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Maddie’s Pharm > Antiplatelets, Anticoagulants and Thrombolytics > Flashcards

Antiplatelets, Anticoagulants and Thrombolytics Flashcards

1
Q

List five common thromboembolic diseases. (5)

A

DVT, PE, TIA, MI, stroke.

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2
Q

Explain the differences between a thrombus and an embolus. (2)

A

Thrombus: a clot adhered to a vessel wall.
Embolus: intraluminal clot that is distal to the site of origin.

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3
Q

Describe a venous thrombosis.
Causes (2)
Clot features. (3)
Treatments (2)

A

Associated with stasis of blood or abnormalities of the vessel wall.
Low platelet content, high fibrin content, called “red”.
Prescribe anticoagulants to prevent (warfarin or heparin).

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4
Q

Describe an arterial thrombosis.
Causes (1)
Clot features (3)
Treatments. (2)

A

Associated with atherosclerotic plaque rupture.
Platelet rich, but low fibrin, called “white”
Prescribe antiplatelet or fibrinolytic drugs.

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5
Q

Describe the effects of aspirin in low doses. (3)

A

Anticoagulent - irreversible COX-1 inhibition to inhibit thromboxane.

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6
Q

Explain why aspirin must be given in low doses to be an anticoagulent. (4)

A

Because at high doses, it inhibits COX-1 and COX-2, which blocks prostacyclin production, meaning it acts as an antipyretic and analgesic but can be pro-thrombotic.

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7
Q

Describe the pharmacokinetics of aspirin. (3)

A

t1/2 is 20 mins unless hydrolysed in the liver to salicylic acid which has a t1/2 of 3-12 hours.

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8
Q

Describe the ADRs of aspirin. (3)

A

Bleeding time is prolonged, increased risk of haemorrhagic stroke, peptic ulcer bleeding.

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9
Q

Explain why aspirin has to be stopped about a week before a surgery. (3)

A

Because aspirin inhibition of COX-1 is irreversible, so you have to wait until all of the platelets that have been inhibited have been destroyed. The lifespan of a platelet is about 7 days.

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10
Q

Describe 4 indications for aspirin therapy. (4)

A

Secondary prevention of stroke or TIA if other agents contraindicated.
Secondary prevention of acute conronary syndrome.
Post primary percutaneous coronary intervention or stent
Secondary prevention of MI in stable angina or peripheral vascular disease.

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11
Q

Describe the mechanism of action of P2Y_12 receptor antagonists (2)

A

Inhibit binding of ADP to P2Y_12 receptors. This inhibits the activation of GP IIb / IIIa receptors.

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12
Q

Name three P2Y_12 receptor antagonists. (3)

Give the common feature of the names of these drugs. (2)

A

Clopidogrel, prasugrel, ticagrelor.

Have -grel- in them, normally at the end but not always.

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13
Q

Describe the pharmacokinetics of clopidogrel. (3)

A

A prodrug with hepatic metabolism and a t1/2 of 7-8 hours.

Needs a loading dose for predictability of effect.

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14
Q

Describe the common indications for clopidogrel prescription. (4)

A

Reduces morbidity and mortality following an embolus stroke.
Reduces secondary events post MI (only prescribed for one year with aspirin)
Useful for prophylaxis in patients intolerant to aspirin.

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15
Q

Describe the pharmacokinetics of prasugrel. (3)

A

A prodrug with hepatic metabolism and a t1/2 of about 8 days.

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16
Q

Describe the pharmacokinetics of ticagrelor and explain why it is not commonly used. (3)

A

Given in active form and has active metabolites.

Very expensive.

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17
Q

Describe the MoA and effectiveness of GP IIb / IIIa inhibitors. (2)

A

Targets the final common pathway of complete aggregation. Results in an 80% reduction in aggregation.

