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There is also a form where you can submit your comments about any question & this will be posted on the website for the use of all. Thanks in advance for contributing in this way. [3] Separate Physiology & Pharmacology files The MCQs have been split into these 2 sections. This is the Pharmacology file. This decreases the size of the file to minimise download time which can be long with large attachments if you have a slow connection. [4] Why . DOC files OR . RTF files? The files can be downloaded from the site in several formats: either .
DOC (MS Word format) or as . RTF files. Download the type you require. Please read the details on the site about why you may prefer the . RTF format. [5] Marker Questions Questions that have a lot of symbols (meaning they have been asked multiple times) are probably all ‘Marker Questions’ – The score from these questions are used to do a comparison between the groups sittting different papers. These questions are more likely to be on the paper you sit so it is worth your while to know these well. [6] Thank your colleagues.
This collection has been made possible by the efforts of your colleagues who have sat the exam & have written down the questions they have been able to recall. Please thank them for their efforts and please assist by sending along the questions you remember after your paper. (Email is the preferred method for submission of questions) [7] Many questions are incomplete In some the question wording may be misleading. In any case the examiners are prone to change some of the options at different exams.
SO: The best strategy is to read around the topics suggested by the questions and not try to rote learn answers. A substantial number of these questions will definitely appear on your paper. [8] Contribute yourself If you find this collection useful & would like to help in improving this ‘Memory Bank’ of Actual Primary MCQs, could you please send along to me the questions that you can remember after you sit your exam. The question codes remain the same so just use the Question Code to indicate the repeat questions. [9] Primary Email List.
This collection gets updated usually after each exam (ie at least twice per year) as I receive new questions or other collections. If you would like to receive these updates, contact me with your email address and I’ll add you to the Mailing List for Primary Updates [10] FREE There is no charge for this collection.
This is a group effort which I am happy to coordinate. Please copy & distribute to assist other registrars with their primary study. [11] “The Physiology Viva: Questions & Answers” This book is currently out of print: sold out!.
A second edition should be available by 2002. This book was written especially for the Primary ANZCA exam. Contact me for further details or queries if required. Thanks, Best wishes with the exam, Kerry Brandis (8 September 2001) Preferred email: kbrandis@bigpond. net. au Post : 204 Heeb Street, Benowa, Qld 4217 AUSTRALIA. Phone : Work 07 55718378 (Intl: +61 7 55718378 ) Fax: 07 55975824 (Intl: +61 7 55975824 ) ————————————————————————————————————————-Please copy this collection & distribute to your colleagues
Primary ANZCA MCQ Bank – Update after July 2001 exam- Pharmacology v2- kbrandis@bigpond. net. au Pharmacology – Question Classification GP General Pharmacology IN General Anaesthetics – Inhalational IV General Anaesthetics – Intravenous LA Local Anaesthetics MR Muscle Relaxants & Antagonists OP Major Analgesics / Opioids AC Anticholinergics/Antimuscarinics PS Psychotherapeutic Drugs CD Cardiovascular Drugs EN Endocrine Drugs MD Miscellaneous Drugs ST Statistics Coding Letters The letters (from a to k) within the square brackets [ ] after the question code indicate which paper(s) the question was on.
The key is: a = Mar 96 paper b = Jul 96 paper c = Mar 97 paper d = Jul 97 paper e = Mar 98 paper f = Jul 98 paper g = Mar 99 paper h = Jul 99 paper i = Feb 00 paper j = Jul 00 paper k = Apr 01 paper l = Jul 01 paper Eg: question CV01 [adgi] . . . was on the papers in Mar 96 (indicated by the ‘a’),Jul 97 (‘d’), Mar 99 (‘g’) & Feb 00 (‘i’) General Pharmacology GP01 [a] A drug is given at a dose of 50 mg/kg to a 70 kg man. The plasma concentration after giving it is 10 mg/ml. The elimination half-life is 8 hours. Clearance would be: CL ln 2 A. 1. 3 l/h = kel = B.
