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Barbar S generic lasix 100 mg visa heart attack jarren benton, Noventa F buy discount lasix 100mg on line arrhythmia vs palpitations, Rossetto V, et al: A risk assessment model for the identification of hospitalized medical patients at risk for venous thromboembolism: the padua prediction score. Nendaz M, Spirk D, Kucher N, et al: Multicentre validation of the geneva risk score for hospitalised medical patients at risk of venous thromboembolism. Coutance G, Cauderlier E, Ehtisham J, et al: the prognostic value of markers of right ventricular dysfunction in pulmonary embolism: a meta-analysis. Vuilleumier N, Le Gal L, Verschuren F, et al: Cardiac biomarkers for risk stratification in non-massive pulmonary embolism: a multicenter prospective study. Lankeit M, Jimenez D, Kostrubiec M, et al: Predictive value of the high-sensitivity troponin T assay and the simplified pulmonary embolism severity index in hemodynamically stable patients with acute pulmonary embolism: a prospective validation study. Jimenez D, Kopecna D, Tapson V, et al: Derivation and validation of multimarker prognostication for normotensive patients with acute symptomatic pulmonary embolism. Konstantinides S, Geibel A, Heusel G, et al: Heparin plus alteplase compared with heparin alone in patients with submassive pulmonary embolism. Meyer G, Vicaut E, Danays T, et al: Fibrinolysis for patients with intermediate-risk pulmonary embolism. Chatterjee S, Chakraborty A, Weinberg I, et al: Thrombolysis for pulmonary embolism and risk of all-cause mortality, major bleeding, and intracranial hemorrhage: a meta-analysis. Birn J, Vedantham S: May-thurner syndrome and other obstructive iliac vein lesions: Meaning, myth, and mystery. Usoh F, Hingorani A, Ascher E, et al: Prospective randomized study comparing the clinical outcomes between inferior vena cava greenfield and TrapEase filters. Decousus H, Leizorovicz A, Parent F, et al: A clinical trial of vena caval filters in the prevention of pulmonary embolism in patients with proximal deep-vein thrombosis. Iorio A, Kearon C, Filippucci E, et al: Risk of recurrence after a first episode of symptomatic venous thromboembolism provoked by a transient risk factor: a systematic review. Jang T, Docherty M, Aubin C, et al: Resident-performed compression ultrasonography for the detection of proximal deep vein thrombosis: fast and accurate. Vieillard-Baron A, Page B, Augarde R, et al: Acute cor pulmonale in massive pulmonary embolism: incidence, echocardiographic pattern, clinical implications and recovery rate. Nazerian P, Vanni S, Volpicelli G, et al: Accuracy of point-of-care multiorgan ultrasonography for the diagnosis of pulmonary embolism. Mathis G, Blank W, Reissig A, et al: Thoracic ultrasound for diagnosing pulmonary embolism: a prospective multicenter study of 352 patients. While these patients are at high risk for developing arterial and venous thrombosis due to underlying comorbidities, central venous catheter placement, and immobility, they are also at high risk for hemorrhagic complications resulting from gastrointestinal stress ulcerations, invasive procedures, liver dysfunction, uremia, or coagulopathy [2]. These divergent features often complicate antithrombotic treatments for the prevention or management of thrombosis. Limitations in administration routes, hemodynamic instability, alterations in renal and hepatic function, and drug interactions further complicate the administration of these high-risk medications [3]. This chapter focuses on the mechanisms of action, pharmacokinetics, pharmacodynamics, clinical indications, complications of therapy, and reversal options for antithrombotic pharmacotherapy in critically ill patients. Platelet activation involves four mechanisms: adhesion to sites of vascular injury, release of stimulatory compounds, aggregation, and priming of coagulation. Antiplatelet ‘resistance’ and ‘nonresponse’ are terms applied to clinical outcomes characterized by failure to prevent a thrombotic event due to inadequate platelet inhibition [4]. While several methods are available for measuring the overall and drug-specific