Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHRM 844 Therapeutics > Exam 4 - Antiplatelets Hockerman > Flashcards

Exam 4 - Antiplatelets Hockerman Flashcards

1
Q

arrest of bleeding from a damaged blood vessel

a. hemostasis
b. coagulation

A

a. hemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

multi-step process to “plug” the leaking vessel

a. hemostasis
b. coagulation

A

b. coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

true or false: platelets have organelles and secretory granules, but no nucleus

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

3 steps of platelet activation

A

-platelet adhesion and shape change
-platelet secretion
-platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

platelet adhesion is mediated by:

-_____ binding to collagen
-_____ binding to von Willebrand Factor bridged to collagen
-shape change facilitates receptor binding

A

GP Ia (glycoprotein Ia)
GP Ib (glycoprotein Ib)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

intact endothelial cells secrete _____ (aka prostacyclin) to inhibit thrombogenesis

A

PGI2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

platelet secretion: platelet granules release what 3 things?

A

-ADP
-thromboxane A2 (TXA2)
-serotonin (5-HT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

platelet aggregation: ADP, 5-HT, and TXA2 activation induces conformation of GPIIb/IIIa receptors to bind __________

A

fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

platelet are cross-linked by

a. plasminogen
b. fibrinogen
c. TXA2
d. ADP

A

b. fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

aspirin is a _____ inhibitor

a. COX-1
b. ADP receptor
c. GP11b/IIIa receptor
d. PDE-3
e. protease-activated receptor

A

a. COX-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

inhibition of _____ synthesis in platelets is the key to anti-platelet activity of ASA

A

TXA2 (thromboxane)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

true or false: aspirin reduces bleeding time

A

false (prolongs it)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

aspirin indication

A

prophylaxis and treatment of arterial thromboembolic disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

after taking aspirin, hemostasis returns to normal ___ hours after last dose

A

36

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

aspirin can cause upper GI bleeding, due to inhibition of _____ mediated prostaglandins

a. COX1
b. COX2

A

a. COX1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

acute aspirin overdose can be induced by doses above _____ mg/kg

a. 50
b. 150
c. 250
d. 500

A

b. 150

(doses above 500 mg/kg can be fatal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

_____ produces prostacyclin in endothelial cells -> leads to vasodilation and inhibition of platelet aggregation

a. COX-1
b. COX-2
c. TXA2

A

b. COX-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

_____ produces TXA2 in the platelets -> which leads to vasoconstriction and platelet aggregation

a. COX-1
b. COX-2

A

a. COX-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

selective _____ inhibitors block synthesis of prostacyclin while not preventing synthesis of TXA2 -> leads to CV risk

a. COX-1
b. COX-2
c. 5-HT

A

b. COX-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what two ADP receptors are involved in activating platelets?

A

P2Y1
P2Y12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

P2Y1 is coupled to which GPCR?

a. Gi
b. Gs
c. Gq

A

c. Gq

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

P2Y12 is coupled to which G protein?

a. Gi
b. Gs
c. Gq

A

a. Gi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

activation of which ADP receptor is required for platelet activation by ADP?

a. P2Y1
b. P2Y12
c. both

A

c. both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

ticlopidine (Ticlid) and clopidogrel (Plavix) are both prodrugs that irreversibly block ___ receptor on platelet and subsequent activation of __________ complex

A

ADP; GPIIb/IIIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how long does the action of ticlopidine and clopidogrel last?

A

several days after last dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

which has a lower toxicity profile?

a. Ticlopidine (Ticlid)
b. Clopidogrel (Plavix)

A

b. Clopidogrel (Plavix)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

ADP receptor inhibitors uses (5 of them)

A

-acute coronary syndrome
-recent MI
-stroke
-established peripheral vascular disease
-stent procedures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

which drug may induce thrombotic thrombocytopenia purpura (TTP)?

a. clopidogrel
b. ticlopidine
c. prasugrel
d. ticagrelor

A

b. ticlopidine

29
Q

prasugrel (Effient) and ticagrelor (Brilinta) is approved for treatment of _____ _____ _____, and _____ _____ _____

A

acute coronary syndrome; percutaneous coronary intervention (PCI)

30
Q

prasugrel is a prodrug that requires _____ + CYP___/___ to generate active metabolite

A

esterases
CYP3A4/2B6

31
Q

does prasugrel bind irreversibly or reversibly?

A

irreversibly

(long duration of action; it is a prodrug)

32
Q

prasugrel and ticagrelor are NOT recommended before what procedure?

A

CABG

33
Q

ticagrelor has __________ binding

a. irrev
b. reversible

A

b. reversible

(binds to an allosteric site)

34
Q

Cangrelor (Kangreal) has a fast onset of action. What is the half-life range?

A

3-5 min

(it is given IV)

35
Q

true or false: cangrelor (Kangreal) requires bioactivation by metabolic enzymes

A

false

36
Q

route of administration for cangrelor (Kangreal)

A

IV

37
Q

cangrelor (Kangreal) is used as an adjunct to _____

A

PCI

38
Q

SELECT ALL THAT APPLY: which of these do not require bioactivation by metabolic enzymes?

a. clopidogrel
b. prasugrel
c. ticagrelor
d. cangrelor

A

c. ticagrelor
d. cangrelor

39
Q

what structural feature makes clopidogrel and prasugrel irreversibly bind to the P2Y12 ADP receptor?

A

they have thiol groups which make disulfide crosslinks, which makes it irreversible

40
Q

what class of drug’s mechanism is to inhibit fibrinogen crosslinking of platelets?

a. ADP receptor inhibitors
b. COX inhibitors
c. GP IIb/IIIa receptor inhibitors
d. PDE-3 inhibitors

A

c. GP IIb/IIIa receptor inhibitors

41
Q

A chimeric mouse-human monoclonal antibody directed against the human GPIIb-IIIa

a. abciximab
b. eptifibatide
c. tirofiban

A

a. abciximab

42
Q

A synthetic peptide which selectively blocks GPIIb-IIIa in a reversible manner

a. abciximab
b. eptifibatide
c. tirofiban

A

b. eptifibatide

43
Q

A nonpeptide tyrosine analogue which is specific for the GPIIb-IIIa and inhibits fibrinogen binding

a. abciximab
b. eptifibatide
c. tirofiban

A

c. tirofiban

44
Q

true or false: eptifibatide binds reversibly to block GPIIb-IIIa receptor

A

true

45
Q

eptifibatide duration of action (range)

A

6-12 hours

46
Q

eptifibatide use

a. combined with heparin to treat acute coronary syndrome
b. prevent thromboembolism in unstable angina and angioplastic coronary procedures
c. prevent thromboembolism in coronary angioplasty

A

b. prevent thromboembolism in unstable angina and angioplastic coronary procedures

47
Q

eptifibatide has what three amino acids as part of its structure?

A

arg (R), gly (G), asp (D)

48
Q

where is eptifibatide derived from?

A

rattlesnake venom

49
Q

which does not reversibly bind to the GP IIb/IIIa receptor?

a. abciximab
b. eptifibatide
c. tirofiban

A

a. abciximab

50
Q

which is combined with heparin to treat acute coronary syndrome?

a. abciximab
b. eptifibatide
c. tirofiban

A

c. tirofiban

51
Q

abciximab use

a. prevent thromboembolism in coronary angioplasty
b. to prevent thromboembolism in unstable angina and angioplastic coronary procedures
c. combined with heparin to treat acute coronary syndrome

A

a. prevent thromboembolism in coronary angioplasty

52
Q

which is combined with t-PA for early treatment of acute MI?

a. abciximab
b. eptifibatide
c. tirofiban

A

a. abciximab

53
Q

how many hours does it take for platelet function to come back with abciximab?

A

48 hours

54
Q

abciximab binds to GP IIb/IIIa to inhibit __________ __________

A

platelet aggregation

55
Q

PDE-3 inhibitor drugs (2 of them)

A

dipyridamole (Persantine)
cilostazol (Pletal)

(dipyridamole mainly inhibits PDE5, but also PDE3 to lesser extent)

56
Q

which drug, when combined with warfarin, can prevent embolization from prosthetic heart valves?

a. dipyridamole (Persantine)
b. cilostazol (Pletal)

A

a. dipyridamole (Persantine)

57
Q

which drug, when combined with ASA, can prevent cerebrovascular ischemia?

a. dipyridamole (Persantine)
b. cilostazol (Pletal)

A

a. dipyridamole (Persantine)

58
Q

which PDE-3 inhibitor is used for intermittent claudication?

a. dipyridamole (Persantine)
b. cilostazol (Pletal)

A

d. cilostazol (Pletal)

(intermittent claudication is muscle pain when exercising; usually in legs bc of reduced blood flow due to atherosclerosis)

59
Q

thrombin activates __________ at nanomolar concentrations. It does this via proteolytic cleavage of PAR-1 receptors on __________ surface (same word in each blank)

A

platelets

60
Q

PARs (protease activated receptors) are _____ coupled to release of ___ from stores

A

GPCRs; Ca2+

61
Q

PAR (protease activated receptor) inhibitor drug

A

vorapaxar

62
Q

is vorapaxar (Zontivity) reversible or irreversible?

A

reversible

(it competitively inhibits PAR-1 receptor)

63
Q

how does vorapaxar (Zontivity) work?

A

inhibits thrombin interaction with PAR, thereby inhibiting thrombin activation of platelet aggregation

64
Q

what is vorapaxar (Zontivity) used for?

A

prophylactic to prevent thrombosis in pts with previous MI or PAD

65
Q

vorapaxar is used with _____ or _____

A

aspirin or clopidogrel

66
Q

contraindications for vorapaxar (3 of them)

A

history of stroke, TIAs, or intracranial hemorrhage

67
Q

half-life of vorapaxar (Zontivity) (range)

A

3-4 days

(very long; antiplatelet effect lasts days after discontinuation)

68
Q

common indication for cilostazol

A

PAD

(intermittent claudication is a typical symptom of PAD)

PHRM 844 Therapeutics (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions