Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmaco Yr 2 Term 2 > Anti-thrombotic Drugs > Flashcards

Anti-thrombotic Drugs Flashcards

1
Q

What is the life cycle of a thrombus?

A 
Damage Vessel
--> Platelet Aggregation
White Thrombus
--> Coagulation Factors
Red Thrombus
--> Plasmin Fibrinolysis
Fibrin Dissolution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 3 types of anti-thrombotic Drugs?

A
  1. Anti-platelet Drugs
    Aspirin
    Clopidogrel
    Fibrinogen Receptor Antagonists
2. Anti coagulants
Unfractionated Heparin (UFH)
LMW Heparin (LMWH)
Warfarin
Rivaroxaban, Apixaban, Dabigatran
  1. Fibrinolytics
    Streptokinase
    Urokinase
    Tissue Plasminogen Factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does Aspirin work as an antiplatelet drug?

A

It is a irreversible cox inhibitor. It blocks more thromboxane (promotes platelet aggregation) in platelets than prostacycline (inhibits platelet aggregation) in endothelial cells, as the effect in platelets is more permanent due to platelets not being a full cell and having no nucleus hence being unable to synthesise new COX enzymes.

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

What are the uses of Aspirin?

A

To prevent arterial thrombosis (in myocardial infarction and stroke)

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

What is the dosage of aspirin used?

A

81mg/day

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

What are the side effects of Aspirin?

A

Peptic Ulcer, GI Bleeding (esp elderly), Allergy

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

What is the mechanism of action of clopidogrel (antiplatelet drug)

A

Clopidogrel (pro drug) is first converted in the liver by CYP2C19 enzymes into active metabolites. These active metabolites are P2Y12 Receptor Irreversible Antagonists, and inhibit ADP-induced platelet aggregation. This effect is active for the entire life-span of the platelet (7-10 days)

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

Why does Clopidogrel have a slow onset and variable effects?

A

This is because it is a pro drug and must first be metabolised by the liver

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

What are the uses of clopidogrel?

A

Prophylaxis of Arterial Thrombosis

Alternative to Aspirin

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

What are the side effects of clopidogrel?

A

Haemorrhage, Dypsnea (shortness of breath), Dizziness, Headache, Nausea

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

What are the different generation variations of clopidogrel?

A

1st gen: Ticlopidine - has more side effects eg. neutropenia, thrombotic thrombocytopenia purpura
Monitoring of WBC is necessary in the first 3 months

2nd gen: Clopidogrel (Pro-drug, slow onset)

3rd gen:
Prasugrel (Pro-drug, fast onset, irreversible)
Ticagrelor (Active drug, reversible)

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

What is an example of a fibrinogen receptor antagonist?

A

Abciximab

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

What is abciximab (fibrinogen receptor antagonist) used for?

A

Combination therapy in high risk patients undergoing angioplasty procedure (opening narrow blood vessel): Aspirin + Heparin + Abciximab

It helps to reduce ischaemic complications as well as prevent restenosis

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

What are the side effects of fibrinogen receptor antagonists?

A

Bleeding

Thrombocytopenia

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

What is a fibrinogen peptide analogue (Fibrinogen receptor antagonist)?

A

Eptifibatide

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

What is a non-peptide inhibitor (Fibrinogen receptor antagonist)?

A

Tirofiban

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

What is the mechanism of action of heparin?

A
  1. Binds and activates anti-thrombin III (through conformational change) which is a plasma protease inhibitor. This enhances anti-thrombin III interaction with clotting factors 2a, 9a, 10a by 1000 folds to form inactive complexes.
  2. Stimulates Tissue Factor Pathway Inhibitor (TFPI) release from endothelium.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is Heparin given?

A 
IV (immediate onset)
Subcutaneous injection (20-60 mins)

In the hospital

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

What is the HMW Fraction of standard heparin?

A

5-30kDa

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

Does Heparin cross the placenta?

A

no hence can be used in pregnant women

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

What are the uses of Heparin (Anti-coagulant)?

A
  1. Treatment and prophylaxis of Venous Thromboembolism, Deep Vein Thrombosis (DVT) and Pulmonary Embolism
  2. Also used in arterial thrombosis: Myocardial Infarction
  3. Induces Anticoagulant therapy followed by oral anticoagulant (warfarin)
  4. Used in pregnant women at risk of thrombosis
22
Q

What are the side effects of Heparin

A
  • Narrow Therapeutic Window
  • Bleeding (8-10%)
  • Allergy - from animal sources
  • Heparin-Induced Thrombocytopenia (HIT), transient (25%) and severe (5%)
    Platelet counts should be performed
    Causes paradoxical Thromboembolism

Long term use:

  • Osteoporosis/Spontaneous Fractures
  • Transient Reversible Alopecia (hair loss)
  • Mineralocorticoid Deficiency
23
Q

What is the management option for Heparin Induced Thrombocytopenia (HIT)/Allergy?

