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Prednisone

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By C. Avogadro. Menlo College. 2019.

Based on the results of these two trials discount prednisone online master card, clopidogrel should now routinely be added to standard fibrinolytic regimens in patients younger than 75 years [27] purchase genuine prednisone line. Prasugrel is a second-generation thienopyridine that is more rapidly acting cheap prednisone 40mg without prescription, more potent, and associated with less response variability than clopidogrel. In addition, there were two important subgroups in whom prasugrel was associated with excess bleeding that nullified clinical benefit, including patients >75 years of age and those <60 kg [77]. This agent provides more rapid onset (and offset) of action and a more potent and predictable antiplatelet response than clopidogrel. Ventricular pauses may also be triggered by ticagrelor early after treatment initiation, but these pauses also decrease in frequency over time, are rarely symptomatic, and have not required an excess of clinical intervention. Morphine administration also appears to reduce absorption of P2Y12 inhibitors and contribute to delayed onset of action [79–81]. Cangrelor is a novel intravenous, fast-acting, and reversible P2Y12 inhibitor that may offer an alternative strategy for patients to achieve rapid P2Y12 inhibition. Given the high cost, at the present time, we generally limit cangrelor use to patients unable to take oral P2Y12 inhibitors. In a meta- analysis involving 3,266 patients enrolled in four randomized trials comparing abciximab with placebo, patients receiving abciximab had a 46% reduction in 30-day death, reinfarction, and urgent target vessel revascularization compared to those who received placebo [83]. Moreover, data are very limited in the current era of more potent and rapidly acting P2Y12 inhibitors. An issue of concern was an increased risk of stent thrombosis within the first 24 hours in the bivalirudin group. Compared with bivalirudin, heparin reduced the incidence of major adverse ischemic events in the setting of primary percutaneous coronary intervention, with no increase in bleeding complications. The availability of P2Y12 inhibitors has virtually eliminated the past reliance on warfarin for aspirin-allergic patients. It should be noted that the newer direct oral anticoagulants have not been evaluated in this clinical context, so their use cannot be recommended. An increasingly challenging scenario relates to the combination of aspirin, a P2Y12 inhibitor, and warfarin. It may be expected that risks will be even higher with combinations that include the newer and more potent antiplatelet agents such as prasugrel and ticagrelor. Surprisingly, the group randomized to withhold aspirin also had markedly lower rates of all-cause mortality than the triple therapy group (2. Ongoing research efforts continue to search for the optimal risk/benefit profile in this complex patient population. The fact that β-blockers were particularly effective in reducing sudden death and reducing mortality among patients with complex ventricular ectopy at baseline suggests that β-blockers exert much of their beneficial effect by reducing the frequency and severity of arrhythmias [96]. Post hoc analyses indicate that this increased risk was predominantly among patients with indicators of or risk factors for hemodynamic compromise. Parenteral β-blockers should be used only if there is a clear indication such as ongoing chest pain or an atrial tachyarrhythmia with normal or elevated blood pressure [27]. Aldosterone antagonists should be avoided in patients with hyperkalemia or significant renal dysfunction (Table 187. Nitrates Nitrates dilate large coronary arteries and arterioles, peripheral veins, and to a lesser extent, peripheral arterioles. Neither study found a significant reduction in mortality with nitrates, although the ability to detect such a difference may have been reduced because more than 50% of patients received off-protocol nitrates. Calcium Channel Blockers Calcium channel blockers block the entry of calcium into cells via voltage- sensitive calcium channels. Sustained-release preparations of nifedipine, on the other hand, can be used safely in combination with a β- blocker. It should be emphasized that there have not been studies comparing the efficacy of verapamil or diltiazem to a β-blocker. Underlying metabolic and electrolyte abnormalities must be corrected, and ongoing ischemia should be addressed. Lidocaine remains an effective alternative if amiodarone is not tolerated or is unsuccessful in controlling the arrhythmia. Bradyarrhythmias the usual cause of bradycardia is increased vagal tone or ischemia/infarction of conduction tissue. Sinus bradycardia is typically caused by irritation of cardiac vagal receptors, which are located most prominently on the inferior surface of the left ventricle (Table 187. Atropine should be reserved for patients with hypotension or symptoms, and temporary pacing is rarely required. Continuing care must be individualized using lifestyle interventions, disease-modifying pharmacological therapies, and additional coronary revascularization when indicated. All patients should undergo a transthoracic echocardiogram prior to hospital discharge to assess ventricular systolic function and to ensure that appropriate medications are initiated prior to discharge (i. In addition, all patients without contraindications should be initiated on high-intensity statin therapy, and considered for ezetimibe, prior to discharge. The objectives of exercise-based cardiac rehabilitation are to increase functional capacity, decrease or alleviate anginal symptoms, reduce disability, improve quality of life, and reduce morbidity and mortality rates [109]. All of these interventions, together with appropriate patient and family education regarding medication adherence and timely follow-up, will serve to reduce rates of rehospitalization and improve patient outcomes (Table 187. Ito H, Tomooka T, Sakai N, et al: Lack of myocardial perfusion immediately after successful thrombolysis. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Kastrati A, Dibra A, Spaulding C, et al: Meta-analysis of randomized trials on drug-eluting stents vs. Palmerini T, Biondi-Zoccai G, Della Riva D, et al: Stent thrombosis with drug-eluting and bare-metal stents: evidence from a comprehensive network meta-analysis. Valgimigli M, Gagnor A, Calabró P, et al: Radial versus femoral access in patients with acute coronary syndromes undergoing invasive management: a randomised multicentre trial. Widimsky P, Groch L, Zelízko M, et al: Multicentre randomized trial comparing transport to primary angioplasty vs immediate thrombolysis vs combined strategy for patients with acute myocardial infarction presenting to a community hospital without a catheterization laboratory. Widimsky P, Budesínský T, Vorβc D, et al: Long distance transport for primary angioplasty vs immediate thrombolysis in acute myocardial infarction. Zeymer U, Uebis R, Vogt A, et al: Randomized comparison of percutaneous transluminal coronary angioplasty and medical therapy in stable survivors of acute myocardial infarction with single vessel disease: a study of the Arbeitsgemeinschaft Leitende Kardiologische Krankenhausarzte. Nielsen N, Wetterslev J, Cronberg T, et al: Targeted temperature management at 33 degrees C versus 36 degrees C after cardiac arrest. Roux S, Christeller S, Ludin E: Effects of aspirin on coronary reocclusion and recurrent ischemia after thrombolysis: a meta- analysis. Antithrombotic Trialists Collaboration: Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. Yusuf S, Peto R, Lewis J, et al: Beta blockade during and after myocardial infarction: an overview of the randomized trials. Pitt B, Remme W, Zannad F, et al: Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. Wilson K, Gibson N, Willan A, et al: Effect of smoking cessation on mortality after myocardial infarction: meta-analysis of cohort studies. The latter condition is usually caused by acute total obstruction of a coronary artery [2,3], and urgent reperfusion is the mainstay of therapy.

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An electrocardiogram and serial cardiac biomarkers should be obtained in all patients to evaluate the possibility of myocardial ischemia or infarction purchase prednisone in india. Sulfur dioxide 2015 Case crossover 849 order prednisone 10 mg on-line,127 Based on data [88] pollution and about deaths increased from incidence of cardiovascular cardiovascular diseases in mortalities buy cheap prednisone 40 mg. The half-life of carboxyhemoglobin decreases as the partial pressure of oxygen in the blood increases. If myocardial ischemia is present, most experts believe cardiac catheterization with stenting of the blocked vessel to be the urgently required procedure. In a clinical study, normocapnic2 hyperoxic hyperpnea reduced the half-life of carboxyhemoglobin to 31 minutes compared with 78 minutes for individuals treated with 100% oxygen at normal minute ventilation [43]. The likelihood for cyanide toxicity in smoke inhalation victims increases with increasing carboxyhemoglobin levels and increasing acidosis [44]. It is also part of jewelry making and various manufacturing processes (metal plating) and in the reclamation of silver from photographic and radiographic film. Cytochrome a3 is a key enzyme in the cytochrome oxidase system that is important for carrying out and sustaining aerobic metabolism within cells. Hyperpnea, dyspnea, tachycardia, agitation, anxiety, dizziness, headache, confusion, nausea, muscle weakness, and trembling are common. Hypotension, flushing, seizures, and Parkinson-like symptoms may occur among cases of severe intoxication. Coma, apnea, and cardiac dysrhythmias are poor prognostic signs unless prompt treatment is given [49,50]. It should be suspected in every individual with any of the above signs or symptoms for which there is no other obvious cause and a pertinent history such as smoke inhalation victims, victims of industrial accidents in which cyanide could have been released, and victims of terrorist attacks. Blood and urine cyanide concentrations can be obtained, but because these tests are not routinely performed in most laboratories, results take days to return and, therefore, are only be used to confirm the diagnosis. Treatment for this potentially life-threatening poisoning must be initiated immediately based on diagnostic suspicion alone. Arterial and venous blood gases can provide potentially useful information, with a high index of suspicion when the arteriovenous O difference is far less than normal. Because of poor2 cellular extraction and utilization of oxygen, the arterial oxygen tension is usually above 90 mm Hg, whereas venous oxygen tension may be significantly elevated above the normal range of 35 to 45 mm Hg. Similarly, arterial oxygen saturation is typically in the normal range of 95% to 100%, whereas the oxygen saturation of mixed venous blood may be in the vicinity of 85% or greater, significantly higher than the normal range of 60% to 80%. Hydroxocobalamin has no adverse effect on the oxygen-carrying capacity of the red blood cells and no negative impact on the patient’s blood pressure—significant benefits when treating victims of smoke inhalation. The mechanism of action is surprisingly simple: hydroxocobalamin binds to cyanide forming vitamin B12 (cyanocobalamin), a nontoxic compound excreted in the urine. Victims presenting with seizures, hypotension, or a coma in a setting consistent with cyanide toxicity should be considered candidates for empiric administration of hydroxocobalamin 5 g intravenously over 15 minutes through two intravenous or intraosseous lines. The most common adverse reactions (>5%) include transient chromaturia, erythema, rash (predominantly acneiform), hypertension, nausea, headache, decreased lymphocyte percentage, and injection site reactions. Less common allergic reactions include anaphylaxis, chest tightness, angioneurotic edema, and dyspnea. Because of its deep red color, hydroxocobalamin may cause hemodialysis machines to shut down because of an erroneous detection of a “blood leak. Sodium nitrite generates methemoglobin by changing the normal ferrous state of iron in the heme +2 +3 molecule of hemoglobin (Fe ) to the ferric state (Fe ). The adult dose of sodium nitrite is 300 mg in 10 mL of diluent (30 mg per mL) administered intravenously over 2 to 4 minutes, and the pediatric dose is 0. Following the administration of sodium nitrite, sodium thiosulfate should be administered intravenously. The inhalation of amyl nitrite from ampules can be used as a temporizing measure until venous access for the administration of sodium nitrite and sodium thiosulfate is obtained. The inhalation of amyl nitrite should never be considered a substitute for the administration of intravenous sodium nitrite and sodium thiosulfate. These effects are more pronounced in children, the elderly, and in patients with cardiopulmonary diseases. Dose regimen is difficult to control and could even result in exposure of the health care provider to amyl nitrite’s adverse effects. For these reasons, administration of amyl nitrite may be unwarranted, especially because hydroxocobalamin is now available [59]. The administration of sodium bicarbonate should be considered for the treatment of severe lactic acidosis in patients who are unconscious or hemodynamically unstable. Arterial blood gas analysis should be used to guide the need for repeat doses of sodium bicarbonate to ensure that metabolic alkalosis does not develop. Hydrogen Sulfide Pathophysiology Hydrogen sulfide (H S) is a colorless, highly flammable gas that has the2 characteristic odor of “rotten eggs. It’s noxious, “rotten eggs” odor is detectable by smell at low concentrations but may not be detectable at high concentrations or after prolonged exposure because of olfactory fatigue. As such, it can produce a variety of clinical effects, including central nervous system dysfunction [63], cardiac dysrhythmias, and pulmonary edema as a result of acute lung injury. After absorption through the lungs,2 H S easily dissolves in the blood and is rapidly distributed to tissues2 throughout the body. The respiratory system and organs with high oxygen demand, such as the brain and heart, are particularly vulnerable. The severity of clinical signs and symptoms associated with H S2 toxicity depends on the exposure dose. Local irritant effects dominate at low exposure doses, whereas pulmonary edema and life-threatening chemical asphyxiation dominate at higher exposure doses. Clinically detectable eye, mucous membrane, and respiratory tract irritation begin to occur at low exposure doses in the vicinity of 50 parts per million (ppm). Low-dose exposures in the range of 50 to 200 ppm are typically characterized by burning of the eyes, increased lacrimation, sore throat, nausea, cough, and occasional wheezing. Because olfactory function is lost at around 100 to 200 ppm, if exposed individuals can still smell the “rotten eggs” odor of H S, the2 concentration is usually not high enough to cause severe asphyxiation or irritant injury. At exposure concentrations of 200 to 250 ppm, H S2 produces intense irritation of mucous membranes, corneal ulceration, blepharospasm, and dyspnea. Pulmonary edema may occur at these concentrations as a result of irritant-induced acute lung injury [64]. At concentrations greater than 500 ppm, chemical asphyxiation of the brain may produce headache, seizures, delirium, confusion, and lethargy. The central nervous system effects of H S toxicity may be exacerbated by2 hypoxemia secondary to severe pulmonary edema. In survivors, long- term neurologic sequelae, such as ataxia, intention tremor, sensorineural hearing loss, muscle spasticity, and memory impairment, have been reported [61]. Myocardial ischemia, arrhythmias, and dilated cardiomyopathy have all been reported after significant exposures [65,66].

