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My Notes > Blood d/o drugs > Flashcards

Blood d/o drugs Flashcards

1
Q

What do oral anticoagulants generally do?

A

Inhibit hepatic synthesis of factors 2, 7, 9, 10, C, S

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2
Q

Which factors do C and S deactivate?

A

Va, VIIIa

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3
Q

What activates the intrinsic clotting cascade?

A
  1. damage → exposure of SEC

2. inflammation → kinin activation (prekallikrein, kininogen)

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4
Q

What activates the extrinsic pathway?

A

Any cellular damage in any tissue will release tissue factor (and activate factor VII)

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5
Q

What two factors can activate factor X?

A

IXa or VIIa

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6
Q

What factors does heparin act on?

A

all activated factors of intrinsic and common pathway (XIIa, XIa, IXa, Xa, IIa) - this is why we use PTT to monitor heparin

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7
Q

What factors does warfarin act on?

A

NOT the activated factors, but the synthesis of vitamin K dependent factors in liver

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8
Q

What factor does argatroban block?

A

IIa aka thrombin (catalyzes fibrinogen → fibrin)

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9
Q

What drug has the sole activity of blocking thrombin (factor IIa)?

A

Argatroban

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10
Q

What drugs activate plasminogen → plasmin? What are they called as a class?

A

Streptokinase and alteplase; called fibrinolytics (because plasmin degrades fibrin clot)

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11
Q

What property of heparin makes it deliverable by IV only?

A

water soluble

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12
Q

Heparin or warfarin: large polysaccharide? small molecule?

A 
Heparin = large polysaccharide
Warfarin = small molecule
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13
Q

As a small, lipid soluble molecule, what properties do you expect warfarin to have?

A

orally deliverable, metabolized by the liver, crosses placenta, highly plasma protein bound, long half life

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14
Q

Which has a longer half life: heparin or warfarin?

A

heparin: 2 hr
warfarin: 30+ hr
(remember, warfarin is lipid soluble and heparin is water soluble)

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15
Q

What is the action of heparin?

A

catalyzes the binding of antithrombin III (a serine protease inhibitor) to inactivate activated factors in intrinsic and common pathway: IIa, IXa, Xa, XIa, XIIa

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16
Q

What is the action of warfarin?

A

prevents gamma carboxylation of 1972, and CS; no effect on factors already activated

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17
Q

Do heparin or warfarin inhibit clotting in vitro?

A

heparin only (remember that warfarin only acts in the liver on factor synthesis)

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18
Q

What is INR?

A

PT of patient / PT of control → standardized measure of PT with no units

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19
Q

What would a target INR be in a patient on warfarin?

A

1.5 - 2.5 (this means it takes about twice as long for the patients blood to clot in a tube as a control patient)

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20
Q

What are the antidotes for warfarin and heparin?

A

Warfarin - fresh frozen plasma, (or vitamin K on STEP1 but not done in practice because this would require synthesis of new factors to normalize PT, takes way too long)
Heparin - protamine sulfate

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21
Q

What type of hypersensitivity response is HIT?

A

II

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22
Q

What property of heparin → HIT?

A

as a large sugar, very immunogenic when bound to protein (platelet factor IV in this case)

23
Q

Describe the pathogenesis of HIT

A

platelet factor IV is on membrane of platelets → opsonization by heparin in 5-10% of patients on heparin → destruction of platelets by splenic Mø → thrombocytopenia

24
Q

What is the advantage of LMW heparins?

A

As smaller sugar molecules, they are less likely to cause HIT (remember, the large sugar of heparin + protein (PF4) → immunogenicity)

25
Q

What drug do you use in place of heparin for patients with HIT? Why?

A

Argatroban; it is not a sugar like heparin, so low risk of immunogenicity

26
Q

What drugs would cause decreased absorption of warfarin?

A

drugs that bind bile, preventing its reuptake (eg. cholestyramine) because warfarin is a lipid that requires emulsification by bile salts to be absorbed

27
Q

What effect would warfarin have on the fetus if taken during pregnancy?

A

bone damage

28
Q

Where do factors V and VIII fit into the coagulation story?

A

they are not part of the cascade; clotting starts slowly without these factors and are activated by thrombin → acceleration of common pathway; VIIIa activates X and Va activates II (prothrombin); Remember V and VIII as accelerators

29
Q

How do factors C and S work?

A

If V and VIII are the accelerator, C and S are the brakes that inactivate both V and VIII

30
Q

Why does warfarin have an ↑ risk of clotting initially?

A

removes the brakes before the clotting factors (i.e. protein C which inhibits the accelerators V and VIII) because protein C has a half life of about 14 h and factors have a much longer half life (e.g. IIa T1/2 = 60 h)

31
Q

What is the order of loss of the following after warfarin administration: intrinsic pathway, protein C, extrinsic pathway?

