Pharmacology - Anti-platelet drugs Flashcards
Pathological formation of a haemostatic plug within the vasculature in the absence of bleeding is known as?
a. haemostasis
b. clotting
c. thrombosis
d. embolism
e. aneurysm
c.thrombosis
which of these is not part of virchows triad?
a. injury to vessel wall
b. stasis of flow
c. abnormal coagubility
d. vasoconstriction
d.vasoconstriction
stasis of flow, abnormal coagubility and injury to vessel wall make up which triad?
a. virchows
b. henrys
c. ficks
a.virchows
which of virchows triad is mainly arterial?
a. stasis of flow
b. injury to vessel wall
c. abnormal coagubility
b.injury to vessel wall
which of virchows triad is mainly venous?
a. stasis of flow
b. injury to vessel wall
c. abnormal coagubility
a.stasis of flow
pregnancy, oral contraceptives and inherited thrombophilia contribute to which elemwnt of virchows triad?
a. injury to vessel wall
b. stasis of flow
c. abnormal coagulability
c.abnormal coagulability
a ruptured atheromatous plaque would make up which element of virchows triad?
a. injury to vessel wall
b. stasis of flow
c. abnormal coagulability
a.injury to vessel wall
what type of abnormal coagulability is part of virchows triad?
a. hypocoagubility
b. hypercoagubility
b.hypercoagubility
virchows triad refers to factors contributing to which process?
a. haemostasis
b. thrombosis
c. clotting
d. platelet aggregation
b. thrombosis
what part of virchows triad is targetted by anti platelet drugs?
a. abnormal coagulation
b. vessel wall injury
c. stasis of flow
b.vessel wall injury
arterial thrombi development targetted
which two substances amplify the process of platelet aggregation?
a.thromboxane A2 and ADP
b, thromboxane A2 and ATP
c. endothelin and thrombin
d. thrombin and von willebrand factor
a.thromboxane A2 and ADP
what is a thrombus stabilised by?
a. conversion of prothrombin to thrombin
b. conversion of thrombin to prothrombin
c. conversion of fibrin to fibrinogen
d. conversion of fibrinogen to fibrin
d.conversion of fibrinogen to fibrin
what type of antiplatelet drug is aspirin?
a. ADP receptor pathway inhibitor
b. cyclo ocygenase inhibitor
c. phosphodiesterase inhibitors
d. glycoprotein IIb/IIa receptor antagonists
b.cyclo ocygenase inhibitor
what type of antiplatelet drug is clopidogrel?
a. ADP receptor pathway inhibitor
b. cyclo ocygenase inhibitor
c. phosphodiesterase inhibitors
d. glycoprotein IIb/IIa receptor antagonists
a.ADP receptor pathway inhibitor
what type of antiplatelet drug is dipyridamole?
a. ADP receptor pathway inhibitor
b. cyclo ocygenase inhibitor
c. phosphodiesterase inhibitors
d. glycoprotein IIb/IIa receptor antagonists
c. phosphodiesterase inhibitors
which type of circulation do anti platelet drugs decrease platelet aggregation and inhibit thrombus in?
a. arterial
b. venous
a.arterial
in faster flowing vessels thrombi composed mainly of platelets with little fibrin
what is true of thrombus in faster flowing vessels eg arteries?
a. composed mainly of fibrin
b. composed mainly of thrombin
c. composed mainly of platelets
c.composed mainly of platelets
true or false anti platelet drugs are not beneficial in venous circulation?
a. true
b. false
a.true
which enzyme is inhibited by aspirin?
a. phosphodiesterase
b. cox 2
c. cox 3
d. cox 1
d.cox 1
which is true of aspirin?
a. selectively and irreversibly inhibits cox 1
b. non selectively and irreversibly inhibits cox 1
c. selectively and reversibly inhibits cox 1
a.selectively and irreversibly inhibits cox 1
what does inhibition of cox 1 in platelets by aspirin prevent ?
a. thromboxanes and endothelin
b. thromoboxane A2 and ADP
c. thromboxanes and prostaglandins
d. prostaglandins and prothrombin
c.thromboxanes and prostaglandins
higher doses of aspirin irreversibly inhibit cox 1 and which other enzyme?
