Thrombosis & Hemostasis Flashcards
PT and PTT are used to detect disorders of secondary hemostasis. What is the difference between the 2 measures?
PT measures extrinsic pathway — normal: 10-13 seconds
PTT measures intrinsic pathway — normal: 25-40 seconds
Causes of prolonged PT
Warfarin or dicoumarol use
Deficiencies of factor II, V, VII, X
Vitamin K deficiency
Fibrinogen deficiency
Liver disease
Causes of PTT prolongation
Heparin
Lupus anticoagulant (predisposes to thrombosis)
Vonwillebrand disease
Deficiencies in factors VIII, IX, XI, or XII
Causes of prolongation of both PT and PTT
Supratherapeutic dose of heparin or warfarin
DIC (PT prolonged first)
Liver disease
Factor V or X deficiency
Prothrombin or fibrinogen deficiency
Direct thrombin inhibitor
Thrombin time tests the rate of conversion of ____
Fibrinogen—>fibrin
Causes of prolonged thrombin time
Heparin
Direct thrombin inhibitor
Factor Xa inhibitor
Fibrin degradation product
Hypo- or dysfibrogenemia
Platelet aggregation studies are important in determining platelet abnormalities when platelet count is normal. The most common abnormality is seen in pts who have taken ___ or ____ due to impaired arachidonate metabolism
ASA; NSAIDs
Platelet aggregation studies assist in dx of vonwillebrand disease, storage pool disease, bernard-soulier disease, and other congenital plt d/o. In addition, what defects in platelet function are associated with uremia, dysproteinemia, and autoimmune d/o?
Uremia — impaired platelet adhesion
Dysproteinemias — interference w/platelet membrane function
Autoimmune d/o — multiple abnormalities
_____ levels are used to identify excessive fibrinolysis
_____ may be more specific than PTT-related testing and is used when antiphospholipid syndrome is suspected
Fibrinogen
DRVVT (dilute russell viper venoma time)
Presentation of hemophilia
Typically presents in childhood w/ muscle hematomas, hemarthrosis, and persistent delayed bleeding after trauma or surgery
What are target joints?
Joints which have recurrent bleeds; typically associated with hemophilias
Inheritence and deficiency associated with Hemophilia A and B
Both are X-linked
Hemophilia A = factor VIII deficiency
Hemophilia B = factor IX deficiency
Assessing factor VIII and IX levels is indicated in any male who presents with a prolonged ____ that corrects with a mixing study
aPTT
Treatment for hemophilia A or B
Factor VIII and IX deficiencies are treated w/factor replacement (recombinant or purified)
FFP is a diluted source of clotting factors with limited efficacy for high-level replacement
Describe testing for pts suspected of having vonwillebrand disease
Includes platelet function analysis (PFA), vWF antigen level, vWF activity assay, factor VIII level, and multimer study
[note: PFA and factor VIII level may be normal in mild cases]
Lab results in vonwillebrand disease concerning PT/INR, aPTT, TT, fibrinogen, D-dimer, platelet count, PFA, platelet aggregation tests, blood smear
Normal PT/INR
Normal or increased aPTT (dependent on factor VIII activity)
Normal TT, fibrinogen, D-dimer, and platelet count
PFA increased
Platelet aggregation tests are abnormal (esp to ristocetin)
Normal blood smear
Most common inherited bleeding disorder
VonWillebrand disease
Inheritance and presentation of vonwillebrand disease
Autosomal dominant
Presents w/mild to moderate bleeding evidenced by epistaxis, menorrhagia, gingival bleeding, easy bruising, and bleeding associated with surgery or trauma
General management strategies for pts with von willebrand disease
Desmopressin (DDAVP) — releases stored vWF and factor VIII from endothelial cells
Intermediate purity factor VIII concentrates — contain vWF
Cryoprecipitate — rich in vWF but risk of transfusion-transmitted infection
Testing for pts suspected of having bleeding from advanced liver disease includes PT/INR, aPTT, mixing study, TT, fibrinogen, D-dimer, platelet count, and PFA. What are the results of these tests in the case of advanced liver disease?
Prolonged PT/INR and aPTT — corrects with mixing study
TT and D-dimer increased
Fibrinogen decreased
Platelet count decreased; PFA normal or increased
[note: PT is sensitive indicator of hepatic synthetic function d/t short half life of factor VII (6 hrs), which a failing liver cannot maintain]
General management for pts with bleeding from advanced liver disease
FFP transiently replaces all coag factors but is short-lived
Cryoprecipitate is useful if fibrinogen level is <100 mg/dL
DIC is a disorder of primary and secondary hemostasis, involving widespread activation of coagulation that leads to formation of fibrin clots. Secondary fibrinolysis dissolves these fibrin clots leading to consumption of platelets and coag factors —> thrombocytopenia, clotting factor deficiencies, bleeding, and vascular injury. What are conditions associated with the development of DIC?
Infection — most commonly gram-negative sepsis but can occur with gram-positive or viral infections (i.e., HIV)
Cancer — usually mucin-producing adenocarcinomas
Obstetric complications
How would the following typically be expected to change in the setting of DIC?
PT/INR and aPTT Thrombin time Fibrinogen D-dimer Platelet count PFA Blood smear
Prolonged PT/INR and aPTT — corrects with mixing study
Prolonged TT
Decreased fibrinogen
Increased D-dimer
Decreased platelet count
Increased PFA
Schistocytes on PB
General treatment strategies for DIC
Correct the underlying cause
Pts may require FFP/cryoprecipitate to replace coag factors, or transfusion of platelets or erythrocytes
Antithrombin III is occasionally useful
Generalized d/o of microcirculation characterized by thrombocytopenic purpura, microangiopathic hemolytic anemia, fluctuating neurological signs, renal dysfunction, and fever
TTP
2 major forms of TTP
Hereditary — mutation of ADAMSTS13 gene
Acquired — autoantibodies to ADAMSTS13
Clinical features of TTP and HUS
TTP: MAHA + thrombocytopenia (<50,000) + fever + neuro sxs
Add renal failure = HUS
Pathologic lesion and peripheral blood smear finding associated with TTP
Pathologic lesion = hyaline thrombi which occlude capillaries of virtually every organ in body
PB shows schistocytes (helmet cells) d/t MAHA — “Waring blender effect”
Treatment plan for TTP
Treat causative d/o
Plasmapheresis is lifesaving in ~100%
What are the vitamin-K dependent coag factors and how does deficiency present?
Deficiency of factors II, VII, IX, X, protein C and S
Presents with bleeding and prolonged PT
Autosomal dominant condition d/t defects in gene encoding endoglin (CD105) on Chr 9 leading to thinning of vessel walls w/telangiectatic formations, AV malformations, and aneurysmal dilatations throughout the body
Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)
Clinical features of hereditary hemorrhagic telangiectasia
Telangiectasias and bleeding (epistaxis is most frequent symptom)
Usually a benign clinical course
Pathophysiology of thromboembolic risk in pts with Factor V leiden mutation
Factor V leiden mutation leads to resistance to activated protein C
Thus protein C is unable to inactivate factor V and VIII —> unregulated prothrombin activation
Heterozygous Factor V leiden mutation leads to 7x increased lifetime risk for VTE, while homozygous risk increases 20-80%. Prothrombin 20210 mutations are treated similarly to Factor V Leiden mutations. How are these conditions treated?
