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Pharmacology > Anticoagulants COPIED > Flashcards

Anticoagulants COPIED Flashcards

1
Q

Key mechanism of Warfarin (coumarin compounds)

A

Vitamin K antagonist

Vitamin K is used to synthesis coagulation factors II (prothrombin), VII, IX, and X

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2
Q

Name three LMWHs

A

enoxaparin

dalteparin

tinzaparin

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3
Q

What’s the management of acute thromboembolic disorders?

A

LMWH (Low molecular weight heparin) plus warfarin, and then withdraw LMWH when warfarin is effective.

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4
Q

Does Warfarin act immediately?

A

No because pool of circulating clotting factors needs to be depleted first.

Synthesis of new factors is then inhibited.

(takes 3-5 days to reach maximal effect)

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5
Q

What’s the advantages of LMWH compared to standard heparin?

A

can be administered subcutaneously.

more predictable anticoagulation activity (aPTT monitoring not required)

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6
Q

What is the INR for recurrent embolization or artificial heart valves?

What is the INR for warfarin (generally)

A

3 - 4.5

2-3

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7
Q

What is HIT?

A

Heparin-induced-thrombocytopenia

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8
Q

Name three LMWH

A

enoxaparin

dalteparin

tinzaparin

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9
Q

Tell me about HIT 2

A

less common, more serious.

Immunoglobulin mediated platelet inactivation.

High risk of thrombotic complications and mortality.

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10
Q

What’s the antidote for warfarin-induced bleeding

A

Phytonadione (vitamin K1)

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11
Q

What are the key adverse effects of Heparin?

A

Bleeding

thrombocytopenia

(hyperkalemia)

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12
Q

Tell me about HIT 1

A

occurs in 25% of patients. Direct interaction between heparin and platelets, leading to platelet aggregation. Mild and reversible.

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13
Q

Clinicial uses for Warfarin

A

Long term management of DVT, AF, and artificial heart values.

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14
Q

What is the principal component of fibrinolysis?

A

Enzyme plasmin

(generated from inactive precursor plasminogen)2

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15
Q

Can Warfarin be used in pregnancy?

A

No because it crosses the placenta

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16
Q

How does Dabigatran work?

A

Direct thrombin inhibitor

(thrombin is used in the pathway of transforming fibrinogen to fibrin)

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17
Q

How does LMWH compare to unfractionated heparin in it’s modus operandi?

A

Primarily deactive factor X

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18
Q

How does Fondaparinux work?

A

Indirect Factor Xa inhibitor

It selectively binds to antithrombin (an endogenous anticoagulant)

which

inactivates Xa resulting in a strong inhibition of thrombin generation and clot formation.

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19
Q

What is antithrombin?

A

an endogenous anticoagulant (potent inhibitor of coagulation)

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20
Q

Key mechanism of heparin

A

inactivates clotting factors by potentiating the activity of an endogenous anticoagulant (antithrombin III)

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21
Q

Can Heparin be given orally?

A

No because heparin and related anticoagulants are not absorbed from the gut (large molecules) and so much be administered by IV.

22
Q

Patient advise for Warfarin

A
  • Any signs of bleeding, including ecchymoses.
  • Contraindicated in pregnancy (fetal warfarin syndrome)
  • Avoid physical activities such as kick boxing
  • Don’t >>> green vegetables (vit K)
  • Avoid grapefruit juice, cranberry juice
  • Avoid major weight changes
  • Avoid aspirin, NSAIDs
23
Q

Some common uses of Warfarin

A

Long-term treatment of DVT

Patients with AF

Patients with artificial heart valves.

24
Q

How Warfarin monitored?

A

Prothrombin Time (PT)

25
Q

What does INR stand for?

A

International normalized ratio

INR = (PT observed / PT control)

PT = prothrombin time

26
Q

What is the antidote to unfractionated heparin and LMWH?

