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Pharmacology > 10 Haemostasis and thrombosis > Flashcards

10 Haemostasis and thrombosis Flashcards

1
Q

10.01 IRREVERSIBLE COX-1 INHIBITOR

Aspirin - actions

A

antiplatelet (also analgesic and anti-inflammatory)

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2
Q

10.01 IRREVERSIBLE COX-1 INHIBITOR

Aspirin - MOA

A

irreversibly inactivates cyclo-oxygenase (COX)-1
alters balance between thromboxane A2 (TXA2) and prostacyclin (PGI2) in the platelet/vascular endothelium axis

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3
Q

10.01 IRREVERSIBLE COX-1 INHIBITOR

Aspirin - abs/distrib/elim

A

given orally in small doses
excretion in urine, increased if urine is alkalinised

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4
Q

10.01 IRREVERSIBLE COX-1 INHIBITOR

Aspirin - clinical use

A

acute treatment of ACS and stroke
secondary prevention of arterial thrombosis after cardiovascular and cerebrovascular events, including after arterial stents
prevention of pre-eclampsia in pregnancy

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5
Q

10.01 IRREVERSIBLE COX-1 INHIBITOR

Aspirin - adverse effects

A

GI bleeding because the cytoprotective action of PGs (namely ↓acid secretion, ↑mucus and bicarbonate) is decreased
bronchospasm in some individuals
toxic doses cause respiratory alkalosis followed by acidosis

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6
Q

10.01 IRREVERSIBLE COX-1 INHIBITOR

Aspirin - special points

A

interactions: effects increased by anticoagulants and thrombolytic drugs

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7
Q

10.02 ADENOSINE (P2Y12) ANTAGONISTS

Clopidogrel, prasugrel, ticagrelor - actions

A

prevent platelet activation

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8
Q

10.02 ADENOSINE (P2Y12) ANTAGONISTS

Clopidogrel, prasugrel, ticagrelor - MOA

A

clopidogrel and prasugrel irreversibly inhibit the binding of ADP to the purine receptor on platelets, thus inhibiting ADP-mediated platelet activation and interfering with GPIIb/IIIa-mediated platelet aggregation
ticagrelor is a reversible, non-competitive inhibitor of the P2Y12 receptor

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9
Q

10.02 ADENOSINE (P2Y12) ANTAGONISTS

Clopidogrel, prasugrel, ticagrelor - abs/distrib/elim

A

given orally, loading dose first then once daily
metabolised to an active compound
irreversible actions of clopidogrel and prasugrel mean the effects last several days until platelets are replaced

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10
Q

10.02 ADENOSINE (P2Y12) ANTAGONISTS

Clopidogrel, prasugrel, ticagrelor - clinical use

A

to prevent/treat MI and other vascular disorders
often given with aspirin

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11
Q

10.02 ADENOSINE (P2Y12) ANTAGONISTS

Clopidogrel, prasugrel, ticagrelor - adverse effects

A

bleeding, GIT discomfort, rashes, rarely neutropenia
ticagrelor can cause dyspnoea

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12
Q

10.03 GPIIb/IIIa RECEPTOR ANTAGONISTS

Abciximab, tirofiban, eptifibatide - actions

A

inhibit platelet activation

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13
Q

10.03 GPIIb/IIIa RECEPTOR ANTAGONISTS

Abciximab, tirofiban, eptifibatide - MOA

A

abciximab is a monoclonal antibody Fab fragment against the platelet GPIIb/IIIa receptor
it binds and inactivates the receptor to prevent the binding of fibrinogen, thus inhibiting platelet aggregation
tirofiban is a synthetic non-peptide and eptifibatide is a cyclic peptide based on the Arg-Gly-Asp (‘RGD’) sequence that is common to ligands for the GPIIb/IIIa receptors

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14
Q

10.03 GPIIb/IIIa RECEPTOR ANTAGONISTS

Abciximab, tirofiban, eptifibatide - abs/distrib/elim

A

given by IV injection
half-life 10-30 min

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15
Q

10.03 GPIIIb/IIIa RECEPTOR ANTAGONISTS

Abciximab, tirofiban, eptifibatide - clinical use

A

used in patients with ACS or undergoing coronary intervention to unblock artery
prevents restenosis and reinfarction

