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Pharmacology > Blood Coagulation > Flashcards

Blood Coagulation Flashcards

1
Q

What is thrombosis associated with in the arteries and in the veins?

A

Arterial: atherosclerosis
Venous: DVT

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2
Q

Describe the extrinsic pathway of blood coagulation.

A

Utilises pre-formed factors hence, is rapid and short-lasting. In vivo pathway including tissue factor and factor VIIa.

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3
Q

Describe the intrinsic pathway of blood coagulation.

A

Longer to activate compared to the extrinsic pathway, longer lasting. Includes factors XII and XI.

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4
Q

Release of which mediators assists in platelet aggregation?

A

ADP, TXA2, PAF.

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5
Q

What is the major endogenous inhibitor of blood coagulation?

A

Antithrombin III

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6
Q

Where does ATIII act in the thrombosis pathway?

A

Factors XIIa, XIa, iXa, Xa, IIa and thrombin.

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7
Q

Which factors released by the vascular endothelial cell layer inhibit player aggregation?

A

PGi2 and NO

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8
Q

What is the route of administration of heparin?

A

I.v. or s.c.

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9
Q

What is the molecular weight of heparin?

A

Daltons

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10
Q

Can heparin be used in vitro or in vivo?

A

Both, in vitro and in vivo

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11
Q

What is the endogenous form or haparin?

A

Heparan sulfate in endothelium.

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12
Q

What is the mode of action of heparin?

A

Binds to ATIII as ATIII binds to serine site of clotting factors IIa (thrombin), IXa, Xa, XIa and XIIa to inhibit clotting.

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13
Q

List two examples of LMWH.

A

Dalteparin and enoxaparin.

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14
Q

What is the molecular weight of LMWH and heparin?

A

LMWH: 4000-15000
Heparin: 3000-40000

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15
Q

What are the advantages of LMWH over heparin?

A

Greater bioavailability, longer 1/2 life, lower effect on platelet function.

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16
Q

Which clotting factors does LMWH most affect?

A

Factor Xa, does not reach others.

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17
Q

List the indications for heparin.

A

Surgery, IV device patency, unstable angina, prevention of arterial thrombosis in coronary angioplasty.

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18
Q

List the common side effects of heparin.

A

Haemorrhage, bruising, pain
Thrombocytopaenia (reduce platelet count, reduced with LMWH) - can be transient-severe in 25% of patients or severe rarely, involving Ab formation.

19
Q

What is the antidote to heparin?

A

Protamine - basic protein that forms inactive complex with heparin.

20
Q

What is the route of administration of warfarin?

A

Oral

21
Q

How is vitamin K involved in thrombosis?

A

Its oxidation clotting factors are activated into gamma-carboxyglutamic acid residue forms.

22
Q

What is the mechanism of action of warfarin?

A

Vitamin K antagonist

23
Q

Regarding warfarin, what contributes to drug interactions, what is the 1/2-life and onset time and can it be used in vivo or in vitro?

A

Binds to plasma proteins
Variable 1/2-life, days for onset as clotting factors degrade
In vivo only

24
Q

List the indications for warfarin.

A

Treatment/prophylaxis of throboembolic disorders and cardiac complications:
PE, DVT, unstable angina, atrial fibrillation caused stroke

25
Q

What are the adverse effects of warfarin?

A

Bleeding, haemorrhage, (nose, urine, faeces)

Dose-monitoring required.

26
Q

What is the antidote for warfarin?

A

Oral or i.v. vitK, slow onset

27
Q

Why is dose monitoring important in warfarin use?

A

Large variability in response due to variable onset, long 1/2-life, drug interactions, diet.

28
Q

What is the normal INR range for warfarin?

A

0.9-1.3

29
Q

List factors that increase and decrease the response to warfarin.

A

Increase: vitK deficiency, liver disease, ageing.
Decrease: pregnancy (avoid in early and late stages), poor patient compliance, vitK (green leafy vegetables), alcohol.

30
Q

List drugs that decrease the effect of warfarin.

A

Barbituates, rifampicin, carbamazepine (anti-epileptic), alcohol, vitK

31
Q

List drugs that increase the effect of warfarin.

A

Cimetidine (anti-ulcer), amiodarone

Salicylates (NSAID aspirin) due to displacement and anti-platelet effect.

32
Q

When are anticoagulant drugs used?

A

Surgery, DVT, atrial fibrillation, prosthetic heart valves, unstable angina.

33
Q

What is the mechanism of action of dabigatran?

A

Direct inhibition of thrombin

34
Q

Compare dabigatran to warfarin.

A

Increased stroke reduction, similar/reduced bleeding, no need for INR or dose monitoring, no/minimal drug and diet interactions, potentially hidden side ADRs and deaths.

35
Q

List classes of anti-platelet agents.

A

COX inhibitors, phosphodiesterase inhibitors, inhibitors of platelet binding/adhesion.

36
Q

List the adverse events of aspirin.

A

GI: dyspepsia, nausea, vomiting, bleeding

Gout (uncommon)

37
Q

What are the indications for low-dose aspirin therapy?

A

Prevention of stroke and MI, high-risk patients, unstable angina, post-MI, post-surgery

38
Q

List “other” anti-platelet compounds

A

Adenosine P2Y12 receptor blockers on platelents, inhibit ADP-induced aggreagtion (clopidogrel, ticlopidine)

Abciximab - glycoprotein IIb/IIIa receptor antagonist on platelets, prevents binding of fibrinogen to platelets

Phosphodiesterase inhibitors, increase cAMP, inhibit thromboxane A2 synthesis, vasodilate (dipyridamole)

39
Q

What are the indications for antiplatelet drugs?

A

Thromboembolic disorders, cardiac complications.

40
Q

List the ADRs of antiplatelet drugs?

A

Bleeding (severe - clopidogrel), headache, nausea (dipyridamole), antibody development, thrombocytopenia (low platelets) (abciximab).

41
Q

What is the mechanism of action of fibrinolytic drugs, such as tPA?

A

Converts plasminogen to plasmin.

42
Q

What factor gives tPA some selectivity?

A

Targets plasminogen adsorbed to fibrin.

43
Q

What are the indications for fibrinolytic agents?

A

AMI <12 hours
PE
Acute thrombotic stroke <4.5 hours

Pharmacology (14 decks)

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