MCQs PHARMACOLOGY: Cardiovascular Drugs

34.1 Under physiological conditions the rate limiting enzyme in the generation of angiotensin II is:
A. Renin
B. Angiotensin converting enzyme
C. Aminopeptidase
D. Angiotensinase

34.2 Angiotensin II causes rise in blood pressure by:
A. Direct vasoconstriction
B. Releasing adrenaline from adrenal medulla
C. Increasing central sympathetic tone
D. All of the above

34.3 Angiotensin III is equipotent to angiotensin II in:
A. Releasing aldosterone from adrenal cortex
B. Promoting Na+ and water reabsorption by direct intrarenal action
C. Causing vasoconstriction D. Contracting intestinal smooth muscle

34.4 The following is a pressor peptide that can be generated both in circulation as well as locally in certain tissues:
A. Bradykinin
B. Angiotensin
C. Kallidin
D. Plasmin
34.1 A
34.2 D
34.3 A
34.4 B

 

34.5 The following factors enhance renin release from the kidney except:
A. Fall in blood pressure
B. Reduction in blood volume
C. Enhanced sympathetic activity
D. Volume overload

34.6 Angiotensin II plays a key role in the following risk factor for ischaemic heart disease:
A. Hypercholesterolemia
B. Ventricular hypertrophy
C. Carbohydrate intolerance
D. Cardiac arrhythmia

34.7 Ventricular remodeling after myocardial infarction involves the mediation of:
A. Angiotensin II
B. Prostaglandin
C. Bradykinin
D. Thromboxane A2

34.8 Captopril pretreatment:
A. Inhibits the pressor action of angiotensin I
B. Inhibits the pressor action of angiotensin II
C. Potentiates the depressor action of brady-kinin
D. Both ‘A’ and ‘C’ are correct

34.9 Captopril produces greater fall in blood pressure in:
A. Diuretic treated patients
B. Patients having low plasma renin activity
C. Sodium replete normotensive individuals
D. Untreated CHF patients

34.5 D
34.6 B
34.7 A
34.8 D
34.9 A

 

34.10 Potentiation of bradykinin appears to play a role in the following effects of angiotensin converting enzyme inhibitors except:
A. Fall in BP in the short term
B. Fall in BP in the long term
C. Cough in susceptible individuals
D. Angioedema in susceptible individuals

34.11 Enalapril differs from captopril in that:
A. It blocks angiotensin II receptors
B. It does not produce cough as a side effect
C. It is less liable to cause abrupt first dose hypotension
D. It has a shorter duration of action

34.12 Enalapril differs from captopril in the following features except:
A. It is dose to dose more potent
B. Its oral absorption is not affected by food in stomach
C. It acts more rapidly
D. It has longer duration of action

34.13 The following angiotensin converting enzyme inhibi-tor can reduce cardiac contractility:
A. Captopril
B. Enalapril
C. Perindopril
D. Lisinopril

34.10 B
34.11 C
34.12 C
34.13 D

 

34.14 Advantages of angiotensin converting enzyme inhi-bitors as antihypertensive include the following except:
A. They tend to reverse left ventricular hyper-trophy
B. Their efficacy is not reduced by nonsteroidal antiinflammatory drugs
C. They do not worsen blood lipid profile
D. They do not impair work performance

34.15 The following drug increases cardiac output in congestive heart failure without having any direct myocardial action:
A. Captopril
B. Digoxin
C. Amrinone
D. Dobutamine

34.16 Angiotensin converting enzyme inhibitors reduce the following haemodynamic parameters in conges-tive heart failure except:
A. Systemic vascular resistance
B. Right atrial pressure
C. Cardiac output
D. Heart rate × pressure product

34.17 Angiotensin converting enzyme inhibitors afford maximum protection against progression of heart failure when used:
A. At the higher therapeutic dose range over long term
B. At the maximum tolerated dose only till haemodynamic compensation is restored
C. At low doses over long term
D. At low doses along with diuretics/digoxin

34.14 B
34.15 A
34.16 C
34.17 A

 

34.18 In post-myocardial infarction and other high cardio-vascular risk subjects but without hypertension or heart failure, prolonged ACE inhibitor medication has been found to:
A. Increase the chances of sudden cardiac death
B. Reduce the incidence of fatal as well as non-fatal myocardial infarction or stroke
C. Lower the risk of developing heart failure and diabetes
D. Both ‘B‘ and ‘C’

34.19 Which of the following statements most closely describes the current status of angiotensin con-verting enzyme inhibitors in congestive heart failure:
A. They are the first choice drugs unless con-traindicated
B. They are used when diuretics alone fail
C. They are a substitute for digitalis
D. They are to be used as adjuncts only in resistant cases

34.20 Long term ACE inhibitor therapy may retard the progression of:
A. Diabetic nephropathy
B. Diabetic retinopathy
C. Hypertensive nephropathy
D. All of the above

34.21 The following drug has been demonstrated to retard progression of left ventricular dysfunction and prolong survival of congestive heart failure patients:
A. Digoxin
B. Furosemide
C. Enalapril
D. Amrinone

34.18 D
34.19 A
34.20 D
34.21 C

 

34.22 Losartan is a:
A. Selective AT1 receptor antagonist
B. Selective AT2 receptor antagonist
C. Nonselective AT1 + AT2 receptor antagonist
D. AT1 receptor partial agonist

34.23 Clinically, the angiotensin antagonists share the following features of angiotensin converting enzyme inhibitors except:
A. Antihypertensive efficacy
B. Potential to reverse left ventricular hyper-trophy
C. Lack of effect on carbohydrate tolerance
D. Potential to induce cough in susceptible individuals

34.24 Choose the drug that selectively blocks AT1 subtype of angiotensin receptors:
A. Ramipril
B. Lovastatin
C. Candesartan
D. Sumatriptan

34.25 An elderly hypertensive was treated with hydro-chlorothiazide 50 mg daily. Even after a month, his BP was not reduced to the desired level and another antihypertensive was added. After 2 hours of taking the other drug his BP fell precipitously. The most likely other drug given to him is:
A. Atenolol
B. Captopril
C. Methyldopa
D. Amlodipine

34.22 A
34.23 D
34.24 C
34.25 B

 

34.26 Indications of angiotensin converting enzyme inhibi-tors include the following except:
A. Evolving myocardial infarction
B. Diabetic nephropathy
C. Scleroderma crisis
D. Stable angina pectoris

34.27 Losartan differs from enalapril in the following res-pect:
A. It does not potentiate bradykinin
B. It depresses cardiovascular reflexes
C. It impairs carbohydrate tolerance
D. It does not have fetopathic potential

34.28 Bradykinin and angiotensin II have the following feature common to both:
A. They both cause fall in BP
B. They both are degraded by Kininase II
C. Their precursor proteins are plasma α2 globu-lins
D. They both release aldosterone from adrenal cortex

34.29 Select the nonapeptide which can be generated from plasma globulin by snake venom enzymes, causes fall in BP and intense pain when applied to blister base:
A. Kallidin
B. Bradykinin
C. Angiotensin II
D. Angiotensin III

34.30 Actions of bradykinin include the following except:
A. Fall in blood pressure
B. Cardiac depression
C. Increase in capillary permeability
D. Bronchoconstriction

34.26 D
34.27 A
34.28 C
34.29 B
34.30 B

 

34.31 The following kinin action is mediated primarily by the kinin B1 receptor:
A. Intestinal contraction
B. Bronchoconstriction
C. EDRF release and vasodilatation
D. Production of Interleukin, TNFα and other inflammatory mediators

35.1 Digitalis in creases the force of contraction of ventricles by:
A. Increasing the duration of systole
B. Increasing the rate of contraction without affecting the duration of systole
C. Increasing the rate of contraction, but reduc-ing the duration of systole
D. Increasing both the rate of contraction as well as the duration of systole

35.2 In a failing heart therapeutic dose of digoxin has no effect on the following parameter:
A. Cardiac output
B. Heart rate
C. Tone of ventricular fibres
D. Cardiac vagal tone