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Prophylaxis and Treatment Drug treatment exploits unique targets in the parasite not found in host cells order prednisone uk. The aminoquinolines purchase on line prednisone, chloroquine 5 mg prednisone overnight delivery, quinine, mefloquine, primaquine, and halofantrine inhibit proteolysis of hemoglobin in the food vacuole and inhibit the heme polymerase that Plasmodium requires for production of malaria pigment. Artemisinin derivatives bind iron in the malarial pigment to produce free radicals that damage parasite proteins. These derivatives are faster-acting than quinine, and they have activity against all stages of the intraerythrocytic life cycle. In recent years, many areas of Africa, northern South America, India, and Southeast Asia have become populated with chloroquine-resistant P. These strains contain an energy-dependent chloroquine efflux mechanism that prevents the drug from concentrating in the parasite. Resistance to mefloquine and halofantrine has also developed, being seen primarily in Southeast Asia. Chemoprophylaxis should start 2 weeks before departure to an endemic area when taking chloroquine and mefloquine, and 1-2 days before travel for atovaquone–proguanil as well as doxycycline. Prophylaxis should be continued for 4 weeks after return if taking chloroquine and mefloquine and for 7 days if taking atovaquone-proguanil or doxycycline. The adult dosage is 300 mg base (500 mg of chloroquine phosphate) orally once per week. In areas of chloroquine-resistance, atovaquone–proguanil (atova-quone 250 mg combined with proguanil 100 mg, the combination tablet is called Malarone) orally once per day, mefloquine 250 mg (228 mg base) orally once per week, or doxycycline 100 mg orally once per day. Mefloquine should be avoided in individuals with psychiatric disorders, seizure disorders, or cardiac conduction abnormalities. Determine if the traveler will be visiting areas with chloroquine-resistant strains (check www. Begin prophylaxis 2 weeks or 1-2 days before travel (depending on the medication). Atovaquone-proguanil, doxycycline, or mefloquine recommended for chloroquine-resistant areas. All individuals without previous immunity who contract falciparum malaria should be hospitalized, because their clinical course can be unpredictable. This agent kills dormant hepatic hypnozoites, preventing their subsequent development into infective schizonts. Before the primaquine is administered, the patient should be tested for glucose-6- phosphate dehydrogenase deficiency, because patients with this deficiency are at risk of severe hemolysis during primaquine treatment. Given the worldwide prevalence of chloroquine resistance, unless absolute assurance can be obtained that travel was only in regions with chloroquine- sensitive P. Artemisinin derivatives have shown superior efficacy for severe chloroquine-resistant P. Their use therefore decreases infectivity after treatment, and can eliminate malaria transmission in endemic areas. The first dose should be followed by a second dose 8 hours later, then 1 dose twice a day for the next 2 days. Artesunates are short-acting, and they should always be combined with one or more other classes of antimalarial agents such as lumefantrine, pyronaridine, atovaquoneproguanil or mefloquine to prevent the development of resistance. Determine whether the traveler came from a chloroquine-resistant area: a) For chloroquine-sensitive strains, use chloroquine. Determine whether the patient is too ill to take oral medicines (requires intravenous quinidine). Determine whether the patient has Plasmodium vivax or ovale (requires primaquine, if not deficient in glucose-6-phosphate dehydrogenase). Refer to Web sites run by health authorities for the most current antimalarial regimens (Table 12. Quinine has a bitter taste and can result in reversible tinnitus and high-frequency hearing loss, hypoglycemia, and cardiac arrhythmias. Mefloquine administration is associated with vertigo (10-20%), gastrointestinal disturbances, seizures, and (less commonly) psychosis. Levels of parasitemia above 5% constitute a medical emergency and require immediate institution of antimalarial treatment. Hematocrit, blood sugar, volume status, cardiac rhythm, renal function, central nervous system function, and arterial oxygenation must all be closely monitored. The severity of organ damage and risk of death correlate with the level of parasitemia. If a patient is too ill to take oral medicines, intravenous quinidine is the treatment of choice. This drug is three to four times more active than is