Pharmacology VIVAs 2003 – 2013

April 2013
Room 2 (I think!) - Monday PM (Old syllabus)

"Question 1" Can you tell me about heparin? How does it work? How is it's mechanism of action different to LMWH? Why is
it's MOA different? (Different molecular weights) How are they administered? Is their excretion different? Why? How do you
monitor their effects? What are their adverse side effects? Mechanism of HIT 1 and 2. How can you reverse them? Can you
reverse heparin with protamine? Why only partially? How could you improve coagulation in a trauma patient? FFP/
tranexamic acid/ aprotinin/ Factor VIIa etc

"Question 2" Sheet of paper with made up analgesic agent with pharmacodynamic/ pharmacokinetic things written down
(basically like tramadol with different name) Went through each point and why this would be a useful/ disadvantageous point
for an analgesic agent in recovery. Quirky bits like "would low oral bioA be a problem?" - no, as long as you adjusted dose etc.
Talked a bit about activating descending inhib. pain pathways with 5-HT and NA reuptake inhibition. Conversion between oral
& IV morphine and this agent.

"Question 3" Tell me about inotropes Classified. Did you mention digoxin ('yes in cardiac glucosides..') ah yes, tell me how
that brings about increased contractility. Does it do anything else? Decreased chronotropy.. mechanism of effect.. direct or
indirect. Can you give me some examples of phosphodiesterase inhibitors? Which subtype is milrinone specific for? Do you
know any non-selective ones? How do they cause increased inotropy? Didn't ask about side effects really. Have you heard of
calcium sensitisers? ('Yes, I mentioned that and gave levosimendan as an example') Excellent, how does it work? What are it's
side effects? (arrythmias and hypotension) Common? Not really.. Why isn't it used more often? I said that it is usually used
when other inotropes have failed and usually you wanted to change preload/afterload as well as contractility so other agents are
usually appropriate but I personally liked its rather elegant MOA (i.e. increasing contractility with no increase in CMRO2) and
he seemed very pleased by this..

"Question 4" Statistics - not much point going through this in detail as now off the syllabus, but went through null hypothesis,
P values& CI- definition and comparison, Alpha and Beta errors, how to calculate power, a bit about normal distribution. Not
too taxing.

Overall a nice viva, not much feedback from examiners during the questions but the questions were all logical and fair game I
thought.

Room 4 - Monday PM

Question 1 Can you tell me about Ketamine? What is its mechanism? - wanted to know about NMDA activation and other
mechanisms What dose would you give for IV and IM and why the higher dos? What kind of anesthesia does it produce? i said
dissociative anesthesia and explained the symptoms. They asked how can you determine the depth of anaesthesia for ketamine
- i said i did not know What is the cardiovascular affect of Ketamine? What happens if you give a shocked hypotensive patient
Ketamine - talked about Norad depletion and unmasking of its negative ionotropic effects leading to decreased BP

Question 2 Can you classify Anti emetics? Tell me about droperidol? - went through Physicochemical, Mech and uses and got
cut off. What dose do we use? - 0.5mg, What is the half life? i said i dont know, they said if the half life is short and the
duration of action is long, how does that work? - Spoke about receptor binding etc What are the side effects - EPS and long QT
- they moved on before i could mention others Tell me about the 5HT channel? Tell me about ondansetron - What are its side
effects

Question 3 Classify topical local anesthetics - Amides/esters Tell me about EMLA? I totally forgot that lignocaine was in it
and i wasted a lot of time trying to remember it. What does Eutectic mean? how does it affect the properties of the Topical
agent. Talked about lower melting point. What else is in the EMLA cream - it took a while but i said Emulsifying agent then
were happy and moved on. What are the side effects of EMLA - mentioned O toludine and the MethHb Mechanism (should
have classified into local and systemic). What risk factors increase the toxicity - Anaemia, Pregnancy, G2PD def? How does
G2PD affect increase.... Didnt get a chance to answer (didnt know anyway!)

Question 4 Can you classify oxytocics? oxytocin, ergot alkaloids, PG-miso and PGF2alpha. What other drugs.... we may have
already discussed? KETAMINE (note examiners are really nice and try to help you pass! i know everyone says it but i actually
experienced it) Tell me about oxytocin - got through physiochem, kinetics. What are the CVS side effects - Got a bit confused
here. eventually settled on Brady and hypotension. What is the mechanims of Hypotension - fluffed around a bit talked about
B2 receptors (prob totally wrong) If we gave a slow infusion instead of a bolus how would that improve the CVS side effects -
i said it would lessen them, they asked How? - i had no idea

Then the bell rang.

Question 1

Can you tell me some of the uses of ketamine?

How does it work? What exactly does it antagonise? Besides the NMDA receptor effects, does it act by any other mechanism?
(Was looking for opioid receptor actions)

What sort of doses would you give somebody for induction with ketamine? Why is the IM dose higher than the IV dose?

