3.B-Antiplatelets Flashcards

1
Q

What can arterial thrombosis cause?

A

ischemic necrosis of tissue supplied by the artery

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2
Q

What does arterial thrombosis often result in?

A

MI
stroke
limb gangrene

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3
Q

What is the appearance of a desired artery?

A

open
no blockage of blood flow
sheet of endothelial cells

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4
Q

What can enter the sub endothelial space of an artery if that artery has been damaged by hypertension?

A

LDL

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5
Q

Where do atherosclerotic plaques form?

A

arteries

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6
Q

What causes atherosclerosis?

A

infiltration of the sub-endothelial space by LDL

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7
Q

What can happen if an atherosclerotic plaque ruptures?

A

ischemia or infarction

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8
Q

What are platelets?

A

circulating cells that aggregate on damaged blood vessel walls

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9
Q

What do you we mean when we say that a ruptured atherosclerotic plaque “fools” platelets?

A

the rupture makes platelets think there is damage to the vessel wall, resulting in the aggregation of platelets on the wall and blocking blood flow

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10
Q

What is ischemia?

A

inadequate blood supply to a tissue

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11
Q

What is infarction? Give an example.

A

a complete version of ischemia, cell death results
ex: myocardial infarction (heart attack)
-death of cardiac muscle as a result of insufficient blood flow

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12
Q

What are the three possible consequences of ischemia? List the artery being affected.

A

myocardial infarction (heart attack)
-occurs in coronary artery (coronary artery disease)
cerebrovascular accident (stroke)
-occurs in cerebral arteries
peripheral arterial disease
-occurs in arteries of limbs

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13
Q

What are some characteristics of platelets?

A

fragments of larger multinucleated cells
no nucleus
contain granules in cytoplasm
contain COX-1

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14
Q

What are the three jobs of platelets?

A

adhere to damaged vessel walls
aggregate to form a platelet plug
activate coagulation cascade & other platelets

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15
Q

How do platelets adhere to injured areas?

A

activation of glycoprotein Ib receptors
-constitutively expressed on platelet surface
-affinity for collagen and vWF

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16
Q

What are the mechanisms for platelet activation?

A

exposure to subendothelial surfaces
exposure to chemical activators

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17
Q

Which receptors emerge once a platelet has become activated?

A

glycoprotein IIb/IIIa

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18
Q

What is the job of the GP IIb/IIIa receptor?

A

promote platelet aggregation

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19
Q

What is the main target of the GP IIb/IIIa receptor?

A

fibrinogen

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20
Q

What is the role of fibrinogen?

A

precursor of fibrin
links platelets to ensure aggregation
localizes substrates for clot formation

21
Q

Which granules do activated platelets release? What happens after they are released?

A

ADP and TXA2
activation of resting platelets and initiates coagulation cascade

22
Q

What is the precursor of prostacyclin? Which cells produce prostacyclin?

A

arachidonic acid
endothelial cells

23
Q

What does prostacyclin promote?

A

vasodilation
decreases platelet aggregation

24
Q

What are the products of cyclooxygenase in arteries?

A

arachidonic acid is the precursor to both
COX-1 –> thromboxane A2
COX-2 –> prostacyclin

25
Q

Which enzyme does ASA inhibit?

A

COX-1 and COX-2
50-100x more potent for COX-1 at 81mg

26
Q

What type of inhibitor is ASA?

A

irreversible inhibitor
-platelets cannot regenerate COX
-allows OD dosing

27
Q

What are the ADP receptor antagonists?

A

clopidogrel
prasugrel
ticagrelor

28
Q

True or false: clopidogrel is a prodrug that requires activation in the liver by CYP 2C19

A

true

29
Q

What does clopidogrel do?

A

inhibits ADP receptor
*remember that ADP can activate platelets

30
Q

What kind of inhibitor is clopidogrel?

A

irreversible inhibitor

31
Q

What does prasugrel do?

A

ADP receptor antagonist

32
Q

True or false: prasugrel is a prodrug but it has way more intra-subject variability compared to clopidogrel

A

false
yes its a prodrug but there is less variability than clopidogrel

33
Q

With prasugrel there is concern for serious bleeding in some patients, what are the risk factors?

A

older than 75
less than 60kg

34
Q

What is different about ticagrelor compared to the other ADP receptor antagonists?

A

it is a reversible inhibitor
not a prodrug

35
Q

Where is ticagrelor commonly seen?

A

post-MI

36
Q

What are the common agents to prevent MI/stroke?

A

ASA
clopidogrel
ticagrelor
prasugrel

37
Q

True or false: ASA, clopidogrel, prasugrel, and ticagrelor can reduce the risk of atherosclerotic plaque rupture

A

false
they prevent the consequences following rupture

38
Q

Where are glycoprotein IIb/IIa inhibitors used? What is the dosage form?

A

hospital
parenteral (IV)

39
Q

What are the glycoprotein IIb/IIIa inhibitors?

A

abciximab
eptifibatide
tirofiban

40
Q

What is the role of nitroglycerin in CAD?

A

manage or prevent angina

41
Q

What is angina?

A

pain or discomfort resulting from inadequate supply of blood to cardiac muscle

42
Q

How can preload be decreased with nitroglycerin?

A

nitroglycerin acts on veins, more blood can pool in veins
consequently decreases workload which reduces pain from angina

43
Q

What are all the options for the management/prevention of angina?

A

nitroglycerin spray or patch
beta blockers and non-DHP CCBs
DHP CCB

44
Q

Which tissue is affected by atherosclerosis?

A

arteries

45
Q

What is the final product of the coagulation cascade?

A

fibrin

46
Q

How strong of an effect does ASA 81mg have on prostacyclin?

A

very minimal effect

47
Q

True or false: just like ASA, all NSAIDs are irreversible inhibitors of COX-1 and are indicated for antiplatelet actions?

A

false
most NSAIDs are reversible inhibitors, COX-2 selective, and not indicated for antiplatelet action

48
Q

What would happen to a person with stable angina at rest? What about during exercise?

A

at rest: perfusion of cardiac muscle is adequate, no angina
exercise: perfusion cannot match increased cardiac workload,
angina develops