intravenous quinine, and serum levels can be measured. Quinidine gluconate salt 10 mg/kg loading dose (maximum 600 mg) in normal saline should be infused slowly over 1-2 hours, followed by a continuous infusion of 0. Given the rapid changes in malaria resistance patterns and newly reported clinical trials, health care providers should refer to excellent Web sites operated by recognized authorities that outline up-to-date treatment regimens (Table 12. The risk of end-organ damage and death increases with the patient’s level of parasitemia. Levels above 5% constitute a medical emergency, and patients with these levels require intensive treatment. However, patients with levels of parasitemia of greater than 50% have survived without blood exchange. Intravenous steroids have been shown to be harmful in cases of cerebral malaria, and those agents should therefore be avoided. Because of the risk of arrhythmias associated with quinine, quinidine, mefloquine, and halofan–trine, cardiac function should be monitored in patients treated with those agents. How do patients with visceral leishmaniasis usually present clinically, and which diseases can this infection mimic? Prevalence, Epidemiology, and Life Cycle Leishmania has caused major epidemics in eastern India, Bangladesh, and East Africa. A small number of American military personnel contracted leishmaniasis during the Persian Gulf War in 1991 and in Afghanistan more recently. Sandflies breed in cracks in the walls of dwellings, in rubbish, and in rodent burrows. Because they are weak fliers, sandflies remain close to the ground near their breeding sites, resulting in localized pockets of infectious insects. The sandfly bites the infected host and ingests blood containing the nonflagellated form called an amastigote. In the digestive tract of the insect, the amastigote develops into a flagellated spindle-shaped promastigote.

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Calciphylaxis presents with intensely painful indurated erythematous papules order genuine prednisone on-line, plaques and subcutaneous nodules that may develop a livedoid pattern discount 20mg prednisone mastercard. A distal buy cheap prednisone 10 mg on-line, proximal, or mixed distribution may occur, with distal lesions on the lower legs being most common. Proximal presentations involve the upper thighs, buttocks, and lower abdomen, and are associated with a worse prognosis [128,129]. Calcification is seen primarily in the medial layer of arterioles in the subcutaneous fat, associated with endovascular fibrosis, thrombosis, and necrosis of the subcutaneous fat and overlying skin. Laboratory studies addressing causes of hypercoagulability can be helpful as can plain radiographs or technetium 99 bone scans showing vascular calcification. Treatment should be multidisciplinary with involvement of nephrology, dermatology, wound care, pain control, and nutrition. Most sources recommend normalization of calcium and phosphorus levels using diet, binding agents, low-calcium dialysis, and cinacalcet or parathyroidectomy if hyperparathyroidism is present [130]. Precipitating factors such as intravenous infusions, oral calcium supplements, or corticosteroids should be avoided or discontinued. Although the mortality of calciphylaxis is still high at 60% to 80%, it may be changing with more successful therapies [133]. The most characteristic eruption is transient facial erythema involving the malar area and the bridge of the nose that follows sun exposure. The redness, which may be accompanied by edema, lasts between hours and several weeks before resolving without scarring. Erythema and poikiloderma (hyperpigmentation, hypopigmentation, telangiectasia, and atrophy) also occur over other sun-exposed surfaces such as the V neck area of the chest and the back. The presence of Raynaud’s phenomenon, periungual telangiectasias, purplish plaques over the tips of fingers and toes with cold exposure, and persistent erythema over the palms, soles, elbows, knees, or buttocks should prompt a search for systemic disease. Vasculitis involving postcapillary venules in the skin manifests as palpable purpura or hemorrhagic wheals. The presence of livedo reticularis, thrombosis, and cutaneous infarction also warrants consideration of a prothrombotic state. Other connective tissue diseases should be considered in the differential diagnosis of the acute lupus syndrome. Eruptions of lupus localized to the head and neck may be difficult to differentiate from rosacea, dermatomyositis, drug-induced photosensitivity, and sunburn. Strict sun protection along with topical