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37 Cards in this Set

  • Front
  • Back
Blockade of the open inactivated sodium channel will
a. slow deplarisation
b. slow repolaristion
c. prevent expression of the action potential
d. lengthen the refractory period
e A &C
Blockade of potassium channel will
a. slow deplarisation
b. slow repolaristion
c. prevent expression of the action potential
d. lengthen the refractory period
e B & D
Blockade of the calcium channel will
a. slow deplarisation
b. slow repolaristion
c. prevent expression of the action potential
d. lengthen the refractory period
e A &D
Mechanistically, quinidine exerts its anti-arrhythmic effects by
a. blocking open, activated sodium channels
b. blocking open, inactivated sodium channels
c. blocking calcium channels
d. A & B
e. all of the above
Mechanistically, lidocaine exerts its anti-arrhythmic effects by
a. blocking open, activated sodium channels
b. blocking open, inactivated sodium channels
c. blocking calcium channels
d. A & B
e. all of the above
Mechanistically, phenytoin exerts its anti-arrhythmic effects by
a. blocking open, activated sodium channels
b. blocking open, inactivated sodium channels
c. blocking calcium channels
d. A & B
e. all of the above
____ is an oral version of lidocaine that may also be used to treat diabetic neuropathy
a. Flecainide
b. Propafenone
c. Disopyramide
d. Procainamide
e. Mexiletine
______ produces a negative inotrophy that may cause heart failure even patients with no pre-existing cardiomyopathy
a. phenytoin
b. propafenone
c. disopyramide
d. procainamide
e. mexiletine
____ can produce a lupus-like effect as a potentially sever ADR
a. flecainide
b. propafenone
c. disopyramide
d. procainamide
e. mexiletine
Mechanistically, propafenone is anti-arrhythmic though ______ blockade
a. sodium channel
b. calcium channel
c. potassium channel
d. beta adrenergic
e. all of the above
in addition to its primary MOA, flecainide may also block the __________
a. sodium channel
b. calcium channel
c. potassium channel
d. beta adrenergic receptor
e. all of the above
Side effects associated with __________ include GI upset, tinnitus, psychoses, and typical anti-cholinergic effects
a. phenytoin
b. mexiletine
c. propafenone
d. procainamide
e. quinidine
Flecainide differs from quinidine by
a. interacting with Na channel for a longer period of time
b. blocking open, activated Na channels
c. also blocking Ca channels
d. A & B
e. B & C
Lidocaine should never be used
a. to treat arrhythmias post- MI
b. to prevent arrhythmias post-MI
c. parenterally
d. A & B
e. none of the above (it make be used all those ways)
Pharmacodynamically, the anti-arrhythmic effects of propranolol are due to its
a. negative inotropy
b. negative chronotropy
c. inhibition of renin release
d. a &B
e. all of the above
_____ is necessary for the anti-arrhythmic effects of acebutolol
a. b-1 selectivity
b. intrinsic sympathomimetic activity
c. sodium channel blocking activity
d. all of the above
e. none of the above
b adrenergic antagonists should not be used in _______ because _________
a. ectopic arrhythmias- will cause cardiac asystole
b. re-entry arrhythmias- cause cardiogenic shock
c. wolf-Parkinson - white arrhythmias- increased risk of /worsen the arrhythmia
d. A&C
e. B&C
Concerning the type III anti-arrhythmics
a. dofetilide and ibutilide are least likely to cause torsades de pointes
b. bretylium produced an initial negative ino& chrono-tropy
c. dronedarone use is safe-during pregnancy
d. all of the above
e. none of the above
ADRs associated with amiodarone include
a. pulmonary fibrosis
b. thyroid toxicity
c. photoallergic reactions
d. all of the above
e. none of the above
Mechanistically, verapamil is effective as an anti-arrhythmic by
a. blocking the T type calcium channels
b. blocking the L type calcium channels
c. Blocking calcium and potassium channels
d. A & B
e. all of the above
#47 Pharmacodynamically adenosine is used as an anti-arrhythmic to
a. hyperpolarize SA nodal tissue
b. produce chemical cardioversion
c. cause cardiac asystole
d. A&C
e. all of the above
Pharmacodynamically, adenosine achieves the effect noted in #47 by
a. blocking sodium influx
b. enhancing calcium efflux
c. enhancing calcium influx
d. enhancing potassium efflux
e. enhancing potassium influx
Mechanistically, _______ exerts its effect by activating lipoprotein lipase
a. simvastatin
b. colestipol
c. fenofibrate
d. A & B
e. A &C
Mechanistically, __________ exerts its effect by binding to bile acids in the intestine.
