1) Infusion of potassium chloride is indicated in digitalis toxicity when the manifestation(s) is/are:
A. Vomiting, hyperapnoea and visual disturbance
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
2) 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
3) Select the most suitable antiarrhythmic drug for counteracting ventricular extrasystoles due to digoxin toxicity:
A. Lignocaine
B. Quinidine
C. Verapamil
D. Amiodarone
4) The following drug given concurrently can enhance toxicity of digoxin:
A. Phenobarbitone
B. Metoclopramide
C. Quinidine
D. Magnesium hydroxide
5) Digoxin is contraindicated in:
A. Angina pectoris patients
B. Ventricular tachycardia
C. Hypertensive patients
D. Complete heart-block
6) 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
7) 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
8) 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
9) Long-term maintenance therapy with digoxin is the best option in the following category of CHF patients:
A. Hypertensive patients
B. Patients with hypertrophic cardiomyopathy
C. Patients with associated atrial fibrillation
D. Patients having cardiac valvular defects
10) A patient of CHF was treated with furosemide and digoxin. He became symptom-free and is stable for the last 3 months with resting heart rate 68/min in sinus rhythm but left ventricular ejection fraction is
low. Which of the following lines of action is warranted:
A. Stop above medication and start an ACE inhibitor
B. Continue all medication as before
C. Continue the diuretic but stop digoxin
D. Continue digoxin but stop the diuretic
11) The following action of digoxin is responsible for beneficial effect in auricular fibrillation:
A. Increased myocardial contractility
B. Suppression of SA node
C. Depression of A-V conduction
D. Enhanced Purkinje fibre automaticity
12) Select the drug that can help restore cardiac performance as well as prolong survival in CHF patients:
A. Spironolactone
B. Furosemide
C. Dobutamine
D. Metoprolol
13) The following drug can relieve symptoms of CHF but does not retard disease progression or prolong survival:
A. Digoxin
B. Carvedilol
C. Spironolactone
D. Ramipril
14) Which of the following drugs can afford both haemodynamic improvement as well as disease modifying benefits in CHF:
A. Furosemide
B. Milrinone
C. Losartan
D. Digoxin
15) What is the usual response to digoxin in a patient ofatrial fibrillation:
A. Restoration of normal sinus rhythm
B. Conversion of atrial fibrillation to atrial flutter
C. Increase in atrial fibrillation frequency, but decrease in ventricular rate
D. Decrease in atrial fibrillation frequency, bu increase in ventricular rate
16) Digoxin produces the following effect(s) in atrial flutter:
A. Reduces ventricular rate
B. Prevents shift of A-V block to a lower grade
C. Converts atrial flutter to atrial fibrillation
D. All of the above
17) The preferred diuretic for mobilizing edema fluid in CHF is:
A. Hydrochlorothiazide
B. Furosemide
C. Metolazone
D. Amiloride
18) Beneficial effect/effects of diuretics in CHF patients include the following:
A. Symptomatic relief
B. Regression of pathological changes
C. Prolongation of life expectancy
D. Both ‘A’ and ‘C’
19) Glyceryl trinitrate is used in CHF for:
A. Routine treatment of mild to moderate chronic heart failure
B. Rapid symptom relief in acute left ventricular failure
C. Arresting disease progression
D. Both 'A' and 'B'
20) Vasodilators are used to treat:
A. Acute heart failure attending myocardial infarction
B. Chronic heart failure due to diastolic dysfunction
C. Chronic heart failure due to both systolic as well as diastolic dysfunction
D. All of the above
21) The following type of vasodilator is not beneficial in CHF due to systolic dysfunction:
A. Calcium channel blocker
B. Angiotensin converting enzyme inhibitor
C. Nitrate
D. Hydralazine
22) Which vasodilator is most suitable for a patient of CHF who is symptomatic even at rest and has a central venous pressure of 25 mm Hg and cardiac index 1.8 L/min/m2:
A. Glyceryl trinitrate
B. Enalapril
C. Hydralazine
D. Nifedipine
23) Beneficial effects of □-adrenoceptor blockers in CHF include the following except:
A. Antagonism of ventricular wall stress enhancing action of sympathetic overactivity
B. Antagonism of vasoconstriction due to sympathetic overactivity
C. Prevention of pathological remodeling of ventricular myocardium
D. Prevention of dangerous cardiac arrhythmias
24) The following is true of □-adrenergic blocker therapy in CHF:
A. They are added to conventional therapy after cardiac compensation is restored
B. They are indicated only in severe (NYHA class IV) heart failure
C. They are to be used only at low doses
D. All of the above
25) Choose the correct statement about use of □- adrenergic blockers in CHF:
A. All □□blockers are equally effective in CHF
