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Cardiovascular Theme πŸ«€ > Antiplatelets, Anticoagulants , Fibrinolytics, Coagulation/Hemostatic > Flashcards

Antiplatelets, Anticoagulants , Fibrinolytics, Coagulation/Hemostatic Flashcards

1
Q

Arterial Side

A

High flow
High pressure
Platelet-rich
White thrombi

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1
Q

Venous Side

A

Low pressure
Fibrin-rich
Red thrombi

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2
Q

What is the mechanism by which aspirin affects platelet function?

A

Aspirin acetylates and irreversibly inactivates COX-1 in platelets.

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3
Q

How does Triflusal impact platelet aggregation?

A

Triflusal inhibits cAMP phosphodiesterase, leading to increased levels of cAMP, which, in turn, decrease platelet aggregation

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4
Q

What is the primary effect of Indobufen on platelet function?

A

Indobufen is a nonsteroidal anti-inflammatory drug that also has a potent reversible inhibitory effect on platelet COX-1.

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5
Q

NSAIDs Adverse Effects

A
  • Bleeding
  • GI ulcers (COX important to make stomach mucus layer)
  • Renal tox
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6
Q

How are NSAIDs eliminated?

A

Renally

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7
Q

NSAIDs Clinical uses

A

Indications: Arterial
* MI (during & post MI)
* Stroke
* Peripheral arterial disease
* Angina
* A-fib
* During and post PCI

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8
Q

What is the primary mechanism of action of Clopidogrel?

Anti-platelet drug

A

Clopidogrel is an irreversible ADP receptor antagonist.

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9
Q

Why is Clopidogrel considered a prodrug?

A

it requires activation by cytochrome P450 (CYP) enzymes to become active.

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10
Q

What is the typical onset time for the effects of Clopidogrel?

A

approximately 2 hours.

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11
Q

What adverse effects are associated with Clopidogrel use?

A

neutropenia, thrombotic thrombocytopenic purpura (TTP), and bleeding.

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12
Q

How is Clopidogrel eliminated from the body?

A

primarily eliminated through hepatic metabolism.

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13
Q

What is the time to off for the irreversible binding of Clopidogrel?

A

Clopidogrel’s irreversible binding effect has a time to off of 5-7 days.

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14
Q

How does Clopidogrel’s efficacy vary in relation to pharmacogenetics (pgx)?

A

Clopidogrel’s efficacy can be lower in poor metabolizers, demonstrating variable effects, and is influenced by pharmacogenetics.

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15
Q

Clopidogrel Indication:

A
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16
Q

What is the primary target of Clopidogrel in platelets?

A

Clopidogrel primarily targets platelet P2Y purinergic (ADP) receptors.

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17
Q

How does ADP initiate platelet aggregation, and how does Clopidogrel interfere with this process?

A

ADP initiates platelet aggregation by inhibiting adenylate cyclase. Clopidogrel interferes with this process by irreversibly blocking the P2Y purinergic receptors on platelets.

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18
Q

How is (S)-Clopidogrel metabolized in the body?

A

(S)-Clopidogrel is metabolized by CYP3A4 and CYP2C19 enzymes to form thiol metabolites.

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19
Q

What is the significance of CYP2C19 in Clopidogrel metabolism?

A

CYP2C19 plays a crucial role in metabolizing Clopidogrel, and patients deficient in CYP2C19 may be less responsive to the drug, increasing the risk of treatment failure.

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20
Q

For what medical conditions is Clopidogrel (Plavix) commonly prescribed?

A

prevention of ischemic stroke, myocardial infarction (MI), peripheral arterial disease, and it is often used in combination with aspirin.

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21
Q

What is the typical onset time for the effects of Clopidogrel after oral administration?

A

The onset time for the effects of Clopidogrel is approximately 2 hours after oral administration.

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22
Q

How long does it take for Clopidogrel’s irreversible binding to P2Y receptors to reverse?

A

The irreversible binding of Clopidogrel to P2Y receptors takes approximately 1 week to reverse.

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23
Q

What is the primary mechanism of action for Clopidogrel, Prasugrel, and Ticagrelor?

A

lopidogrel, Prasugrel, and Ticagrelor are all ADP receptor antagonists, which means they inhibit platelet activation by irreversibly binding to ADP receptors.

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24
Q

How is Clopidogrel activated in the body, and what is its primary limitation in terms of genetic variability?

A

Clopidogrel is an oral prodrug that requires activation by CYP enzymes, primarily CYP2C19. The limitation is that individuals with CYP2C19 deficiency may have reduced efficacy.

25
Q

How does Prasugrel differ from Clopidogrel in terms of genetic variability?

A

Prasugrel uses the same mechanism as Clopidogrel but has a different prodrug, eliminating the issue of CYP2C19 genetic variability.

26
Q

What is Ticagrelor’s unique feature regarding its prodrug status and onset of action?

A

Ticagrelor is not a prodrug; it has a direct action and offers a faster onset of action compared to prodrugs like Clopidogrel and Prasugrel.

27
Q

How long is the typical duration of action for Clopidogrel, Prasugrel, and Ticagrelor?

A

The typical duration of action for Clopidogrel, Prasugrel, and Ticagrelor is approximately 5-7 days.

28
Q

What is Cangrelor, and how does it differ from the oral antiplatelet medications in terms of pharmacokinetics?

A

Cangrelor is an intravenous (IV) medication that is highly polar, leading to rapid on/off effects. Its half-life is very short (2-3 minutes) due to rapid dephosphorylation.

29
Q

Why are some antiplatelet medications administered orally, and what factors, like size and polarity, influence this choice?

A

Oral administration is chosen for some antiplatelet medications because it offers convenience for long-term use. The size and polarity of molecules can influence their oral administration, as they must be able to pass through the gastrointestinal tract and be absorbed effectively.

30
Q

What is the primary target of RGD Mimetic inhibitors of GP IIb/IIIa?

A

RGD Mimetic inhibitors primarily target the GP IIb/IIIa receptor on platelets.

31
Q

Name three RGD Mimetic inhibitors used for antiplatelet therapy.

A

Three RGD Mimetic inhibitors used for antiplatelet therapy are Eptifibatide (Integrelin), Tirofiban (Aggrastat), and Abciximab (ReoPro).

32
Q

How does Eptifibatide work, and what is its chemical nature?

A

Eptifibatide is a cyclic hexapeptide that inhibits GP IIb/IIIa by mimicking the RGD (Arginine-Glycine-Aspartic Acid) sequence, which is essential for platelet aggregation.

33
Q

What is the unique feature of Tirofiban in comparison to other RGD Mimetic inhibitors?

A

Tirofiban is a non-peptidic mimic of the RGD loop of fibrinogen, which distinguishes it from the peptide-based inhibitors like Eptifibatide.

34
Q

What is the mechanism of action of Abciximab, and what makes it different from other inhibitors in terms of targets?

A

Abciximab is an antibody that binds to GPIIb/IIIa but can also bind to Ξ±VΞ²3. It has a longer duration of action, approximately 1 month.

35
Q

Why was Roxifiban, an oral compound, not successful in clinical trials?

A

Roxifiban, despite being an oral compound, failed in clinical trials due to mechanism-based toxicity, which included issues like bleeding and platelet count reduction.

36
Q

Why does aspirin have the strongest antiplatelet effect of all NSAIDS?
A. It has the highest affinity for COX-1
B. It is an irreversible inhibitor of COX-1 & 2
C. It is selective for COX in platelets
D. It is selective for COX in the endothelium

A

B. It is an irreversible inhibitor of COX-1 & 2

37
Q

Which of the following could decrease the ability of clopidogrel to reduce risk of stroke and MI in a patient after stent placement?
A. Addition of aspirin
B. High cholesterol levels
C. Loss of CYP2C19 function
D. Slow acetylator phenotype

A

C. Loss of CYP2C19 function

38
Q

Warfarin MOA

A

Prevent regeneration of Vit K

39
Q

What is the role of vitamin K in the coagulation process?

A

Vitamin K is an essential cofactor for the carboxylation of glutamate residues. This carboxylation process is crucial for the activation of various coagulation factors, making vitamin K vital for blood clotting.

40
Q

How is vitamin K used in the context of coagulation?

A

Vitamin K is used as a coagulant because of its role in promoting the carboxylation of clotting factors, which leads to their activation.

41
Q

What is the significance of inhibitors of vitamin K in the field of anticoagulants?

A

Inhibitors of vitamin K are commonly used as anticoagulants. They work by interfering with the vitamin K-dependent carboxylation process, reducing the activity of coagulation factors and preventing excessive blood clotting.

