Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology > Antiplatelet and Antithrombotics > Flashcards

Antiplatelet and Antithrombotics Flashcards

1
Q

What is aspirin?

A

COX I and II inhibitor

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

What is clopidogril?

A

ADP receptor antagonist

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

What is abciximab?

A

GPIIb/IIIa antagonist

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

What is heparin?

A

Antithrombin III activator

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

What is LMW heparin?

A

Antithrombin III activator

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

What is protamine sulfate?

A

Binds heparin and LMW heparin

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

What is warfarin?

A

Vitamin K antagonist

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

What is dabigatran?

A

Direct thrombin inhibitor

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

What is idarucizumab?

A

Binds direct thrombin inhibitors

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

What is rivaroxaban?

A

Direct factor Xa inhibitor

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

What is andexanet alfa?

A

Binds direct factor Xa inhibitors

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

What is tissue plasminogen activator

A

Activates plasminogen

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

What is hemostasis?

A

The process of arresting the loss of blood from injured vessels

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

What is hemostatic plug?

A

Formed by aggregated platelets and then stabilized by cross-linked fibrin fibres

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

What is thrombosis?

A

Unwanted formation of a hemostatic plug or clot inside a blood vessel or heart chamber

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

What is good and bad about the formation of a clot in a blood vessel?

A

It is beneficial to stop bleeding (normal hemostasis)

But may also obstruct blood flow

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

What is a thrombus?

A

Blood clot attached to a blood vessel
It may obstruct flow
Pieces may break off which then “plug” capilllaries

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

What is an emboli?

A

Portion of thrombus that breaks away
Clot floating in the blood
If “mobilized” it will get stuck in the capillaries
The damage depends on where it lodges (heart, brain, lung)

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

How are the arterial and venous sides of circulation different (from a blood clotting perspective)?

A

Arterial side is platelet rich

Venous side is rich in red blood cells

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

What is atherosclerosis? Why is it problematic?

A

It the build of cholesterol and it may partially obstruct blood flow in the arteries. Eventually the plaque damages the endothelium (thrombus forms)
Blood flow is blocked by the atherosclerosis and the thrombus.
If the thrombus ruptures it’s called an embolus and it can lodge in the capillary and block flow

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

What happens if there is damaged endothelium in the parties? What damages the endothelium?

A

The damaged endothelial layer stimulates thrombus formation
Atherosclerosis damages the endothelial layer
Physical damage can be caused by ballon angioplasty, stenting

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

What happens if an artery perfuses a the brain and there’s thrombosis?

A

The emboli can lodge in the cerebral capillaries and cause an acute ischemic stroke

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

What happens if an artery perfuses the heart muscle and there’s thrombosis?

A

The emboli can lodge in coronary arteries and cause an acute myocardial infarction