A

Discontinuation use of Heparin: Fondaparinux

New direct reversible thrombin 2a inhibitor (DTI): Argatroban

24
Q

What is the MW of LMW heparin?

A

2-6 kDa by fractionation of UFH

25
Q

What is the difference between LMW heparin and UFH?

A
  1. LMWH can be given as outpatient medication while UFH is given in the hospital
  2. LMWH is more homogenous than UFH
  3. Heparin Anti-thrombin III complex inhibits more factor 10a than 2a
  4. Greater bioavailability - LMWH: 90%
  5. Longer plasma half life - LMWH: 4hrs
26
Q

What are the uses of LMWH?

A

Prophylaxis and treatment of deep vein thrombosis

27
Q

What is an example of a LMWH?

A

Enoxaparin

28
Q

What is the efficiency of LMWH?

A

Same as HMW Heparin (UFH)

29
Q

What is the dosage/method of administration of LMWH?

A

Subcutaneous injection only (once or twice daily)

30
Q

What are the side effects of LMWH?

A
  • Similar risk of bleeding
    LESS
  • thrombocytopenia
  • osteoporosis
31
Q

What is an Oral Anticoagulant?

A

Warfarin

32
Q

What is Warfarin?

A

A Racemic mixture of 2 equal amounts of optical isomers (S-Warfarin (4x more potent) and R-Warfarin)

33
Q

What are Direct Anticoagulants - Factor 10a Inhibitors?

A

Rivaroxaban, Apixaban

34
Q

What are Direct Anticoagulants - Factor 2a Inhibitors?

A

Argatroban, Dabigatran

35
Q

What is the mechanism of action of Warfarin?

A

It inhibits the Vitamin K Epoxide Reductase enzyme which is needed to convert KO (inactive epoxides) into KH2 (Active hydroquinones) which is needed to convert non-functional coagulation factors into functional coagulation factors with y-Carboxylase enzyme.

36
Q

What is the onset, peak effect, plasma halflife and duration of action of Warfarin?

A

Onset: Slow (8-12 hrs)
Peak effect: 1-3 days
Plasma half life: 36 hrs
Duration of Action: 4-5 days

37
Q

How is warfarin metabolised?

A

Hepatic Microsomal

S-Isomer is more rapidly metabolised than R isomer

38
Q

Does warfarin cross the placenta?

A

Yes, hence it is contraindicated in pregnancy

39
Q

What are the uses of warfarin?

A
  1. Maintenance of anticoagulant therapy
  2. Prophylaxis and treatment of venous thromboembolism (DVT and PE)
  3. Patients who suffered an MI, Stroke or transient ischemic attack (TIA)
  4. Potent Rodenticide
40
Q

What are the side effects of warfarin?

A
  • Narrow Therapeutic Window
  • Bleeding
  • Cutaneous necrosis and rarely infarction of breast, buttock, intestine, extremities
In babies:
Teratogen: Fetal Warfarin Syndrome
Severe Birth defects: Bone/CNS
Hemorrhagic Fetus
Abortion
41
Q

What are some examples of drugs that cause enhanced anticoagulant effects?

A
  • metronidazole
  • fluconazole
  • co-trimoxazole
  • aspirin
  • cephalosporin (3rd gen)
  • heparin
42
Q

What are some examples of drugs that cause reduced anticoagulant effects?

A
  • barbituates (eg. thiopentone) –> GA
  • phenytoin, carbamezapine, phenobarbitone
  • rifampicin (antibiotic)
43
Q

What is the treatment for overdose of anticoagulant?

A

Discontinuance

Heparin Antidote: Protamine Sulfate - highly basic peptide forming stable complex with heparin
Warfarin Antidote: Vitamin K1 (Phytonadione) re-establishes normal activity of clotting factors

44
Q

What are 3 examples of Fibrinolytics?

A

Streptokinase, Urokinase, Tissue plasminogen Activator

45
Q

What is the mechanism of action of Fibrinolytics?

A

It activates the conversion of Plasminogen to Plasmin

46
Q

What is the route of administration of Fibrinolytics?

A

IV

47
Q

What is the source of Fibrinolytics?

A

Streptokinase: Streptococci
Urokinase: Human Kidney
Tissue plasminogen activator: Human Recombinant

48
Q

What is the type of plasminogen activation of fibrinolytics?

A

Streptokinase: free and fibrin bound
Urokinase: free and fibrin bound
Tissue plasminogen activator: fibrin bound

49
Q

What is the side effects of fibrinolytics?

A

Haemorrhage

Allergy (Streptokinase)

50
Q

What are the uses of fibrinolytics?

A
  1. Acute myocardial infarction
  2. Acute ischaemic stroke
  3. Acute pulmonary embolism
51
Q

What are the efficacies of the fibrinolytics?

A

All are comparable in reperfusion rate, LVF preservation and overall survival
Tissue plasminogen activator lyses clots faster

Pharmaco Yr 2 Term 2 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions