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74 Cards in this Set
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CD01 [Mar96] [Mar98] [Mar99] [Jul01] Milrinone:
A. Decreases pulmonary vascular resistance B. Increases systemic vascular resistance C. Is poorly absorbed when given orally D. Chronic use causes thrombocytopaenia |
ANSWER A
* A. Decreases pulmonary vascular resistance - true; milrinone is a vasodilator. "In the peripheral vasculature, the result is dilation of both resistance and capacitance vessels, leading to reduction of both afterload and preload." Goodman and Gilman Ch 33 * B. Increases systemic vascular resistance - false; * C. Is poorly absorbed when given orally - false, can be given orally, but long term use has been associated with increase mortality, therefore no longer available * D. Chronic use causes thrombocytopenia occurs in 10% of patients receiving inamrinone but is rare with milrinone |
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Milrinone causes:
A. Chronic use causes thrombocytopaenia B. Pulmonary vasoconstriction C. Not effective orally D. Typically administered for 7 days E. Adverse effects include hypotension, SVT and ventricular arrythmias |
ANSWER E
* A. Chronic use causes thrombocytopenia occurs in 10% of patients receiving inamrinone but is rare with milrinone * B. Pulmonary vasoconstriction - false; potent vasodilator of all vessels * C. Not effective orally - false; can be given orally, but not pharmaceutically available * D. FALSE: short term treatment only and should generally not be used for longer than 72 hours * E. TRUE |
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CD01b [Mar97] Milrinone:
A. Cannot be given orally B. Is a phosphodiesterase III inhibitor that decreases cyclic AMP C. Decreases peripheral vascular resistance D. Increases pulmonary vascular resistance |
ANSWER C
* A. Cannot be given orally - false * B. Is a phosphodiesterase III inhibitor that decreases cyclic AMP -false increases cAMP * C. Decreases peripheral vascular resistance - true; * D. Increases pulmonary vascular resistance - false; |
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CD01c [Feb00] Milrinone, which is FALSE:
A. Is structurally related to thyroid hormone B. Is arrhythmogenic C. Has its effects via cAMP mediated increase in intracellular Ca2+ D. Increases myocardial oxygen consumption |
ANSWER A
A. Is structurally related to thyroid hormone - False; milrinone is a bipyridine. B. Is arrhythmogenic - true; "Milrinone appears less likely to cause bone marrow and liver toxicity than inamrinone, but it does cause arrhythmias." C. Has its effects via cAMP mediated increase in intracellular Ca2+ - true; "The bipyridines increase myocardial contractility by increasing inward calcium flux in the heart during the action potential; they may also alter the intracellular movements of calcium by influencing the sarcoplasmic reticulum. They also have an important vasodilating effect. Inhibition of phosphodiesterase results in an increase in cAMP and the increase in contractility and vasodilation" Katzung Ch 13 D. Increases myocardial oxygen consumption - maybe true; milrinone acts to increase cardiac contractility and therefore O2 demand, but it also decreases preload and afterload. "The O2 consumption by the heart is determined primarily by the intramyocardial tension, the contractile state of the myocardium, and the heart rate." |
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CD02 [Mar96] [Mar03] Sodium nitrite used in cyanide toxicity:
A. Increases methaemoglobinaemia B. To produce increased hepatic sulphydryl groups C. Increases conversion to cyanocobalamin (?hydroxycobalamin) D. Displaces cyanide from haemoglobin E. Enhances oxidative phosphorylation |
ANSWER A and E
* A. Correct, converts Hb to Meth-Hb which acts as antidote by converting cyanide to cyanometh-Hb * B. Incorrect, Na-Thiosulphate does this: sulfur donor * C. Incorrect, incr. cyano-meth-Hb but can give hydroxycobalamine which binds cyanide to form cyanocobalamine. * D. Incorrect, converts Hb to Meth-Hb which binds cyanide to form cyanometh-HB * E. correct, as reversal of cyanide toxicity should improve the impaired oxidative phosphorlylation |
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CD03 [Mar96] [Jul96] [Jul98] [Jul99] [Feb00] [Apr01] [Mar03] [Jul04] Ephedrine:
A. Is resistant to metabolism by MAO B. Is metabolised by COMT C. Action is totally indirect D. Acts via direct & indirect beta effect E. Action is purely alpha agonist |
ANSWER A
A. ephedrine is resistant to metabolism by MAO due to methyl at metabolised by MAO B : false, no COMT metabolism as no OH at '4 C : false, direct effects as alpha (lacks 3 OH) and indirect effects at beta by displacing adrenaline D: as above E: as above D: |
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Ephedrine:
A. Has direct alpha actions only B. Has direct beta actions only C. Has indirect (alpha) actions only D. ? E. Has both indirect & direct actions on alpha & beta receptors |
ANSWER E
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CD03b [Apr01] [Mar02] Ephedrine:
A. Decreases skeletal muscle blood flow B. Acts only by indirect effects C. Not metabolised by GIT MAO D. Not metabolised by COMT E. Increase renal blood flow |
ANSWER D
A. FALSE Increases skeletal muscle blood flow (also increases coronary blood flow, but decreases renal and splanchnic blood flows) B. False- see above C. RESISTANT to GIT MAO- not sure whether this means it doesn't happen at all D. True: resistent to monoamine oxidase and COMT, mostly excreted unchanged in urine E. False- see above |
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CD03c [Jul01] [Jul04] Ephedrine has:
A. Direct agonist on alpha receptors B. Direct and indirect effects on alpha and beta receptors C. Indirect actions on alpha receptors D. Direct actions on beta receptors E. Indirect actions on beta receptors |
