The patient demonstrates several risk factors for thrombosis, including oral contraceptive use, a recent long airplane trip (venous stasis), and a presumptive family history of an inherited thrombophilia (father is on anticoagulation therapy)

The patient demonstrates several risk factors for thrombosis, including oral contraceptive use, a recent long airplane trip (venous stasis), and a presumptive family history of an inherited thrombophilia (father is on anticoagulation therapy). This will require further testing but not as a prerequisite to beginning appropriate therapy. Based on the radiological studies, the patient has a deep vein thrombosis and bilateral pulmonary emboli with significant clot burden in her lungs to lower her arterial 02 saturation. She is therefore a potential candidate for thrombolysis, especially in light of her presenting within 3 days of developing symptoms and the absence of comorbid conditions that would increase her risk of bleeding. Following thrombolysis, she will need to be anticoagulated, beginning with heparin, and then transitioned to warfarin therapy with an INR target of 2-3 for a prolonged period (>6 months). A search for other underlying thrombophilic defects is warranted in a young patient like this one. Without specific symptoms, an extensive workup for an occult mal ignancy is not efficacious. However, testing for an inherited/metabolic defect is in order. Therefore, a battery of coagulation tests needs to be sent from the emergency room, prior to thrombolysis/anticoagulation, including tests for APC resistance (APC-R/factorV Leiden), prothrombin G202 / OA mutation, a lupus anticoagulant, and AT, protein C, and protein S levels. This patient's results are as follows: Prothrombin G202 / 0 mutation – not detected AT = 65% (SO'Yo- 1 20%) Protein C = 60% (?O'Yo- 1 40%) Protein S = 35% (50'Yo- 1 50%) APC-R = 1 .80 (>2.20) dRVVT = 1 .22 (< 1=”” .20)=”” these=”” coagulation=”” panel=”” results=”” point=”” out=”” the=”” difficulty=”” in=”” evaluating=”” studies=”” drawn=”” during=”” an=”” acute=”” thrombosis=”” episode.=”” aii=”” of=”” the=”” natural=”” anticoagulants-at,=”” protein=”” c,=”” and=”” protein=”” s-are=”” sl=”” ghtly=”” lower=”” than=”” the=”” normal=”” range,=”” a=”” finding=”” that=”” is=”” common=”” due=”” to=”” consumption=”” of=”” factors=”” with=”” an=”” acute=”” clot.=”” when=”” repeated=”” once=”” the=”” patient=”” finished=”” her=”” anticoagulation,=”” they=”” are=”” found=”” to=”” be=”” normal.=”” similarly,=”” testing=”” for=”” the=”” lupus=”” anticoagulant=”” with=”” the=”” dilute=”” rvvt=”” can=”” also=”” be=”” affected=”” by=”” acute=”” stress=”” or=”” thrombosis.=”” the=”” most=”” common=”” inherited=”” causes=”” of=”” thrombophilia=”” are=”” the=”” factor=”” v=”” lei=”” den=”” and=”” prothrombin=”” 20210=”” mutations;=”” the=”” latter=”” was=”” not=”” detected=”” in=”” this=”” patient,=”” but=”” the=”” screening=”” apc-resistance=”” test=”” for=”” leiden=”” was=”” abnormal.=”” unlike=”” the=”” natural=”” anticoagulant=”” activities,=”” apc-r=”” is=”” not=”” affected=”” by=”” acute=”” thrombosis=”” or=”” anticoagulation.=”” when=”” the=”” apc-r=”” result=”” was=”” confirmed=”” by=”” mutational=”” analysis,=”” the=”” patient=”” was=”” found=”” to=”” be=”” heterozygous=”” for=”” the=”” v=”” lei=”” den=”” mutation,=”” as=”” was=”” her=”” father=”” on=”” subsequent=”” analysis.=”” the=”” heterozygous=”” v=”” leiden=”” mutation,=”” by=”” itself,=”” does=”” not=”” increase=”” the=”” incidence=”” of=”” recurrent=”” thrombosis=”” in=”” otherwise=”” healthy=”” individuals.=”” therefore,=”” the=”” duration=”” of=”” her=”” anticoagulation=”” need=”” not=”” be=”” extended=”” and=”” lifelong=”” therapy=”” is=”” not=””>

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Based on smear morphology and the red blood cell indices (mean cell volume [MCV], mean cell hemoglobin [MCH], mean corpuscular hemoglobin concentration [MCHC]), the patient has a severe microcytic, hypochromic anemia most likely caused by iron deficiency (see Chapter 5).

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Given the diagnosis of HHT, how should this patient be managed?

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