42
Q

Warfarin affects factors

A

Activation of FACTORS
X, IX, VII, II
β€œ1972” is often used to remember.

43
Q

Warfarin intereferes with

A

modification of clotting factors AND
protein C & S, thus it takes 3-5 days for all factors to be at lowest level (depends on t1/2)

44
Q

How is Warfarin eliminated from the body?

A

Warfarin is hepatically eliminated primarily by the enzymes CYP2C9 and CYP3A4.

45
Q

What is the half-life (T1/2) of Warfarin, and how long does its effect typically last?

A

Warfarin has a relatively long half-life of approximately 40 hours, and its anticoagulant effect can last for 2 to 5 days.

46
Q

What is monitored to assess the anticoagulant effect of Warfarin, and how is it measured?

A

The anticoagulant effect of Warfarin is monitored using prothrombin time (PT) tests, and the results are typically reported as the International Normalized Ratio (INR).

47
Q

What are some adverse effects associated with Warfarin use?

A

Adverse effects of Warfarin include an increased risk of bleeding. It is also contraindicated for use during pregnancy due to potential harm to the developing fetus.

48
Q

In cases of acute overdose or excessive anticoagulation with Warfarin, what can be used as a rescue treatment?

A

In cases of acute overdose or excessive anticoagulation with Warfarin, Vitamin K and Prothrombin Complex Concentrates (PCC) can be administered as rescue treatments to reverse its effects.

49
Q

What is the primary clearance mechanism for Heparin, and why is it considered β€œsticky”?

A

Heparin is primarily cleared by sticking to the surface of endothelial cells, macrophages, and other cells. It is considered β€œsticky” because it is a large, highly anionic polysaccharide that binds to many basic proteins in solution and on cell surfaces.

50
Q

What is the secondary clearance mechanism for Heparin, and when does it become more important?

A

The secondary clearance mechanism for Heparin is renal clearance, and it becomes more important with higher doses of Heparin, leading to an increase in its clearance half-life.

51
Q

How do Low Molecular Weight Heparins (LMWHs), such as enoxaparin, differ from traditional Heparin in terms of size and clearance?

A

LMWHs have a smaller and more homogeneous size, typically in the 4-6 kDa range, and they are fully cleared in the kidney with a half-life of about 3 hours. They are not administered orally and are typically given via intravenous (i.v.) or subcutaneous routes.

52
Q

What is the primary advantage of Heparin in certain medical situations, such as surgery?

A

Heparin still has a place in surgery due to its short half-life, which allows for rapid reversal of its anticoagulant effects using an antidote called protamine.

53
Q

Which of the following drugs interfere with
platelet activation through binding to the ADP
receptor?
A. Aspirin
B. Clopidogrel
C. Cangrelor
D. Abciximab

A

B. Clopidogrel
C. Cangrelor

54
Q

How does clopidogrel block the receptor
A. Acetylation of Cys in receptor
B. Disulfide formation with Cys in receptor
C. Gamma carboxylation of Cys in receptor
D. Protonation of Cys in receptors

A

B. Disulfide formation with Cys in receptor

55
Q

Why does it take about a week to reverse?

clopidogrel

A

The thiometabolite forms a covalent nonreversible bond to the ADP receptor, permanently inhibiting its activity. Platelets don’t have ability to express new proteins; new platelet production takes about a week.

56
Q

Which of the following is true about warfarin?
A. It interferes with hepatic modification of clotting factors
B. It interferes with hepatic modification of anticlotting factors
C. A & B
D. None of the above

A

C. A & B

57
Q

Which of the following anticoagulants
and monitoring test are paired correctly?
A. Warfarin aPTT
B. Heparin PT
C. Warfarin INR
D. Heparin INR

A

C. Warfarin INR

58
Q

A person with hemophilia B also called
factor IX deficiency is more likely to have an
abnormal value for which of the following
tests?
A. aPTT
B. PT/INR
C. Platelet count

A

A. aPTT

59
Q

Which receptor is responsible for linking platelets together?

A

GPIIb-IIIa Fibrinogen receptor

60
Q

Decide which receptor links to collagen through VWF

A

GPIb-IX-V

61
Q

Talk to your neighbor and decide which receptor is targeted by aspirin

A

TXA2 Receptor

Cardiovascular Theme πŸ«€ (15 decks)

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