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Bloc C - Circulation > Anticoagulant and Fibrinolytic Drugs Nov21 M2 > Flashcards

Anticoagulant and Fibrinolytic Drugs Nov21 M2 Flashcards

1
Q

goal of these drugs

A

prevent thromboembolism

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2
Q

3 steps of normal coagulation

A
  1. retraction of vessel
  2. platelets activation after factor exposure from endothelium
  3. coagulation cascade
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3
Q

white vs red thrombus

A

white in arterial blood

red in venous blood bc stasis, slow flow. more blood stuck in fibrin

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4
Q

normal procoagulant vs anticoagulant factors present

A

pro: platelet adhesion, aggregation. fibrin clot formation
anti: fibrinolysis + natural inhibitors of coagulation

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5
Q

anticoagulant drugs discussed

A

UF heparin, LMWH heparin, oral anticoagulants (warfarin, dabigatran, rivaroxaban, apixaban)

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6
Q

fibrinolytic drugs discussed

A

alteplase (tissue plasminogen activator, a tPA), tenecteplase

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7
Q

heparin descript

A

sulphated mucopolysacch occuring in mast cells

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8
Q

heparin normal fct

A

cofactor of antithrombin III

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9
Q

antithrombin III functions (3)

A 
inhibits thrombin (IIa) and factor Xa
traps other coag factors, other proteases (suicide substrate)
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10
Q

how express UF heparin dose

A

USP units

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11
Q

heparin administration and why

A

IV or subcutaneous (latter = 1-2hr effect delay)

can’t GI bc mast cells destroy it

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12
Q

how heparin degraded

A

macrophages. reticulo-endothelial system

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13
Q

how monitor heparin dose

A

with activated partial thromboplastin time (aPTT)

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14
Q

normal aPTT value

A

30-50 seconds

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15
Q

uses of IV UF heparin

A

hospital. PE after DVT. DVT above knee joint. unstable angina. MI.

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16
Q

uses of subcut UF heparin

A

bed-ridden or hosp patients not receiving IV heparin for prevention of DVT

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17
Q

important UF heparin toxicities

A
  • bleeding
  • thrombocytopenia
  • allergies
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18
Q

why thrombocytopenia possible in UF heparin

A

transient + harmless in 25% of patients
5% get heparin-induced-anti-platelet antibodies (HIT) can lead to serious bleeding: emergency, can give paradoxical clotting

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19
Q

contraindications of heparin

A

thrombocytopenia, bleeding disorders, active peptic ulcer disease, severe htn

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20
Q

UF heparin antagonist and when

A

protamine sulfate. when severe bleeding only. (binds to heparin tightly and inactivates it)

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21
Q

LMWH 2 examples

A

enoxaparin, dalteparin

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22
Q

LMWH effect compared to UF heparin

A

On Xa but not IIa. LMWH catalyze Xa inhib by antithrombin III but not IIa (thrombin) inhibition

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23
Q

why LMWH can’t inhib IIa too

A

lacks tail to bind to IIa too when it’s bound to antithrombin III

24
Q

LMW vs UF heparin effectiveness

A

same

25
Q

LMWH monitoring

A

none

26
Q

LMWH effect on aPTT

A

increased

27
Q

LMWH something better than UF heparin

A

less incidence of HIT

28
Q

LMWH antagonist

A

not really. (partial effect only from protamine sulfate)

29
Q

new heparin replacement

A

fondaparinux (indirect inhibitors of Xa through antithrombin III)

30
Q

fondaparinux: admin, monitoring, HIT risk

A

s.c once a day, no monitoring, no HIT risk

31
Q

fondaparinux problem

A

no antagonist

32
Q

2 members of warfarin family

A

Coumadin (warfarin), sintrom (acenocoumarol)(more in Europe but same)

33
Q

Warfarin and acenocoumarol fct

A

antagonizes vitamin K and affects synthesis of factors where it is involved

34
Q

factors affected by warfarin and sintrom

A

II, X, IX, VII

35
Q

warfarin vs heparin: which crosses placenta

A

warfarin

36
Q

warfarin monitoring how

A

prothrombin time (PT), now INR

37
Q

INR therapeutic level and why boundaries

A

2 to 3. minimal therapeutic effect but don’T want bleeding

38
Q

warfarin best for what

A

prevent stroke in patients with prosthetic heart valves or mitral stenosis

39
Q

2 other uses of warfarin (less now)

A

prevent DVT above knee + PE complication AFTER HEPARIN TREATMENT
prevent stroke if a fib

40
Q

warfarin major toxicity + cause + other toxicity

A

bleeding. drug interactions. can cross plancenta too

41
Q

warfarin antagonist (how to treat bleeding)

A

plasma + concentrated K1

42
Q

what type of conditions interact dangeroulsy with warfarin

A
  • bad uptake or metabo of vitK or warfarin
  • bad synth, fct, clearance of clotting, hemostasis, fibrinolysis factors
  • bad integrity of epithelia
43
Q

most used new oral anticoag

A

rivaroxaban

44
Q

dabigatran effect

A

direct thrombin inhibitor

45
Q

dabigatran used in what

A
  • prevent stroke in non-valvular a fib
  • prev or treat PE after DVP AFTER OR WITH heparin or LMWH
  • PE after hip knww replacement
46
Q

dabigatran

inhibitor + fct

A

idarucizumab, (humanized monoclonal Ab)

47
Q

rivaroxaban effect

A

direct Xa inhibitor

48
Q

rivaroxaban use

A
  • prev or treat PE, DVT
  • prevent stroke in a fib
  • after knee hip replacement
49
Q

new rivaroxaban findings in coronary disease

A

low dose rivaroxaban + aspirin useful in coronary disease

50
Q

which new anticoagulants don’t need start on heparin

A

rivaroxaban and apixaban

51
Q

apixaban fct

A

Xa inhibitor

52
Q

edoxaban fct + something to note

A

like rivaroxaban (Xa inhibitor) but need to start on heparin

53
Q

problem with direct factor Xa inhibitors

A

no antagonist for now

54
Q

antagonist in dev for Xa inhibitors

A

Andexanet alfa

55
Q

fibrinolytic drugs effect and why good and bad

A

catalyse plasmin formation from plasminogen, to lead to lysis of thrombi

56
Q

fibrinolytic drugs main use

A

acute MI with ST elevation in 6 hrs after infarction if PCI not available

57
Q

danger of fibrinolytic

A

can lyse physiological thrombi. systemic lytic state

Bloc C - Circulation (29 decks)

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