If no prior episodes — monitor; consider DVT prophylaxis and risk reduction
If prior episodes — consider lifelong anticoagulant therapy
Pathophysiology of thromboembolic risk in pts with prothrombin gene mutation
G-A mutation in prothrombin gene at position G20210 —> increased levels of prothrombin —> excess thrombin formation
Increases VTE risk 3-4x
Inheritance and pathophysiology of thromboembolic risk in pts with protein C deficiency
Autosomal recessive
Protein C normally inactivates factors VIII and V. Thus, increased factor VIII and V levels —> increased production of prothrombin, fibrinogen and eventual fibrin clots
______ has a half life of 6 hrs and decreases to low levels shortly after starting therapy; it is associated with the cause of warfarin-induced skin necrosis in some pts
Protein C
Inheritance and pathophysiology of thromboembolic risk in pts with protein S deficiency
Autosomal dominant (RARE!)
Protein S is a cofactor of protein C, so decreased levels —> less protein C activity —> increased fibrin formation
Treatment for proteins C and S deficiency
Warfarin
[note: the most common cause of hypercoagulable state d/t S and C deficiency is initiation of warfarin therapy — since S and C are depleted prior to any other factors resulting in temporary increase in coagulability]
Inheritance and pathophysiology of thromboembolic risk in pts with antithrombin III deficiency
Autosomal dominant
Antithrombin normally decreases production of factors X and II (prothrombin). Thus, increased factor X and II levels —> increased production of fibrinogen and fibrin clots
________ deficiency should be suspected in a pt whose clot does not respond to heparin therapy, since heparin requires its presence
Antithrombin III
Clinical presentation of antithrombin III deficiency
Varies from minimal symptoms to early death from recurrent PE
Recurrent LE thrombophlebitis and DVT, venous insufficiency, and chronic leg ulcers
Significantly increased risk in pregnancy
Dx by demonstrating diminished levels of AT-III in serum (<50% of normal activity)
Treatment for antithrombin III deficiency
Prophylaxis w/anticoagulants
Pts with DVT should receive heparin, but much higher doses are required
AT-III replacement for those with DVT unresponsive to heparin
The American College of Chest Physicians recommends discontinuing anticoagulant therapy after 3-6 months in a pt with factor V leiden or prothrombin G20210A mutation, but advise extending therapy (1 year to lifetime) only in those with what other conditions?
Active cancer
Persistently elevated anticardiolipin antibodies
Antithrombin deficiency
Most common form of acquired thrombophilia caused by development of antibodies to plasma proteins bound to phospholipids —> disruption of normal coagulation and an increased risk of thrombosis
Antiphospholipid antibody syndrome
Presentation of antiphospholipid antibody syndrome
Can present w/one or more arterial or venous thrombosis in any tissue or organ, thrombocytopenia, cerebral ischemia and recurrent strokes (esp. in young pts), recurrent miscarriages, or premature births
Associated clinical features/conditions with antiphospholipid Ab syndrome
Connective tissue disease in 50%
Valvular heart disease and/or coronary artery disease in some
3 tests used in dx of antiphospholipid Ab syndrome
- Prolonged PTT (or DRVVT)
- Lack of correction in mixing studies using normal plasma
- Neutralization of inhibitor with excess phospholipid
[Note: multiple positive tests over 3-12 month period required to make dx]
What are some Abs that may be found in association with antiphospholipid antibody syndrome?