a. exetimibe
b. colestipol
c. fenofibrate
d. A & B
e. A & C
Mechanistically, ___________ exerts its effect by inhibiting HMG-CoA reductase
a. Simvistatin
b. colestipol
c. fenofibrate
d. A& B
e. A& C
Mechanistically, ______ exerts its effect by inhibiting the NPC 1L1 transporter
a. exetimibe
b. colestipol
c. fenofibrate
d. A & B
e. A & C
Pharmacodynamically, _____ lowers circulating lipids, but the specific mechanism is unknown
a. niacin
b. icoaspent
c. ezetimibe
d. a & B
e. A & C
Pharmacodynamically, _______ effectively lowers circulating lipids by increasing hepatic LDL receptor density (up-regulating)
a. simvastatin
b. colestipol
c. fenofibrate
d. A & B
e A & C
Pharmacodynamically, _________ effectively lowers circulating lipids by cleaving free fatty acids from circulating fat packages
a. ezetimibe
b. colestipol
c. fenofibrate
d. A & B
e. A & C
As a part of its pharmacodynamics effects, _____ inhibits the absorption of dietary fat
a. ezetimibe
b. colestipol
c. fenofibrate
d. A & B
e. A & C
___________ is a pregnancy category X drug and should never be given during pregnancy
a. fluvistatin
b. ezetimibe
c. nicacin
d. clofibrate
e. colesevelam
Adverse effects associated with atorvastatin include
a. hepatotoxicity
b. myotoxicity
c. cataracts
d. A& B
e. all of the above
______ is less likely than other drugs of the class to participate in drug interaction
a. pravastatin
b. colesevelam
c. gemfibrozil
d. A & B
e. B & C
______ is effective in lowering LDL, triglycerides and increasing HDL
a. Niacin
b. Pitavastatin
c. clofibrate
d. A & B
e. B & C
Problems associated with colestyramine may include
a. diarrhea
b. constipation
c. impaired absorption
d. all of the above
e. none of the above
Problems associated with ezetimibe include
a. animal evidence of birth defects
b. dyspepsia/burping
c. myptoxicity
d. a & B
e. none of the above
problems associated with niacin include
a. myotxicity
b. hepatotoxicity
c. flushing/rash/pruritis
d. all of the above
e. none of the above
Mechanistcially, heparin acts by binding to and inhibiting
a. thrombin
b. factor Xa
c. anti-thrombin III
d. A & B
e. B & C
Concerning heparin therapy
a. bovine heparin is less likely to cause idiopatic thromboctopaenic purpura
b. porcine heparin is more allergenic than low molecular weight heparin
c. all heparins are approved for treatment of deep vein thrombosis
d. A&B
e. none of the above
The treatment of choice for heparin overdoes is
a. pralidoxime
b.phytonadione
c.protamine
d. piroxicam
e.pentazole
Pharmacodynamically heparin inhibits
a. activated Stuart factor
b. thrombin
c. converstion of fibrinogen to fibrin
d. A&B
e. all of the above
______ therapy is monitored used the activated partial thromboplastin time
a. heparin
b. warfarin
c. bivalirudin
d. A & C
e. all of the above
Concerning the MOA of desirudin
a. factor IIA is inhibited
b. its actions are are dependent upon anti-thrombin III
c. it inhibits both free thrombin and thrombin bound to fibrinogen
d. A & C
e. all of the above
Concerning the MOA of argatroban
a. thrombin is inhibited
b. it acts in a manner similar to lepirudin
c. it inhibits both free thrombin & thrombin bound to fibrinogen
d. A & C
e. all of the above
Concerning the anti-coagulant dabigatran
a. it is a direct Xa inhibitor
b. it is orally effective
c. its mechanism is the same as enozaparin
d. A & C
e. None of the above
____ is a direct factor Xa inhibitor that carries a black box warning for potential subdural haematoma
a. fondipariunux
b. rivaroxaban
c. apixaban
d. B & C
e. all of the above
_______ is a direct factor Xa inhibitor that only administered parenterally and may potentially cause idiopathic thrombocytopaenia similar to heparin
a. fondipariunux
b. rivaroxaban
c. apixaban
d. B & C
e. all of the above
_______ excerts its anticoagulant effect by inhibiting vitamin K epoxide reductase
a. fonaparinux
b. otamixaban
c. warfarin
d. drotecogin
e. enoxaparin
Pharmacodynamically inhibition of vitamin K epoxide reductase prevents
a. regeneration of diol form of vitamin K
b. reduction of the dione version of vitamin K
c. synthesis of clotting factors II, VII, IX, and X
d. A & C
e. B & C
Concerning potential drug interactions with warfarin
a. ibuprofen could increase its effect by displacement from plasma proteins
b. ibuprofen could increase its effect by inhibiting COX-I
c. cimetidine could increase its effect by inhibiting metabolism
d. A & C
e. all of the above
Reteplase exerts its effect by ______ mechanistically
a. inhibiting ADP at its binding site
b. glycoprotein IIb/IIIa antagonism
c. converting plasminogen to plasmin
d. inhibiting COX-I
e PGI2 agonist actions
Aspirin exerts its anti-platelet effect by
