Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Therapeutics P2 > Anticoagulation > Flashcards

Anticoagulation Flashcards

1
Q

drugs used in coagulation disorders

A

Antiplatelets
anticoagulants
thrombolytics
coagulants

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

role platelets play in homeostasis

A

They arrest bleeding from a damaged BV

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

What happens when a BV is injured?

A

Exposure of the materials inside the BV will act as a catalyst to kick off a number of processes that lead to plugging the hole. BV constricts and platelet aggregation occurs.

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

platelets are derived from

A

megakaryocytes, they have no nucleus

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

What are the 3 steps to thrombus formation?

A

Adhesion and shape change
secretion
aggregation

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

The adhesion step of thrombus formation is driven

A

The presence of collagen behind the endothelial layer of the BV

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

WHat happens when there is damage to the endothelium

A

Platelets and clotting factors will find things that they normally do not see (collagen), kicking off coagulation.

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

Exposure of platelets to what will allow platelets to adhere to collagen

A

VWF (vonwillebrand factor)

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

What does GP1a bind? What does GP1b bind?

A

GP1a binds collagen
GP1b binds VWF

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

How do endothelial cells inhibit platelet aggregation?

A

Prostacyclin (PGI2) is secreted to inhibit platelet aggregation
PGI2 also causes vasodilation

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

What happens when we have damage to the endothelial layer

A

We lose the ability to locally inhibit platelet aggregation and lose the ability to locally cause vasodilation

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

What is the 2nd step of platelet aggregation called?

A

secretion

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

Platelets adhere to damaged portion of BV through

A

GP1a and GP1B

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

What things are secreted after the adhesion of platelets

A

Platelets undergo degranulation and secrete ADP, thromboxane A2 (TXA2) and serotonin, which are pre-stored in platelet

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

WHat do the secreted factors from platelet do?

A

These factors bind to receptors on other platelets and recruit these platelets to site of damageWhich factors are potent vasoconstrictors

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

Thromboxane A2 and Serotonin

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

degranulation leads to secretion of

A

ADP, txA2 and serotonin.
These bind to other platelets

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

What receptor is an important pcol target to prevent platelet aggregation

A

ADP receptors

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

TXA2 stimulates

A

recruitment of platelets to site of damage

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

what is the final step in platelet aggregation

A

Platelatelet aggregation

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

What happens to platelets in platelet aggregation phase

A

Platelets undergo a shape change that activates their GP IIb/IIIa receptor.

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

What factors activate GP IIB/IIIa receptors

A

They are activated by the stimulation of ADP, TXA2 and serotonin, They can crosslink platelets to each other.

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

What is fibrinogen? what does it do?

A

Fibrinogen crosslinks platelets via fibrinogen binding to its BIVALENT receptors

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

What happens after platelets are cross linked by fibrinogen?

A

They fuse together and compact around site of damage. This becomes the substrate for formation of fibrin clot.

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

WHat are some targets to inhibit platelet aggregation?

A

Inhibit GP IIb/IIIa receptors, TXA2, ADP receptors or inhibit thrombin

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

WHat are some drugs that have actions related to platelets

A

COX-1 inhibitors, ADP receptor inhibitors, PDE 3 inhibitors, protease activated receptor inhibitors

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

What does aspirin (ASA) inhibit

A

COX-1 (covalently)

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

How does aspirin interfere with platelet aggregation? what effects will that have on the body? WHat is its use?

A

inhibits TXA2 production. Prolongs bleeding time. Prevents arterial thrombin formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Dose of aspirin that is used to inhibit platelet selectivity? Why this specific dose?

A

50-320 (81mg). At this dose, it leaves the prostacyclin production in endothelium alone and selectively inhibits thromboxane A2 production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is produced by COX2

A

PHI 2 (prostacyclin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

indication of aspirin

A

prophylaxis and tx of arterial thromboxane disorders

prevents thrombosis in unstable angina
Can be used with thrombolytic therapy
Prevents recurrence of strokes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Side effects of aspirin

A

prolongs bleeding
GI bleeding due to cox-1 ihibition (increased risk of this in in NSAID pts)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

WHat does COX 2 pruduce and what is its use?

A

Produces prostaglandin in endothelial cells. Vasodilation and inhibiton of platelet aggregation

34
Q

What does COX 1 produce? What is its use?

A

Produces thromboxane A2 in platelets. Used for vasoconstriction and platelet aggregation.

35
Q

What do selective COX 2 inhibitors do? what effect does this have?

A

They block synthesis of prostacyclin in endothelial cells, while not blocking TXA2. This leads to pro-platelet aggregation, increasing CV events.

36
Q

What is the name of the two adp receptors involved in activating platelets

37
Q

what receptors are P2Y1 and P2Y12 coupled to

A

P2Y1- GQ
P2Y12- Gs

38
Q

How does P2Y12 work?