3 l/hr – The answer, based on the above should be 30. 3 mL/h Vd t1 / 2 C. ? D. 125 l/hr ? 50 ? 70 ? ln 2 ? Vd CL = = t1 / 2 0. 693 ? ? ? 10 8 ? ? = 30. 3ml / h GP02 [a] A drug is given orally and 95% absorbed. Only 25% reaches the general circulation due to hepatic first pass metabolism. If hepatic blood flow is 1500 mls/min, the hepatic clearance is: A. 400 mls/min B. ? C. 1100 mls/min – Correct ((0. 95-0. 25)/0. 95 = 1st pass metabolism * hepatic flow rate = 1105 ml/min) D. ? E. 1425 mls/min GP03 [d] Histamine release (no other details) GP04 [d] Rectal administration of drugs: A.
Gives predictable blood levels – No, inherently unpredictable B. From lower 1/3rd avoids first pass & upper 2/3rds doesn’t – Well, that is the theory, but in reality?? C. None undergoes first pass metabolism – No, never say never… D. All of it undergoes first pass metabolism – No, not always GP05 [gjk] LD50 is: A. Median lethal dose – Yes Page 2 Update from questions submitted by your colleagues http://www. qldanaesthesia. com Primary ANZCA MCQ Bank – Update after July 2001 exam- Pharmacology v2- kbrandis@bigpond. net. au B.
Determined in phase I clinical trial – No, this involves human volunteers C. Determined from log-dose response curve – No, it is determined from (dose)/(quantal response) curves – not LOG dose. D: Dose causing death in 50% of animals within ? 1/? 4 hours – No E. Half the mean lethal dose – No, it is the median lethal dose GP06 [gi] Which of the following crosses the blood-brain barrier? A. GABA – No, but GABApentin does… B. Propranolol – Yes, side effects include sleepiness & depression C. Suxamethonium – No D. Edrophonium – No E.
Dopamine – No GP07 [fhk] With regard to drug-receptor binding: A. A competitive antagonist has no intrinsic activity – True, it shouldn’t B. A partial agonist has less receptor affinity than a full agonist – No, not necessarily. It may have more affinity for the receptor but less INTRISIC ACTIVITY… therefore less effect C. KD is maximal intrinsic efficacy – No, it is the equilibration dissociation constant. It is equal to the concentration of drug (D) at which 50% of the receptors are occupied. It doesn’t reflect efficacy at all GP07b [i] A partial agonist: A.
Always antagonises a full agonist – No, not if the dose is low enough B: Can never be used to antagonise a full agonist – No, it is possible C: Has a dose response curve similar to that of a full agonist in the presence of a non-competitive antagonist. – Yes, this is correct (or more correctly – in the presence of a competitive irreversible antagonist… ) D. ? GP08 [fl] Placental transfer of drugs: A. Increases in late pregnancy – Probably the most correct option B. Increases late because of decreased albumin – Possibly correct for some drugs but not the whole picture C.
Do not cross because > 600 daltons – No, but drugs with MW >500 have ‘incomplete’ transfer D. ? E. ? Ref: Clin Pharmacokinet. 1995 Mar; 28(3): 235-69 GP09 [fh] Regarding pharmacokinetics: A. ? B. Half-life is inversely proportional to clearance – correct C. ? D. Half-life is proportional to steady-state – ? time to steady state E. B & D – Most correct based on the wording GP10 [h] An ether bond:
A. Formed from condensation of 2 alcohols – Yes, 2 ethanols -> diethyl-ether + H2O B. Hydroxyl group on middle bond – No, R-O-R C. ? GP11 [i] The NMDA receptor A. Ketamine is an agonist – No, it is a non-competitive antagonist B.
Requires glycine as a modulating protein (“YES PROTEIN ! ”) to have its effect – No C. Mg+2 blocks the receptor – Yes, in the resting state D. Is not permeable to Calcium – No, it is a CALCIUM channel! GP12 [i] Activated charcoal:
A. Should be given with sorbitol – No, while it often is (to reduce the risk of constipation) it shouldn’t ALWAYS be given with sorbitol (especially in children) Page 3 Update from questions submitted by your colleagues http://www. qldanaesthesia. com Primary ANZCA MCQ Bank – Update after July 2001 exam- Pharmacology v2- [email protected]. au B. Is not effective against theophylline – No, it IS effective in acute theophylline overdose C. Should be given with ipecac – No, ipecac may make it difficult to give charcoal.