Anticardiolipin Abs — react w/proteins associated with cardiolipin; also responsible for false positive syphilis test
Lupus anticoagulants — antiphospholipid Abs that, when bound to their target proteins, prolong clotting times (such as PT and aPTT) — despite prolonged clotting time, these Abs are thrombophilic
Anti-B2M Abs — prevent normal B2M inhibition of coagulation and platelet aggregation
Describe results of mixing study in which pts with antiphospholipid Ab syndrome (w/lupus anticoagulant) have their plasma mixed with plasma containing all normal clotting factors
Because lupus anticoagulants act as inhibitors, PT and aPTT do NOT correct when mixing study is performed
Outline management plan for pts with antiphospholipid Ab syndrome and/or lupus anticoagulant
No benefit of anticoagulant therapy in those without hx of thromboembolic disease
For those with a hx — consider lifelong anticoagulation
Anticoagulate during pregnancy w/ SC heparin
Hydroxychloroquine may help reduce thromboembolism in pts with APS and SLE
Pathophysiology of thromboembolic risk in pts with heparin-induced thrombocytopenia (HIT)
Type 1 — occurs rapidly after onset of therapy and self-resolves (sometimes despite continuing therapy); most likely d/t direct platelet-aggregating effect of heparin
Type 2 — occurs 5-14 days after onset of therapy and parodoxically leads to venous and arterial thromboses; caused by Abs that recognize heparin complexed to platelet factor 4 — binding leads to platelet activation and thrombosis, even in the setting of thrombocytopenia
Four T’s score to assess risk for having HIT
Thrombocytopenia — platelet count <50% AND platelet nadir >20 = +2; platelet count 30-50% OR platelet nadir 10-19 = +1; platelet count fall<30% OR platelet nadir <10 = 0
Timing of platelet count fall — clear onset between days 5-10 or <1 day (prior heparin exposure w/i 30 days) = +2; consistent with days 5-10 but not clear onset OR onset after day 10 OR fall <1 day (prior exposure 30-100 days ago) = +1; platelet count fall <4 days w/o recent exposure = 0
Thrombosis or other sequelae — new thrombosis OR skin necrosis, acute systemic post-IV reaction = +2; progressive or recurrent thrombosis, non-necrotizing skin lesions, suspected thrombosis = +1; none = 0
Other causes for thrombocytopenia — none = +2, possible = +1, definite = 0
Score: <3 points is low probability, 4-5 points is intermediate probability, and 6-8 points is high probability for HIT
Describe testing for pts suspected of having HIT
Heparin-PF4 antibody testing
Functional HIT antibody tests like heparin-induced platelet aggregation (HIPA), serotonin-release assay SRA), and flow cytometric assays that detect platelet microparticle release
Management approach for anticoagulation in pt with HIT
Discontinue heparin promptly
Direct thrombin inhibitor such as lepirudin or argabotran may be used for tx of thromboses
Fondaparinux also effective
DO NOT use LMWH
17 y/o F presents c/o easy bruising. She has petechiae on her shins. She reports being sick with a URI 4 weeks ago. She is not on any medications. The best explanation for her physical findings is:
A. Decreased serum fibrinogen B. Decreased levels of factor VII C. Decreased platelet functionality D. Elevated plasminogen activator E. Decreased platelet numbers
E. Decreased platelet numbers
[most likely dx is Immune thrombocytopenia (ITP)]
17 y/o F presents c/o easy bruising. She has petechiae on her shins. She reports being sick with a URI 4 weeks ago. She is not on any medications. The best explanation for her physical findings is:
A. Medication-related suppression of platelet production B. Defective or deficient ADAMTS13 C. Platelet clumping D. Use of NSAIDs E. Ab interaction with platelet surface
E. Ab interaction with platelet surface
17 y/o F presents c/o easy bruising. She has petechiae on her shins. She reports being sick with a URI 4 weeks ago. She is not on any medications. The best explanation for her physical findings is ITP. Her CBC should demonstrate:
A. WBC count of 1500/cc
B. Hb of 7.2 g/dL
C. An absolute eosinophil count of 1200/cc
D. A platelet count of 35,000/cc
E. An absolute lymphocyte count of 10,000/cc
D. A platelet count of 35,000/cc
17 y/o F presents c/o easy bruising. She has petechiae on her shins. She reports being sick with a URI 4 weeks ago. She is not on any medications. The best explanation for her physical findings is immune thrombocytopenia. She should be treated with
A. Vincristine 2 mg IVP B. IV immune globulin C. Hydroxyurea 10 mg/kg/day D. Plasmapheresis E. Observation
E. Observation
71 y/o F w/ 4 day hx of progressive fatigue and malaise. She is critically ill in the ICU, intubated, on vasopressors, febrile at 102.6; N/G tube is draining coffee-ground material. Her labs indicate WBC 28.6, 69% segs, 18% bands, 12% lymphs, 2% monos, Hb/Hct 10.6/32; plts 42K. Na 132, K 3.8, Cl 105, CO2 19; Alb 2.8, ALT/AST normal; T.bili 1.3; BUN 55/Cr 1.4. PT 17.8, PTT 45.
