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CVS > anti clotting drugs > Flashcards

anti clotting drugs Flashcards

1
Q

classes of drugs for anti clotting

A
  1. antiplatelet
  2. anticoagulants
  3. thrombolytics
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2
Q

name the 4 antiplatelet drugs

A
  1. aspirin
  2. GP2b/3a receptor blockers
  3. ADP receptor blockers
  4. PDE inhibitors
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3
Q

which prostanoids are heavily involved in primary hemostasis

A

PGI2 (anti thrombotic)

TXA2 (pro thrombotic)

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4
Q

what does PGI2 do in primary hemostasis

A
  1. helathy intact endothelium release PGI2 into plasma
  2. PGI2 blinds to platelet membrane receptors –> conversion of ATP to cAMP
  3. cAMP inhibits release of granules containing aggregating agents (serotonin, ADP)
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5
Q

what does TXA2 do in primary hemostasis

A
  1. thrombin + TXA2 + subendothelial collagen cause release of arachidonic acid from platelet membrane
  2. TXA2 is synthesised from archidonic acid in platelet, then released
  3. TXA2 binds to receptors on other platelets, inititaes release of additional aggregating agents (serotonin, ADP)
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6
Q

aspirin MOA

A
  1. irreversible nonselective COX inhibitor –> no production of prostanoids from arachidonic acid
  2. antiplatelet effect as PGI2 can be restored, TXA2 cannot
    => overall antiplatelet effect
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7
Q

aspirin PK

A

rapid inhibitory effect that lasts for the platelet lifespan (7-10 days) as it is irreversible inhibitor

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8
Q

aspirin clinical uses

A
  1. prophylactic treatment of transient cerebral ischemia (BUT recent studies indicate against use if there is no history of cerebral infarct, MI, etc.)
  2. reduce incidence of recurrent MI
  3. decrease mortality in post MI patients
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9
Q

aspirin adverse effects

A
  1. gastic upset and ulcers
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10
Q

what do gp2b/3a receptors do in primary hemostasis

A

for platelet aggregation

  1. for fibrinogen and vitrionectin binding - cross link platelets
  2. for fibronectin and vWF binding
  3. activation of this receptor is final common pathway for platelet aggregation
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11
Q

name 3 gp2b/3a receptors blockers

A

abciximab, eptifibatide, tirofiban

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12
Q

gp 2b/3a receptor blockers MOA

A

displace fibrinogen that is cross linking platelets on existing thrombi –> prevent further platelet cross linking and thrombosis

=> prevents clot formation

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13
Q

how does abciximab displace fibrinogen

A

humanised Ab that reversibly inhibits binding of fibrinogen and other ligands

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14
Q

how does eptifibatide displace fibrinogen

A

analog of sequence at C terminal of delta chain of fibrinogen, which mediates binding of fibrinogen to receptor
thus preventing binding between fibrinogen and receptor

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15
Q

how does tirofiban displace fibrinogen

A

tirofiban is a small molecule receptor blocker

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16
Q

gp 2b/3a receptor blocker clinical uses

A
  1. prevent restenosis after coronary angioplasty

2. acute coronary syndromes (to prevent possible thrombus formation)

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17
Q

name 2 ADP receptor blockers

A

clopidogrel, ticlopidine

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18
Q

ADP receptor blocker MOA

A

prevent binding of ADP to ADP receptors –> reduce platelet aggregation

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19
Q

name 1 PDE inhibitor

A

dipyridamole

20
Q

PDE inhibitor MOA

A

prevent conversion of cAMP to 5’AMP –> accumulation of cAMP –> inhibits release of granules containing aggregating agents (serotonin, ADP)