a. cox 2
b. cox 3
c. phosphodiesterase
a.cox 2
why are other NSAIDS not used instead of aspirin for anti platelet tasks?
a. reversible,short duration
b. irreversible, short duration
c. reversible , long duration
d. irrerversible, long duration
a.reversible,short duration
which of these does not happen when levels of thromboxane A2 are reduced by aspirin?
a. vasoconstriction
b. vasodilation
c. increased bleeding time
d. reduced platelet aggregation
a.vasoconstriction
which of these is increased by reduced thromboxane A2 levels following aspirin ?
a. bleeding time
b. platelet aggregation
c. cox 1 action
a.bleeding time
which of these causes aggregation and vasoconstriction?
a. PGI2
b. Cox 2
c. cox 1
c. cox 1
which of these causes reduced aggregation and vasodilation?
a. PGI2
b. Cox 2
c. cox 1
a. PGI2
true or false platelets cannot regenerate cox 1 as they have no nucleus ?
a. true
b. flase
a.true
how long is the anti aggregatory effect of aspirin irreversible for?
a. 1-2 days
b. 5-10 hours
c. 7-10 days
d. 25-27 hrs
c.7-10 days
lifespan of platelet
how many days following cessatio on aspirin is most of platelet function recovered?
a. 1-2 days
b. 7-10 days
c. 4-5 days
c.4-5 days
how many platelets are generated each day?
a. 25%- 30%
b. 10-14%
c. 2-5%
b.10-14%
why is inhibition of pgI2 synthesis less marked with aspirin and recovers faster?
a. selectively for cox 2> cox 1
b. selectively for cox 1> cox 2
b.selectively for cox 1> cox 2
what is used for secondary prevention in atrial fibrillation if warfarin is contra inidcated?
a. clopidogrel
b. dipyridamole
c. aspirin
c. aspirin
aspirin is used for 2 prevention following MI?
a. short term
b. long term
b.long term
what drug is used for 2 prevention following ischaemic stroke, angina pectoris and acute coronary syndrome ?
a. clopidogrel
b. dipyrimadole
c. aspirin
c.aspirin
gastric irritation / bleeding , reyes syndrome in children and what else is an adverse effect of aspirin?
a. headache
b. nausea
c. hypersensitivity
d. first dose hypotension
c. hypersensitivity
skin and resp
Reyes syndrome in children includes a rash, vomiting, damage to brain and liver. This is an adverse effect of which drug?
a. clopidogrel
b. ezetemibe
c. aspirin
d. dipyrimadole
c. aspirin
aspirin in conjunction with which of these drugs would not increase the risk of gastric irritation and bleeding?
a. corticosteroids
b. opiods
c. NSAIDS
d. anticoagulants
e. antiplatelets
b.opiods
aspirin resistance is often associated with..
a. old age
b. poor adherence
c. comorbidities
d. reyes syndrome
b. poor adherence
why is their a continued risk of bleeding some time after stopping aspirin?
a. selective to cox 1
b. irreversible effects
c. reversible effects
d. inhibition of cox 2 at higher doses
b. irreversible effects
what receptor does ADP bind to in order to unmask glycoprotein GPIIb/IIIa receptors ?
a. P2Y12 receptors
b. nicotinic receptors
c. muscarinic receptors
d. cox receptors
a.P2Y12 receptors
what binds to the P2Y12 receptors?
a. ATP
b. thromboxanes
c. prostaglandins
d. ADP
d. ADP
what do GPIIb/IIIa receptors become exposed to in order to enhance platelt aggregation?
a. thrombin
b. prothrombin
c. fibrin
d. fibrinogen
d.fibrinogen
which of these drugs is a thienopyridine?
a. clopidogrel
b. aspirin
c. dyprimadole
a.clopidogrel
how does clopidogrel inhibit ADP mediated platelet activation and aggregation?
a.unselectively, reversibly
b,selectively, reversibly
c.unselectively, irreversibly
d.selectively, irreversibly
d.selectively, irreversibly
what is inhibited by clopidogrel?
a. Cox 1
b. ADP mediated platelet activation
c. P2Y12 receptors
b. ADP mediated platelet activation
how is clopidogrel given?
a.IM
b.iv
C.oral
C.oral
85 % of clopidogrel is hydrolysed by esterases after absorption to what?
