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MOHD3 Exam 2 > Bleeding and Clotting Disorders > Flashcards

Bleeding and Clotting Disorders Flashcards

1
Q

Intrinsic Pathway
Starts with factor ___
Tested by:

A

12

PTT (Partial thromboplastin time) or APTT

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2
Q

Extrinsic Pathway
Start at factor ___
Tested by:

A

7

prothrombin time

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3
Q

Prothrombin time prolonged by deficiencies in: (5)

A

Factor 7, 10, 5
Prothrombin (II)
Fibrinogen (I)

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4
Q

International Normalized Ratio (INR)

A

Standardize method developed to compensate for variation among reagent and instrument systems in prothrombin time.

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5
Q

PTT prolonged by deficiencies in:

A

any plasma clotting factor except 7 or 13

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6
Q

Most common inherited deficiencies associated with bleeding with prolonged PTT

A

Factor 8, Factor 9

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7
Q

Specific factor inhibitor associated w/ ____ which leads to ____. Causes prolonged ___

A

antibody to factor 8
severe bleeding diathesis
PTT

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8
Q

Deficiency associated with long PTT w/o risk of bleeding

A

Factor 12

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9
Q

Antiphospholipid antibody:
Prolonged ___
Cause:

A

Antibodies against phospholipid protein complexes
PTT
Paradoxically: hypercoagulatibility, thrombosis

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10
Q

PT and PTT prolonged seen in:

A

Common pathway deficiency

Multiple factor decificiencies

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11
Q

PT prolonged, normal PTT seen in:

A

Factor 7 deficiency

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12
Q

PTT prolonged, normal PT seen in:

A

Factor 8, 9, 11, 12 deficiency

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13
Q

Mixing study: Correction of PT or PTT to normal suggests:

A

Factor deficiency

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14
Q

Mixing study: Test remains prolong suggest:

A

inhibitor, antibody

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15
Q

D-dimer increased when:

Evaluates:

A

Increased fibronolysis –> excessive generation of products of digestion of fibrin by plasmin
DVT, disseminated intravascular coagulation, PE

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16
Q

Platelet function analysis (PFA-100) used to:

2 tests:

A

assess how effectively platelets work to close hole in membrane
Collagen/Epinepherine
Collagen/ADP

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17
Q

Long closure time w/ Col/Epi, normal Col/ADP caused by:

A

Drugs (aspirin, NSAIDS)

18
Q

Long closure time w/ Col/Epi and Col/ADP caused by:

A

Qualitative platelet disorders
Von Willebrand disease
Thrombocytopenia
Anemia

19
Q

____ more likely to cause mucocutaneous bleeding (epistaxis, menorrhagia, pectechia) than hematomas

A

Platelet abnormalities

20
Q

Thrombocytopenia =

A

decrease in number of platelets in peripheral circulation

21
Q

Mechanisms of causing thrombocytopenia:

A

Decreased platelet production
Splenic sequestration
Increased peripheral destruction of platelets

22
Q

Increased peripheral destruction of platelets causes
Non-immune destruction:

Immune destruction:

A
  1. Disseminated intravascular coagulation
  2. Microangiopathic hemolytic anemia: vasculitis
  3. Alloimmune destruction: maternal fetal incompatibility, after blood transfusion
  4. Drug inducted: absorption of drug on platelet surface –> ab formation –> platelet removed in liver and spleen
    Quinine
    Heparin: ab directed against heparin and platelet factor 4 –> platelet aggregation
23
Q

Acute immune thrombocytopenic purpura=
Typically in: (age, sex)
Associated w/:
Treatment:

A

Acute onset w/ severe thrombocytopenia

2-6 y/o, both M and F

Viral infection: cross reactivity of ab b/w viral infection and platelets

Steroids, IVIG, Rh immune globulin

24
Q

Chronic immune thrombocytopenic purpura =
Typically in: (age, sex)
Associated with:
Treatment:

A

Not as severe thrombocytopenia. Insidious onset w/ remissions and relapses

20-40 y/o, F

Other autoimmune disorders

Steroids, splenectomy, Rituximab

25
Q

Clinical presentation of thrombotic thrombocytopenic purpura (5)