ANSWER B
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CD04 [Mar96] [Jul98] The principal (?urinary) metabolite of adrenaline is:
A. Normetanephrine B. Metanephrine C. 3,4-dihydroxy-mandelic acid D. 3-methoxy, 4-hydroxymandelic acid E. 3-Methoxy 4-hydroxy phenylalanine |
ANSWER D
Adrenaline is a COMT and MAO substrate which is conjugated with glucaronide to form mandelic acid |
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CD05 [Mar96] [Jul97] [Jul98] [Mar99] [Feb00] [Apr01] [Jul01] [Feb04] Thiazide diuretics:
A. Work mainly on PCT B. Not effective if severely sodium depleted C. Action is independent of acid-base balance D. Increase GFR immediately E. Decrease BP by decreasing contractility F. Cause hypoglycaemia |
A: False, works on DCT
B: True, blocks NaCl cotransporter at luminal membrane causing naturesis and duiresis C: true D: False, but chronic use, through an unknown mechanism, results in decreased SVR. Therefore maintaining hypotensive effect despite returning to euvolaemic. E: false F: false, causes hyperglycaemia, can unmask glucose intolerance |
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CD05 [Mar96] [Jul97] [Jul98] [Mar99] [Feb00] [Apr01] [Jul01] [Feb04] Thiazide diuretics:
A. Interferes with kidney concentrating mechanisms B. Causes hypocalcaemia C. Used to treat hypercalcaemia D. Potentiate hyperglycaemia E. Are effective as antihypertensives by decreasing cardiac output L. Cause hypernatraemia M. Washes out the medullary concentration gradient |
ANSWER C
A: false, block NaCl cotransporter at DCT therefore attenuates kidney's ability to excrete a dilute urine during water diuresis. it is not involved in medullary concentrating gradient B: false, increased Ca reabsorption in collecting ducts C. TRUE D: FALSE, does not decrease CO E : FALSE, not involved in medullary concentrating gradient |
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Thiazide diuretics:-
A. Increase calcium excretion in the urine. B. Decreased efficacy in sodium depletion. C. Main site of action is the proximal tubule. D. Cause equivalent amount of diuresis to frusemide E. Causes hyperkalemia by blocking reabsorption of Na and Cl from the distal convuluted tubules |
ANSWER B
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CD06 [Mar96] Sodium nitroprusside in healthy patient:
A. Decreases venous more then arterial resistance B. Has no effect on control of pulmonary vascular resistance C. Decreases cerebral blood flow D. Causes uterine relaxation E. Does not inhibit hypoxic pulmonary vasoconstriction |
ANSWER D
A : FALSE, SNP is potentent veno and vasodilator, while GTN preferential venodilator at low dose 2mcg/ kg/ min B : FALSE , SNP is dilator of all SM C : FALSE, vasodilatory action over comes the metabolic autoregulation D : TRUE E: FALSE |
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CD07 [Mar96] [Mar97] [Jul97] [Mar98] [Jul98] [Jul99] [Feb00] [Apr01] [Mar03] Which one of the following statements about clonidine is correct?
A. Increase MAC requirements B. Cause transient hypertension with IV administration C. 65% is excreted in the faeces D. Is more efficious than pethidine in reducing shivering E. Is not absorbed transdermally |
ANSWER B
A: FALSE, decreases MAC due alpha agonist activity at the spinal level B: TRUE, IV administration causes transient hypertension due to direct alpha1 vasoconstriction followed by vasodilation caused by decreased adrenaline release mediated by alpha2 (presynaptic) agonist activity. C: FALSE: 65% excreted unchanged in the urine and 20% in the faeces D: FALSE: false, both are equally efficacious. http://dig.pharm.uic.edu/faq/Dec10/shivering.aspx E: is formulated as a patch |
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CD08 [Mar97] [Mar99] Regarding Digoxin:
A. The aglycone portion causes the cardiac effects B. The glycone portion causes the cardiac effects C. Antibodies to the glycone portion can be used to treat digoxin toxicity D. Side effects do not occur within the therapeutic range E. Intramuscular absorption is similar to oral absorption |
Best Answer - A
Structurally, cardiac glycosides consist of 2 parts: * aglycone (or 'genin')- this is the steroid and the lactone ring * glycone - the attached sugar residues Both are required for the drug to be useful clinically. It is said that the the intrinsic cardiac activity resides in the aglycone portion (see below for structure-activity), but that the glycone (sugar) portion is responsible for pharmacokinetic factors (eg uptake into tissues). Digoxin consists of 3 molecules of beta(1,4)-D glycoside linked digitoxose linked to digoxigenin. ('genin' is a suffix used to indicate the aglycone. The cardiac activity of cardiac glycosides is a consequence of inhibition of the cell membrane Na+-K+ ATPase ('sodium pump'). Digoxin specifc antibody fragments are available for treatment of digoxin toxicity. Side effects are common and occur within the therapeutic range but especially if above the therapeutic range. Absorption after IM injection is erratic |
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CD09 [Mar97] [Jul99] Digoxin:
A. Decreases ventricular response due to vagal stimulation in AF B. Decreases myocardial oxygen consumption C. Increases the R-T interval D. Decreases AV conduction |
ANSWER D
A : digoxin slows AV conduction directly by inhibition of the NaKATPase and indirectly by vagal stimulation B: digoxin increases contractility which increases the demand, but then also slows the HR??? C false - Shortens QT interval D true - see above |
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CD10 [Jul97] [Jul00] [Apr01] [Jul02] Which of the following ECG changes would be most likely in digoxin toxicity:
