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3 complications of hemophilia the severity of bleeding associated with hemophilia correlates with the degree of factor viii or factor ix deficiency as measured against the normal plasma standard. Table 67–1 summarizes the age at onset and laboratory and clinical manifestations of hemophilia a and b. 4 1003 1004  section 14  |  hematologic disorders treatment intrinsic pathway »» pk hk xii xiia hk xi xia ix extrinsic pathway ixa viia tf viiia x xa x va prothrombin xiii thrombin xiiia fibrinogen fibrin cross-linked fibrin figure 67–1. Cascade model of coagulation demonstrates activation via the intrinsic or extrinsic pathway. This model shows successive activation of coagulation factors proceeding from the top to the bottom where thrombin and fibrin are generated.

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Patients typically present with a sensation of chest pressure or heaviness that is provoked by exertion and relieved with rest or sublingual nitroglycerin. Chronotropic. Pertaining to the heart rate. Chvostek sign. Noted when a tap on the patient’s facial nerve adjacent to the ear produces a brief contraction of the upper lip, nose or side of the face. Chylothorax. The presence of lymphatic fluid (chyle) in the pleural cavity. Circadian rhythm. 24-hour cycles of behavior and physiology that are generated by endogenous biologic clocks (pacemakers). Circulatory shock. A condition wherein the circulatory system is inadequately supplying the oxygen and vital metabolic substrates to cells throughout the body. Cirrhosis. Hepatic fibrosis and regenerative nodules that have destroyed the architecture of the liver, scarring the liver tissues. Progressive scarring of the liver resulting in nonfunctional hepatocytes. Clonal expansion. An immunologic response in which lymphocytes stimulated by antigen proliferate and amplify the population of relevant cells. Closed comedo. A plugged hair follicle of sebum, keratinocytes, and bacteria that remains beneath the surface of the skin. Also referred to as a “whitehead. ” clotting cascade. A series of enzymatic reactions by clotting factors leading to the formation of a blood clot. The clotting cascade is initiated by several thrombogenic substances. Each reaction in the cascade is triggered by the preceding one and the effect is amplified by positive feedback loops. Clotting factor. Plasma proteins found in the blood that are essential to the formation of blood clots.

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5) norethindrone (1) ee (35) ethynodiol diacetate (1) ee (50) norgestrel (0. 5) ee (50) ethynodiol diacetate (1) mestranol (50) norethindrone (1) biphasic preparations ee (10) norethindrone acetate (1,0) ee (20,0,10) desogestrel (0. 15) ee (35) norethindrone (0. 5,1) triphasic preparations ee (20,30,35) northindrone acetate (1) ee (30,40,30) levonorgestrel (0. 05,0. 075,0. 125) ee (35) norgestimate (0. 18,0. 215,0. 25) ee (35) norethindrone (0. 5,1,0. 5) ee (35) norethindrone (0. 5,0. 75,1) ee (25) norgestimate (0. 18,0. 215,0. 25) ee (25) desogestrel (0. 1,0. 125,0. 15) quadriphasic preparations estradiol valerate dienogest (0,2,3,0) (3,2,2,1) extended cycle preparations ee (20) levonorgestrel (0. 09) ee (20) levonorgestrel (0. 1) ee (30) levonorgestrel (0. 15) ee (20,25,30,10) levonorgestrel (0.

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The nomenclature for dmards was proposed by an international leader price of viagra at costco canada in rheumatology to distinguish the different types of dmards. Figures 57–1 and 57–2 outline the course of treatment for adult ra according to the acr 2012 recommendations. 19 the recommendations are based on the disease activity level, presence or absence of poor prognostic features, and duration of disease activity (early vs established). Figure 57–1 applies to patients who have had ra for less than 6 months. Csdmard monotherapy includes hydroxychloroquine, leflunomide, methotrexate, minocycline, or sulfasalazine. Examples of combination therapy for patients with moderate or high disease activity with evidence of poor prognostic features are methotrexate/hydroxychloroquine, methotrexate/sulfasalazine, or methotrexate/ sulfasalazine/hydroxychloroquine. Figure 57–2 outlines the course of treatment for patients with established ra (disease duration 6 months or longer). Bodmards are usually considered in patients with established ra following inadequate response to csdmards. Figure 57–2 establishes a progression for switching from one agent to another in a patient who experiences an inadequate response or adverse event. Because of treatment expense, bodmards should be considered only in patients who have no limitations due to cost or insurance coverage. There is no evidence that the benefits of combination bodmard therapy outweigh the potential risks, especially the increased risk of infections. Nonpharmacologic therapy all patients should receive education about the nonpharmacologic and pharmacologic measures to help manage ra and jia. Empowered patients take an active role in care by participating in therapy-related decisions. Certain forms of nonpharmacologic therapy benefit all levels of severity, whereas others (ie, surgery) are reserved for severe cases only. Early ra low disease activitya high moderate target. Low disease activity or remission without dmard monotherapy features of poor prognosis with combination dmard therapy (double and triple therapy)b without features of poor prognosis dmard monotherapy or hcq and mtx with anti-tnf with or without mtx or combination dmard therapy (double and triple therapy)b figure 57–1. Recommendations for the treatment of early ra (disease duration < 6 months). Dmard, disease-modifying antirheumatic drug (in this figure, “dmard” refers to conventional synthetic dmards or csdmards). Asee ref. 19 for definitions of disease activity. Bcombination dmard therapy. Methotrexate + leflunomide, methotrexate + hydroxychloroquine, methotrexate + sulfasalazine, sulfasalazine + hydroxychloroquine. Triple dmard therapy. Methotrexate + hydroxychloroquine + sulfasalazine. (reproduced, with permission, from singh ja, furst de, bharat a, et al. 2012 update of the 2008 american college of rheumatology recommendations for the use of disease-modifying antirheumatic drugs and biologic agents in the treatment of rheumatoid arthritis. Arthritis care res.