Based on her clinical findings she most likely has:
A. ITP B. DIC C. TTP D. HELLP E. Pseudothrombocytopenia
B. DIC
[clinical findings also indicate metabolic acidosis, and prerenal kidney injury likely d/t GI bleed]
71 y/o F w/ 4 day hx of progressive fatigue and malaise. She is critically ill in the ICU, intubated, on vasopressors, febrile at 102.6; N/G tube is draining coffee-ground material. Her labs indicate WBC 28.6, 69% segs, 18% bands, 12% lymphs, 2% monos, Hb/Hct 10.6/32; plts 42K. Na 132, K 3.8, Cl 105, CO2 19; Alb 2.8, ALT/AST normal; T.bili 1.3; BUN 55/Cr 1.4. PT 17.8, PTT 45. Her clinical findings suggest DIC.
She should be managed by:
A. Blood product support alone B. Correction of the underlying problem C. Repeat labs in heparin or citrate tubes D. Plasmapheresis E. IVIG
B. Correction of the underlying problem
16 y/o F presents with easy bruisability, epistaxis, and menometrorrhagia. Her exam demonstrates lightly ecchymotic areas over the arms and legs, no petechiae or purpura; no hemarthrosis. CBC demonstrates WBC 9.4 w/ 71% segs, 27% lymphs, 2% monos, Hb/Hct 11.9/36; plts 102K. She most likely has
A. DIC B. Qualitative platelet d/o C. TTP D. Adenocarcinoma of the uterus E. Hemophilia
B. Qualitative platelet d/o
[Note: menometrorrhagia = heavy menses occurring frequently]
16 y/o F presents with easy bruisability, epistaxis, and menometrorrhagia. Her exam demonstrates lightly ecchymotic areas over the arms and legs, no petechiae or purpura; no hemarthrosis. CBC demonstrates WBC 9.4 w/ 71% segs, 27% lymphs, 2% monos, Hb/Hct 11.9/36; plts 102K. She most likely has a qualitative platelet disorder.
Peripheral smear exam will likely show
A. Fragmented RBCs and diminished numbers of normal-appearing platelets B. Agranular platelets C. Microplatelets D. Cabot rings E. Giant platelets
E. Giant platelets
[agranular platelets would be gray platelet syndrome; giant platelets seen in bernard soulier]
16 y/o F presents with easy bruisability, epistaxis, and menometrorrhagia. Her exam demonstrates lightly ecchymotic areas over the arms and legs, no petechiae or purpura; no hemarthrosis. CBC demonstrates WBC 9.4 w/ 71% segs, 27% lymphs, 2% monos, Hb/Hct 11.9/36; plts 102K. She most likely has a qualitative platelet disorder. Platelet aggregation studies reveal absent aggregation to ristocetin, normal aggregation to ADP, collagen, arachidonic acid, epinephrine.
The dx is:
A. Hermansky-Pudlak syndrome B. Chediak-Higashi syndrome C. Glanzmann thrombasthenia D. Bernard-Soulier syndrome E. Gray platelet syndrome
D. Bernard-Soulier syndrome
[ristocetin is Gp1b]
67 y/o M w/bleeding from multiple sites. PMH includes cirrhosis secondary to Hepatitis C for which he declined therapy. There is also a hx of alcohol abuse for many years. He is in the ICU with ecchymoses over the trunk and extremities. He has anasarca and coffee-ground material in his NG tube.