21
Q

what are the main anticoagulants

A
  1. heparin
  2. warfarin (coumarin derivative)
  3. lepirudin and hirudin
22
Q

what does thrombin do in hemostasis

A
  1. activates upstream factors esp 5, 8, 11
  2. cleaves fibrinogen to form fragments that polymersise to form fibrin
  3. 8 is a fibrinoligase that strengthens fibrin-fibrin cross links, stabilising coagulum
  4. causes platelet aggregation, stimulate cell proliferation, modulates SM contraction
23
Q

what does antithrombin III do

A

is an endogenous anticlotting protein:

irreversibly inactivates factors 2, 9, 10, (11, 12) by forming equimolar stable complexes

24
Q

what are heparins

A

a family of sulfated glycosaminoglycans

25
Q

heparin MOA

A
  1. bind to ATIII –> conformational change that exposes its active sites for more rapid interaction with factors (proteases)
    - inhibtion of thrombin: heparin needs to bind both thrombin and ATIII
    - inhibition of 10: heparin binding to ATIII alone is enough
26
Q

what is the difference between LMWH and normal heparin

A

LMWH increases action of ATIII on factor 10 but not its action on thrombin
LMWH has longer doa than regular heparin

27
Q

heparin PK

A

IV or SC administration

28
Q

can heparin be given IM?

A

No. will result in hematomas

29
Q

heparin clinical uses

A
  1. DVT, PE, MI - use together with thrombolytics for revascularisation (heparin is just anticoagulant, wont do anything against thrombi that have already formed)
  2. angioplasty and placement of coronary stents (use together with GP2b/3a inhibitors)
  3. if anticoagulant must be used in pregnancy
30
Q

which drug combination is used for thrombotic events

A

heparin/warfarin and thrombolytics

31
Q

which drug combination is used for angioplasty and coronary stents

A

heparin/warfarin and GP2b/3a inhibitors

32
Q

which anticoagulant is still safe to use in pregnancy

A

heparin

33
Q

heparin adverse effects

A
  1. hemorrhage –> stop heparin therapy, give protamine sulfate (binds and inhibits heparin)
  2. thrombosis
  3. thrombocytopenia
34
Q

how can heparin cause thrombosis

A

platelet factor 4:heparin complex can form immune complexes with IgM/IgG –> activate platelets, more relase PF4 –> cause endothelial damage with antibodies

35
Q

warfarin MOA

A

inhibits vit K reductase –> cannot regenerate reduced Vit K which is needed for carboxylation of glutamic acid –> cannot produce functional factors 2, 7, 9, 10

36
Q

warfarin PK

A

oral, absorbed quickly
small Vd, strongly bound to albumin
metabolised by hepatic CYP450 (DDIs!)

37
Q

warfarin clinical uses

A
  1. DVT, PE, MI - use together with thrombolytics for revascularisation (heparin is just anticoagulant, wont do anything against thrombi that have already formed)
  2. angioplasty and placement of coronary stents (use together with GP2b/3a inhibitors)
38
Q

warfarin adverse effects

A

bleeding

39
Q

warfarin contraindications

A

pregnancy

  • crosses placenta –> hemorrhagic disorder in fetus
  • fetal proteins with gamma-carboxyglutamate residues found in bone and blood get affected
40
Q

how to reverse effects of warfarin?

A

give reduced vit K (can prevent hemorrhagic disease of newborn)

41
Q

what are thrombolytics

A

plasminogen activators

42
Q

name 4 thrombolytics

A

alteplase (tPA), urokinase, streptokinase, anistreplase

43
Q

thrombolytics MOA

A

convert plasminogen to plasmin

  • main: plasmin breaks down fibrin to fibrin degradation products
  • plasmin breaks fown fibrinogen to fibrinogen degradation products
44
Q

thrombolytics administration

A

intracoronary injection, IV

45
Q

thrombolytics clinical uses

A
  1. emergency treatment of coronary artery thrombosis (can use with anticoagulants)
  2. peripheral arterial thrombosis and emboli
46
Q

thrombolytics adverse effects

A

bleeding

47
Q

thrombolytics contraindications

A

pregnancy, presence of healing wound

CVS (6 decks)

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