corticosteroids and calcineurin inhibitors are the mainstay of treatment for cutaneous lupus. Antimalarial agents with or without corticosteroids or steroid-sparing immunosuppressants may be required for systemic or severe skin disease [135]. Dermatomyositis Dermatomyositis is a rare disease characterized by a proximal muscle myositis with skin changes. Initial cutaneous manifestations include swelling of the face and eyelids with a characteristic violaceous erythema (heliotrope rash). These changes become more widespread with erythema and telangiectasia spreading to the neck, sun-exposed area of the chest and back in a shawl distribution, as well as to the scalp, elbows, and knees. Gottron’s sign, which consists of scaly reddish papules over the knuckle, is considered pathognomonic of dermatomyositis. Hands may take on the appearance of mechanics’ hands with hyperpigmentation, scaling, fissuring of the fingertips, ragged cuticles, and enlarged proximal nail fold capillaries. Aggressive treatment at an early stage allows for better disease control with lower immunosuppression. Early treatment also reduces the development of disfiguring calcium deposition in the skin and muscle. Initial treatment of skin disease includes sunscreens with topical corticosteroids or calcineurin inhibitors, but resistant skin disease may require methotrexate or antimalarials. With appropriate and timely therapy, patients may become disease-free and off therapy within 2 to 4 years. Of note, patients should be surveyed for an occult visceral malignancy which is associated with dermatomyositis in up to 25% of adult cases. Poor prognostic factors include malignancy, older age, initiating therapy after 24 months of muscle weakness, extensive cutaneous lesions, dysphagia, and cardiac or pulmonary disease [137]. A discussion of myositis and systemic disease associated with dermatomyositis is detailed in Chapter 66. First, recipient tissue damage from conditioning regimens leads to inflammatory cytokines, this activates donor lymphocytes, and finally, alloreactive T cells expand into cytotoxic T cells [139]. Skin findings begin with painful or pruritic erythematous macules which can arise on the palms, soles, and ears, and evolve into a diffuse morbilliform eruption which is often folliculocentric. Histopathology of involved skin classically shows an interface dermatitis and apoptotic keratinocytes. The lichenoid variant is characterized by erythematous and violaceous papules and plaques, often distributed on flexural surfaces that resemble lichen planus. The sclerodermoid form presents with sclerotic, indurated white to yellow plaques that involve the dermis. The oral mucosa is often involved and may demonstrate redness and atrophy of mucosal surfaces, lacy white reticulations of buccal mucosa, and ulcerations. A furuncle represents an abscess associated with a hair follicle and a carbuncle is a collection of multiple furuncles. The clinical presentation consists of a small red papule that evolves into a tender, erythematous deep-seated nodule that may become fluctuant. The differential diagnosis includes an inflamed epidermal inclusion cyst, hidradenitis suppurativa, and arthropod bite. Infectious folliculitis is usually caused by staphylococci, Pseudomonas, or Malassezia furfur, whereas noninfectious folliculitis is the result of trauma to or occlusion of the pilosebaceous unit. The lesions may be pruritic and are most often found on the face, scalp, thighs, axillae, and inguinal area. Pseudomonal folliculitis may be more inflammatory and localized to a distribution that would be covered by a bathing suit. Pityrosporum folliculitis may be localized to the upper back and chest and be extremely pruritic [146]. Most cases will respond to appropriate topical and/or oral antibiotics (most commonly anti-staphylococcal). Pityrosporum folliculitis requires topical or oral antifungals and pseudomonal folliculitis is often self-limited, but may require fluoroquinolones in immunosuppressed patients. Peripheral Edema Peripheral edema, which is commonly seen among elderly and hospitalized patients, occurs when capillary hydrostatic pressure and filtration exceeds the lymphatic drainage rate. Common causes of edema include heart failure, renal failure, nephrotic syndrome, cirrhosis, venous thrombosis, or medications, particularly calcium channel blockers. Acute exacerbations of chronic edema may cause edema blisters which present as asymptomatic, noninflammatory tense vesicles and bullae with clear fluid, usually on the distal lower extremities.

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