How would the patient behave? What would they be doing? You mentioned their eyes would be open, would they be doing
anything characteristically? (Wanted REM/nystagmus)

So we’ve talked about all these uses of ketamine and it sounds like a pretty wonderful drug, why don’t we use it more often?

Question 2

Can you tell me about some of the drugs we can use to treat intraoperative hypertension? (Mentioned drugs that act
centrally/on the heart/on the peripheries)

That list of drugs is quite specific, is there anything else we can do during the operation to drop the blood pressure? (Turn up
volatiles, give a bolus of propofol)

Let’s talk about GTN – how does it work? You say it needs to be metabolised in the liver first, do you know what the name of
that enzyme is? (Wanted glutathione-s-transferase) How exactly does GTN cause a fall in blood pressure? Does it act primarily
on the arterial or venous system?

Let’s talk about SNP – how is that different from GTN? Between the two, which one is more potent?

Question 3

Let’s talk about the student’s t-test – what does it measure? What sort of data do we use it on? What do you mean by
parametric data? What is a normal distribution? Is there any situation where we can also use the t-test despite the underlying
population distribution not being normally distributed? That number of 100 is quite conservative, what is the name of this
effect?

Can we use the student’s t-test to test more than 2 groups? Say you have groups A, B and C can you use the t-test? If you test
them in pair i.e. A/B, A/C, B/C what is the risk with doing this? What type of error is this? Let’s talk about when we want to
test more than 2 groups – do you know what test we can use? Can the ANOVA test be used for less than 2 groups, say I have a
2x2 table and I want to compare the means. Does it still work? Back to using the t-test for more than 2 groups: How can we
compensate for this (besides using another test?) Can you tell me what a Bonferroni correction is?

Question 4
Let’s talk about pharmacokinetics in a patient who has taken an overdose of an unknown orally ingested drug. What PK
parameters can we alter in this patient?

A – activated charcoal, lavage, emesis How does activated charcoal work? How exactly does it bind drugs?

Let’s talk about D now (mentioned IV chelating agents) What IV chelating agents do you know? Besides that, have you heard
of digibind? What about something used in the management of local anaesthetic toxicity? How about metabolism? (talked
about replacing precursors in paracetamol toxicity) Can you walk me through the pharmacology of paracetamol toxicity?

What about E? (Talked about alkalinising urine) What drug are you specifically referring to here? What is the mechanism of
aspirin toxicity?

1) Define pain. list types of analgesia and mechanism of action. Mechanisms of action of tramadol. Is tramadol directly acting
at all these receptors? ( no prodrug at mu receptor). What is the compound acting at mu then? what enzyme metabolises mu? Is
this enzyme present in everyone ( talked about genetic variability and enzyme inducers and inhibitors). Name some enzyme
inhibitors.

2) Mechanism of action of NSAIDS. what is the difference between cox 1 and 2? Side effects of NSAIDS. types of nsaids
( non selective, relative selectivity and selective cox 2). name a cox 2 inhibitor.

3) what Factors speed up inhalation induction with sevo in a 5 year old child? why does a leak in gas circuit decrease speed of
induction? ( because of entrainment of atmospheric air diluting the volatile concentration). Why does increased cardiac output
slow induction? how do you reduce cardiac output in a 5 year old child? Draw a wash in curve for desflurane. Superimpose a
wash in curve for 70% nitrous oxide? What is happening at the shoulder and at the top of the nitrous curve? why is nitrous rise
faster and higher than the desflurane curve? ( use alot, 70%)

4) Stats. Given a bunch of data. Which of these data is likely to be subject to a chi square test? (the only categorical type data
on the paper). The other data are interval data and subject to variance analysis, how else can you analyse this data ( said T test).
What is the difference between the T test and variance analysis? What other tests can you use? Is population age really a
normal distribution? Shown another bunch of data but bell rang.

Monday pm 1) What is the fate of epidurally administered fentanyl, and morphine. What percentage of the dose gets into the
spinal cord for both. In what layer is the blood brain barrier. What is an epidural and an intrathecal dose of fentanyl or
morphine. Asked about side effects of epidural morphine, how would you treat the itch? When do you get respiratory
depression and how would you check for it.

2) How does dexamethasone exert it's effect as an antiemetic. At what point in a case would you give it. How much of
dexamethasone is glucocorticoid/mineralocorticoid, same Q for hydrocortisone. Why do we use hydrocortisone for adrenal
replacement. What happens in an adrenal crisis. Why. What dose of hydrocortisone would you give, does it depend on the
procedure?

3) Draw an FA/FI curve for isoflurane, at what ratio does it stabilise. Why. What about halothane and sevoflurane. Would it
eventually reach 1, why not. What speeds induction. If I decreased CO to 0 what would happen to the curve.

