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A 71-year-old woman presents with 1 day of headache and left-sided weakness after complaining for several days of dyspnea and confusion. Her history is notable for non-valvular atrial fibrillation and hypertension; she denies any prior history of thrombosis or bleeding. Her medications include a beta-blocker and warfarin (coumadin). Examination is notable for partial left hemiplegia; ecchymoses are noted over both forearms. The remainder of the examination demonstrates rales over both lung bases, an irregularly irregular heart rhythm, and a heave at the left sternal border.

CBC: Hemoglobin/hematocrit - 12 g/dL/35%

MCV - 89 fL  MCH - 30 pg  MCHC - 27 g/dL

RDW-CV - 10%  WBC count 6,500/μL

Platelet count - 225,000/μL

PT = 55.1 seconds (<14 seconds)

INR = 7.1 (<1.3)

PTT = 39 seconds (22–35 seconds)

  • Do the screening coagulation test results point to a specific cause for a bleeding tendency in this patient?

  • Are additional studies warranted for diagnosis or determining therapy?

An abnormality in the extrinsic or common pathways can result in a significant bleeding tendency. Inherited deficiencies of a single coagulation factor, including factors VII, V, X, and prothrombin, are rare. More commonly, bleeding results from acquired deficiencies in several factors. This reflects the fact that most vitamin K–dependent factors are produced by the liver, so liver disease or vitamin K deficiency (from any of multiple causes) can be expected to produce a multifactor abnormality.


Interactions of the factors involved in the extrinsic and common pathways are illustrated in Figures 34-1 and 34-2. The extrinsic pathway begins with circulating activated factor VII (VIIa) combining with tissue factor (TF) that is derived from damaged tissues or expressed on activated monocytes. In the presence of tissue factor, VIIa provides a potent stimulus for the activation of factor X to Xa. This is the pathway that initiates physiologic hemostasis, generating small amounts of thrombin, which then feeds back to activate the intrinsic coagulation factors and subsequently generate higher thrombin levels. The tissue factor-VIIa-Xa complex is rapidly inhibited by tissue factor pathway inhibitor (TFPI); thus, further factor X activation and adhesive fibrin formation depend on the intrinsic pathway, which explains the severity of hemophilia A (factor VIII deficiency) and hemophilia B (IX deficiency; see Chapter 33).


The extrinsic pathway. The extrinsic pathway (and physiologic hemostasis) is initiated by release of microsomal lipoproteins (tissue factor) from damaged tissue. This tissue factor (TF) combines with the normal small amounts of circulating activated factor VII (VIIa) to activate factors X and IX.


The common pathway. Both the intrinsic and extrinsic pathways lead to activation of the common pathway. Factor X is activated to Xa, which then stimulates the conversion of prothrombin to thrombin, facilitated by the presence of phospholipid ...

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