a. inactive COOH
b. active COOH
a.inactive COOH
15% of clopidogrel undergoes a 2 step oxidation activation by which liver enzymes?
a. cox 1
b. cox 2
c. phosphodiesterase
d. CYP2C19
e. P2Y12
d. CYP2C19
where are the CYP2C19 enzymes that activate clopidogrel by 2 step oxidation found?
a. kidney
b. blood vessels
c. heart
d. spleen
e. liver
e.liver
how many days after cessation of clopidogrel is platelet function inhibited for?
a. 7-8
b. 4-5
c. 7-10
a. 7-8
what drug is used as secondary prevention in patients intolerant of aspirin?
a. clopidogrel
b. prasrugrel
c. ticagrelor
d. dipyridamole
a.clopidogrel
what drug is given with aspirin 3 months after acute coronary sydrome and following CABG/stents to prevent thrombosis?
a. clopidogrel
b. prasrugrel
c. ticagrelor
d. dipyridamole
a.clopidogrel
which of these us not an adverse effect of clopidogrel?
a. GI irritation and bleeding
b. reyes syndrome
c. hypersensitivity reactions
d. dyspepsia and GI upset
b.reyes syndrome
with which anti platelet drug is gi irritation and bleeding most common?
a. clopidogrel
b. aspirin
c. ticagrelor
d. dipyridamole
b. aspirin
where do the hypersentivity reactions associated with clopidogrel occur?
a. skin and resp
b. skin and liver
b.skin and liver
how is the delayed onset of action of clopidogrel overcome?
a. giving aspirin prior
b. loading dose of 300 mg
c. loading dose of 50 mg
d. gradually increasing dose
b. loading dose of 300 mg
why does response to clopidogrel vary between individuals?
a. genetic variation of platelets
b. genetic variation of liver enzymes CYP2C19
c. genetic variation in number of P2Y12 receptors
d. genetic variation in number of GPIIb/IIIa receptors
b.genetic variation of liver enzymes CYP2C19
which of these drugs interacts with clopidogrel?
a. NSAIDS
b. PPI
c. cORTICOSTEROIDS
d. anticoagulants
b.PPI
what does clopidogrel inhibit ?
a. platelets
b. liver enzymes CYP2C19
c. P2Y12 receptors
d. GPIIb/IIIa receptors
e. ADP
c. P2Y12 receptors
how long is there a continued bleeding risk for 7-8 days after stopping taking clopidogrel?
a. 5 days
b. 7-8 days
c. 7-10 days
d. 4-5 days
b.7-8 days
how many steps of oxidation are required to convert prasugrel to an active metabolite?
a. 1
b. 3
c. 2
a. 1
which drug has less dependence on cytochrome p 450 enzymes than clopidogrel?
a. clopidogrel
b. aspirin
c. ticagrelor
d. dipyridamole
e. prasugrel
e. prasugrel
true or false prasugrel gives a more predictable antiplatelet response than clopidogrel ?
a. true
b. false
a.true
what drug is used in Percutaneous coronary intervention / coronary angiography and acute coronary syndromes?
a. clopidogrel
b. aspirin
c. ticagrelor
d. dipyridamole
e. prasugrel
e. prasugrel
where does ticagrelor bind on the platelet?
a. ADP binding site on P2Y12 receptor
b. GPIIb/IIIa reveptors
c. separate site on P2Y12 receptor
c.separate site on P2Y12 receptor
to inhibit g protein signalling
which of these applies to ticagrelor inhibition of the P2Y12 receptor?
a.unselectively, reversibly
b,selectively, reversibly
c.unselectively, irreversibly
d.selectively, irreversibly
b,selectively, reversibly
rapid onset of action
true or false ticagrelor has a rapid onset and offset of action?
a. true
b. false
a.true
which of these is correct in terms of potency ?
a. clopidogrel> ticagrelor
b. ticagrelor > clopidogrel
b. ticagrelor > clopidogrel
but increased bleeding risk
what drug is used in patients with acute coronary syndrome undergoing PCI when thrombosis risk is higher than bleeding risk?
a. clopidogrel
b. aspirin
c. ticagrelor
d. dipyridamole
e. prasugrel
c. ticagrelor
which of these drugs is not a pro drug
a. clopidogrel
b. prasugrel
c. ticagrelor
c.ticagrelor
how does cangrelor bind to the P2Y12 receptor ?