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16
Q

10.03 GPIIIb/IIIa RECEPTOR ANTAGONISTS

Abciximab, tirofiban, eptifibatide - adverse effects

A

bleeding
thrombocytopaenia

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17
Q

10.04 OTHER ANTIPLATELET DRUGS

Dipyridamole

A

causes vasodilation and inhibits platelet aggregation
prevents platelet adenosine uptake and cyclic GMP phosphodiesterase action
used in some patients with aspirin for secondary prevention of ischaemic stroke and TIAs (if clopidogrel not tolerated or contraindicated)

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18
Q

10.04 OTHER ANTIPLATELET DRUGS

Epoprostenol

A

agonist at prostanoid IP receptors
causes vasodilation and inhibits platelet aggregation
added to blood entering the haemodialysis circuit to prevent thrombosis, especially for patients in whom heparin is contraindicated

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19
Q

10.05 PLASMINOGEN ACTIVATORS

Alteplase, duteplase, reteplase, streptokinase - actions and MOA

A

enzymically activate plasminogen to give plasmin, which digests fibrin and fibrinogen, lysing the clot

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20
Q

10.05 PLASMINOGEN ACTIVATORS

Alteplase, duteplase, reteplase, streptokinase - abs/distrib/elim

A

given by IV injection or infusion
short half-life (except for reteplase)

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21
Q

10.05 PLASMINOGEN ACTIVATORS

Alteplase, duteplase, reteplase, streptokinase - clinical use

A

MI, acute ischaemic stroke and other arterial thrombosis
ideally given as soon as possible after the onset of thrombosis
occasionally used in severe cases of DVT and PE

22
Q

10.05 PLASMINOGEN ACTIVATORS

Alteplase, duteplase, reteplase, streptokinase - adverse effects

A

bleeding (most important), reperfusion dysrhythmias, nausea and vomiting, hypersensitivity reactions

23
Q

10.05 PLASMINOGEN ACTIVATORS

Alteplase, duteplase, reteplase, streptokinase - special points

A

streptokinase is a plasminogen-activating protein extracted from cultures of streptococci
alteplase and duteplase are single- and double-chain recombinant tissue plasminogen activators (tPA)
more active on the fibrin-bound plasminogen than on the plasma plasminogen (‘clot selective’)
action blocked by antibodies which appear about 4 days after initial dose - use of either agents should not be repeated after this time has elapsed

24
Q

10.06 PLASMINOGEN INHIBITOR

Tranexamic acid - actions and MOA

A

inhibits plasminogen activation and thus prevents fibrinolysis

25
Q

10.06 PLASMINOGEN INHIBITOR

Tranexamic acid - abs/distrib/elim

A

given orally and by IV injection or infusion

26
Q

10.06 PLASMINOGEN INHIBITOR

Tranexamic acid - clinical use

A

to reduce haemorrhage following dental extraction, major surgery or trauma
for menorrhagia, epistaxis, hereditary angioedema

27
Q

10.06 PLASMINOGEN INHIBITOR

Tranexamic acid - adverse effects

A

GIT disturbances
rare: hypersensitivity skin reactions, disturbed colour vision

28
Q

10.06 PLASMINOGEN INHIBITOR

Tranexamic acid - special points

A

do not use in patients with massive haematuria as this may cause ureteric obstruction

29
Q

10.07 ANTICOAGULANTS

Heparin - actions

A

inhibit blood coagulation

30
Q

10.07 ANTICOAGULANTS

Heparin - MOA

A

accelerates action of antithrombin III (ATIII), increasing its inactivation mainly of factors IIa (thrombin) and Xa
also affects IXa, XIa and XIIa

31
Q

10.07 ANTICOAGULANTS

Heparin - abs/distrib/elim

A

given by SC or IV injection
elimination half-life 40-90 min
renal excretion

32
Q

10.07 ANTICOAGULANTS

Heparin - clinical use

A

to treat DVT, PE, unstable angina, acute peripheral arterial occlusion

33
Q

10.07 ANTICOAGULANTS

Heparin - adverse effects

A

main adverse effect: bleeding
thrombocytopaenia, hypersensitivity reactions, osteoporosis

34
Q

10.07 ANTICOAGULANTS

Heparin - special points

A

dosage is adjusted according to the activated partial thromboplastin time
overdose treated with protamine sulfate