A 
Thrombocytopenia
Microangiopathic hemolytic anemia
Neurologic symptoms
Fever
Renal insufficiency
26
Q

Thrombotic thrombocytopenic purpura =

Etiology:

Treatment:

A

Deposition of platelet thrombi in small vessels –> schistocytes in peripheral blood

Deficiency of protease ADAMTS13 that cleaves von Willebrand multimers –> aggretate platelets –> deposit of thrombi

Plasmapheresis

27
Q

Drugs that induce platelet disorders:

A

Aspirin, indomethacin, NSAIDs

Clopidogrel (Plavix): block ADP receptor on platelets

28
Q 
Hemophilia A = deficiency of \_\_\_\_
Genetics:
Clinical manifestation:
Lab evaluation:
Treatment:
A

Factor 8
Sex-linked: inversion mutation of X chromosome

Delayed bleeding from small wounds
Bleeding into joints, hematomas, hematuria
Joint destruction, muscle atrophy

Prolonged PTT, normal PT
Factor assay

Factor replacement

29
Q 
Hemophilia B = deficiency of \_\_\_
Genetics:
Clinical manifestation:
Lab evaluation:
Treatment:
A

Factor 9
Sex-linked: point mutation

Mild hemophilia

Prolonged PTT, normal PT
Factor assays

Recombinant factor 9 replacement

30
Q

Factor 12 deficiency

A

Rare, benign

Increase PTT but no increase risk of bleeding

31
Q 
Von Willebrand Disease =
Genetics:
Symptoms:
Lab evaluations:
Treatment:
A

Plasma deficiency of von Willebrand factor

Autosomal dominant

Mucocutaneous bleeding: epistaxis, menorrhagia, easy bruising

Long closure time by PFA
Decreased vW antigenic level and activity
Decrease Factor 8

Desmopressin: release vWF from endothelial cells
vWf replacement

32
Q

Subtypes of Von Willebrand Disease:

A

Type 1: most common: mild-moderate quantitative decrease in vWf
Type 2: qualitative defect in vWF
Type 3: rare: severe quantitative deficiency of vWf. Autosomal recessive. No factor 8 at all.

33
Q 
Liver disease lab values:
PT, PTT:
FDPs, D-Dimers:
Fibrinogen:
Platelet count:
Factor 8
A 
Increase PT, PTT
Increased FDP, D-Dimer
Decreased fibrinogen
Decreased platelet count
Increased factor 8: activated endothelial cells
34
Q

Disseminated Intravascular Coagulation =

Coagulation factors level:
Inhibitors of coagulation level:

End result:

A

Extensive intravascular thrombin formation –> deposition of fibrin in microvasculature and thrombosis of small and medium sized vessels

Depleted coag factors
Inhibitors (antithrombin 3, protein C and S) consume and fail to control coagulation process

Ischemic tissue injury
Hemorrhage: consumption of clotting factors

35
Q

2 mechanisms for triggering acute DIC

A

Widespread release of tissue factor into blood

Widespread injury to endothelial cells

36
Q 
Lab values of DIC
PT, PTT:
FDPs, D-Dimers:
Fibrinogen:
Platelet count:
Smear:
A 
Increased PT, PTT
Increased FDPs, D-dimers: increased fibrinolysis
Decreased fibrinogen: consumption
Decreased platelet: consumption
Fragmented RBCs
37
Q

Most common cause of acquired thrombophilia that can be tested

A

Antiphospholipid antibody syndrome

38
Q

Antiphospholipid antibody syndrome =

Associated w/: (3)

Labs:

A

Development of ab against plasma proteins w/ affinity for anionic phospholipids
Acquired thrombophilia

  1. Venous and arterial thrombosis
  2. Recurrent fetal loss
  3. Thrombocytopenia

Prolonged PTT
Presence of lupus anticoagulant

39
Q

Factor V Leiden =

A

Inherited thrombophilia
Factor V can’t be cleaved by activated Protein C
Increased levels of factor V

40
Q

Prothrombin gene mutation =

A

inherited thrombophilia

Mutation of G20210A

MOHD3 Exam 2 (13 decks)

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