D. Should be given in a drug:charcoal ratio of 1:10 – No… no good evidence. The United States Pharmacopeia (USP DI, 1997) recommends the following oral dosage regimen. – Children up to one year of age:1 g/kg – Children 1 to 12 years of age:25 to 50 g – Adolescents and adults:25 to 100 g (A) could be the ‘most correct’ answer given this bunch of clowns… GP13 [k] Therapeutic index: A.
Easy to determine in humans – No – how many humans do the ethics committees allow you to kill? O B. ? C. D. E. Derived from LD50/ED50 – Yes, the ratio of the two In that order GP14 [k] (A Basic drug with a pKa of 8. 7) A. ? B. ? C. Will be predominantly ionised at plasma pH – Correct BH+ will predominate, and at a lower pH than pKa, more will be protonated/ionised GP15 [k] Oxygen toxicity A. Causes convulsions at less than 100 kPa – No, that’s only one atmosphere B. Causes lipid peroxidation at less than 100 kPa – Yes (Nunn p502)… GP16 [l] With regard to log/dose response curves: A.
The response is fairly linear over the 20-80% range – This is probably the most correct, albeit confusing B. The Dose is fairly linear over the 20-80% range – No, the LOG(dose) is though C. The ED50 and slope are characteristic for each drug – No. For example, adding competitive antagonist will shift the curve to the right; adding a non-competitive (or competitive, irreversible) antagonist will change the slope for the same drug (Technically, this should be the EC50 not ED50 as referred to here – ED50 is from a DOSE/%RESPONDING curve not a LOG DOSE/RESPONSE curve… there is a difference) D.
? E. ? GP17 – renumbered to another section. GP18 [l] With regards to diffusion through a membrane: A. Directly proportional to thickness – No, inversely B. Inversely proportional to thickness – Yes C. Inversely proportional to Surface area – No, directly D. Inversely proportional to concentration difference – No directly E. ? General Anaesthetics – Inhalational IN01 [a] Which compound(s) is/are broken down in soda-lime? A. Nitrous oxide – Not sure, but contaminants (such as nitric oxide N3O) …may cause problems…BOC gases state the the nitrous oxide cylinders contain AT LEAST 99. 5% N2O B.
Halothane – Yes, and product is a volatile compound – a diflourovinyl compound which is nephrotoxic in rats – but not humans… (temp & humidity dependent) C. Sevoflurane – Yes, unstable in soda lime but products apparently non-toxic in humans (Compound A) – temperature dependent – increase temp -> increase degradation D. Desflurane – Yes, produces CO (related to the CHF2- moiety) E.
All of the above – YES… (therefore N20 by default MUST do something!! ) Page 4 Update from questions submitted by your colleagues http://www. qldanaesthesia. com Primary ANZCA MCQ Bank – Update after July 2001 exam- Pharmacology v2- kbrandis@bigpond.
net. au IN02 [a] Regarding nitrous oxide at 70%: – assuming the other 30% is oxygen! A. Synthetised from ? & N2 at 273C – No, produced by heating ammonium nitrate to 240-270? C B. Decreases muscle blood flow by 30% – No C. Decreases cerebral autoregulation 24% – Possibly, provided there are no other inhalational agents (they tend to blunten N2Os effect on increasing CBF and ICP) D. ? IN02b [d] Nitrous Oxide: A. ?Increases/decreases CBF – Increases when used alone (effect blunted/abolished with other agents present) B. Is an effective oxidant – Yes, and will in fact support combustion.
It will even enable combustion of agents that would not be flammable in air (don’t forget that people use it in their cars to increase performance! ) C. Is made by heating nitrogen and oxygen in an iron retort – No, heated ammonium nitrate D. Decreases pulmonary artery pressure in neonates – No, it actually increases pulmonary artery pressure by increasing PVR (thereby increasing the chance of persistant R->L shunt) IN03 [abdfh] The following drugs are (potent) triggers for malignant hyperthermia EXCEPT: A. Decamethonium – Yes (triggers MH) B. Suxamethonium – Yes (triggers MH) C.