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18
Q

Name three GP IIb / IIIa inhibitors and describe their mechanisms of action. (6)

A

Abciximab - monoclonal antibody irreversibly blocks GP IIb / IIIa to prevent fibrinogen binding.
Eptifibatide - synthetic peptide that binds irreversibly.
Tirofiban - reversible antagonist.

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19
Q

Describe the main ADR of GP IIb / IIIa inhibitors. (1)

A

Thrombocytopenia.

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20
Q

Name one phosphodiesterase inhibitor. (1)

A

Dipyridamole

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21
Q

Describe the MoA of a phosphodiesterase inhibitor. (6)

A

Inhibits cellular uptake of adenosine to increase plasma levels leading to platelet aggregation inhibition through A2 receptors.
Also a phosphodiesterase inhibitor which prevents the degeneration of cAMP and cGMP which inhibits the expression of GP IIb / IIIa.

22
Q

Describe the pharmacokinetics of a phosphodiesterase inhibitor. (2)

A

Hepatic metabolism with a t1/2 if around 12 hours.

23
Q

Describe the common indications of a ohosphodiesterase inhibitor, and it’s ADRs. (4)

A

Secondary prevention of a TIA or stroke.
With other anticoagulents following valve replacement.
ADRs include flushing and headaches.

24
Q

Name the two types of fibrinolytic agents and describe their MoAs. (4)

A

Streptokinase and plasminogen activator - targets plasminogen to encourage formation of plasmin, which breaks down fibrin.

25
Q

Name one plasminogen activator and give the common feature of the names of this class. (2)

A

Alteplase

-telplase

26
Q

Explain the considerations made when deciding whether do to primary percutaneous coronary intervention or use thrombolytics. (2)

A

Depends on symptom development, and time until PPCI can occur.

27
Q

Define anticoagulent. (2)

A

Prevent thrombus formation and thrombus propagation.

28
Q

Name the most common vitamin K antagonist prescribed. (1)

A

Warfarin.

29
Q

Explain the MoA of warfarin. (3)

A

Inhibits the synthesis of vitamin K dependent clotting factors - II (prothrombin), VII, IX and X. Stops the reduction of vitamin K to its active form.

30
Q

Describe the pharmacokinetics of warfarin. (6)

A 
t1/2 is 36-48 hours. 
Good oral bioavailability. 
Carried on plasma albumin. 
Hepatic metabolism through CYP2C9
Needs constant monitoring through INR.
31
Q

Explain why warfarin is not immediately effective. (2)

A

Circulating active vitamin K and activated clotting factors have to be cleared.

32
Q

Describe the therapeutic uses for warfarin. (5)

A 
DVT prophylaxis and treatment 
PE prophylaxis and treatment 
AF with high risk of stroke 
Protein C and S deficiency
Following orthopaedic surgery.
33
Q

Define INR. (1)
Describe what it is (3).
Describe the target values for INR. (4)
Describe why we need to measure INR regularly. (4)

A

International normalised ratio.
It is a measure of prothrombin time, a measure of how effective factor VII is working (as this is the most vitamin K dependant).
Targets differ depending on reason for therapy:
DVT, PE, AF - 2.5 +/- 0.5
Recurrent DVT/PE, mechanical heart valves - 3.5 +/- 0.5.
Warfarin effectiveness varies based on vitamin K intake, coagulation problems, CYP2C9 action, and other drugs.

34
Q

Describe the commonest ADR of warfarin, and why this is important. (2)

A

Bleeding - warfarin therapy can take weeks to wear off, so alternative therapy may be needed before surgery.

35
Q

Describe why warfarin is not advised in pregnancy. (2)

A

Can cross the placenta, and will encourage bleeding in foetus and mother at birth.

36
Q

Describe methods of reversal for warfarin. (2)

A

Vitamin K, especially with fresh frozen plasma.