A. Increased PR interval B. Increased QT interval C. Peaked T waves D. ST elevation E. Ventricular extrasystoles |
ANSWER E
he ECG signs of prolonged PR interval, characteristic ST segment depression, T wave flattening, and shortened QT interval are not signs of toxicity. PVR and bigemeny most common sign of toxicity. occur due to increased automaticity of the Purkinje and decreased AV conduction. Brady's and heart block also common. VT is a late sign. Gastrointestinal symptoms are common, but the abdominal examination is usually nonspecific. Visual changes occur, but the pupils are spared, and objective findings are few. |
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July 2000 version: Digoxin toxicity, which is FALSE
A. Inverted T waves B. Prolonged PR interval C. Xanthopsia D. Prolonged PT interval E. heart block |
ANSWER D
Various ECG changes are associated with the use of digoxin: ST depression and T wave inversion in V5-6 in a reversed tick pattern. Changes are more extensive in digoxin toxicity. Other changes that may occur: bradycardia prolonged PR shortened QT arrhythmias, especially heart block or bigemini |
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CD11 [Jul97] [Jul98] Regarding digoxin overdose/toxicity:
A. Serum level > 2.1 ng/ml is toxic B. Hyperkalaemia increases risk C. Causes a long PR interval D. Causes xanthochromia E. Causes a long QT interval and bigeminy |
ANSWER A
A : narrow therapeutic range of 0.5-2ng/ml, >2.5ng/ml is the toxic range B: false, hypokalaemia increases risk C : false, a prolonged PR interval is a theraputic effect, but also occurs in toxicity D: false, xanthopsia is evidence of toxicity (predominance of yellow in vision due to a yellowing of the optic media of the eye) E: false, bigeminy is a sign of toxicity, but long QT does not occur |
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CD12 [Jul97] [Mar02] [Jul02] [Jul04] Clonidine:
A. Elimination half-life of 3 hours (??or 3 to 6 hrs) B. Excreted 50% unchanged in the urine (or 50% renally excreted) C. Oral bioavailability 50% D. Cannot be absorbed topically E. Is highly protein bound |
ANSWER B
A : false, elimination is 6-15 hours B: True 50% excreted unchanged C: false, bioavailablity of 100% D : false, it is formulated as patches E: false 20% protein bound |
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CD14 [Jul97] [Jul98] [Jul00] [Jul04] Adenosine:
A. Slows conduction velocity and increases refractory period B. Is metabolised in plasma C. Decreases urate levels D. Methylxanthines increase response E. Activation of the Gi-protein, opens potassium channels, which hyperpolarizes the cell |
ANSWER E
A - False: adenosine slows AV conduction, hence its use to treat SVT. BUT refractory period is shortened by adenosine, and consequently it may induce AF or flutter. B - incorrect. It's taken up via a specific nucleoside transporter by RBCs and is metabolised by enzymes on the lumenal surface of the vascular endothelium C - incorrect: "Uric acid levels may increase 10% to 20% when adenosine is used D - incorrect: methylxanthines such as theophylline block A1 receptors E. True |
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CD15 [Jul97] [Jul99] Catecholamine substituition:
A. Alpha carbon CH3 substituition gives beta selectivity B. Beta-hydroxy substituition gives increased affinity C. D-dobutamine antagonist, L-dobutamine agonist D. ? |
ANSWER C
A incorrect. alpha carbon CH3 substitution blocks metabolism by MAO, and increases indirect activity. B possibly correct as beta -OH substitution gives increased potency of direct actions C correct if discussing actions at a1 receptor. levo dobutamine potent alpha 1 agonist dextro dobutamine alpha 1 antagonist, beta 1 agonist; hence the combination of the two gives selective b1 agonist activity. |
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CD16 [Mar96] [Jul96] [Jul97] [Jul98] Esmolol:
A. Active at beta-1 & beta-2 receptors B. Half-life < 2 minutes C. Has methanol as a metabolite D. Is metabolised by (?acetyl/?plasma) cholinesterase E. Is excreted unchanged in the urine F. Is a non-selective beta-1 receptor antagonist |
* A: esmolol is beta 1 selective
* B: t1/2 is about 10 min * C: true * D: metabolised by esterases in RBCs (not plasma cholinesterases) * E: see above * F: partly true - see A above |
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CD16b [Feb04] [Jul04] Esmolol
A. Is a non-selective beta antagonist B. Has intrinsic sympathomimetic activity C. Does not have membrane stabilising activity D. Has no effect on the pharmacokinetics of morphine E. Metabolised by red cell esterases to ethanol |
ANSWER D
A. FALSE: acts by competitive blockade of beta-adrenoceptors and is relatively selective for beta 1 B. FALSE: has no intrinsic sympathomimetic activity C. FALSE D. TRUE E. FALSE: metabolised by red cell esterases to methanol |
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CD17 [Jul97] [Jul98] [Mar99] [Jul99] [Jul01] [Jul04] Osmotic diuretics (?Mannitol):
A. Less sodium delivered to distal tubule B. Hypotonic medulla C. Increased sodium loss D. Urine osmolality > plasma osmolality E. MW greater than 600 |
ANSWER C
A Incorrect. More delivered at a lower concentration. B Incorrect. Isotonic. C Correct D Incorrect. Their osmolalities will be the same. E. Incorrect. MW 182.17 |
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MCQ-16 on July 2001]] paper:
Osmotic diuretics: A. Include mannitol and the dextrans. B. Wash out the medullary osmotic gradient. C. Cause sodium retention D. Is hypertonic E. Have a molecular weight >600 |
ANSWER B
A Incorrect. Mannitol and urea B Correct C Incorrect. Causes sodium loss. D Incorrect. It is isotonic E MW 182.17 |
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CD18 [Jul97] Guanethidine:
A. Causes sedation as a side effect B. Postural hypotension occurs C. Decreases reuptake of catechols presynaptically D. ? |