His labs would likely show
A. Platelet count of 675,000/cc B. Hb 15 g/dL C. PT 17 sec D. Bilirubin 0.4 IU/dL E. PTT 20 sec
C. PT 17 sec
67 y/o M w/bleeding from multiple sites. PMH includes cirrhosis secondary to Hepatitis C for which he declined therapy. There is also a hx of alcohol abuse for many years. He is in the ICU with ecchymoses over the trunk and extremities. He has anasarca and coffee-ground material in his NG tube. His GI bleeding is exacerbated by:
A. NG suction B. Coagulopathy C. Erythrocytosis D. Obstructive jaundice E. PNH
B. Coagulopathy
[PNH is complement-mediated hemolysis]
67 y/o M w/bleeding from multiple sites. PMH includes cirrhosis secondary to Hepatitis C for which he declined therapy. There is also a hx of alcohol abuse for many years. He is in the ICU with ecchymoses over the trunk and extremities. He has anasarca and coffee-ground material in his NG tube. His GI bleeding might be minimized with the use of:
A. Eculizumab B. Plasmapheresis C. Platelet transfusion D. FFP E. Fondaparinux
D. FFP
[eculizumab is used for PNH; fondaparinux is an anticoagulant]
31 y/o F c/o menometrorrhagia and recurrent epistaxis. She also complains of low energy. Recent labs demonstrated iron deficiency anemia and she is taking oral ferrous sulfate. She notes easy bruising and relates a family hx of similar complaints. She most likely has
A. Hx of substance abuse B. Hx of abusive relationship C. Acquired coagulopathy D. Hereditary coagulopathy E. Bleeding secondary to medications
D. Hereditary coagulopathy
31 y/o F c/o menometrorrhagia and recurrent epistaxis. She also complains of low energy. Recent labs demonstrated iron deficiency anemia and she is taking oral ferrous sulfate. She notes easy bruising and relates a family hx of similar complaints. She most likely has a hereditary coagulopathy. Her CBC is normal. The best test(s) to evaluate further include:
A. PT B. PTT C. PT and PTT D. PT and TT E. Platelet aggregation studies
C. PT and PTT
[normal CBC eliminates possibility of thrombocytopenia]
31 y/o F c/o menometrorrhagia and recurrent epistaxis. She also complains of low energy. Recent labs demonstrated iron deficiency anemia and she is taking oral ferrous sulfate. She notes easy bruising and relates a family hx of similar complaints. She most likely has a hereditary coagulopathy. CBC is normal. PT is normal, but PTT is mildly prolonged at 44 sec. The best test(s) to evaluate further include:
A. Mixing studies B. Dilute Russell Viper Venom Time (DRVVT) C. Thrombin time D. Reptilase time E. Bleeding time
A. Mixing studies
[DRVVT used to look for lupus anticoagulant antiphospholipid antibodies]
31 y/o F c/o menometrorrhagia and recurrent epistaxis. She also complains of low energy. Recent labs demonstrated iron deficiency anemia and she is taking oral ferrous sulfate. She notes easy bruising and relates a family hx of similar complaints. She most likely has a hereditary coagulopathy. CBC is normal. PT is normal, but PTT is mildly prolonged at 44 sec and corrects with a 1:1 mix. The best test(s) to evaluate further include:
A. Platelet aggregation studies B. Antiphospholipid antibody levels C. Factor VIII-inhibitor level D. Factor XII level E. Factor IX level
E. Factor IX level
[this presentation could also be seen with factor XII deficiency but that is extremely rare]
31 y/o F c/o menometrorrhagia and recurrent epistaxis. She also complains of low energy. Recent labs demonstrated iron deficiency anemia and she is taking oral ferrous sulfate. She notes easy bruising and relates a family hx of similar complaints. She most likely has a hereditary coagulopathy. CBC is normal. PT is normal, but PTT is mildly prolonged at 44 sec and corrects with a 1:1 mix. Platelet aggregation studies demonstrate a depressed response to ristocetin with a normal vWF multimer pattern. The pts diagnosis is:
