinetics and drug effect observed in population studies. Three of the best-studied polymorphisms are the debrisoquine/sparteine, N-acetylation, and mephenytoin polymorphisms. These are each associated with an autosomal recessive inheritance and together are responsible for the metabolism of approximately 40 drugs (Table 26-4). Individuals with autosomal recessive genes are "poor metabolizers" with potentially altered pharmacokinetics that result in elevated plasma drug concentrations and can lead to toxicity. Other genetic defects do not specifically affect metabolism and hence do not produce a range of quantitative changes. These defects can produce "qualitative" defects and are often associated with structural defects. Individuals who are deficient in this enzyme cannot tolerate oxidative stress that is produced by some drugs, leading to hemolysis (see Chapter 164). Drugs that can produce this clinical picture include aspirin, nitrofurantoin, primaquine, probenecid, quinidine, quinine, sulfonamides, sulfones, and vitamin K. Another similar defect is deficiency of methemoglobin reductase, which results in an inability to maintain iron in hemoglobin in the ferrous state, causing methemoglobinemia after exposure to oxidizing drugs such as nitrites, sulfonamide, or sulfones. This type of adverse drug response is not predictable and is not obviously due to either an increase in drug concentration (pharmacokinetic) or drug effect (pharmacodynamic). With other drugs, metabolism of the drug to an active intermediate must first occur. With a standard dose of acetaminophen, no untoward effects occur because the relatively small amount of reactive metabolite formed by oxidative metabolism is rapidly detoxified by reduced glutathione. In the presence of an overdose, the glutathione is depleted and the remaining reactive metabolite can then damage the liver. Understanding the mechanism of this toxicity has provided a rationale for treating acetaminophen overdose. Immunologic reactions to drugs (Table 26-5) in general are not produced by the drug alone. Like other small molecular weight compounds (<1000 daltons), they are typically not antigenic themselves.

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More than 60% (39% of those in patients who would otherwise succumb) can be prevented by defibrillation initiated by a bystander or a first-responding rescuer symptoms gluten intolerance discount liv 52 200 ml with mastercard. Additional objectives of prehospital care by paramedical and emergency personnel include adequate analgesia (generally with morphine) medications54583 buy liv 52 200 ml line, reduction of excessive sympathoadrenal and vagal stimulation pharmacologically treatment gonorrhea cheap 60 ml liv 52, treatment of hemodynamically significant or symptomatic ventricular arrhythmias (generally with lidocaine) medicine buy liv 52 cheap online, and support of cardiac output, systemic blood pressure, and respiration. It is indicated for patients in whom thrombolysis will be the preferred approach to coronary reperfusion. Refractory or severe pain should be treated symptomatically with intravenous morphine, meperidine, or pentazocine. Repeated intravenous doses of 4 to 8 mg of morphine at intervals of 5 to 15 minutes can be given with relative impunity until the pain is relieved or toxicity is manifested by hypotension, vomiting, or depressed respiration. Blood pressure and pulse must be monitored in an attempt to keep the systolic blood pressure above 100 mm Hg and, optimally, below 140 mm Hg. Relative hypotension may be treated with elevation of the lower extremities or administration of fluids, except in patients with concomitant pulmonary congestion, in whom treatment for cardiogenic shock may be required (see Chapter 95). Atropine, in doses similar to those given in the prehospital phase, may increase blood pressure if hypotension reflects bradycardia or excess vagal tone. High concentrations may be counterproductive because of vasoconstriction and lack of augmented myocardial oxygen delivery in normoxemic patients. Patients requiring mechanical ventilation require special measures (see Chapter 93). Lower-risk patients without obvious ischemia should be observed and monitored in either a step-down/intermediate care unit or a chest pain evaluation/observation unit (see above). Alternatives for coronary recanalization include intravenous thrombolytic agents or catheter-based approaches. Thrombolysis can be accomplished with a variety of intravenous medications and regimens (see Chapter 188), with or without the use of adjunctive therapies. Catheter-based approaches also avoid the risk of bleeding, including intracerebral bleeding, seen with thrombolytic medications. It is clearly the treatment of choice in patients with contraindications to thrombolytic agents (see below). First-generation drugs invariably elicit a systemic lytic state characterized by depletion of circulating fibrinogen, plasminogen, and hemostatic proteins, and by marked elevation of concentrations of fibrinogen degradation products in plasma. In optimal regimens, they induce clot lysis without inducing a systemic lytic state, are less prone to predispose to hemorrhage that requires transfusion compared with non-clot-selective agents, and are effective in inducing recanalization in 80 to 90% of infarct-related arteries within 90 minutes. Adequate beta-adrenergic blockade should then be established; when this is not possible or contraindications exist, a calcium antagonist can be considered. High-risk patients should be triaged to cardiac catheterization with plans for revascularization if they are clinically suitable; patients who are clinically stable can be treated more conservatively, with continued observation in the hospital and consideration of a stress test to screen for myocardial ischemia. The risks of coronary thrombolysis include bleeding, much of which is confined to sites of vascular access. Marked depletion of fibrinogen or prolongation of the bleeding time may be markers of pharmacologic effects that lead to bleeding. With thrombolysis, the incidence of hemorrhagic stroke is increased, but the risk of thrombotic or embolic stroke is somewhat reduced, and overall any small increase in fatal cerebrovascular accidents is more than offset by the favorable impact on survival. Plasminogen activators should not be given to patients with active internal bleeding or a bleeding diathesis, suspected aortic dissection, recent trauma, intracranial neoplasm, or hypertensive crisis. Relative contraindications include prolonged or traumatic cardiopulmonary resuscitation, peptic ulcer disease, remote cerebrovascular accident, and hepatic failure. Safety has not been established for pregnant women, although it has been for menstruating women. Treatment may be helpful in some patients first seen 6 to 12 hours after the onset of symptoms, particularly those with stuttering infarcts. Clinical efficacy of coronary thrombolysis depends on the frequency, rapidity, and persistence of recanalization, all of which depend not only on the intensity of fibrinolysis, but also on the inhibition of coagulation and platelet-induced thrombosis, which undoubtedly occur concomitantly. Presently, intravenous heparin is the agent of choice, coupled with orally administered aspirin. These and similar agents are undergoing intense evaluation for assessment of their potential utility alone or in various combinations with fibrinolytic agents. They are particularly promising because platelet activation results in profound augmentation of thrombin generation. Even optimally effective coronary thrombolysis is compromised by early thrombotic reocclusion in 6 to 20% of patients with initial recanalization unless vigorous conjunctive anticoagulation is initiated immediately. Treatment may require use of thrombolytic medications and mechanical revascularization.

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