35.3 Digitalis slows the heart in congestive heart failure by:
A. Increasing vagal tone
B. Decreasing sympathetic overactivity
C. Direct depression of sinoatrial node
D. All of the above

35.4 The electrophysiological effects of digitalis on Purkinje fibres include the following except:
A. Enhancement of resting membrane potential
B. Decrease in the slope of phase-0 depolari-zation
C. Increase in the rate of phase-4 depolarization
D. Abbreviation of action potential duration

34.31 D
35.1 C
35.2 C
35.3 D
35.4 A

 

35.5 Digitalis induced increase in refractory period of myocardial fibres is most consistent and pronounced in the:
A. Atria
B. Ventricles
C. A-V node
D. Purkinje fibres

35.6 What is/are the consequence(s) of myocardial Na+ K+ ATPase inhibition by digoxin:
A. Increased intracellular Na+ ion concentration
B. Increased cytosolic Ca2+ ion concentration
C. Increased intracellular K+ ion concentration
D. Both ‘A’ and ‘B’ are correct

35.7 The positive inotropic action of digoxin takes several hours to develop because:
A. Binding of digoxin to Na+K+ATPase is slow
B. After Na+K+ATPase inhibition by digoxin, Ca2+ loading of myocardial fibres occurs progressively with each contraction
C. Digoxin inhibits Na+K+ATPase through modi-fication of gene function which takes time
D. Both ‘A’ and ‘B’ are correct

35.8 Among all cardiac glycosides, digoxin is the most commonly used, because:
A. It is the most potent and fastest acting glycoside
B. It has the highest and most consistent oral bioavailability
C. It is the longest acting and the safest glycoside
D. It has intermediate plasma half life so that dose adjustments are possible every 2-3 days and toxicity abates rather rapidly after discontinuation

35.5 C 35.6 D 35.7 D 35.8 D

 

35.9 The most important channel of elimination of digoxin is:
A. Glomerular filtration
B. Tubular secretion
C. Hepatic metabolism
D. Excretion in bile

35.10 Infusion of potassium chloride is indicated in digitalis toxicity when the manifestation(s) is/are:
A. Vomiting, hyperapnoea and visual distur-bance
B. Pulsus bigeminus with heart rate 110/min in a patient on maintenance digoxin therapy
C. Ventricular tachycardia in a child who has accidentally ingested 10 digoxin tablets
D. 2:1 A-V block with occasional ventricular extrasystoles

35.11 Potassium therapy tends to counteract the cardiac toxicity of digitalis by:
A. Reducing the affinity of sarcolemal Na+ K+ATPase for digitalis
B. Suppressing ectopic automaticity enhanced by digitalis
C. Promoting A-V conduction
D. Both 'A' and 'B' are correct

35.12 Select the most suitable antiarrhythmic drug for counteracting ventricular extrasystoles due to digoxin toxicity:
A. Lignocaine
B. Quinidine
C. Verapamil
D. Amiodarone

35.9 A 35.10 B 35.11 D 35.12 A

 

35.13 The following drug given concurrently can enhance toxicity of digoxin:
A. Phenobarbitone
B. Metoclopramide
C. Quinidine
D. Magnesium hydroxide

35.14 Digoxin is contraindicated in:
A. Angina pectoris patients
B. Ventricular tachycardia
C. Hypertensive patients
D. Complete heart-block

35.15 Digitalis is most suitable for treatment of CHF when it is due to:
A. Cor pulmonale
B. Arterio-venous shunt
C. Thiamine deficiency
D. Long-standing uncontrolled hypertension

35.16 The dose of digoxin in congestive heart failure is adjusted by monitoring:
A. Electrocardiogram
B. Heart rate and symptoms of CHF
C. Blood pressure
D. Plasma digoxin levels

35.17 Digoxin affords the following benefit/benefits in CHF:
A. Restores cardiac compensation and relieves symptoms
B. Reverses the pathological changes of CHF
C. Prolongs survival of CHF patients
D. Both ‘A’ and ‘B’ are correct

35.13 C 35.14 B 35.15 D 35.16 B 35.17 A

 

hi, from where did you get these questions?

pls post link