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ABSITE Review > ABSITE Review - Hematology > Flashcards

ABSITE Review - Hematology Flashcards

1
Q

What are the three initial responses to vascular injury?

A

Vascular vasoconstriction, Platelet adhesion, Thrombin generation

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2
Q

What is the convergence point betweem the intrinsic and extrinsic pathway?

A

Factor X

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3
Q

Which coagulation factor helps with fibrin crosslinking?

A

Factor XIII

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4
Q

What are the functions of thrombin?

A

Key to coagulation
Converts fibrinogen to fibrin and fibrin split products
Activates factors V and VIII
Activates platelets

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5
Q

What are the functions of antithrombin III?

A

Key to anticoagulation
Binds and inhibits thrombin
Inhibits factors IX, X, XI
Heparin binds AT-III

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6
Q

What are the functions of protein C?

A

Degrades factors V and VIII

Degrades fibrinogen

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7
Q

What is the function of tissue plasminogen activator?

A

It is released from the endothelium and converts plasminogen to plasmin

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8
Q

What is the function of plasmin?

A

Degrades factors V, VIII, fibrinogen and fibrin –> lose platelet plug

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9
Q

What coagulation factor has the shortest half life?

A

Factor VII

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10
Q

Which are the labile coagulation factors?

A

Factors V and VIII, activity is lost in stored blood but not in FFP

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11
Q

Which is the only factor not synthesize in the liver?

A

Factor VIII which is synthesized in the endothelium

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12
Q

Name the vitamin K-dependent factors.

A

II, VII, IX, X, protein C and protein S

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13
Q

How long it takes to witamin K to take effect?

A

6 hours

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14
Q

How long FFP lasts?

A

Effect is immediate and lasts 6 hours

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15
Q

Describe the half-life of RBCs, PLTs, PMNs.

A

RBCs 120 days
PLTs 7 days
PMNs 1-2 days

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16
Q

Where protacyclin is produce and what is its function?

A

Comes from endothelium.

Decreases platelet aggregation and promotes vasodilation.

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17
Q

Where thromboxane is produce and what is its function?

A

Comes from platelets.
Increase platelets aggregation and promotes vasoconstriction.
Triggers release of calcium in platelets –> exposes GpIIB/IIIa receptor and causes PLT to PLT binding, PLT to collagen binding

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18
Q

What coagulation factors are present in cryoprecipitate?

A

Contains the highest concentration of vWF VIII and fibrinogen

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19
Q

What coagulation factors are present in FFP?

A

High levels of all factors, protein C, protein S and AT-III

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20
Q

What cause release of VIII and vWF from endothelium?

A

DDAVP and conjugated estrogens

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21
Q

What PT measures?

A

Measures II, V, VII and X; fibrinogen; best for liver synthetic function

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22
Q

What PTT measures?

A

Measures most factors except VII and XIII; fibrinogen

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23
Q

What is ACT and what arange is needed for anticoagulation?

A

Activated clotting time
ACT 150-200s for routine anticoagulation
ACT 460s for CABG

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24
Q

What is the MC congenital bleeding disorder?

A

von Willebrand’s disease

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25
Q

What is the function of vWF?

A

Links GpIb receptor on PLTs to collagen

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26
Q

What are the diagnostic lab findings on vWF disease?

A

Normal PT
Normal or abnormal PTT
Long bleeding time (ristocetin test)

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27
Q

What is the most common and/or severe type of vWF disease?

A

MC type - Type I (autosomal dominant)

Most severe type - Type III (autosomal recessive)

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28
Q

Describe the genetics and diagnostic lab findings for Hemophilia A.

A 
VIII deficiency
Sex-linked recessive
Need levels 100% preop and keep at 30% after surgery
Dx - Prolonged PTT and normal PT
Factor VIII crosses placenta
29
Q

Describe the genetics, diagnostic lab findings and treatment for Hemophilia B.

A 
IX deficiency
Sex-linked recessive
Need levels 100% preop
Dx - Prolonged PTT and normal PT
Factor VIII crosses placenta
Tx - recombinant factor IX concentrate or FFP
30
Q

Mention the diagnostic lab findings and treatment for Factor VII deficiency.

A

Dx - Prolonged PT, normal PTT, bleeding tendency

Tx - recombinant factor VII concentrate, FFP

31
Q

What medications can cause Acquired thrombocytopenia?

A

H2 blockers, heparin

32
Q

What is the defect in Glanzmann’s thrombocytopenia and treatment?

A

GIIb/IIIa receptor deficiency on platelets

Tx - platelets

33
Q

What is the defect in Bernard Soulier thrombocytopenia and treatment?

A

GpIb receptor deficiency on platelets

Tx - platelets

34
Q

What is the MOA of Ticlopidine?

A

Decreases ADP in platelets, prevent exposure of GpIIb/IIIa

35
Q

What is the MOA of Dipirydamole?

A

Inhibits cAMP PDE, increases cAMP, decreases ADP-induced PLT aggregation

36
Q

What is the MOA of Pentoxifylline?