B. They are used as alternative to conventional therapy with ACE inhibitors ± digitalis/ diuretic
C. They are most useful in mild to moderate cases with systolic dysfunction due to dilated cardiomyopathy
D. They are indicated only in asymptomatic left ventricular dysfunction
26) The following drug is used for short-term control of emergency heart failure, but not for long-term treatment of congestive heart failure:
A. Digoxin
B. Ramipril
C. Dobutamine
D. Spironolactone
Answer- C
27) The principal action common to all class I antiarrhythmic drugs is:
A. Na+ channel blockade
B. K+ channel opening
C. Depression of impulse conduction
D. Prolongation of effective refractory period
28) The antiarrhythmic drug which decreases both rate of depolarization (phase 0) as well as rate of repolarization (phase 3) of myocardial fibres is:
A. Lignocaine
B. Propranolol
C. Quinidine
D. Verapamil
29) Quinidine has the following action on electrophysiological properties of the heart
except:
A. Decreases automaticity of Purkinje fibres
B. Abolishes after depolarizations
C. Prolongs refractory period of atrial fibres
D. Decreases membrane responsiveness of atrial and ventricular fibres
30) The limitations of quinidine in the treatment of cardiac arrhythmias include the following except:
A. It has narrow spectrum antiarrhythmic activity
B. It is not tolerated by many patients
C. It can precipitate myocardial decompensation
D. It can cause marked hypotension
31) The following is not true of quinidine:
A. It blocks myocardial Na+ channels primarily in the open state
B. It has no effect on myocardial K+ channels
C. It produces frequency dependent blockade of myocardial Na+ channels
D. It delays recovery of myocardial Na+ channels
32) Quinidine can cause paradoxical tachycardia in a patient of:
A. Sick sinus syndrome
B. Atrial extrasystoles
C. Atrial fibrillation
D. Ventricular extrasystoles
33) Quinidine is now used primarily for:
A. Conversion of atrial fibrillation to sinus rhythm
B. Control of ventricular rate in atrial flutter
C. Termination of ventricular tachycardia
D. Prevention of recurrences of atrial fibrillation/ ventricular tachycardia
34) The following antiarrhythmic drug has the most prominent anticholinergic action:
A. Disopyramide
B. Quinidine
C. Procainamide
D. Lignocaine
35) Procainamide differs from quinidine in the following respect(s):
A. It does not cause paradoxical tachycardia
B. It has no α adrenergic blocking activity
C. It has little antivagal action
D. Both ‘B’ and ‘C’ are correct
36) The following is true of procainamide except:
A. It generates an active metabolite in the body
B. Its plasma half-life is longer than that of quinidine
C. On long-term use, it can cause systemic lupus erythematosus like illness
D. It is effective in many cases of ventricular extrasystoles, not responding to lignocaine
37) The most significant feature of the antiarrhythmic action of lignocaine is:
A. Suppression of phase-4 depolarization in ventricular ectopic foci
B. Prolongation of action potential duration
C. Prolongation of effective refractory period
D. Depression of membrane responsiveness
38) Myocardial Na+ channel blockade by lignocaine has the following characteristic:
A. It blocks inactivated Na+ channels more than activated channels
B. It blocks activated Na+ channels more than inactivated channels
C. It delays rate of recovery of Na+ channels
D. It produces more prominent blockade of atrial than ventricular Na+ channels
39) Lignocaine is the preferred antiarrhythmic for emergency control of cardiac arrhythmias following acute myocardial infarction because:
A. It has a rapidly developing and titratable antiarrhythmic action
B. It causes little myocardial depression and hypotension
C. It has broad spectrum antiarrhythmic efficacy in atrial as well as ventricular arrhythmias
D. Both ‘A’ and ‘B’ are correct
40) Lignocaine is effective in the following cardiac arrhythmia(s):
A. Atrial fibrillation
B. Paroxysmal supraventricular tachycardia
C. Digitalis induced ventricular extrasystoles
D. All of the above
41) Absorption of oral iron preparations can be facilitated by coadministering:
A. Antacids
B. Tetracyclines
C. Phosphates
D. Ascorbic acid
42) The gut controls the entry of ingested iron in the body by:
A. Regulating the availability of apoferritin which acts as the carrier of iron across the mucosal cell
B. Regulating the turnover of apoferritin-ferritin interconversion in the mucosal cell
C. Complexing excess iron to form ferritin which remains stored in the mucosal cell and is shed off
D. Regulating the number of transferrin receptors on the mucosal cell
43) In the iron deficient state, transferrin receptors increase in number on the:
A. Intestinal mucosal cells
B. Erythropoietic cells
C. Reticuloendothelial cells
D. All of the above
44) The percentage of elemental iron in hydrated ferrous sulfate is:
A. 5%
B. 10%
C. 20%
D. 33%
45) Select the oral iron preparation which does not impart metallic taste and has good oral tolerability despite high iron content but whose efficacy in treating iron deficiency anaemia has been questioned:
A. Iron hydroxy polymaltose
B. Ferrous succinate
C. Ferrous fumarate
D. Ferrous gluconate
46) The daily dose of elemental iron for maximal haemopoietic response in an anaemic adult is:
A. 30 mg
B. 100 mg
C. 200 mg
D. 500 mg
47) The side effect which primarily limits acceptability of oral iron therapy is:
A. Epigastric pain and bowel upset
B. Black stools
C. Staining of teeth
D. Metallic taste
48) Choose the correct statement about severity of side effects to oral iron medication:
A. Ferrous salts are better tolerated than ferric salts
B. Complex organic salts of iron are better tolerated than inorganic salts
C. Liquid preparations of iron are better tolerated than tablets
D. Tolerability depends on the quantity of elemental iron in the medication
49) The following is not a valid indication for parenteral iron therapy:
A. Inadequate response to oral iron due to patient noncompliance
B. Anaemia during pregnancy
C. Severe anaemia associated with chronic bleeding
D. Anaemia in a patient of active rheumatoid arthritis
50) Iron sorbitol-citric acid differs from iron dextran in that:
A. It cannot be injected i.v.
B. It is not excreted in urine
C. It is not bound to transferrin in plasma
D. It produces fewer side effects
51) Choose the correct statement about iron therapy:
A. Haemoglobin response to intramuscular iron is faster than with oral iron therapy
B. Iron must be given orally except in pernicious anaemia
C. Prophylactic iron therapy must be given during pregnancy
D. Infants on breastfeeding do not require medicinal iron
52) A patient of iron deficiency anaemia has been put oniron therapy. What should be the rate of rise in haemoglobin level of blood so that response is considered adequate:
A. 0.05 – 0.1 g% per week
B. 0.1 – 0.2 g% per week
C. 0.5 – 1.0 g% per week
D. More than 1.0 g% per week
53) The following chelating agent should not be used systemically to treat acute iron poisoning in a child:
A. Desferrioxamine
B. Calcium edetate
C. Dimercaprol
D. Calcium disodium diethylene triamine penta acetic acid
54) Megaloblastic anaemia occurs in:
A. Vitamin B12 but not folic acid deficiency
B. Folic acid but not Vitamin B12 deficiency
C. Either Vitamin B 12 or folic acid deficiency
D. Only combined Vitamin B12 + folic aciddeficiency
55) The metabolic reaction requiring vitamin B12 but not folate is:
A. Conversion of malonic acid to succinic acid
B. Conversion of homocysteine to methionine
C. Conversion of serine to glycine
D. Thymidylate synthesis
56) The daily dietary requirement of vit B12 by an adult is:
A. 1-3 □g
B. 50-100□g
C. 0.1-0.5 mg
D. 1-3 mg
57) The following factor(s) is/are required for the absorption of dietary vitamin B12:
A. Gastric acid
B. Gastric intrinsic factor
C. Transcobalamine
D. Both ‘A’ and ‘B’
58) A 60-year-old patient presented with anorexia, weakness, paresthesia and mental changes. His tongue was red, tendon reflexes were diminished, haemoglobin was 6 g% with large red cells and neutrophils had hypersegmented nuclei. Endoscopy revealed atrophic gastritis. Deficiency of which factor is likely to be responsible for his condition:
A. Folic acid
B. Vitamin B12
C. Pyridoxine
D. Riboflavin
59) Features of methylcobalamin include the following:
A. It is an active coenzyme form of vit B12
B. It is required for the synthesis of S-adenosyl methionine
C. It is specifically indicated for correcting neurological defects of vit B12 deficiency
D. All of the above
60) Hydroxocobalamin differs from cyanocobalamin in that:
A. It is more protein bound and better retained
B. It is beneficial in tobacco amblyopia
C. It benefits haematological but not neurological manifestations of vit B12 deficiency
D. Both ‘A’ and ‘B’ are correct Answer- D
ANSWER KEY:
1-B 11-C 21-A 31-B 41-D 51-C
2-D 12-D 22-B 32-C 42-C 52-C
3-A 13-A 23-B 33-D 43-B 53-C
4-C 14-C 24-A 34-A 44-C 54-C
5-B 15-C 25-C 35-D 45-A 55-A
6-D 16-D 26-C 36-B 46-C 56-A
7-B 17-B 27-A 37-A 47-A 57-D
8-A 18-A 28-C 38-A 48-D 58-B
9-C 19-B 29-B 39-D 49-B 59-D
10-A 20-D 30-A 40-C 50-A 60-D
1) Osmotic diuretics are contraindicated in
a) Increased intracranial tension
b) Increased intraocular tension
c) Established acute renal failure
d) Poisonings
2) The antidiuretic action of Desmopressin is due to activation of:
a) V 1a receptor
b) V 2 receptor
c) V 1b receptor
3) Furosemide increases the excretion of all of the followings except
a) Sodium
b) Potassium
c) Uric acid
d) Calcium and magnesium
4) A group of college students is planning a mountain climbing trip. Which of the following drugs would be appropriate for them to take to prevent mountain sickness?