platelet aggregation, standard testing protocols have yet to be established [5]. Aspirin and Aspirin Derivatives Pharmacology, Pharmacodynamics, and Monitoring Aspirin, or acetylsalicylic acid, is a prodrug of salicylic acid that blocks platelet activation. Consequently, there is a 50- to 100-fold variation between the daily doses required to suppress inflammation and inhibit platelet function [7]. Enteric-coated and delayed release formulations have diminished bioavailability, take 3 to 4 hours to reach peak plasma levels, and have delayed onset. Rectally administered aspirin has variable absorption with a bioavailability of 20% to 60% over a 2- to 5-hour retention time [8]. There are currently no data suggesting inferiority of lower (75 to 100 mg) to higher (>100 mg) maintenance dosing in preventing thromboembolic events [9,10]. Recurrent vascular thrombotic episodes despite aspirin therapy occur at rates between 2% and 6% of patients per year [11] Aspirin resistance occurs in 5. Possible mechanisms of aspirin resistance include extrinsic factors (adherence, absorption, dosage formulation, and smoking) and intrinsic factors (pharmacodynamic alterations, receptor polymorphisms, up regulation of nontargeted platelet activation pathways). Clinical Indications Aspirin is indicated for the primary and secondary prevention of arterial and venous thrombosis (Table 93. Aspirin provides effective thromboprophylaxis in patients on warfarin with prosthetic heart valves and in patients with nonvalvular atrial fibrillation [13]. The recommended interval for discontinuation of aspirin prior to elective surgery or procedures is 7 to 10 days. Therapy can be resumed approximately 24 hours or the next morning after surgery when there is adequate hemostasis [14]. For patients exhibiting clinically significant bleeding or requiring emergent surgery, platelet transfusion may be warranted (Table 93. Intravenous desmopressin antagonizes aspirin’s effect, suggesting a role in emergent situations as well [15]. Aspirin produces gastrointestinal ulcerations and hemorrhage through direct irritation of the gastric mucosa and via inhibition of prostaglandin synthesis. Enteric-coated and buffered aspirin doses ≤325 mg do not reduce the incidence of gastrointestinal bleeding [17]. Aspirin-induced gastric toxicity can be prevented with concurrent use of acid-suppressive therapy [16]. Underlying aspirin allergy can exacerbate respiratory tract disease, angioedema, urticaria, or anaphylaxis and is estimated to occur in 10% of the general population. Leukotriene-modifying agents may reduce aspirin- provoked respiratory reactions but do not eliminate the risk. For patients with a compelling indication for therapy, aspirin desensitization may be considered [18]. While thienopyridine metabolites have a short plasma elimination half- life (1 to 8 hours), their irreversible activity at P2Y12 receptors spans the life of the platelet (7 to 10 days). The onset of action, duration of antiplatelet effect, and unpredictable levels of platelet inhibition led to the development of newer agents [21]. Ticagrelor is a nonthienopyridine P2Y12 inhibitor that does not require hepatic activation resulting in immediate, short-acting, dose-dependent inhibition of platelet activation aggregation [22]. Ticagrelor binds reversibly at P2Y12 receptors resulting in a shorter duration of antiplatelet activity compared to thienopyridines [22]. Resistance to clopidogrel occurs in 4% to 34% of patients and depends on the agent, type, and timing of platelet function test, as well as underlying comorbidities such as diabetes and obesity [20]. Monitoring the antiplatelet effect of P2Y12 inhibitors using platelet function testing is an evolving area of research [5]. Recent literature does not show significant improvements in clinical outcomes with platelet-function monitoring and treatment adjustment for coronary stenting, as compared with standard antiplatelet therapy without monitoring [24]. For patients with threatened in-stent thrombosis and presumed or confirmed clopidogrel resistance, maintenance dosing up to 150 mg daily could be attempted with platelet function testing.