A

Protamine sulfate

(+ve charged protein than combines with -ve charged heparin)

** measure aPTT to monitor **

27
Q

How do you monitor

(a) Heparin
(b) Warfarin
(c) Dabigatran

A

(a) Heparin - aPTT

(b) Warfarin - PT - Prothrombin Time (remember the INR equation for warfarin)

(c) Dabigatran - TT (thrombin clotting time)

28
Q

What initiates the formation of platelets along the vascular wall?

A

injury and the expose of the blood to extravascular collagen.

29
Q

What activates the intrinsic pathway?

A

surface contact with a foreign body or extravascular tissue (i.e. collagen)

30
Q

What activates the extrinsic pathway in the coagulation cascade?

A

a complex tissue factor called thromboplastin.

31
Q

Where does the intrinsic and extrinsic pathways converge?

A

Factor X - major rate-limiting step

32
Q

What does the activation of factor X lead to?

A

the formation of Thrombin

33
Q

What three factors combined often lead to thrombic changes?

A
  • sluggish blood flow
  • inflammation
  • abnormalities in vascular endothelium
34
Q

What’s the difference between arterial thrombi and venous thrombi?

A

arterial thrombi (white); more platelet aggrevation driven

venous thrombi (red); more coagulation driven

35
Q

Aspirin; clinical usages and action as an antiplatelet drug

A

Acute coronary syndrome

Thrombic strokes; acute and prophylaxis

shown to prevent MI with angina.

Artificial heart valves, percutaneous coronary angioplasty.

ACTION: inhibits the synthesis of prostaglandins from arachidonic acid.

36
Q

What’s the most important prostaglandin affecting platelet aggregation?

A

prostacyclin and TXA2

(prostaglandin I2 (PGI2)

Aspirin irreversibly inhibits cyclooxygenase; enzyme that catalyzes TXA2 synthesis.

37
Q

Adverse effects of aspirin

A

GI bleeding

hypoprothrombinaemia; therefore increased bleeding risks

38
Q

When is clopidogrel indicated?

A
  • px who can’t tolerate aspirin
  • used in COMBINATION with aspirin for ACS
39
Q

When are the representative drugs steptokinase, alteplase indicated?

A

intravenously to degrade thrombi in px with

MI, thromvotic stroke, PE

Primary means of restoring coronary blood flow if angioplasty facilities not available.

40
Q

Adverse reactions with aspirin?

A

GI irritation, bleeding,

hypersensitivity reactions,

tinnitus

41
Q

Adverse reactions to streptokinase

A

bleeding, hypersensitivity reactions,

and reperfusion arrhymias (of interest)

anaphylactic shock can occur with streptokinase, therefore cannot be used repeatedly on same patient.

42
Q

what is t-PA and give an example drug

A

Alteplase

drugs that are ‘recombinant forms of human tissue plasminogen activator’

tissue-Plasminogen Activator

43
Q

How do Rivaroxaban, Apixaban, Edoxaban work?

A

Direct Factor Xa inhibitor

44
Q

How does Dagibatran work?

A

Direct thrombin inhibitor.

45
Q

What’s best for arterial thrombosis? Anticoagulants or antiplatelets?

A

Antiplatelets

46
Q

Some advantages of NOACs/ DOACs

A
  • few interactions with food/ drugs
  • predictable anticoagulant effect
  • no need for routine monitoring
47
Q

Which pathway does Warfarin affect?

A

Both intrinsic and extrinsic

48
Q

MOA of Heparin

A

binds to body’s own anticoagulant (antithrombin III)

This complex inhibits factor Xa (and other factors)

49
Q

What is Dipyridamole?

What is it indicated for?

A

Dipyridamole a coronary vasodilator and a relatively weak antiplatelet drug.

Dipyridamole is used in COMBO with aspirin to prevent ischaemic stroke in px with history of thrombotic stroke, and persons experiencing TIAs.

50
Q

What is Dipyridamole?

A

Dipyridamole is an antiplatelet medication that also has vasodilating properties that can make it unsuitable for use in those with severe coronary artery disease, unstable angina, recent myocardial infarction.

Can be combined with aspirin as an option to prevent occlusive vascular events in patients who have had a TIA, or ischaemic stroke.

Pharmacology (13 decks)

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