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

Describe venous thrombosis

A

It involves red blood cells and not platelets
It is more related to stagnant flow in the veins and/or atria
Problems post surgery, long term bed rest or just sitting (long plane rides)
Clots form and if dislodges (emboli) the flow in the capillaries in the lungs can be obstructed (pulmonary embolism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are the two major sites of venous clot formation?
``` Lower leg veins (deep vein thrombosis) Right atria (if atria is not contracting properly) ```
26
What is the platelet response to vascular injury?
1. Formation of a platelet plug 2. Coagulation (clot formation) 3. Fibrinolysis
27
How does a platelet plug form?
Platelet adhesion Platelet activation Platelet aggregation
28
Describe coagulation
It stabilizes the clot (platelet plug) | Thrombin increases fibrin formation (re-infroces platelet plug)
29
What is fibrinolysis?
Clot dissolving (as would heals the clot is removed)
30
What drugs affect the formation of a platelet plug?
Platelet inhibitors - COX inhibition (aspirin) - ADP receptor blockers (clopidogrel) - GPIIb/IIIa block (abciximab)
31
What drugs affect coagulation?
Anticoagulants - thrombin inhibition (heparin) - vitamin K antagonist (warfarin) - thrombin antagonist (dabigatran) - factor Xa inhibitor (rivaroxaban)
32
What drugs affect fibrinolysis?
Thrombolytic agents | -fibrin breakdown (tissue plasminogen activator)
33
How does prostacyclin affect platelet aggregation?
Healthy, intact endothelium releases prostacyclin (PGI2) into the plasma It binds to the platelet membrane receptors, causing the synthesis of cAMP cAMP stabilizes inactive GPIIb/IIIa receptors and inhibits platelet aggregation agents or calcium
34
What are platelet activating mediators?
Thromboxane A2 ADP Serotonin PAF
35
What are the steps to the formation of a platelet plug?
Damaged endothelium causes the exposure of collagen Platelets stick to exposed collagen Platelets are activated and release mediators to excite other platelets Released mediators activate resting platelets and recruit to the platelet plug Activation of GPIIb/IIIa receptors binds fibrinogen linking platelets Avalanche of platelet aggregation (which releases more mediators)
36
How do we prevent plug formation?
Selective change in prostaglandin levels -increase/maintain endothelial prostacyclin -decrease thromboxane A2 levels in platelets Block effects of released mediators (block ADP receptor) Prevent GPIIb/IIIa receptor coupling (block the receptor)
37
How does aspirin prevent the formation of platelet plugs?
Aspirin inhibits cyclo-oxygenase (irreversibly blocks it) COX is the enzyme necessary for the formation of prostaglandins Prostaglandins are ubiquitous and do many things
38
Why does the inhibition of COX enzymes prevent platelet formation?
In platelets, COX produces thromboxane A2 which promotes aggregation In vascular endothelium, COX produces PGI2, which acts on platelets to increase stability (less likely to aggregate) A balance between TxA2 and PGI2 determines how "sticky" the platelets will be
39
If COX produces TxA2 and PGI2, how does aspirin impede aggregation?
Aspirin irreversibly blocks COX, so a cell needs to produce new COX to be able to synthesize TxA2 and prostaglandins Platelets lack a nucleus so they cannot generate new COX. The lifespan of a platelet is 7-10 days, so throughout, there won't be any new TxA2 Vascular endothelial cells have nucleus and are able to generate more COX and therefore more PGI2 So the balance shifts towards PGI2
40
What are the problems associated with the use of aspirin?
Can cause problems associated with increased bleeding - hemorrhagic stroke - GI bleeding - easy bruising
41
What does clopidogrel do?
It prevents ADP from binding to platelets (ADP binding to platelets activates the GPIIb/IIIb receptors) Fibrinogen is now unable to link platelets and aggregation is significantly decreased It is effective in preventing ischemic stroke and myocardial infarction It is given routinely during stent insertion during a MI
42
What is the problem with clopidogrel?
``` Bleeding may be prolonged and hard to stop Easy bruising (bleeding) ```
43
What does abciximab do?
It's a monoclonal antibody against the GPIIb/IIIa receptor. This prevents fibrinogen from binding and "joining" platelets and aggregation of platelets can not occur Potential problems for bleeding and bruising Given IV
44
What is the goal of the coagulation pathway?
There are two pathways that result in thrombin activation and ultimately fibrin formation. Both pathways involve a number of coagulation factors and the purpose of both it to convert prothrombin into thrombin. Thrombin in turn converts fibrinogen into fibrin
45
What activates the intrinsic pathway of coagulation?
Factors released from the site of damage
46
What activates the extrinsic pathway of coagulation?
Tissue factors released from elsewhere (not the site of damage)
47
Why is vitamin K important?
Vitamin K is an important factor in the synthesis of many of the coagulation factors (factors II, VII, IX and X) Low vitamin K is associated with bleeding disorders
48
What does antithrombin III do?
It naturally inactivates thrombin and Factor Xa (decreasing fibrin formation)
49
What does heparin do?
It is usually given as unfractionated heparin and low molecular weight heparin Heparin leads to thrombin inactivation by binding to antithrombin and increasing its activity It prevents expansion of the thrombi by blocking fibrin formation
50
When do we use heparin?
Used in the prevention of arterial and venous thrombosis (post-op venous thrombosis, coronary re-thrombosis following thrombolytic treatment) Used in the treatment of pulmonary embolism and acute MI Anticoagulant choice in pregnancy (does not cross the placenta)
51
How do we treat excessive bleeding (due to heparin)?
Antidote: protamine sulfate, given IV
52
How is heparin given (not LMWH)? What is the IV half life? When is the anticoagulant response? What is the bioavailability? What is the major adverse effect? What is the setting for therapy?
``` IV or SC 2 hours Variable 20% Frequent bleeding Hospital ```
53
How is low molecular weight heparin given? What is the IV half life? When is the anticoagulant response? What is the bioavailability? What is the major adverse effect? What is the setting for therapy?
``` IV or SC 4 hours Predictable 90% Less frequent bleeding Hospital and outpatient ```
54
What is warfarin?
It is a vitamin K antagonist
55
Why is warfarin losing popularity?
It requires constant monitoring and visits to the clinic (International Normalized Ratio needs to be measured) LMWH is given easily SC and has predicable/reproducible effects Newer oral anticoagulants are now available (NOACs)
56
What are the adverse effects of warfarin?
``` Effects are variable Bleeding disorders (major problem) Many drug interactions Dietary interactions Avoid during pregnancy (teratogenic and may cause abortion) ```
57
What are dabigatrin and rivaroxaban?
They are novel oral anticoagulants (NOACs) Dabigatran directly inhibits thrombin Rivaroxaban directly inhibits factor Xa
58
When do we use novel oral anticoagulants?
``` Percutaneous cardiac interventions Venous thromboembolism (prophylaxis and management) Hip/knee replacement (post surgery) ```
59
Why are NOACs superior to heparin and warfarin?
Heparin and warfarin have very narrow therapeutic windows | These can be used without measuring drug levels or coagulation times
60
Why are dabigatrin and rivaroxaban so great?
They are orally active direct thrombin inhibitors (decrease in fibrin formation, natural dissolution of clot) Used post-op for knee and hip replacements to prevent/manage venous thromboembolism Rapid, predictable response and orally active
61
What is the response to excessive bleeding due to dabigatrin?
Intravenous antidote: idarucizumab | It's monoclonal antibody fragment that binds to dabigatrin
62
What is the response to excessive bleeding due to rivaroxaban?
Andexanet alfa | It's a modified Factor Xa molecule that binds directly to to factor Xa inhibitors
63
What does plasmin do?
It breaks down fibrin, dissolving the clot
64
What is tPA?
Tissue plasminogen activator | Can be used as a fibrinolytic drug (alteplase)
65
What does tPA do?
It activates tissue plasminogen that is bound to fibrin | The increase in plasmin breaks down the clot
66
What do we use tPA for?
MI Massive pulmonary embolism Acute ischemic stroke

Pharmacology (15 decks)

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