37
Q

Describe the common DDIs for warfarin.
6 categories
14 drugs

A

Inhibition of hepatic metabolism by CYP2C9 - amioderone, clopidogrel, ethanol, quinolone, metronidazole.
Acceleration of heptic metabolism by CYP2C9 - barbiturates, phenytoin, rifampicin, St Johns Wort.
Inhibition of platelet function - aspirin
Externally reduced vitamin K through eliminating gut bacteria - cephalosporin
Externally reduced vitamin K through reducing absorption - NSAIDS
Displacement of warfarin from plasma albumin - rifampicin, aspirin

38
Q

Describe the endogenous roles of heparin. (3)

A

Heparin is produced naturally in mast cells and vascular endothelium, and inhibits the action of coagulation factors.

39
Q

Explain the differences in production between unfractionated and low molecular weight heparins (3)

A

Unfractionated heparin has a weight of 5-30 kDa.

Low molecular weight heparins are prepared from unfractionated heparin by chromatography and weigh 1-5 kDa.

40
Q 
Describe unfractionated heparin.
MoA (4)
Pharmacokinetics (5)
Mixture (1)
Advantages. (1)
Disadvantages. (2)
A

Binds to antithrombin, causing a conformational change to catalyse inhibition of thrombin (IIa), Xa, and others to a lesser extent.
Given IV in emergencies, or subcut in prophylaxis even though bioavailability is low. t1/2 is 30 mins at low dose and 2 hours at higher dose.
Typically around 45 polysaccharides in a mixture.
Very fast anticoagulation.
Thrombocytopenia common, and needs monitoring with PTT.

41
Q 
Describe low molecular weight heparins. 
MoA (1)
Pharmacokinetics. (3)
Advantages over unfractionated heparins. (3)
Disadvantages. (1)
Mixture. (1)
A

Targets only Xa.
Over 90% bioavailability subcut and t1/2 of 2 hours, cleared renally.
Thrombocytopenia less likely, needs less monitoring, absorbed more uniformly so only needs mg/kg dosing.
Slower in onset.
Typically 15 polysaccharides.

42
Q

Describe the naming of heparins. (5)

A

Unfractionated heparin - called heparin.

Low molecular weight heparins - eg bempiparin - all end in -parin

43
Q

Describe the uses of heparins. (4)

A

DVT, AF and PE common while warfarin kicks in.
Also if warfarin is contraindicated eg before surgery.
Used in ACS to reduce MIs.
Can be used in pregnancy as does not cross placenta.

44
Q

Describe the ADRs of heparin. (7)

A

Bruising and bleeding - intracranial, epistaxis, GI, injection site.
Heparin induced thrombocytopenia - autoimmune response leads to thrombus.
Osteoporosis - long term UFH or in pregnancy
Rare hypersensitivity.

45
Q

Describe the reversal of heparins. (4)

A

Protamide sulphate; dissociates heparin from ATIII, given IV. UFH more reversible than LMWH.

46
Q

Describe fondaparinux. (6)

A

Synthetic pentasaccharide that selectively inhibits Xa by binding to ATIII. Given sc, t1/2 is 18 hours, needs little monitoring.

47
Q

Define DOAC and NOAC. (2)

A

Direct acting oral anticoagulent

Novel oral anticoagulant

48
Q

Describe the two classes of DOAC, and give examples. (5)

A 
Direct Xa inhibitors - apixaban. 
Direct thrombin (IIa) inhibitors - dabigatran, argatroban.
49
Q

Describe the pharmacokinetics of Apixaban. (4)

A

Hepatic metabolism, renal excretion, taken oral, t1/2 of 10h.

50
Q

Describe the pharmacokinetics of Dabigatran. (3)

A

Active metabolites have a t1/2 of 30-60 mins, taken orally.

51
Q

Describe the uses and contraindications of DOACs (4)

A

For use in AF, stroke prevention, PE, DVT.

Not for use in mechanical heart valves or in HF with vascular disease.

Maddie’s Pharm (23 decks)

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