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Memory Functions Memory functions include immediate memory span buy lasix 100mg online blood pressure chart systolic diastolic pulse, learning capacity and retention purchase lasix amex hypertension vasoconstriction, and retrieval of previously learned information (recent and remote). For example, three or four unrelated words are presented and the patient is instructed to remember them. Nonverbal learning can be assessed in a similar fashion using line drawings of simple geometric figures or by pointing to three or four objects in the room and asking the patient to recall them a few minutes later. Visuospatial and Visuoconstructive Abilities Visuoconstructive ability is tested by having the patient copy simple figures (e. Left-sided visual inattention or hemispatial neglect is suggested if the patient places all the numerals on one side of the clock, or omits all numerals normally on one side. Capacity to process number/time relationships can be tested by having the patient “Set the time to 10 minutes past 11 o’clock. An example of an easy similarity test pair is “broccoli–cauliflower”; a more difficult pair is “fish–dandelion. Insight and judgment can be approximated when discussing the patient’s recent medical care, their understanding of their status; and their ability to manipulate data, make and maintain a decision regarding the next steps. The hallmark features of delirium are inattentiveness, confusion, and psychomotor agitation, as well as sleep– wake alterations, and in many patients hyper-alertness, with hallucinations or visual misinterpretation of common objects. Fever, sepsis, metabolic and endocrine disturbances, as well as medication use or withdrawal are among the causes of delirium; this is discussed in more detail in Chapters 145 and 157. Focal Syndromes Stroke is another adverse neurologic outcome from surgery—especially cardiac surgery [2] or endovascular procedures, such as angioplasty—and is usually recognized by the presence of focal or lateralizing deficits of sudden onset with motor weakness or sensory deficits (see Chapters 149 and 150). These changes can, however, persist beyond the immediate postoperative period when the effects of anesthesia and analgesia directly affecting cognitive functions have clearly worn off. Most mental status changes improve, but in some cases may continue following discharge, even weeks, months, and years later with associated impaired quality of life and increased mortality [4,18]. Other individual features that increase the risk of mental status dysfunction include previous cerebrovascular disease, previous and undetected cognitive impairment or dementia, and cardiovascular risk factors such as hypertension, diabetes, and peripheral vascular disease [2,19–23]. Atherothromboembolic phenomena (microemboli) and hypoxia with watershed area injury secondary to hypoperfusion are possible causative mechanisms of postoperative cognitive dysfunction due to intraoperative events during surgery [2]. The approach to testing should be flexible and targeted to the individual patient’s complaints and level of functioning. Postoperative cognitive changes can range from obvious deficits in concentration and memory to subtle deficits in executive functions. Anoxic damage can be caused by circulatory collapse; respiratory failure; or inadequate hemoglobin or its ability to bind and release oxygen. Prognosis and management of the anoxic patient depend in part on which of these mechanisms has caused the injury. The continuous availability of oxygen is secured by the cerebral vasculature’s autoregulatory mechanisms [1], which control the rate of blood flow over a wide range of blood pressures. If blood pressure drops too low for autoregulatory mechanisms to operate, oxygen extraction from the blood increases. In cardiovascular collapse, loss of venous outflow leads to the accumulation of lactic acid and pyruvate, the end products of anaerobic metabolism. Metabolic causes, including anoxic encephalopathy, should be suspected when patients with impaired consciousness present with a nonfocal examination. Acute decrease in the partial pressure of oxygen to less than 40 mm Hg causes confusion, and to less than 30 mm Hg results in coma [2]. Associated abnormalities that potentiate anoxic damage include anemia, acidosis, hypercapnia, hyperthermia, and hypotension. The internist or neurologist is often consulted to evaluate the patient who has impaired consciousness after well-documented cerebral hypoperfusion event that has occurred during surgical operations requiring the use of extracorporeal circulation. Because surgical patients with such a history often have preexisting illnesses (vascular disease, borderline renal function, hepatic impairment, and diabetes), it is the obligation of the intensive care physician to determine whether the new deficits are caused by anoxic encephalopathy, or by other treatable conditions secondary to metabolic, infectious, or iatrogenic factors such as sedating medications. Intracerebral hemorrhage and subdural hematomas should also be sought, because they can occur spontaneously in the perioperative period, especially in anticoagulated patients. If anoxia is moderately prolonged, the patient awakens but may have residual deficits, such as cognitive impairment, or later sequelae, including extrapyramidal movement disorders or seizures, which may not develop for days to weeks. A delayed postanoxic syndrome may occur rarely in patients with anoxic insults after the initial coma. Three to 30 days following the initial anoxic insult, after the patient has regained consciousness and cognitive function, there is a secondary decline characterized by irritability, confusion, lethargy, clumsiness, and increased muscle tone; patients may become comatose again and die. The cause is unknown, but it may be caused by alteration of enzymatic processes; edema; or damage to small blood vessels [2,3]. The overall prognosis for a meaningful recovery in patients with nontraumatic coma is guarded; the longer patients are in coma, the worse the outcome [4–6]. Non-anoxic metabolic coma carries the best prognosis, whereas anoxic coma has a better prognosis than coma resulting from structural lesions. Although infrequent seizures or myoclonus do not affect prognosis, myoclonic or nonconvulsive status epilepticus is a grave prognostic sign and is associated with poor recovery [4,7]. Irreversible damage is rarely seen in healthy individuals if the duration of anoxia is less than 4 minutes, although it may occur for individuals with preexisting cerebrovascular disease in shorter periods. In cases of nontraumatic coma, the most valuable prognostic information is obtained from the physical examination. The loss of vestibulo-ocular responses at 12 hours; presence of decerebrate or decorticate posturing at 24 hours; and absent motor response to pain by the third day [5,8,10]. When prognosticating by the clinical criteria alone, one must be careful that no sedative, anesthetic, or anticonvulsant is being used, because these agents can suppress brainstem reflexes. Generalized cerebral anoxia due to respiratory insufficiency, with maintained circulation, carries a better prognosis. A low partial pressure of oxygen does not necessarily convey a bad prognosis in cases of isolated hypoxia, if circulation is carefully maintained [18,19]. Emergency crew–witnessed arrests; consciousness level on admission; and requirement for ventilation are independently useful to predict in-hospital outcome and mortality [23]. Magnetic resonance spectroscopy demonstrating elevated lactate and reduced N-acetyl aspartate peaks is associated with a poor prognosis [24,25]. The longer a patient survived without awakening, the smaller the probability of awakening without deficits [30,31]. To ensure that the oxygen-carrying capacity of the blood is restored, excess oxygen administration is suggested for several hours after anoxic events. The partial pressure of carbon dioxide is kept at the patient’s baseline (usually 40 mm Hg), unless there are active signs of cerebral herniation; if herniation is suspected, the patient should be hyperventilated. Vital signs, hematocrit, electrolytes, blood sugar, and serum osmolality should be maintained in the normal range. They are treated with loading and then maintenance doses of fosphenytoin (loading dose, 15 to 20 mg phenytoin equivalents per kg, rate not to exceed 100 mg phenytoin equivalents per minute; maintenance dose, 5 mg phenytoin equivalents per kg per day). Alternatively, intravenous phenytoin can be used (loading dose, 18 to 20 mg per kg; rate, 50 mg per minute; maintenance dose, 5 mg per kg).