A. Type 2B vonWillebrand disease B. Hereditary hemorrhagic telangiectasia C. Type 1 vonWillebrand disease D. Bernard Soulier syndrome E. Gray platelet syndrome
C. Type 1 vonWillebrand disease
[75% of vonwillebrand disease is type 1]
31 y/o F c/o menometrorrhagia and recurrent epistaxis. She also complains of low energy. Recent labs demonstrated iron deficiency anemia and she is taking oral ferrous sulfate. She notes easy bruising and relates a family hx of similar complaints. She most likely has a hereditary coagulopathy. CBC is normal. PT is normal, but PTT is mildly prolonged at 44 sec and corrects with a 1:1 mix. Platelet aggregation studies demonstrate a depressed response to ristocetin with a normal vWF multimer pattern. The pts diagnosis is type 1 vonwillebrand disease. She can be treated with
A. Intranasal DDAVP daily for prophylaxis
B. Intravenous DDAVP daily for prophylaxis
C. Intranasal DDAVP as needed for bleeding or prophylaxis for procedures
D. IV DDAVP as needed for bleeding or prophylaxis for procedures
E. Cryoprecipitate as needed for bleeding or prophylaxis for procedures
C. Intranasal DDAVP as needed for bleeding or prophylaxis for procedures
[Daily DDAVP for prophylaxis is excessive, will deplete all of your vWF; Cryoprecipitate used if needed for bleeding]
35 y/o F presents for eval of prolonged clotting time. No prior hx of bleeding or clotting d/o. Mild arthralgias and myalgias. PTT is 55 sec. Her only medication is acetaminophen PRN. No menometrorrhagia. PE is normal. Her PTT could be prolonged due to
A. Lab error B. Circulating inhibitor C. Factor deficiency D. Surreptitious medication usage E. Rat poison F. All of the above
F. All of the above
35 y/o F presents for eval of prolonged clotting time. No prior hx of bleeding or clotting d/o. Mild arthralgias and myalgias. PTT is 55 sec. Her only medication is acetaminophen PRN. No menometrorrhagia. PE is normal. The best test to evaluate the PTT is
A. TT B. DRVVT C. 1:1 mix D. PT E. Reptilase time
C. 1:1 mix
35 y/o F presents for eval of prolonged clotting time. No prior hx of bleeding or clotting d/o. Mild arthralgias and myalgias. PTT is 55 sec. Her only medication is acetaminophen PRN. No menometrorrhagia. PE is normal. Her PTT fails to correct with 1:1 mix. The most likely explanation is
A. Lab error B. Type I VW disease C. Bernard-soulier syndrome D. Factor V leiden mutation E. Circulating inhibitor
E. Circulating inhibitor
35 y/o F presents for eval of prolonged clotting time. No prior hx of bleeding or clotting d/o. Mild arthralgias and myalgias. PTT is 55 sec. Her only medication is acetaminophen PRN. No menometrorrhagia. PE is normal. Her PTT fails to correct with 1:1 mix. The best set of tests at this time are:
A. Antiphospholipid Abs and DRVVT
B. DRVVT alone
C. Antiphospholipid Abs alone
D. Antiphospholipid Abs and prothrombin gene mutation
E. DRVVT and platelet aggregation studies
A. Antiphospholipid Abs and DRVVT
35 y/o F presents for eval of prolonged clotting time. No prior hx of bleeding or clotting d/o. Mild arthralgias and myalgias. PTT is 55 sec. Her only medication is acetaminophen PRN. No menometrorrhagia. PE is normal. Her PTT fails to correct with 1:1 mix. Confirmative tests demonstrate an antiphospholipid Ab of the lupus anticoagulant variety. The best course of tx is:
A. Long-term anticoagulation with warfarin
B. Long-term anticoagulation with a Factor Xa inhibitor
C. Observation
D. Long-term use of an antiplatelet regimen
E. IVC filter placement
C. Observation