Isoflurane – Yes (triggers MH) D. Halothane – Yes (triggers MH) E. Calcium – No – how is this possible? F. Sevoflurane – Yes (triggers MH) G. Tubocurarine – Yes (a few cases of MH reported) – interestingly it was originally used to treat MH (I wonder if it worked!? ) H. Nitrous oxide – Yes, apparently it is a WEAK trigger for MH in susceptible patients (but this is HIGHLY debateable) (Different options on different papers) IN04 [a] IPPV with Isoflurane at 1 MAC results in: A. Depresses cardiovascular reflexes more than halothane – No, there is no reflex tachy with Halothane at all B.
Causes decreased conduction velocity – No, in fact may increase conduction velocity via it’s indirect effect on transiently increasing SNS activity C. Maintains cerebral autoregulation – No, but effect is less than that of halothane, and it is responsive to changing pCO2 D. Equal respiratory depression to enflurane – No, it doesn’t change rate whereas enflurane does E. Reduction in cardiac output by 25% – No, usually no change in cardiac output since reflex tachy continues despite decreased SV F. Increased vasodilatation – Yes, but does this really answer the question with the IPPV part??
IN05 [ae] The effect of increased cardiac output on Pa versus time for volatile agents is: A. No effect – No B. Decrease slope – Correct C. Decrease then increase slope – No D. Increase then decrease slope – No, initial slope UNCHANGED but the rest is DECREASED IN06 [adk] Nitrous oxide: A. Supports combustion – Yes it does B. Is flammable – No C. Causes muscle rigidity – No, but it is a WEAK trigger for MH…apparently… D. In tissues is slower to reabsorb than oxygen – No, it diffuses out faster than oxygen E. Has a partition coefficient of 0.
76 – No, for a start which coefficient are we talking about? (BG = 0. 47, OG=1. 2) F. All of the above G. Is formed by heating oxygen & nitrogen – No, ammonium nitrate to 240-270 degrees Page 5 Update from questions submitted by your colleagues http://www. qldanaesthesia. com Primary ANZCA MCQ Bank – Update after July 2001 exam- Pharmacology v2- kbrandis@bigpond. net. au H. Induces methionine synthetase – No, inhibits it I. Oxidises the cobalt in vitamin B12 – Yes IN06b [ef] Nitrous oxide: A. Has MW of 42 – No, (O=16, N=14) therefore MW=44 B. Critical temperature 32 C – No, 36.
5 degrees C C. Formed by using iron as a catalyst – Yes, this is how Priestly first produced it from NO – it’s not how they make it now though… D. Does not support combustion – No, it does support combustion E. ?? has saturated vapour pressure of 24 kPa – No, it’s a little higher than this… O F. Produced using ammonium sulphate in an iron retort – No, ammonium nitrate G. Boiling point 32C – No, boiling point is -89 degrees H. ??. . . ammonium nitrate . . . copper vessel ?? (Multiple options as this represents 2 separate N2O questions on Mar98 paper) IN07 [c] Desflurane A.
Takes 5 minutes to reach equilibrium – No, longer than this >20-30 minutes B. Is fastest to approach equilibrium of any inhaled anaesthetic agent – No, Nitrous Oxide is faster despite the fact that Desflurane’s Blood:Gas coefficient is lower at 0. 45 compared to 0. 47 for N2O) C. Is a fluorinated diethyl ether – No, it is a ethyl-METHYL ether (fluorinated only) D. ? IN08 [cd] Regarding sevoflurane:
A. The vapour pressure is less than enflurane – Yes, SVP is less (the only agents with lower SVPs than Sevoflurane are METHOXYFLURANE & TRICHLOROETHYLENE) B. The vapour pressure is greater than Isoflurane – No, the SVP is less C.
Cardiovascular side effects are similar to Isoflurane – Yes, main effect on SVR, no change in CO, some SNS stimulation D. Molecular weight less then Isoflurane – No, larger (it is the biggest) E. Boiling point greater than enflurane – Yes, 58 compared to 56 degrees for enflurane IN08b [di] Sevoflurane: A.
Is a methylethyl ether – No, it has a propyl-type arrangement B. Is odourless – No, has a slightly pungent/sweet odour C. Is stable in soda lime at 37 degrees – No, undergoes spontaneous degradation (temp dependent) D. Has a boiling point higher than enflurane – Yes, 58 compared to 56 E.