a) Acetazolamide
b) Furosemide
c) Hydrochlorothiazide
d) Spironolactone
5) Drug of choice for nephrogenic diabetes insipidus is:
a) Lypressin
b) Terlipressin
c) Desmopressin
d) Vasopressin
6) Which of the following agent is most e|ective in the treatment of hepatic edema?
a) Chlorthalidone
b) Triamterene
c) Furosemide
d) Spironolactone
7) All of the following drugs are nephrotoxic except
a) Amphotericin
b) Lithium
c) Metronidazole
d) Cocaine
8) The dose related toxicity of loop diuretics is:
a) Allergic reaction
b) Deafness
c) Hypomagnesemia
d) Hyperuricemia
9) Aminoglycosides induced nephrotoxicity is in the order of
a) Gentamicin> Tobramycin>Amikacin>Netilmicin> Streptomycin
b) Streptomycin > Tobramycin >Amikacin>Netilmicin > Gentamicin
c) Gentamicin > Amikacin > Netilmicin > Tobramycin > Streptomycin
d) Tobramycin > Amikacin>Netilmicin> Streptomycin > Gentamicin
10) All of the followings are non-renal actions of antidiuretic hormone except
a) a neurotransmitter in central nervous system
b) promotes haemostasis
c) is a potent vasoconstrictor
d) increases the permeability of the membrane to water
11) Which of the following drugs is used for urinary incontinence?
a) Flavoxate
b) Sodium citrate
c) Trimethoprim
d) Phenazopyridine
12) Concurrent use of Spironolactone & ACE inhibitors should be avoided because of danger of –
a) Hyperglycemia
b) Hyperkalemia
c) Hypokalemia
d) Hypoglycemia
13) Following diuretic promotes calcium reabsorption:
a) Spironolactone
b) Chlorothiazide
c) Furosemide
d) Ethacrynic acid
14) Following are the uses of Amiloride except
a) Adjunct to K+ wasting diuretics
b) Lithium induced nephrogenic diabetes insipidus
c) Congestive heart failure
d) a and b
e) a, b and c
15) Which one of the following diuretics is e|ective in severe renal failure?
a) Loop diuretics
b) K+ sparing diuretics
c) Thiazides
d) Carbonic anhydrase inhibitors
16) Following statements about osmotic diuretics is true except
a) Mannitol gets ltered in glomerulus, but cannot be reabsorbed
b) To maintain osmotic balance, water is retained in the urine
c) None of the above
d) All of the above
17) Which of the following drug and its mechanism of action is not correct?
a) Acetazolamide: epithelial sodium channel blockers
b) Spironolactone: potassium sparing diuretics
c) Hydrochlorothiazide: inhibit sodium chloride symporter
d) Bumetanide: inhibits NA+/K+/2Cl- cotransport
18) Based on V2 receptor, followings are the therapeutic uses of vasopressin except:
a) Diabetes insipidus
b) Bedwetting in children
c) Bleeding esophageal varices
d) Hemophilia
19) Which of the following is a synthetic prodrug of vasopressin?
a) Terlipressin
b) Lypressin
c) Desmopressin
d) None of the above
20) Long term use of loop diuretics causes ………………….
