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Bloc C - Circulation > Nov23 M1-Pharmacology Antiplatelet Drugs > Flashcards

Nov23 M1-Pharmacology Antiplatelet Drugs Flashcards

1
Q

3 drug groups

A
  • inhibit Tx synthesis
  • block ADP receptor
  • inhibit glycoprotein IIB-IIIA
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2
Q

use of anti-platelet drugs

A

prevent thrombosis

alter evolution of ats

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3
Q

2 types of granules found in platelets

A 
delta granules (contain ADP)
alpha granules
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4
Q

mechanism of primary plug formation

A
  1. plts recon vWF and collagen and are activate
  2. activate plts release ADP, TxA2 and 5HT
  3. these substances activate platelets and activate an integrin (glycoprot IIB-IIIA) on their surface
  4. this integrin binds fibrinogen and fibrin
  5. formation of formalin aggregate
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5
Q

what happens to plts when activated

A

change shape and have processes

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6
Q

aspirin action

A

blocks covalently (irreversibly) COX-1 (acetylates serine residue near its active site) so can’t produce TxA2

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7
Q

why aspirin effect irreversible

A

platelet no nucleus, can’T prod new COX 1

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8
Q

why ASA less effective at higher dose (NSAID dose)

A

Also inhibits prostacyclin prod (prostacyclin is an endogenous anti platelet)

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9
Q

where ASA absorbed

A

stomach and upper SI

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10
Q

ASA overdose effect

A

primary metab pathway saturated. elim becomes order 0 (constant rate no matter dose). significant increase in plasma ASA

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11
Q

aspirin effect on bleeding time

A

prolonged in all patients

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12
Q

salicylism def + cause

A

reduce hearing, ringing in ears, dizziness. cause: mild overdose.

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13
Q

aspirin use

A

secondary prevention of cerebral and cardiac ischemia, MI, …

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14
Q

inhibitors of ADP pathway mechanism

A

block ADP receptor on platelet surface

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15
Q

inhibitors of ADP pathway: give drugs

A

clopidogrel, prasugrel, ticagrelor

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16
Q

diff between inhibitors of ADP pathway and ASA

A

they have no effect on PG metabolism

17
Q

2 inhibitors of ADP pathway used and effect

A

clopidogrel, prasugrel. irreversibly block ADP receptor

18
Q

how ADP activates platelets

A

binds two purine receptors. P2Y1 and P2Y12. both must be activated

19
Q

clopidogrel effect

A

irreversibly blocks P2Y12 receptor

20
Q

clopidogrel pharmacokinetics

A

given as prodrug, activated by enzymes in cytochrome P450.

21
Q

why clopidogrel resistance exists

A

genetic variability. some patients have reduced fct variant of CYP2C19 enzyme of the cytochrome P450

22
Q

when clopidogrel used with ASA and when used instead of ASA

A

clopidogrel in stroke

clopidogrel with aspirin in ACS (acute coronary syndrome)

23
Q

prasugrel effect + diff with clopidogrel

A

same effect. P2Y12 blocker irreversibly.

less resistance to it

24
Q

ticagrelor mechanism

A

blocks REVERSIBLY P2Y12

25
Q

ticagrelor when

A

in ACS, to reduce CV death, MI and stroke (better than clopidogrel)

26
Q

glycoprot IIB-IIIA fct

A

receptor fo fibrinogen and vWF

27
Q

glycoprot IIB-IIIA inhibitors: potency and administration

A

best anti plt but replaced by ticagrelor and prasugrel

given by injection

28
Q

abciximab charact and mechanism

A

Fab fragment of humanize monoclonal Ab against the receptor

29
Q

eptifibatide and tirofiban mechanism

A

peptide (2nd is small molecule) blocker of fibrinogen binding site on the receptor

30
Q

major side effect of glycoprot IIB-IIIA inhibitors

A

bleeding and thrombocytopenia

31
Q

arterial vs venous side choice of medication

A

arterial side: anti platelet drug

32
Q

which for stroke

A 
anti platelet (clopidogrel)
dabigatran
33
Q

which for DVT

A

UF heparin and then warfarin

LMWH heparin if good kidney function and then warfarin

34
Q

which prevention of cereb or cardiac and ischemia + MI

A

aspirin

35
Q

which to prevent stroke if prosthetic heart valve or mitral stenosis

A

warfarin

36
Q

which to prevent stroke in a fib

A

rivaroxaban

37
Q

which for 6 hours after after acute STEMI

A

alteplase or tenecteplase

Bloc C - Circulation (29 decks)

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