Has a molecular weight lower than desflurane – No, higher (168 compared to 200) IN08c [fh] Sevoflurane: A. Molecular weight greater then enflurane – Yes, 184 compared to 200 (SEVOFLURANE IS THE BIGGEST) B. MAC less than enflurane – No, less potent therefore higher MAC C. Contains Cl & F – No, only Fluorine groups… D. SVP > enflurane – No IN09 [cfj] Uptake of N2O when breathing 70%: A.
More than one litre absorbed in the first minute – ? Correct option B. Equilibrium (? 90%) is achieved in 3mins – No, usually 5-10 minutes C. Absorb 10 litres ? at time of ? 90% equilibration / ? in first 3 mins D.
At steady state, uptae is 200mls/min – No, at ‘steady state’ the uptake should technically be zero E. Produces surgical anaesthesia – No, this is obvious (It’s MAC is 102% and that is only good for 50% of subjects…) IN10 [cfgl] N2O causes the second gas effect because: A. It is relatively insoluble – Not really – it’s because there is a LOT of it (ie. You need >70% to see the second gas effect).
B. Reaches equilibrium faster than the more soluble second gas – No, this is true but doesn’t account for this effect Page 6 Update from questions submitted by your colleagues http://www.qldanaesthesia. com Primary ANZCA MCQ Bank – Update after July 2001 exam- Pharmacology v2- kbrandis@bigpond. net. au C.
Larger volume – Well… a larger volume is absorbed, hence the effect but (D) probably ‘more correct’ D. Its high concentration – Yes, high concentration required IN11 [d] Desflurane: A. Is non-irritant to the airways – No, it is quite irritating and pungent, hence not much use as an induction agent (can cause broncho/laryngospasm, coughing etc) B. Is more/less potent than Sevoflurane – Less potent (MAC of 6. 0) C. Has a higher molecular weight than ? isoflurane/?
enflurane – No, less (substitutes an F=19 for the Cl=35. 5) D. Is a chlorinated methyl ethyl ether – No, only fluourinated IN12 [dk] Effects of volatile agents include: A. Halothane increases hepatic artery and portal blood flow – No, decreases… B. Isoflurane causes hypotension by reducing cardiac output – No, effect mainly by decreasing SVR, almost no effect on CO C. ? D. ? IN13 [dfhk] Problems with MAC: A. Large interspecies variability – No, but I thought is was only for human subjects… B. Affected by temperature and other factors – Yes C. Affected by obesity – No D.
? IN13b [afil] MAC: A. Is decreased in the elderly – Yes, decreases with increased age B. Is unchanged throughout pregnancy – No, pregnancy decreases MAC C. Increases in hypothermia – No, decreases with decreased temperature D. ?Decreased/? increased with hyper/hypo-kalaemia – No, K doesn’t affect MAC at all E. ? Alt version (Jul 01) All the factors decrease MAC except: A. Pregnancy – Yes, decreases B. Hyperthermia – No, increases MAC C. Hypothermia – Yes, decreases D. Hypoxia – Yes, decreases E. ? IN13c [gkl] MAC: A. Highest between ages 2 to 5 yrs – No, highest below 3 months of age B.
Increases with pregnancy – No, decreases C. MAC BAR is concentration at which 95% do not move – No, it’s to do with Adrenergic Response D. Is 0. 2% halothane in 70% N2O – Most correct, true value is 0. 29% (MAC with 100% oxygen is 0. 75) E. ? Jul 01 version: With regards to MAC: A. The MAC of Halothane with 70%N2O is 0. 29 – Correct B. Concentration at which 95% of patients don’t move after a surgical stimulus – No, this is 1. 3 MAC C. MAC- BAR ?? – To do with adrenergic response D. Decreased by increased CO2 – No, no change if PaCO2 between 15-95mmHg E.