ANSWER B
CD18 * A. ?doesn't cross BB barrier * B. BEST ANSWER - "Therapeutic use of guanethidine is often associated with symptomatic postural hypotension" (Katzung 9th ed p.169) * C. False - Appears to have multiple mechanisms of actions. "Guanethidine inhibits the release of NA from sympathetic nerve endings" (Katzung 9th ed. p.169) |
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CD18b [Jul98] [Jul01] (Q24]] on Jul01]] paper) Guanethidine:
A. Acts primarily at?/on? the CNS B. Produces anti-hypertensive effect primarily by presynaptically inhibiting release of noradrenaline C. Highly lipid soluble D. Mental depression is a troublesome side effect E. Orthostatic hypotension is not a prominent side effect |
ANSWER B
Guanethidine is an antihypertensive drug that reduces the release of catecholamines, such as noradrenaline. Guanethidine is transported by uptake 1 into the presynaptic terminal. (In this it competes with noradrenaline so can potentiate exogenously applied noradrenaline). Once inside the terminal it blocks the release of noradrenaline in response to arrival of an action potential. Spontaneous release is not affected. This drug is no longer used clinically. * A. see above * B. True - see above * C. Probably false if A is false * D. doesn't cross BBB * E. see B above |
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CD19 [Jul97] [Jul99] Labetalol:
A. Alpha agonist & beta agonist B. Alpha agonist & beta antagonist C. Alpha antagonist & beta antagonist D. Is a more potent alpha blocker than phenoxybenzamine E. Alpha > beta effect |
ANSWER C
Labetolol is both alphablocker and betablocker, but the alpha blocking properties are relatively weak. Labetalol is formulated as a recemic mixture of four isomers... Two ...are inactive, a third (S,R) is a potent alpha-blockers, and the last (R,R) is a potent beta-blocker... Labetalol has 3:1 ratio of beta:alpha antagonism |
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CD20 [Mar98] [Jul98] [Jul99] [Feb00] [Apr01] [Jul04] Frusemide:
A. 30% plasma protein binding B. 20% oral absorption C. Elimination half-life less than one hour D. Promotes active secretion E. Affects the uricosuric effect of probenecid F. Effects not decreased until large decrease in GFR G. Causes a diuresis which is dependant on GFR over a wide range |
* A false - 95% protein bound and excreted unchanged in urine (p305 Peck and Hill)
* B False. Sassada and Smith: 60-70% absorption after oral administration, the bioavailability by this route is 43-71% * C true - "The elimination half-time is <1 hour" (Stoelting 3rd ed. p.439) * D false - "inhibit reabsorption of sodium and chloride primarily in the medullary portions of the ascending limbs of the loops of Henle" (Stoelting 3rd ed. p.437) "does not increase GFR or renal tubular secretion" (p.438) * E no idea * F perhaps - nothing in Stoelting for or against * G true - "responsiveness to frusemide is directly related to GFR over a wide range" (Stoelting 3rd ed. p.437-8) |
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Apr 2001 version: Frusemide:
A. Has 30% (?35%) protein binding B. Has an elimination half-life less than 1 hour C. 90% excreted in bile D. Increases rate of secretion in the renal tubules |
ANSWER B
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CD20b [Jul00] [Jul02] Frusemide does NOT cause:
A. Hyponatremia B. Hypokalemia C. Hypouricemia D. Hypomagnesemia E. Hypocalcemia |
ANSWER C
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CD21 [Mar98] [Jul98] The antiarrhythmic effect of lignocaine:
A. Because it incvreases the refractoriness of in cardiac muscle B. Therapeutic level 2-5ng/ml C. ? |
ANSWER A
A. Does increase refractoriness but main efect is slowing of phase 4 depolarisation due to blockage of sodium channels. ?? Class1B decrease ARP. B. 2-5 micrograms/ml not nanograms |
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CD22 [Jul98] [Feb04] [Jul04] The effects of beta blockers – the following is not true
A. Relax uterine muscle B. Increased AV conduction C. Decreased lipolysis D. Increased SVR E. Mask hypoglycaemia F. Negative inotropy G. Opposing effects of insulin H. Lipolysis |
ANSWERS C D F
A. beta 2 stimulation (salbutamol) relaxes uterine smooth muscle, so presumably this is false B. false: decrease C. true (adrenergic agonists stimulate) D. true E. true F. true G. false? (agonists oppose insulin) H. see C above |
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CD23 [Mar96] [Jul96] [Jul00] [Apr01] Phentolamine:
A. Is a selective alpha-1 antagonist B. Binds covalently to the alpha receptor C. Causes bradycardia D. Is a selective alpha-2 antagonist E. Increases cardiac output |
ANSWER E
Phentolamine is a non-selective alpha antagonist. Acts at alpha 1 and 2 It does not bind covalently (phenoxybenzamine does). It is competitive (reversible) antagonist. It decreases systemic blood pressure and causes reflex TACHYCARDIA (via baroreceptor reflex) Also causes tachycardia via its alpha 2 effects - enhanced neural release of noradrenaline. Increase in noradrenaline release also INCREASES CARDIAC OUTPUT. E. is Correct |
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CD24 [Mar96] [Feb00] [Mar03] A non-selective beta-blocker with low extraction ratio, long half-life and ISA:
A. Atenolol B. Propranolol C. Metoprolol D. Labetalol E. ? |
NO ANSWER
Atenolol is selective for beta-1 Propranolol is non-selective but "lacks intrinsic sympathomimetic activity" (Stoelting p.290) Metoprolol is beta-1 selective Labetalol is non-selective for both beta and alpha, does have some intrinsic beta-2 agonist properties, don't know about its extraction ratio (oral bioavailability 100%) |
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CD24b [Mar02] [Jul02] Which ONE of the following is water soluble, half life 6-8hrs, (“and something else”)?
A. Esmolol B. Metoprolol C. Propranalol D. ? E. Atenolol |
ANSWER E?
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CD26 [Jul98] [Mar99] [Mar03] [Feb04] [Jul04] Sotalol:
A. Non-selective beta-blocker B. Contraindicated in long QT C. Increases K+ conductance D. Used in the treatment of torsades E. Class II anti-arrhythmic drug F. Is a selective beta 1 antagonist G. Blocks K+ channels |
ANSWER A B E G
Sotalol is a non-selective beta-blocker with both class II & III activity. It causes prolonged QT interval & precipitates torsades in about 4% of those on it. The class 3 activity is due to K channel block in the myocardium. Major use is for treating ventricular arrhythmias (not torsades) and for atrial fibrillation. |
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CD28 [Mar99] Diazoxide:
A. Has diuretic activity B. Opens ATP-dependent K channels C. Not absorbed orally D. ? |
ANSWER B
Diazoxide is a potassium channel activator, which causes local relaxation in smooth muscle by increasing membrane permeability to potassium ions. This switches off voltage-gated calcium ion channels which inhibits the generation of an action potential. A - False: "Unlike thiazide diuretics, diazoxide causes sodium and water retention" (Stoelting p327) B - True: Diazoxide opens potassium channels (Katzung p 175) C - False: given orally to treat hypoglycaemia (increases catecholamine release) at a dose of 5mg/kg/day. From Yentis A-Z. |
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CD29 [ghj] [Jul00] Phenylephrine:
A. Metabolised by COMT B. Causes mydriasis C. Metabolised by MAO D. Effect lasts (?same time as/?longer than) noradrenaline E. Acts by indirect method only |
ANSWER B C D
A - False: "Because it is not a catechol derivative, (phenylephrine) is not inactivated by COMT" (Katzung p134) B - True: "It is an effective mydriatic" C - True: "metabolised by MAO" (Rang Dale and Ritter p168) D - True if longer than: Phenylephrine "has a much longer duration of action than the catecholamines" (Katzung p134) E - False: "It acts directly on the receptors" (Katzung p135) |
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CD30 [Jul98] Regarding hydrallazine:
A. Fast acetylators have shorter half lives than slow acetylators B. Acts via SNS mechanism C. Slow acetylators decrease half-life D. Has diuretic action E. Clearance > 50ml/kg/min |
ANSWER A
A - true: rapid acetylators have much lower bioavailability and acetylation appears to be the major form of metabolism (Stoelting p310) B: false, direct action of SM C - False: Slow acetylators will increase half-life D - False: Causes sodium and water retention, a property common to most vasodilators E - false: Sasada and Smith - Clearance=1.4 l/kg/hr = 23 mL/kg/min |
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CD32 [Jul99] Which of the following statements about hydrallazine is (?true/false)?:
A. Acts via alpha 1 receptors B. Increases cerebral blood flow C. Increases renal blood flow and urine output D. Decreased renin activity E. Has a duration of action of 1-2 hours |
ANSWER B
A : false direct vasodilatory effects by interfering with Ca entry into cell B. TRUE C. FALSE: increases renal blood flow secondary to increased cardiac output however results in sodium retention and decreased urine volume D. FALSE: increases renin activity E: false, elimination 3 hours, duration of action 2-6 hours |
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CD33 [Jul99] Concerning Dobutamine
A. Levo has alpha 1 antagonist and beta agonist effects B. Levo has partial alpha agonist effect and beta effects C. Is a pure beta agonist D. Selective B1 activity E. Selective B2 activity |
ANSWER D
A. FALSE: The levo (-) isomer has alpha agonist effects which opposes the Dextro (+) isomer which has alpha antagonist and beta 1 agonist effects. (also in Katzung p.135) Thus leaving it a selective beta 1 agonist. * The (-) isomer of dobutamine is a potent agonist at alpha-1 receptors. * The (+)-dobutamine is a potent a1 receptor antagonist, which can block the effects of (-)-dobutamine. The effects of these two isomers are mediated via beta receptors. The (+) isomer is a more potent beta receptor agonist than the (-) isomer (approximately tenfold). Both isomers appear to be full agonists B. FALSE see above C. FALSE see above D. TRUE E: FALSE |
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CD34 [Feb00] [Apr01] [Jul01] Adenosine
A. Causes AV block via action at A1 receptors B. Causes bronchoconstriction via A2 receptors C. Causes renal vasodilation D. Causes profound depression of the SA node E. Decreases AV transmission |
ANSWER A
* A - Correct: Adenosine causes "block of cardiac AV conduction (A1)" (Rang, Dale and Ritter 1995 p189) * B - Incorrect: Bronchoconstriction occurs via A1 receptors (Rang Dale and Ritter 1995 p189) * C - Incorrect: Adenosine causes renal vasoconstriction but vasodilation of most other systems including the coronary vessels (Rang Dale and Ritter 1995 p189) * D - Incorrect: Adenosine "has lesser effects on the sinoatrial node" (Katzung 2004 p236) * E - Correct but I think A is more correct: "Decreases AV transmission" is a quite imprecise term. (However, the exact wording is not important as this is just what people remember, thats where the imprecision probably arises. The actual question will be different.) |
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CD35 [Feb00] Mechanism of action of hydralazine
A. Selective cerebral, coronary, renal vasodilator B. Alpha agonist C. Increases intracellular calcium D. Stimulation of cNOS to increase nitric oxide production E. None of the above |
ANSWER E
Acts directly on vascular smooth muscle by interfering either with calcium entry into the cell or release from intracellular stores |
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CD36 [Jul00] [Jul04] Clonidine:
A. Causes hypertension and tachycardia B. Causes bradycardia C. A single dose given orally is significantly less effective then an intravenous dose D. Counteracts the hypertensive response in phaeochromocytoma E. Transiently decreases systemic vascular resistence |
ASNWER B
A false - causes a decrease in HR B true - "there is a decrease in sympathetic nervous system outflow from CNS to peripheral tissues... manifested as decreases in systemic BP, HR and CO" (Stoelting 3rd ed. p.306) C false - "rapidly absorbed after oral administration and reaches peak plasma concentrations within 60-90min" (Stoelting 3rd ed. p. 306) D false - "Clonidine will decrease the plasma concentration of catecholamines in normal patients but not in the presence of phaeochromocytoma" (Stoelting 3rd ed. p.305) E. SVR is decreased with long term treatment |
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CD37 [Jul00] [Jul04] The first sign of sodium nitroprusside toxicity is:
A. Cyanide toxicity B. Tachyphylaxis C. Hypotension D. Tinnitus E. Abdominal pain |
ANSWER B
A. I understand SNP toxicity is cyanide toxicity B. Tachyphylaxis is a sign of toxicity C. Hypotension is false as a sign of toxicity is when the pt BP does not fall despite maximal therapy. D. |
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CD38 [Apr01] Dexmedetomidine:
A. Alpha-1 antagonist B. No dose adjustment in hepatic failure C. Decrease in intraocular pressure D. Partial alpha2 agonist E. Less selective than clonidine |
ANSWER C
A - false: it is mainly an alpha-2 agonist B - False: undergoes extensive hepatic metabolism to methyl and gluconide conjugates, 95% of metabolites are excreted in the urine. Therefore it requires dose adjustments in both renal and hepatic dysfunction C - true: see BJA 1992;68:570 - single dose of dexmedetomidine prior to cataract surgery under GA - 34% reduction in IOP in dexmedetomidine group D - false: "dexmedetomine is considered a full agonist at the alpha2 receptor" (Stoelting p307) E - false: "Compared with clonidine, dexmedetomine is seven times more selective for alpha2 receptors" (Stoelting p307) |
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CD39 [Jul01] [Jul04] Amiloride:
A. Potassium sparing antidiuretic which blocks the aldosterone receptor B. Blocks luminal sodium channels in the collecting tubules C. Increases potassium excretion. D. Is metabolised by the liver. E. Has a short elimination half time. |
ANSWER B
A- False. Potassium sparing diuretic, blocks sodium channels which have been inserted in response to aldosterone. B- True. Amiloride antagonises the "effects of aldosterone at the late distal tubule and cortical collecting tubule" amd works by "inhibition of Na+ influx through ion channels in the luminal membrane" (Katzung 9th ed. p.250) C- False. It is a potassium SPARING diuretic D- False. "Excreted unchanged in urine" (Katzung 9th ed. p.250) E- False. 18-24 hours. |
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CD40 [Jul01] With regard to sodium nitrite in cyanide (CN) toxicity:
A. Causes MetHb B. Used to create more hydrocobalamin C. Used to displace CN from Hb D. Creates more sulfhydryl groups |
ANSWER A
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CD42 [Feb04] [Jul04]
Which is the initial drug to use in the treatment of ventricular fibrillation? A. Amiodarone B. Lignocaine C. Adrenaline D. Magnesium E. Sotalol |
ANSWER C
Adrenaline then amiodarone then lignocaine then consider others eg, Mg, K with electricity and CPR obviously |
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CD43 [Feb04] All are side effects of Thiazides except:
A. Hypokalaemia B. Hypernatraemia C. Impaired carbohydrate tolerance D. Pancreatitis |
ANSWER B
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CD44 [Feb04] Adrenaline for VF?
A. Coarsens fine VF B. To improve coronary blood flow C. Increase chronotropy D. 1:1,000 is more better than 1:10,000 E. Short half life therefore continue bolus after ROSC |
ANSWER B
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CD46 [Jul04] Which of the following is a sign of SNP toxicity?
A. Tachyphylaxis B. Decreased mixed venous PO2 C. Sudden decrease in arterial PO2 D. Hypotension |
ANSWER A
A: tachyphylaxis is first sign of toxicity due to exhaustion of sulphur donors and methaemoglobin B: increased mix venous PO2 C: unchanged D: not a sign toxicity but overdose |
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CD47 [Jul04] Dihydropyridine Ca channel blocker causes peripheral oedema due to
A. vasodilator causing redistribution of ECF B. has a mild antidiuretic effect, and therefore easily treatable with diuretic C. salt and water retention due to hypotension D. Negative inotropic effect E. Baroreceptor mediated renin and aldosterone release |
ANSWER A
http://www.australianprescriber.com/magazine/20/1/5/8/ Dihydropyridines Nifedipine, felodipine, amlodipine and nimodipine are available in Australia. Nimodipine is marketed only for the treatment of cerebrovascular spasm following subarachnoid haemorrhage. The dihydropyridines are selective for blood vessels as therapeutic doses relax arteriolar smooth muscle without detectable cardio depression. In general, they cause a more profound reduction in peripheral resistance and thus blood pressure than verapamil or diltiazem. Although in vitro the dihydropyridines can depress myocardial contractility, the usual clinically observed effect on the heart is one of reflex- mediated sympathetic stimulation of both heart rate and contractility. This cardiac stimulation has been associated with the precipitation or worsening of angina or even the occurrence of myocardial infarction or sudden death. Reflex-mediated cardiac stimulation is less likely with the longer-acting and slow-release preparations because their slower onset of effect allows baroreflex resetting. It is also effectively blocked by the concomitant administration of a beta blocker. Despite having an intrinsic diuretic effect, the dihydropyridines cause peripheral oedema. The oedema represents a redistribution of extra cellular fluid rather than a net retention of salt and water and hence does not respond to diuretics. |
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CD48 [Jul04] Isoprenaline
A. can be used as a substitute to Metaraminol for treatment of hypotension B. used extensively to treat ischaemic heart disease C. cause decrease SVR D. cause bradycardia E. useful in asthma |
ANSWER C
A. FALSE: Isoprenaline cannot be used as a substitute for metaraminol as it DECREASES systemic vascular resistance. B. FALSE: Not used in ischaemic heart disease as it decreases diastolic BP and therefore coronary blood flow and causes increased contractility and tachycardia (increases O2 requirements) C. TRUE: Does decrease SVR D. FALSE: Powerful positive inotrope and chronotrope E. FALSE: althought it is a potent bronchodilator, it increases deap space and V/Q mismatching resulting in hypoxia. It's use as an inhaler is associated with excessive mortality |
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CD49 Which one of the following is NOT an adverse effect of amiodarone?
A. Pulmonary fibrosis B. Photosensitive rash C. Corneal microdeposits D. cardiomyopathy E. thyrotoxicosis |
ANSWER D
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CD50 The beta blocker with the greatest oral bioavailability is:
A. Atenolol B. Metoprolol C. Sotalol D. Labetalol E. Carvedilol |
ANSWER ? C
Bioavailablity Atenolol 50% Metoprolol 10% Sotolol 100% Labetalol 90% Carvedilol 30% Propanolol 12% |
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CD51 Dexmedetomidine
A. MAC sparing for isoflurane by maximal 30% B. can cause bradycardia & sinus arrest C. increases CBF D. used as a muscle relaxant E. dry mouth is rare |
ANSWER B
A. FALSE MAC reduction by 47% [Aantaa R et al. Anesthesiology 86: 1055, 1997]. B. TRUE C. FALSE: maintains CBF D. FALSE: sedation, anxiolysis and analgesia E. FALSE: hypotension, bradycardia, nausea and dry mouth are common |
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CD52 [Jul08] Acetazolamide:
A. maximum increase in urine pH 8 hours after oral dose B. maximum safe dose causes complete absence of HCO3 reabsorption C. maximum safe dose decreases HCO3 reabsorption (?to) 45% D. causes hypochloraemic acidosis E. is a potassium sparing diuretic |
ANSWER C
A: FALSE maximal at 2 hours after oral dose - Katzung B: FALSE: Inhibition of carbonic anhydrase activity profoundly depresses bicarbonate reabsorption in the proximal tubule. At its maximal safely administered dosage, 85% of the bicarbonate reabsorptive capacity of the superficial proximal tubule is inhibited. Some bicarbonate can still be absorbed at other nephron sites by carbonic anhydrase–independent mechanisms, and the overall effect of maximal acetazolamide dosage is about 45% inhibition of whole kidney bicarbonate reabsorption. - Katzung C: TRUE: above D: false, causes hyperchloremic metabolic acidosis E: false, distal tubules excrete K in exchange for Na |
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CD54 [Mar09] Pharmacokinetics of amiodarone:
A. Oral bioavailability is reliable B. Doses must be reduced in renal and hepatic failure C. Omission of 1 or 2 doses can lead to severe consequences D. Metabolism is via demethylation E. Increases refractory period |
ANSWER E
A - false - "poor absorption and wide inter-patient variability of absorption" (datasheet) B - false - "modification of the dose is not required in the presence of renal impairment" (S+S) although "should be used with extreme caution in patients with hepatic disease" (datasheet) C - false - very long half life so a missed dose or two shouldn't make much difference overall D - False, The principal metabolite of amiodarone... is desethylamiodarone (ie hydroxylated) E - True, "prolongs the effective refractory period in all cardiac tissues" (Stoelting) |
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CD55 Sympathomimetics:
A. Phenylephrine acts only on beta receptors B. Metaraminol acts only on alpha receptors C. Methoxamine in high doses acts on beta receptors D. Pseudoephedrine is an isomer of ephedrine E. ? |
ANSWER D
A. False - acts only on alpha receptors B. False - "stimulates alpha- and beta- receptors by indirect and direct effects" (Stoelting) C. False - "beta adrenergic receptor stimulation is absent" (Stoelting) D. True - "Pseudoephedrine...is a stereoisomer of ephedrine" (datasheet) |
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CD56 Whice ONE of the following is True about vasopressin?
A. Slowly metabolized by renal peptidase B. Does not cause coronary vasoconstriction C. Causes mesenteric vasoconstriction D. Increases plasma level of factor VIII E. Is an orally active derivative of ADH |
ANSWER C
A. False - "rapidly destroyed in the liver and kidneys" (datasheet) B. False - "should not be used in patients with vascular disease, especially disease of the coronary arteries" (datasheet) C. True - Causes profound splanchnic vasoconstriction D. False : Desmopressin can be used to promote release of vWF and F8 E. cannot be given orally as it metabolised by endothelium and liver |
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CD57 Clonidine:
A. Dry mouth and agitation are very common side effects B. Half life is 24-48 hours C. 65% is excreted in the faeces D. Can cause severe hypertension if withdrawn abruptly after long term therapy with large doses E. Therapeutic dose is 2-5mg per day |
ANSWER D
A: false : dry mouth and drowsiness occur commonly B: false : half life 6-23 hours C. False: 65% is excreted in the urine and 20% in the faeces unchanged D: true E: false : 0.15-2mg |
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CD58 Beta adrenergic receptor antagonists
A. Seldom causes inhibition of lipolyisis B. Causes inhibition of gluconeogenesis caused by adrenergic stimulation following hypoglycaemia C. Does not mask the signs of hypoglycaemia D Sudden cessation is not associated with rebound effects E. There is no evidence of cardiac protection for high risk patients pre-operatively |
ANSWER B
A: false , adrenergic stimulation causes lipolysis B: true C: false , parasympathetic effect of hunger and nausea still occur D: false, can cause rebound hypertension E: false, beta blockade has been shown to decrease MI associated mortality, but conversely increases the risk of CVA |
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CD59 Labetalol:
A. Beta and alpha antagonism with partial agonist activity at alpha 2 receptors B. Beta and alpha 1 antagonist C. Alpha agonist and beta 1 antagonist D. Alpha antagonist and Beta agonist E. Partial alpha agonist and beta 1 antagonist |
ANSWER B
A : false, labetalol has alpha and beta antagonism, but no ISA Agents with intrinsic sympathomimetic action (ISA) : Acebutolol, carteolol, celiprolol, mepindolol, oxprenolol, pindolol B: true C: false D. false E. false |
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CD60 GTN is helpful myocardial infarction by:
A. Decreasing left ventricular pressure and mean arteriolar pressure B. Producing methaemoglobinaemia C. improving coronary blood flow by dilating the small arterioles D. antioxidant effect E. Relaxation of vascular smooth muscles by inhibition of cAMP |
ANSWER A
A: true : dilates large capacitance vessels to decrease preload and large arterioles to reduce afterload, overall reducing myocardial oxygen demand B: false, I can't see how this would be of benefit C: false, GTN has no effect on small vessels, however it does dilate large epicardial arteries associated with coronary spasm D. False: no antioxidant effects E. False: GTN is converted to NO in the smooth muscle which increased cGMP through activation of cGMP-dependent protein kinases |
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CD61 Which of the following could cause significant adverse reactions with the MAO-i selegiline?
A. Dopamine B. Phenylephrine C. Ephedrine D. Metaraminol E. Nove of the above |
ANSWER C
MAOI's interact with symphatometics/adrenergic agents especially ephedrine. selegilline is a selective MAO-b inhibitor |
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CD62 Mannitol:
A. Causes loss of medullary tonicity B. Urine hyperosmolar compared to plasma C. Site of action is PCT and DCT D. Tubular fluid is isotonic in descending loop of Henle |
ANSWER A
A : true B: urine and plasma will have the same osmolarity C: false, it does not act in any part of the nephron specifically, but prevents reabsorption of water and abolishes the MCG. D: ??? |
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Catecholamine includes the following EXCEPT
A. Ephedrine B. Adrenaline C. Isoprenaline D. Noradrenaline |
ANSWER A
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Ephidrine decreases intracellular cAMP levels by acting on
A. A1 receptor B. A2 receptor C. B1 receptor D. B2 receptor |
ANSWER B
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Which of the following effects is related to direct B1-adrenoreceptor stimulation
A. Bronchodilation B. Vasodilation C. Tachycardia D. Bradycardia |
ANSWER C
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In which of the following tissues both alpha and beta 1 adrenergic stimulation produces the same effect
A, Blood vessels B. Intestine C. Uterus D. Bronchial muscles E. All of the above |
ANSWER B
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