a) Cirrhosis of liver
b) Deafness
c) Distal nephron hypertrophy
d) Renal insu}ciency
21) Under physiological conditions the rate limiting enzyme in the generation of angiotensin II is:
A. Renin
B. Angiotensin converting enzyme
C. Aminopeptidase
D. Angiotensinase
22) 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
23) 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
24) 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
25) 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 (p. 446, 447)
26) 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
27) Ventricular remodeling after myocardial infarction involves the mediation of:
A. Angiotensin II
B. Prostaglandin
C. Bradykinin
D. Thromboxane A
28) Captopril pretreatment:
A. Inhibits the pressor action of angiotensin I
B. Inhibits the pressor action of angiotensin II
C. Potentiates the depressor action of bradykinin
D. Both ‘A’ and ‘C’ are correct
29) 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
30) 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
31) 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
32) 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
33) The following angiotensin converting enzyme inhibitor can reduce cardiac contractility:
A. Captopril
B. Enalapril
C. Perindopril
D. Lisinopril
34) Advantages of angiotensin converting enzyme inhibitors as antihypertensive include the following except:
A. They tend to reverse left ventricular hypertrophy
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
35) The following drug increases cardiac output in congestive heart failure without having any direct myocardial action:
A. Captopril
B. Digoxin
C. Amrinone
D. Dobutamine
36) Angiotensin converting enzyme inhibitors reduce the following haemodynamic parameters in congestive heart failure except:
A. Systemic vascular resistance
B. Right atrial pressure
C. Cardiac output
D. Heart rate × pressure product
37) 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
38) In post-myocardial infarction and other high cardiovascular 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 nonfatal myocardial infarction or stroke
C. Lower the risk of developing heart failure and diabetes
D. Both ‘B‘ and ‘C’
39) Which of the following statements most closely describes the current status of angiotensin converting enzyme inhibitors in congestive heart failure:
A. They are the first choice drugs unless contraindicated
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
40) Long term ACE inhibitor therapy may retard the progression of:
A. Diabetic nephropathy
B. Diabetic retinopathy
C. Hypertensive nephropathy
D. All of the above
41) 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
42) Losartan is a:
A. Selective AT1 receptor antagonist
B. Selective AT2 receptor antagonist
C. Nonselective AT1 + AT2 receptor antagonist
D. AT1 receptor partial agonist
43) Clinically, the angiotensin antagonists share the following features of angiotensin converting enzyme inhibitorsexcept:
A. Antihypertensive efficacy
B. Potential to reverse left ventricular hypertrophy
C. Lack of effect on carbohydrate tolerance
D. Potential to induce cough in susceptible individuals
44) Choose the drug that selectively blocks AT1 subtype of angiotensin receptors:
A. Ramipril
B. Lovastatin
C. Candesartan
D. Sumatriptan
45) An elderly hypertensive was treated with hydrochlorothiazide 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
46) Indications of angiotensin converting enzyme inhibitors include the following
except:
A. Evolving myocardial infarction
B. Diabetic nephropathy
C. Scleroderma crisis
D. Stable angina pectoris
47) Losartan differs from enalapril in the following respect:
A. It does not potentiate bradykinin
B. It depresses cardiovascular reflexes
C. It impairs carbohydrate tolerance
D. It does not have fetopathic potential
48) 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□2globulins
D. They both release aldosterone from adrenal cortex
49) 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
50) Actions of bradykinin include the following except:
A. Fall in blood pressure
B. Cardiac depression
C. Increase in capillary permeability
D. Bronchoconstriction
51) The following kinin action is mediated primarily by the kinin B 1 receptor:
A. Intestinal contraction
B. Bronchoconstriction
C. EDRF release and vasodilatation
D. Production of Interleukin, TNF□□and other inflammatory mediators
52) 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 reducing the duration of systole
D. Increasing both the rate of contraction as well as the duration of systole
53) 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
54) 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
55) 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 depolarization
C. Increase in the rate of phase-4 depolarization
D. Abbreviation of action potential duration
56) 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
57) 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
58) 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 modification of gene function which takes time
D. Both ‘A’ and ‘B’ are correct
59) 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
60) The most important channel of elimination of digoxin is:
A. Glomerular filtration
B. Tubular secretion
C. Hepatic metabolism
D. Excretion in bile Answer- A
ANSWER KEY:
1-C 11-A 21-A 31-C 41-C 51-A
2-B 12-B 22-D 32-C 42-A 52-C
3-C 13-B 23-A 33-D 43-D 53-C
4-A 14-D 24-B 34-B 44-C 54-D
5-C 15-A 25-D 35-A 45-B 55-A
6-D 16-D 26-B 36-C 46-D 56-C
7-C 17-A 27-A 37-A 47-A 57-D
8-B 18-C 28-D 38-D 48-C 58-D
9-A 19-A 29-A 39-A 49-B 59-D
10-D 20-C 30-B 40-D 50-B 60-A