? IN14 [eg] Systemic vascular resistance is LEAST changed with: A. Isoflurane – No, the decrease in BP is attributable to only the decrease in SVR B. Sevoflurane – No C. Desflurane – No D. Enflurane – No E. Halothane – Correct, minimal change in SVR Page 7 Update from questions submitted by your colleagues http://www. qldanaesthesia. com Primary ANZCA MCQ Bank – Update after July 2001 exam- Pharmacology v2- kbrandis@bigpond. net. au IN15 [efg] MAC awake during emergence when patient will respond to command: A. 0. 1 B. 0. 2 C. 0. 3 – Not quite, see below D. 0.
5 – Correct (see below) E. ?0. 7 ? 0. 8 MAC-awake depends on the rate of ‘expected awakening’: If the agent is ceased abruptly the MAC-awake will vary depending on the agent but it is roughly: Halothane: 0. 5 Isoflurane: 0. 25 Desflurane & Sevoflurane: 0. 33 It depends on the BRAIN -> BLOOD -> ALVEOLI gradient (it is only the alveoli we measure – the concentration at the ‘effect site’ will still be higher as it slowly leaves the brain) The % at the brain will be the same (equivalent to 0. 5 MAC) If the agent is SLOWLY decreased then almost all agents have a MAC-awake of 0.
5 IN16 [fh] Isoflurane & enflurane are: A. Structural isomers – Yes B. Enantiomers – No, these are stereo isomers that are mirror images of each other C. Diastereomers – No, these have more than 1 chiral centre and may differ in ALL properties (stereoisomers that are NOT mirror images) D. Optical isomers – No (? another name for enantiomers) E. Configurational isomers IN17 [ab] Sevoflurane: A. Is broken down in the body to Compound A which has been shown to be toxic to rats – No, broken down by sodalime (KOH & NaOH but not CaOH) B. Has a blood:gas partition coefficient of 2. 3 – No, 0.
65 C. Is a irritant causing coughing on induction – Not usually – this is mainly halothane D. Has a boiling point of 24 degrees centigrade – No, boiling point is 58. 5 degrees E. Has Cl & F atoms in its structure – No, the only halide is flourine F. None of the above – Correct (Note: Compound A is a breakdown product produced in the CO2 absorber; it is not produced by biotransformation) IN18 [gi] With isoflurane anaesthesia, MAC awake is: A. 0. 1% vol B. 0. 3% vol C. 0. 5% vol D. 0. 5% vol – ?? 0. 6% vol E. 1% vol See IN15 comments… not really a straightforward question… If (D) was 0.
6% I’d go for that (MAC isoflurane = 1. 2%)…but it could also be (B) depending on how you interpret the question… I love how MCQs test one’s knowledge… IN19 [g] Isoflurane: A. Is a halogenated methyl ethyl ether – Correct (both F & Cl atoms) B. Higher boiling point than Sevoflurane – No, lower 48. 5 compared to 58. 5 C. No odour – No, pungent odour D. Enantiomer of enflurane – No, enatiomers are mirror image stereoisomers (with 1 chiral centre) IN20 [g] MAC of halothane with 70% N2O is: A. 0. 25% – Correct, approximately 0. 29% B. 0. 5% C. 0. 75% – No, this is 1 MAC with 100% oxygen D. 1. 0%
Page 8 Update from questions submitted by your colleagues http://www. qldanaesthesia. com Primary ANZCA MCQ Bank – Update after July 2001 exam- Pharmacology v2- kbrandis@bigpond. net. au IN21 [g] All reduce MAC except: A. Aminopyridine – No – This drug is presumed to enhance the presynaptic release of acetylcholine by facilitating the entry of calcium ions into nerve endings (mainly at NMJ not muscarinic) B. ? IN22 [f] N2O is NOT relatively contra-indicated with: A. Pneumothorax B. Ear surgery – depends on surgery type though… it can be used to inflate the middle ear by some ENT surgeons C.
Postop nausea & vomiting D. Renal failure – Correct, there is no evidence of renal, hepatic or GIT toxicity IN23 [h] Which of the following does NOT affect the speed of induction with a volatile agent? A. FRC – Yes, this does (decreases FRC means that induction is faster) B. Obesity – Yes, probably by the changes in FRC C. pCO2 – No effect D. Cardiac output – Yes, this does E. ? Alt version: Regarding the time constant for volatile anaesthetic uptake in the lungs A. Affected by agent concentration – Yes B. Affected by obesity – Yes C. Not affected by FRC – No, decreased FRC reduces the time constant D.