a. inhibiting ADP at its biding site
b. glycoprotein IIb/IIIa antagonism
c. converting plasminogen to plasmin
d. inhibiting COX-I
e PGI2 agonist actions
antagonism
c. converting plasminogen to plasmin
d. inhibiting COX-I
e PGI2 agonist actions
Clopidogrel exerts its anti-platelet effect by
a. inhibiting ADP at its biding site
b. glycoprotein IIb/IIIa antagonism
c. converting plasminogen to plasmin
d. inhibiting COX-I
e PGI2 agonist actions
antagonism
c. converting plasminogen to plasmin
d. inhibiting COX-I
e PGI2 agonist actions
Concerning ticlopidine
a. it should not be used in patients who can not tolerate aspirin
b. it may cause idiopathic throbocytopaenia as an ADR
c. it carries a black box warning for subdural haemotoma
d. A&B
e. A&C
Concerning prasugrel
a. clinically it is more effective that clopidogrel
b. it should not be used in patients 75 years of age or older
c. its efficacy is decreased when >100 mg of aspirin at taken concurrently
d. A & B
e. A & C
Concerning ticagrelor
a. clinically it is more effective that clopidogrel
b. it should not be used in patients 75 years of age or older
c. its efficacy is decreased when >100 mg of aspirin at taken concurrently
d. A & B
e. A & C
Concerning drugs affecting haemostasis
a. eptifibitide acts as a gp IIb/IIIa atagonist
b. at low doses, anagrelide inhibits platelet function
c. aminocaproic acid acts in a mechanism opposite that of reteplase
d. A &B
e. A & C
Concerning drugs affecting
a. bleeding is the primary ADR for tirofiban
b. anagrelide may cause arrhythmias & heart failure as ADRs
c. traxenamic acid is used specificially to prevent clotting in intracranial haemorrhage
d. A &B
e. A & C
Pharmacodynamically, pentoxyphylline is thought to be beneficial in intermittent claudication by
a. decreasing platelet aggregation
b. increasing red blood cell flexibility
c. inhibiting the clotting cascade
d. A & C
e. all of the above
Cilostazol differs from pentyoxyphylline by
a. its greater clinical efficacy
b. being more prone to drug interactions
c. its mechanism of action
d. A & B
e. none of the above
Concerning sildenafil
a. mechanistically it inhibits PDF to exert its desired effect
b. it exhibits a low risk of drug interaction
c. it may cause color blindness as an ADR
d. A & C
e. none of the above
______ is an opium-derived inhibitor of PDE, that is used parenterally to treat vascular spasm
a. cyclandelate
b. papaverine
c. isoxsuprine
d. nylidrin
e all of the above
_____ is less likely to cause allergic reactions when used as a parenterally to treat vascular spasm
a. iron dextran
b. ferumoxytol
c. iron sucrose
d. all of the above (all are unlikely)
e. none of the above (all are likely)
Common side effects with oral iron supplementation may include
a. GI upset
b. black stools
c. allergic reaction
d. A&B
e. A & C
Chronic iron toxicity may be ultimately fatal due to
a. organ failure
b. blood loss
c. oxygen toxicity
d. seizures
e. inhibition of ATP
Concerning treatment of iron toxicity
a. the treatment of choice for chronic iron overload is desferioxamine
b. desferrioxamine is doesed orally with 1 mg of chelator for every 1 mg of fe
c. deferasirox may cause liver and kidney damage
d. all of the above
e. none of the above
Hypochromic, microcytic anaemias are more appropriately treated with
a. romiplostim
b.folate
c. iron
d.sargramostim
e.parenteral coblamin
as a treatment of anaemias, ____ functions as a co-factor in methyl group transfer
a. plerixafor
b. tbo-filgrastim
c. folate
d. darbepoietin
e. coblamin
as a treatment of anaemias, ____ functions as a methyl group donor/acceptor
a. plerixafor
b. tbo-filgrastim
c. folate
d. darbepoietin
e. coblamin
______ acts as an agonist at the colony stimulating factor receptor that is responsible for proliferation of both white blood cells and macrophages
a. darbepoietin
b. peginesatide
c. plerixafor
d. sargramostim
e. eltrombopag
_________ is an orally active agonist at the thrombepoietin receptor to increase platelet proliferation
a. darbepoietin
b. peginesatide
c. plerixafor
d. sargramostim
e. eltrombopag
_____________is an agonist at the erythropoietin receptor to increase RBC proliferation, but is not a recombinant version of erythropoietin
a. darbepoietin
b. peginesatide
c. plerixafor
d. sargramostim
e. eltrombopag
________ is used as an adjunct in GCSF agonist therapy to stabilize stem cell proliferation
a. darbepoietin
b. peginesatide
c. plerixafor
d. sargramostim
e. eltrombopag
The primary concern with erythropoietin agonists as an ADR is the increased risk of
a. thromboembolic events
concurrent leucopaenias
c. concomitant platetet proliferation
d. A & B
e A & C