A

Inhibits PLT aggregation

37
Q

What is the MOA of Clopidogrel (Plavix)?

A

ADP receptor antagonist

38
Q

How ticlopidine, dipirydamole, pentoxyfylline and Plavix thrombocytopenia is treated?

A

PLTs

39
Q

Mention the cause of HIT.

A

AntiPLT antibodies (IgG PF4 antibody)

40
Q

What two MC findings in patients with HIT?

A

Thrombocytopenia (decrease of 50% PLTs or below 100) and thrombosis (white clot)

41
Q

What is the treatment for HIT?

A

Stop heparin

Give argatroban, hirudin, ancrod or dextran to anticoagulate

42
Q

What are the lab findings of DIC?

A

Decrease PLTs, prolonged PT, prolonged PTT, low fibrinogen, high fibrin split products, high D-dimer

43
Q

What is the MOA of ASA and how long before surgery it need to be stop?

A

Inhibits COX in PLTs

Stop 7 days prior to surgery, pts will have prolonged bleeding time

44
Q

What PLT level is adequate before and after surgery?

A

Keep > 50,000 before surgery and > 20,000 after surgery

45
Q

When urokinase is release and what is the MOA and treatment?

A

Can be release during prostate surgery and activates plasminogen causing thrombolysis
Tx- aminocaproic acid

46
Q

What is the MC congenital hypercoagulability disorder? What is the defect and treatment?

A

Leiden factor - 30% spontaneous venous thromboses
Resistance to activated protein C, defect on factor V
Tx - heparin, warfarin

47
Q

What is the treatment for Hyperhomocysteinemia?

A

Folic acid and B12

48
Q

What is the treatment for AT-III deficiency?

A

Recombinant AT-III concentrate or FFP followed by heparin or hirudin or ancrod; warfarin

49
Q

What parameters are needed prior to surgery on a patient with polycythemia vera?

A

Keep Hct < 48 and PLTs < 400 before surgery

50
Q

Mention how to diagnose and treat Lupus anticoagulant.

A

Dx- prolonged PTT (but hypercoagulable and does not correct with FFP), positive Russell viper venom time, false-positive RPR test for syphilis
Tx - heparin, warfarin

51
Q

Mention some causes of acquired hypercoagulability.

A

tobacco (MC), malignancy, infammatory states IBD, infections, OCP, pregnancy, RA, postop pts, myeloproliferative disorders

52
Q

What is the etiology of warfarin-induced skin necrosis?

A

Occurs when pt receives coumadin without being heparinized first. Protein C and S has a short half life and are the first to decrease compare with the procoagulatyion factors.

53
Q

What is the Virchow’s triad?

A

Stasis, endothelial injury and hypercoagulability

54
Q

What is the treatment for 1st, 2nd and 3rd DVT or PE?

A

1st - warfarin for 6 months
2nd - warfarin for 1 year
3rd or significant PE - warfarin for lifetime

55
Q

Where is the MC place for DVT and why?

A

LLE due to compression of L common iliac vein by arterial system.

56
Q

What are the indications for a IVC filter?

A
  1. Patients with contraindication to anticoagulation
  2. Documented PE while on anticoagulation
  3. Patients with free-flating iliofemoral, IVC or femoral DVT
  4. Patients s/p pulmonary embolectomy
57
Q

Most PEs come from ____________ region.

A

Iliofemoral

58
Q

What is the MOA of warfarin?

A

Prevents vitamin K-dependent decarboxylation of glutamic residues

59
Q

What is the MOA of SCDs?

A

Improve venous return but also induce fibrinolysis with compression (release of tPA).

60
Q

What is the MOA of heparin? How can it can be reversed?

A

Activates AT-III

Reversed with protamine (1-1.5mg/100U heparin)

61
Q

What is the half-life of heparin? Where heparin is proccesed?

A

60-90 minutes

Cleared by Reticuloendothelial system

62
Q

What is the MOA of hirudin?

A

Irreversible direct thrombin inhibitor - the most potent

63
Q

What is the MOA of argatroban?

A

Direct thrombin inhibitor, half life 50 minutes

64
Q

What is the MOA of bivalirudin (Angiomax)?

A

Reversible direct thrombin inhibitor, half life 25-30 minutes

65
Q

What is the protamine reaction?

A

Hypotension, bradycardia and decreased heart function

66
Q

What is the MOA of aminocaproic acid?

A

Inhibits fibrinolysis by inhibiting plasmin

67
Q

What are the ABSOLUTE contraindications to thrombolytic use?

A

Active internal bleeding; recent CVA (<2 months); Intracranial pathology

68
Q

What are the MAJOR contraindications to thrombolytic use?

A

Recent (<10 days), organ biopsy, or obstetric delivery; L heart thrombus; active peptic ulcer or GI abnormality; recent trauma; uncontrolled HTN

69
Q

What are the MINOR contraindications to thrombolytic use?

A

Minor surgery; recent CPR; Afib w MV disease; bacterial endocarditis; hemostatic defects; diabetic hemorrhagic retinopathy; pregnancy

ABSITE Review (32 decks)

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