Affected by restrictive lung disease – Yes 3 V =m IN24 [i] 22g of Nitrous oxide at STP occupies a volume of: A. 3. 6 L B. 11. 2 L – Correct! C. 22 L (? or 22. 4 L) D. 44. 1 L Here is the equation in case you’re REALLY interested… O P = 101. 3kPa T = 273K n = 0. 5mol R = 8. 31 J K -1 mol -1 V= nRT 0. 5 ? 8. 31? 273 = = 0. 0112m 3 = 11. 2l P 101325 IN25 [j] Wash in (? washout) of volatile anaesthetics is reduced in neonates because: A. Reduced FRC – No, there FRC is proportionately the same as an adult B. Increased cardiac index – Yes, slows the rate of rise of FA/FI C.
Decreased plasma protein levels? – No, nothing to do with this D. (Something about blood:gas partition coefficients being different in neonate) – No, obviously Alt version which probably is the same question remembered differently: The washout of inhalational anaesthetics A.. Increases with elimination by the liver – No B.. Related considerably with the duration of anaesthesia – Yes (tissue uptake & release – notably from animal studies) C. Increases in the neonates compared to an adult – No, decreased due to the increased CO IN26 [l] With regard to compound A: A.
Increased production in Baralyme compared to sodalime – Yes, (Baralyme™ contains Barium octahydrate, CaOH, KOH – Sodalime contains NaOH) B. More likely in children – No, it is related to the CO2 absorber not the patient C. Sevofluranes metabolites cause hepatotoxicity – No, no evidence to support this (no change in LFTs either) D. Sevoflurane is METABOLISED to Compound A in the liver – No E. ? IN27 [l] Concerning the effects of various volatile agents on cerebral blood flow under conditions of 1 Page 9 Update from questions submitted by your colleagues http://www. qldanaesthesia. com.
Primary ANZCA MCQ Bank – Update after July 2001 exam- Pharmacology v2- kbrandis@bigpond. net. au MAC and normocarbia: A. Halothane produces greater increase than enflurane – Yes (see Fig 2. 4 in Stoelting) B. Isoflurane produces greater increase than enflurane – No, other way around C. Any change produced depends upon cerebral metabolic rate – No independent of this D. Change in CBF is due to change in cardiac output – No, not at all E. IN28 [l] Which of the following drugs is not associated with EEG epileptiform activity A. Propofol – No, there is no evidence of epileptiform activity (therefore the ‘correct’ answer) B.
Enflurane – Yes, hence the need to ‘discover’ isoflurane C. ? D. ? E. ? General Anaesthetics – Intravenous IV01 [acd] Propofol: A. Has a pKa of 7 – No, pH is 7 B. Has a pH of 11 – No, pKa is 11 C. Causes hypotension due to myocardial depression – Direct myocardial effects at HIGH doses. Normally, hypotension mainly by reducing sympathetic vasoconstriction and indirect effects on the heart (blunting reflex tachy – may lead to bradys) D. Has 98% protein binding – Yes, highly protein bound E. ? IV02 [adk] Thiopentone causes a decrease in BP by: A. Direct decrease in myocardial contractility – No, it lacks direct effects B.
Fall in systemic vascular resistance – Possibly, by decreased SNS vasoconstriction C. Decrease in venous tone – Yes, ? the main reason, venodilatation and venous pooling does occur therefore decreased VR and decreased CO & BP. There is no blunting of reflex tachy unlike propofol D. ? IV03 [abdg] Ketamine: A. Is a direct inotrope – No, in fact it is a direct NEGATIVE inotrope which is overshadowed by its central SNS stimulation B. Causes bronchodilatation – Yes, by its muscarinic effects C. Less likely to see emergence delirium (? psychotomimetic effects) in ? older/?
younger females – More common in women, less in children D. Reduces pharyngeal secretions – No, if anything it may increase secretions (muscarinic effects) E. Leaves airway reflexes reliably intact – Trick question (‘reliably’), it does leave them intact, but NOT reliably (Miller) (See IV17 for another Ketamine Q) IV04 [ak] With regards the action of midazolam: A. Ring closure occurs immediately on injection – Yes, as soon as pH >4 then the ring closes and becomes highly lipid soluble B. ? C. ? IV05 [dghk] Propofol depresses cardiac output predominantly by: A.