a. reversibly
b. irreversibly
a.reversibly
very rapid onset and offset
how is cangrelor administered during PCI in high risk patients prior to switching to an oraly P2Y12 receptor antagonist?
a. IM
b. IV
c. oral
b.IV
along with oral aspirin
what does dipyridamole inhibit?
a. cox 1
b. P2Y12 receptor
c. phosphodiesterase and thromboxane synthase
c. phosphodiesterase (cAMP) and thromboxane synthase
dipyrimadole inhibits throboxane synthase, phosphodiesterase and what mechanism?
a. ADP reuptake and metabolism
b. ATP reuptake and metabolism
c. Adenosine reuptake and metabolism
c.Adenosine reuptake and metabolism
what does dipyrimadole promote
a. platelet aggregation
b. vasoconstriction
c. vasodilation
c.vasodilation
which drug is given with oral anticoagulants for prevention of thromboembolism in patients with prosthetic heart valves?
a. clopidogrel
b. prasugrel
c. ticagrelor
d. dipyridamole
d. dipyridamole
which drug is given with aspirin for secondary prevention of ischaemic stroke/transient ischaemic attack?
a. clopidogrel
b. prasugrel
c. ticagrelor
d. dipyridamole
d. dipyridamole
which of these is not a side effect of dipyridamole?
a. GI irritation and bleeding
b. dizziness, flushing and headache
c. chest and muscle pain
d. nausea
e. hypersensitivity
d.nausea
where do the hypersensitivtiy reactions occur for dipyridamole?
a. skin and liver
b. skin and resp
c. skin and kidney
c.skin and kidney
interaction with other anti platelet agents and anticoagulants increases risk of which side effect of dipyridamole?
a. chest pain
b. myalgia
c. dizziness, flushing and headache
d. hypersensitivity
e. GI irritation and bleeding
e. GI irritation and bleeding
what is the most significant side effect of anti platelet agents?
ableeding
b. dyspepsia
c. hypersensitivity
d. reyes
ableeding
which anti platelet agent has the least risk of bleeding?
a. clopidogrel
b. ticagrelor
c. dipyrimidole
d. low dose aspirin
e. cangrelor
d.low dose aspirin
how are anti platelet drugs reversed eg in acute bleed?
a. drugs
b. plasma transfusion
c. blood transfusion
b.plasma transfusion
what drug is used for acute coronary syndromes eg NSTEMI/STEMI?
a. clopidogrel
b. ticagrelor / prasugrel
c. dipyrimidole
d. low dose aspirin
b.ticagrelor / prasugrel
what drug is used for occlusive vascular events eg stroke/peripheral vascular disease?
a. clopidogrel
b. ticagrelor / prasugrel
c. dipyrimidole
d. low dose aspirin
a.clopidogrel
what drug is used for secondary prevention eg post MI?
a. clopidogrel
b. ticagrelor / prasugrel
c. dipyrimidole
d. low dose aspirin
d.low dose aspirin
what do fibrinolytic drugs do?
a. inhibit cox 1
b. inhibit P2Y12 receptors
c. inhibit phosphodiesterase and thromboxane
d. promote conversion of plasminogen to plasmin
d.promote conversion of plasminogen to plasmin
dissolves fibrin strands of clot
streptokinase and alteplase are examples of which drugs?
a. fibrinolytic
b. anti platelet
c. anticoagulant
a.fibrinolytic
which of these drugs activates plasminogen?
a. alteplase
b. streptokinase
a.alteplase
what is given IV for acute PE/DVT and to reduce mortality post STEMI MI and ischaemic stroke
a. clopidogrel
b. ticagrelor / prasugrel
c. fibrinolytic
d. low dose aspirin
c.fibrinolytic
when should fibrinolytics be given for acute PE/DVT/post MI?
a. 1 hr after symptoms
b. within 1 hr of symptom onset
c. prophylactic
b.within 1 hr of symptom onset
which of these is not a side effect of fibrinolytics?
a. bleeding
b. breakaway embolus formation
c. reperfusion arrhythmias
d. hypersensitivity
e. dizziness
e.dizziness