A

it inhibits adenylyl cyclase

39
Q

What are drugs that target this receptor

A

Prasgurel, clopidogrel, ticagrelor, cangrelor

40
Q

WHat is the difference between the drugs that target P2Y12?

A

Prasgurel and clopidogrel undergo metabolism to active form (prodrugs) and are irreversible, while ticagrelor and cangrelor do not require activation and are reversible

41
Q

What happens when we block P2Y12

A

Prevents platelet aggregation

42
Q

Clopidogrel binds to? MOA?

A

binds to p2Y12. It is a prodrug that irreversibly blocks ADP receptors, inhibiting platelet activation.

43
Q

Clopidogrel duration of action? indication?

A

Long duration of action.
prevention of heart attack, stroke, peripheral vascular disease

44
Q

What kind of drugs are clopidogrel and prasgurel?

A

Theinopyridine drugs (they are also prodrugs)

45
Q

How is prasgurel activated?

A

Activated by esterase-1 CYP 3A4/2B6

46
Q

prasgurel warnings

A

Old people can not use it due to risk of bleeding

47
Q

Which P2Y12 drugs are reversible

A

Ticagrelor and cangrelor, they also have a short t1/2

48
Q

Ticagrelor is a substrate for____
Onset and duration?

A

CYP3A4.
Fast onset and short half life

49
Q

What is cangrelor used for

A

Used to prevent thrombosis during PCI
It is reversible, fast onset, short t1/s

50
Q

Clopidogrel is activated by

51
Q

prasgurel needs _____ to cleave its bonds

52
Q

What happens to prasgurel in the active form

A

The drug binds P2Y12 receptor and forms a disulfide cross link, becoming irreversible

53
Q

What does dipyridamole do?

A

Inhibits PDE III in platelets and acts as aggregation inhibitor

54
Q

dipyridamole can be used in conjuction with______ and ______ to prevent thrombosis

A

Warfarin and aspirin

55
Q

What does citazole do?

A

Also a PDE III inhibitor. Used in a condition called intermittent claudification.

56
Q

What does fibrinogen bind to? What does it do once bound?

A

Binds to GP IIb/III a to crosslink adjacent platelets

57
Q

What do GPIIb/IIIa inhibitors do?

A

They inhibit the ability of fibrinogen to crosslink the platelets

58
Q

Name GP IIb/IIIa inhibitor drugs

A

Abiciximab
Eptifibatide
tirofiban

59
Q

All of the GPIIb/IIa drugs ROA, they are all used in conjuction with

A

All IV
In conjuction with PCI

60
Q

What type of molecule is eptifibatide

A

Cyclic peptide

61
Q

What does Eptifibatide do?

A

Inhibits fibrinogen binding to decrease platelet aggregation

62
Q

Eptifibatide MOA

A

arginine (R), glycine (G), aspartic acid (D) motif is the basis of binding, which exists in fibrinogen to bind GPIIB/IIIA. So it is a perfect mimic

63
Q

What kind of molecule is tirofiban

A

small molecule

64
Q

MOA of tirofiban

A

R,G,D motif that acts as a mimic to bind to gPIIb/IIIa

65
Q

tirofiban can be compined with____

A

heparin to treat acute coronary syndrome

66
Q

What kind of drug is abriximab

67
Q

What is an important thing about abciximab that we should know

A

long duration of action, increased risk of bleeding

68
Q

Abciximab MOA

A

Binds to GPIIb/IIIa and inhibits platelet aggregation

69
Q

What are eptifibatide, tirofiban,abciximab indicated for?

A

all given IV for unstable angina and stents to prevent thrombosis

70
Q

What does thrombin do?

A

activates platelets

71
Q

how does thrombin activate platelets

A

Via protease activated receptor (PAR)

72
Q

MOA of thrombin on platelets

A

proteolytic cleavage of PAR-1 on platelet surface

73
Q

PAR is activated by

74
Q

why is cox 1 targeted in antiplatelet drugs

A

cox 1 synthesizes txa2,

75
Q

why is GPiib/iiia a target for antiplatelet activity

A

fibrinogen (protein that is cleaved to generate a fibrin clot) is bivalent and binds to two GPIIb/IIIa receptors to crosslink platelets. we can inhibit cross linking of platelets by targeting GPIIb/IIIa

76
Q

why is P2Y12 a target for antiplatelet activity

A

It secretes ADP, stopping this can inhibit aggregation

77
Q

what does thrombin do?

A

cleaves fibrinogen to fibrin.
activates PAR

78
Q

How does thrombin activate platelets

A

cleavage of PAR-1 receptors on platelet surface

79
Q

Vorapaxar MOA

A

inhibits I/A of thrombin with PAR, inhibits thrombin activation of platelet aggregation

80
Q

is vorapaxar reversible?

81
Q

Know structures of the drugs

Therapeutics P2 (41 decks)

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