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This information becomes important when considering how long to observe asymptomatic patients after an overdose order generic lasix online arteria d8. However discount 100mg lasix free shipping arteria thoracoacromialis, several adult patients have developed toxicity and death at doses less than maximum recommended daily doses [18]. Generally, the most significant poisonings are large intentional ingestions, but patients with significant underlying medical diseases or advanced age are prone to effects at lower doses. Minimally intoxicated patients, or those who present soon after ingestion, may demonstrate no signs of toxicity. However, the causes of the hypotension are typically an extension of the drugs’ therapeutic effects (i. This selectivity may be lost in large overdoses such that dihydropyridine poisoning results in bradycardia and/or impaired cardiac conduction [15,16,19–21]. Although overdose experience with dihydropyridines other than nifedipine is limited [15,20–22], they would be expected to have effects similar to nifedipine. Severe poisoning is characterized by hypotension and bradycardia [16,23–25], hyperglycemia [19–21,23,26–32], and metabolic acidosis [2,15,19,21,27,32,33]. Hyperglycemia is caused by the aforementioned alterations in insulin and carbohydrate homeostasis (see “Physiology and Pathophysiology” section). Additionally, tissue hypoperfusion can result in cerebrovascular accidents, seizures, renal failure, myocardial infarction, and noncardiogenic pulmonary edema [35]. However, the differential diagnosis of a patient with hypotension and bradycardia includes other toxicologic causes such as β-blockers, digoxin and other cardiac glycosides, antidysrhythmics, and clonidine. However, nontoxicologic causes such as myocardial disease, hyperkalemia, sepsis, and hypothyroidism should also be considered. Preemptive intubation should strongly be considered for patients with significant ingestions or signs of toxicity because of the potential for rapid deterioration. Among bradycardic patients, administration of atropine before intubation may prevent vagal responses from laryngoscopy. Measurements of renal function, electrolytes, complete blood counts, liver function tests, arterial blood gases, and acetaminophen, salicylate, and digoxin levels should be guided by the clinical picture and medical history. For patients with severe or refractory hypotension, urinary and central venous catheterization are recommended to guide fluid and vasopressor therapy. Finally, early consultation with a medical toxicologist regarding medical therapy, and a cardiologist regarding pacemaker or intraaortic balloon pump placement, is recommended. Risks and benefits should be considered on a case by case basis, and interventions necessary to maintain vital signs take precedence over decontamination. Gastric lavage should not be used routinely, but considered for recent life-threatening ingestions in patients who have not vomited [37]. Cardiovascular Support Hypotension should initially be treated with intravenous crystalloids with close monitoring for fluid overload. Although usually ineffective for severe poisoning [16,17,23,30], atropine should be given for symptomatic bradycardia. Treatment beyond general supportive care, intravenous fluids, and atropine will depend on the clinical situation. Transvenous pacing may be attempted, but in significant poisoning there may be failure to capture, and blood pressure may not improve despite an increase in heart rate [16,17]. However, health care providers generally have the greatest familiarity with dosing and administration of vasopressor agents. Improvements have been noted with dopamine, dobutamine, norepinephrine, isoproterenol, and epinephrine. However, no specific agent has demonstrated superiority, so it is reasonable for clinicians to start with the agent they are most familiar with. Animal models have demonstrated either no improvement in mean arterial pressure [42] or decreased survival [43] with vasopressin compared to saline controls. However, there was improvement in systemic vascular resistance and blood pressure after vasopressin was administered to two patients unresponsive to multiple other therapies [44]. Because vasopressors can result in tachydysrhythmias, increased myocardial oxygen consumption and vasospastic events, these agents should be the first to be weaned from a patient who has stabilized. The exact mechanisms underlying these actions still remain controversial [46], but may be best described in the following animal studies. However, survival with epinephrine [2,47], glucagon [2,47], and calcium [2] was 33%, 0%, and 17%, respectively. Insulin also increased the mean lethal dose of verapamil and time to death compared to epinephrine and glucagon [7]. Insulin improved myocardial metabolism and function without increasing myocardial oxygen consumption [3,7]. One patient had failed to improve with respiratory support, crystalloids, atropine, calcium, and glucagon. Patients responding to insulin therapy demonstrate improved blood pressure, myocardial contractility, and metabolic acidosis, whereas effects on bradycardia and cardiac conduction are variable [46]. Serum glucose and potassium were monitored every 30 minutes until stable and then 1 to 2 hourly thereafter. Aggressive correction of insulin-induced hypokalemia is unnecessary unless the patient is symptomatic or potassium falls below an arbitrarily suggested level of 2. Calcium the goal of calcium therapy is to increase extracellular calcium concentrations thereby increasing calcium influx through any unblocked calcium channels. Calcium has demonstrated effectiveness in animal models [53], and improvement has been reported in human cases [17,54]. However, responses are variable and often short-lived, and patients with significant toxicity often fail to improve with calcium alone [16,23]. Conduction disturbances, contractility, and blood pressure may be improved, but generally there is no increase in heart rate [16,23,30]. Calcium chloride contains three times the amount of elemental calcium of calcium gluconate (10% calcium chloride: 272 mg elemental calcium or 13. The higher elemental calcium content in calcium chloride also poses a greater risk for tissue injury should extravasation occur. Initial doses are generally given as boluses (10 to 20 mL of 10% calcium chloride or 30 to 60 mL of 10% calcium gluconate). Some authors suggest more aggressive dosing of 1 g every 2 to 3 minutes until clinical response is seen [31]. Raising serum ionized calcium to 2 to 3 mEq per L improves canine cardiac performance in verapamil poisoning [2,53], and is a reasonable goal to attain. It may be necessary to continue therapy despite high serum calcium levels if the patient is only responding to calcium administration. Significantly poisoned patients have tolerated high serum calcium levels without untoward effect [39,54], including one patient who obtained a peak serum calcium level of 23. Several case reports noted improvement with glucagon therapy [26,38], but failures are also reported [30,32]. Five to 10 mg (150 μg per kg) given intravenously over 1 to 2 minutes is a typical starting dose [57]. Cardiovascular effects of glucagon last only 10 to 15 minutes [58], so repeat boluses may be required every 5 to 10 minutes followed by a continuous infusion of 2 to 10 mg per hour (50 to 100 μg/kg/h) [57]. However, they can be difficult to titrate and cause vasodilation and hypotension so are not generally recommended.

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Patients are candidates for prophylactic urate-lowering therapy if they have more than two attacks per year or they have chronic kidney disease cheap 100 mg lasix with visa hypertension knowledge test, kidney stones lasix 40mg with visa prehypertension treatments and drugs, or tophi (deposit of urate crystals in the joints, bones, cartilage, or other body structures). Treatment of chronic gout Urate-lowering therapy for chronic gout aims to reduce the frequency of attacks and complications of gout. Treatment strategies include the use of xanthine oxidase inhibitors to reduce the synthesis of uric acid or use of uricosuric drugs to increase its excretion. Xanthine oxidase inhibitors (allopurinol, febuxostat) are first-line urate- lowering agents. Uricosuric agents (probenecid) may be used in patients who are intolerant to xanthine oxidase inhibitors or fail to achieve adequate response with those agents. It is neither a uricosuric nor an analgesic agent, although it relieves pain in acute attacks of gout. Mechanism of action Colchicine binds to tubulin, a microtubular protein, causing its depolymerization. This disrupts cellular functions, such as the mobility of neutrophils, thus decreasing their migration into the inflamed joint. Therapeutic uses the anti-inflammatory activity of colchicine is specific for gout, usually alleviating the pain of acute gout within 12 hours. Colchicine is also used as a prophylactic agent to prevent acute attacks of gout in patients initiating urate-lowering therapy. It undergoes enterohepatic recirculation and exhibits high interpatient variability in the elimination half-life. Adverse effects Colchicine may cause nausea, vomiting, abdominal pain, and diarrhea (ure 38. Chronic administration may lead to myopathy, neutropenia, aplastic anemia, and alopecia. The drug should not be used in pregnancy and should be used with caution in patients with hepatic, renal, or cardiovascular disease. It reduces the production of uric acid by competitively inhibiting the last two steps in uric acid biosynthesis that are catalyzed by xanthine oxidase (see ure 38. Therapeutic uses Allopurinol is an effective urate-lowering therapy in the treatment of gout and hyperuricemia secondary to other conditions, such as that associated with certain malignancies (those in which large amounts of purines are produced, particularly after chemotherapy) or in renal disease. The primary metabolite alloxanthine (oxypurinol) is also a xanthine oxidase inhibitor with a half-life of 15 to 18 hours. Thus, effective inhibition of xanthine oxidase can be maintained with once-daily dosing. Dose adjustment is needed if estimated glomerular filtration rate is less than 30 mL/min/1. Hypersensitivity reactions, especially skin rashes, are the most common adverse reactions. Its adverse effect profile is similar to that of allopurinol, although the risk for rash and hypersensitivity reactions may be reduced. Febuxostat does not have the same degree of renal elimination as allopurinol and thus requires less adjustment in those with reduced renal function. Febuxostat should be used with caution in patients with a history of heart disease or stroke, as this agent may be associated with a greater risk of these events as compared to allopurinol. It is a weak organic acid that promotes renal clearance of uric acid by inhibiting the urate-anion exchanger in the proximal tubule. Adverse effects include nausea, vomiting, and dermatologic reactions, and, rarely, anemia or anaphylactic reactions. It acts by converting uric acid to allantoin, a water-soluble nontoxic metabolite that is excreted primarily by the kidneys. Pegloticase is indicated for patients with gout who fail treatment with standard therapies such as xanthine oxidase inhibitors. Infusion-related reactions and anaphylaxis may occur with pegloticase, and patients should be premedicated with antihistamines and corticosteroids. His medical history includes diabetes, hypertension, hyperlipidemia, gastric ulcer (resolved), and coronary artery disease. This patient is at high risk of future ulcers, due to the history of gastric ulcer. Choices A and B are incorrect because this patient has significant cardiovascular risk and a history of coronary artery disease. Which drug is an oral agent that would target the cause of his acute gout attacks? Probenecid is a uricosuric agent that increases renal excretion by inhibiting the urate–anion exchanger in the proximal tubule, thereby blocking reabsorption of uric acid and facilitating its excretion. Allopurinol and febuxostat are xanthine oxidase inhibitors, which primarily act by decreasing uric acid production. Probenecid is a uricosuric agent indicated to lower serum urate levels to prevent gout attacks. It is not indicated during acute gout flares and should not be started until after the resolution of an acute attack. Naproxen, colchicine, and prednisone all represent viable treatment options that acutely reduce pain and inflammation associated with acute gout attacks. Each of these conditions may be associated with a troublesome cough, which may be the only presenting complaint. Asthma is a chronic disease characterized by hyperresponsive airways that affects over 235 million patients worldwide. This disorder is underdiagnosed and undertreated, creating a substantial burden to individuals and families, and resulting in millions of emergency room visits. Allergic rhinitis is a common chronic disease and is characterized by itchy, watery eyes, runny nose, and a nonproductive cough that can significantly decrease quality of life. Each of these respiratory conditions may be managed with a combination of lifestyle changes and medications. Drugs used to treat respiratory conditions can be delivered topically to the nasal mucosa, inhaled into the lungs, or given orally or parenterally for systemic absorption. Local delivery methods, such as nasal sprays or inhalers, are preferred to target affected tissues while minimizing systemic adverse effects. Medications used to treat common respiratory disorders are summarized in ure 39. Preferred Drugs Used to Treat Asthma Asthma is a chronic inflammatory disease of the airways characterized by episodes of acute bronchoconstriction that cause shortness of breath, cough, chest tightness, wheezing, and rapid respiration. Pathophysiology of asthma Airflow obstruction in asthma is due to bronchoconstriction that results from contraction of bronchial smooth muscle, inflammation of the bronchial wall, and increased secretion of mucus (ure 39. The underlying inflammation of the airways contributes to airway hyperresponsiveness, airflow limitation, respiratory symptoms, and disease chronicity. Asthma attacks may be triggered by exposure to allergens, exercise, stress, and respiratory infections. However, if untreated, asthma may cause airway remodeling, resulting in increased severity and incidence of asthma exacerbations and/or death.