A

extrinsic (8 hr) then protein C (14 hr) then intrinsic (24-60 hr)

32
Q

When is bivalirudin used?

A

direct thrombin inhibitor (like argatroban) used in patients with unstable angina (in combo with asprin) to perform PCTA (percutatneous transluminal coronary angioplasty)

33
Q

What effect would warfarin have on the fetus if taken during pregnancy?

A

bone damage

34
Q

Where do factors V and VIII fit into the coagulation story?

A

they are not part of the cascade; clotting starts slowly without these factors and are activated by thrombin → acceleration of common pathway; VIIIa activates X and Va activates II (prothrombin); Remember V and VIII as accelerators

35
Q

How do factors C and S work?

A

If V and VIII are the accelerator, C and S are the brakes that inactivate both V and VIII

36
Q

Why does warfarin have an ↑ risk of clotting initially?

A

removes the brakes before the clotting factors (i.e. protein C which inhibits the accelerators V and VIII) because protein C has a half life of about 14 h and factors have a much longer half life (e.g. IIa T1/2 = 60 h)

37
Q

What is the order of loss of the following after warfarin administration: intrinsic pathway, protein C, extrinsic pathway?

A

extrinsic (8 hr) then protein C (14 hr) then intrinsic (24-60 hr)

38
Q

When is bivalirudin used?

A

direct thrombin inhibitor (like argatroban) used in patients with unstable angina (in combo with asprin) to perform PCTA (percutatneous transluminal coronary angioplasty)

39
Q

What medication is the recombinant synthetic form of tPA (rTPA)?

A

alteplase

40
Q

What thrombolytic drug is made from the hemolysins produced by streptococcal bacteria?

A

streptokinase

41
Q

4 conditions in which fibrinolytic drugs are used:

A
  1. coronary thrombosis in MI
  2. stroke caused by thrombus (non-hemorrhagic)
  3. DVT
  4. PE
42
Q

What are the differences b/w the fibrinolytics streptokinase and alteplase?

A
  1. streptokinase is antigenic (it comes from bacterial product) → can react with strep antibodies and cause anaphylaxis (hypersensitivity); alteplase does not cause allergy b/c recombinant form of human protein;
  2. streptokinase is very cheap b/c bacterial product and alteplase is very expensive
  3. streptokinase binds to plasminogen → conformational change → activation to plasmin vs. alteplase binds directly to fibrin (more clot specific instead of causing a general lytic state) → activates plasminogen to plasmin
43
Q

What is the time window in which thrombolytics can be used?

A

< 3 hours clinically

44
Q

What is the antidote for thrombolytic OD (excessive bleeding)?

A

Antifibrinolysins: aminocaproic acid (EACA = epsilon aminocaproic acid) or tranexamic acid

45
Q

How does abciximab work?

A

binds gpIIb/IIIa, blocking binding to fibrinogen

46
Q

What drug blocks the synthesis of thromboxane A2 thus preventing platelet activation?

A

asprin - a baby dose is enough to cause irreversible inhibition of platelet aggregation for the life of the platelet

47
Q

What are the uses for direct antiplatelet drugs (e.g. abciximab)?

A

acute coronary syndromes (i.e. in process of developing MI) and post-angioplasty; NOT for chronic management (unlike aspirin or clopidogrel)

48
Q

Path review: which disease has a deficiency in GpIb? GpIIb/IIIa?

A

GpIb: Bernard Soulier syndrome

GpIIb/IIIa: Glanzmann thrombasthenia

49
Q

What patients are prescribed asprin for prevention?

A

Ppl w/ risk for IHD: atherosclerosis, HTN, smokers, diabetics, previous MI, atrial arrhythmias
TIA patients to prevent stroke

50
Q

How many mg is a baby asprin? What are the side effects?

A

81-82 mg; very unlikely to have side effects at such a low dosage

51
Q

When are clopidogrel and ticlopidine used?

A

as an alternative (effects are equal) to baby asprin for post-MI, TIA, and unstable angina patients

52
Q

What is the disadvantage of using ADP receptor blockers in place of asprin?

A

side effects: leukopenia, TTP → risk of hemorrhage

clopidogrel has less risk vs. ticlopidine

53
Q

What are the uses for direct antiplatelet drugs (e.g. abciximab)?

A

acute coronary syndromes and post-angioplasty

54
Q

What are the direct antiplatelet drugs?

A

abciximab, and the “fib” drugs eptifibatide, tirofiban (fib = fibrinogen receptor antagonist)

My Notes (23 decks)

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