35
Q

10.08 ANTICOAGULANTS

Low molecular-weight heparin: enoxaparin, dalteparin, bemiparin - actions

A

inhibit blood coagulation

36
Q

10.08 ANTICOAGULANTS

Low molecular-weight heparin: enoxaparin, dalteparin, bemiparin - MOA

A

accelerate action of antithrombin III (ATIII), increasing its inactivation of factor Xa

37
Q

10.08 ANTICOAGULANTS

Low molecular-weight heparin: enoxaparin, dalteparin, bemiparin - abs/distrib/elim

A

given by SC injection
elimination half-life 130-180 min
renal excretion

38
Q

10.08 ANTICOAGULANTS

Low molecular-weight heparin: enoxaparin, dalteparin, bemiparin - clinical use

A

to prevent VTE
to treat DVT, PE, MI, unstable angina

39
Q

10.08 ANTICOAGULANTS

Low molecular-weight heparin: enoxaparin, dalteparin, bemiparin - adverse effects

A

main adverse effect: bleeding
less likely than heparin to cause thrombocytopaenia, hypersensitivity reactions, osteoporosis

40
Q

10.08 ANTICOAGULANTS

Low molecular-weight heparin: enoxaparin, dalteparin, bemiparin - special points

A

no need to monitor the activated partial thromboplastin time
overdose treated with protamine sulfate

41
Q

10.09 ANTICOAGULANTS

Vitamin K antagonist: warfarin - actions

A

inhibit blood coagulation

42
Q

10.09 ANTICOAGULANTS

Vitamin K antagonist: warfarin - MOA

A

inhibits the reduction of vitamin K and thus prevents the γ-carboxylation of the glutamate residues in factors II, VII, IX, and X

43
Q

10.09 ANTICOAGULANTS

Vitamin K antagonist: warfarin - abs/distrib/elim

A

given orally
slow onset because the circulating γ-carboxylated factors have to be degraded

44
Q

10.09 ANTICOAGULANTS

Vitamin K antagonist: warfarin - clinical use

A

to treat DVT/PE
to prevent embolisation in atrial fibrillation

45
Q

10.09 ANTICOAGULANTS

Vitamin K antagonist: warfarin - adverse effects

A

bleeding - treated by giving natural vitamin K, fresh plasma or prothrombin complex concentrates

46
Q

10.09 ANTICOAGULANTS

Vitamin K antagonist: warfarin - special points

A

prothrombin time must be monitored
action increased (with ↑risk of bleeding) by many drugs, e.g. ciprofloxacin, aspirin
action decreased (with ↑risk of clotting) by many drugs, e.g. rifampicin

47
Q

10.10 DIRECT ORAL ANTICOAGULANTS

Dabigatran, apixaban, rivaroxaban - actions

A

reduce clot formation

48
Q

10.10 DIRECT ORAL ANTICOAGULANTS

Dabigatran, apixaban, rivaroxaban - MOA

A

dabigatran is a direct inhibitor of clot-bound and free thrombin (factor IIa)
apixaban and rivaroxaban are direct inhibitors of factor Xa

49
Q

10.10 DIRECT ORAL ANTICOAGULANTS

Dabigatran, apixaban, rivaroxaban - abs/distrib/elim

A

given orally
half-lives: dabigatran 14-17h, apixaban 8-13h, rivaroxaban 5-9h
dabigatran is a prodrug with low bioavailability
apixaban and rivaroxaban are around 50% renally excreted
dabigatran is 80% renally excreted

50
Q

10.10 DIRECT ORAL ANTICOAGULANTS

Dabigatran, apixaban, rivaroxaban - clinical use

A

to prevent DVT/PE in orthopaedic surgery
to treat VTE
to prevent stroke in atrial fibrillation

51
Q

10.10 DIRECT ORAL ANTICOAGULANTS

Dabigatran, apixaban, rivaroxaban - adverse effects

A

bleeding - treated with specific reversal agents: idarucizumab for dabigatran, andexanet alfa for factor Xa inhibitors

52
Q

10.10 DIRECT ORAL ANTICOAGULANTS

Dabigatran, apixaban, rivaroxaban - special points

A

these drugs are administered in standard doses without monitoring
dabigatran can be removed via haemodialysis
apixaban and rivaroxaban are highly protein bound - limits dialysis

Pharmacology (34 decks)

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