Direct depression of myocardial contractility – No, it has DIRECT cardiac effects but only at high doses… therefore not ‘predominantly’ B. Decreased SVR – Yes, by decreased SNS vasoconstriction C. ? D. ? IV06 [dk] Methohexitone: A. Has a molecular weight of 285 – No… it’s actually 284. 29 Page 10 Update from questions submitted by your colleagues http://www. qldanaesthesia. com Primary ANZCA MCQ Bank – Update after July 2001 exam- Pharmacology v2- kbrandis@bigpond. net. au B. Has a melting point of 158 degrees – No idea/who cares!! C. A 2. 5% solution is isotonic – No… I don’t think it even comes as a 2.
5% solution, only 1%. From what I’ve read concentrations > 1% should not be used IV D. Is yellow – No, it’s a white crystalline powder (in solution pH about 11) E. Has 4 isomers – Yes… IV07 [e] Benzodiazepine binding site on GABA receptor is: A. Near Cl- channel – No B. Inside the channel – No C. Outside the channel – No D. On the alpha subunit – Yes, the 2 alpha subunits IV08 [el] The drug with the largest volume of distribution at steady state is: A. Propofol – 98% ppb, Vd=4L/kg B. Midazolam – Vd=1. 5L/kg C. Etomidate – Vd = 3L/kg D. Thiopentone – 85% ppb, Vd=2. 5L/kg E. Methohexitone – 70% ppb, Vd=2.
2L/kg IV09 [f] GABA: A. Is the principal inhibitory neurotransmitter in the spinal cord – No. While it is present in the spinal cord it is not the principal one… Glycine is… B. Barbiturates decrease the dissociation time between GABA and its receptor – No, they increase the average channel opening time by the action of GABA on GABAA receptors. In hight doses they activate the channel directly. C. ?? A & B types?? – There are three types currently known (A & C – 5 subunit ion channels (Cl), and B – G protein linked receptor (increases K efflux & decreases/blocks Ca influx). A & B in CNS, C in retina exclusively D.
? (see also IV18 ) IV10 [a] Propofol is structurally related to: A. Althesin – No, a mixture of 2 steroids in Cremophor EL B. Etomidate – No C. Ketamine – No D. ? E. None of the above – Correct IV11 [gi] Midazolam: A. Water soluble at physiological pH – No, lipid soluble at pH >4 B. Undergoes oxidative metabolism – No, extensive HYROXYLATION (CYP3A4) in liver C. More lipophilic than lorazepam – No, lorazepam is more lipophilic than midazolam & diazepam D. Causes hypotension – Yes, therefore care in hypovolaemia (similar effect as thiopentone) E. Has a pKa of 7. 4 (or ? 8. 1) – No, pKa is 6.
15 and commercial preparation pH is 3. 5 F. Causes retrograde amnesia – No, anterograde amnesia IV12 [f] Thiopentone: A. Is the sulphur analogue of phenobarbitone – No, sulphur analogue of pentabarbitol B. Has higher protein binding than its oxy analogue – Yes, protein binding parallels lipid solubility C. ? 6% sodium bicarbonate – No, there is 30mg of ANHYDROUS sodium CARBONATE in an ampoule D. Isotonic at 2. 5% concentration – Probably not, given that you can reconstitute it with water or saline… IV13 [f] Propofol clearance is significantly increased in: A. Elderly – No, definitely decreased B.
Metabolic acidosis – No effect C. Pregnancy – Yes, due to general enzyme induction D. ? (See also IN13b) Page 11 Update from questions submitted by your colleagues http://www. qldanaesthesia. com Primary ANZCA MCQ Bank – Update after July 2001 exam- Pharmacology v2- kbrandis@bigpond. net. au IV14 [i] Thiopentone: A. 100% reabsorbed in renal tubule – No, depends on urinary pH and not 100% is reabsorbed – some isn’t obviously… B. Does not cross the placenta in significant amounts due to high plasma protein binding – No, it does (high lipid solubility) C. ?? accumulate in the foetus – No, this is rare, des.