4) Can you calculate a confidence interval. What is it's significance, ie. what does a 95% confidence interval mean. Why don't
we use p values any more (statistical vs clinical relevance). Can we calculate confidence intervals for other things besides
means (ratios).

September 2012
Monday
1. Strengths and weaknesses of a case control trial? Given a set of numbers comparing 2 antiemetics and vomiting in a
case controlled trial. What can you use to compare the two groups? Calculate the odds ratio. What is the difference
between this and relative risk? Why are the numbers different? What happens when vomiting is common vs when it is
uncommon

1. Draw wash in curve for 6% des, for 70% nitrous oxide and for 6% nitrous oxide? Causes for the differences in the
curves. What are the factors that affect speed of gas induction in an infant with sevoflurane? What happens if premed
was given to the infant? - it decreases MV and CO from anxiolytics and sedation but at the same time is MAC
sparing. So will induction be faster or slower overall?

1. Define pain? MoA of morphine? It's sites of action? Morphine's effect on descending pathway? What is gabapentin?
What is its MoA?

1. Given a picture of a graph of rocuronium and atracurium, i found it quite difficult to get my head around it. Y axis is
reduction in contraction depth, x is log dose, each point has 95%CI drawn in and a line connecting the the dots. What
do the points represent? Is it graded or quantal response? How do you define ED95? Where is ED95 on the graph?
Factors that affect the onset of NMB?

Tuesday
1. Define potency. Another type of potency besides ec50 (MAC). Draw quantal dose response curve for sevoflurane (%
response vs MAC). Described effect of fentanyl 1mcg/kg (wanted precise decrease in MAC ??) then 5mcg/kg then 50mcg/kg.

2. Short acting muscle relaxant drugs – mivacurium and suxamethonium. Which would you use. Offset; reversal. Adverse
effects of repeated doses of suxamethonium. How to treat phase 2 block. How to reverse mivacurium.

3. Tell me about phenylephrine. Effects on systolic and diastolic BP, vs adrenaline (particularly effect on diastolic BP.

4. Tell me about Aspirin. How do you measure the effect of aspirin on platelets. By how much does aspirin affect bleeding
time. Does this change with uraemia; how much does bleeding time increase if you give a uraemic patient aspirin. What is the
half life of aspirin? Duration of effect on platelets. Who would you not give aspirin to. What proportion of people exhibit this
bronchoconstriction response. How would you tell who was at higher risk. What is the mechanism.

This viva smashed me, I felt like a fish out of water the whole time. Even things I knew well went out the window - oh well,
next time..

another viva
1st examiner.

 Drugs used in ischemic heart disease /Classification of Beta blockers

 Isomerism /Bioavailability

2nd examiner.)

 S/E of Propofol:what is the apneic dose? how many % of people would be apneic if given 1mg/kg propofol?
 Drugs used in anaphylactic shock

April 2012
my viva on 16/04/12
1. You have a pt needing surgery who is at risk of PONV, what drugs do you use for prophylaxis intraop? Classify them,
pharmacology of Droperidol, MOA of Cyclizine, where are the 5-HT receptors that you are targeting? Any other drugs
targeting 5- HT? apart from CTZ, where else does antimuscarinic targeting-Vestibular, vagus?

2. Why is Propofol a popular GA drug? Is it really fast onset? How long does it take for pt to go to sleep? How long is one arm
brain circulation time? Is the induction really smooth? Do you see excitation symptoms on induction? Can you use Thio for
LMA? Apart from Thio not suppressing airway reflexes, what else does Thio have to contribute to bronchospasm?-Histamine
release. Tell me why propofol have faster waking up vs Thio? What’s CTSH? Why Thio’s CTSH is long vs Propofol?
Anything else contributing to Thio’s long CTSH apart from slow elimination?-zero order kinetics after long infusion. What’s
propofol’s Cl in number? What pt would you not use propofol?

3. How many ways can you classify opioids? Get stopped quickly. How is morphine metabolized? In what setting do you think
M-3-G’s hyperalgesia can be significant? If you give a pt 30mg iv morphine in total on post-op day 1, and the next day you
decide to give the same analgesic dose but in oral, how much do you give and why? If the pt have severe renal impairment say
GFR <30 what dose will you give? I said I’ll try to avoid morphine as I have much better choices in that setting. What drugs
can be your choices? What features of those alternative drugs do you think making them more favourable choices? If you only
have morphine to give him, what dose will you give? No more than half. What else would you do? Increasing dosing interval.

4. Can you classify non depolarizing NMBD for me? Let’s focus on atracurium- what’s the difference btw atrac and cis-atrac?
Isomer, potency, histamine release, metabolism. How many times more potent? How do you compare the potency? What’s
ED95? How do you get 95% twitch depression? How does a nerve stimulator work? What’s the mechanism of post-tetanic
potentiation? Traditionally you obtain ED95 under GA using barbiturates, nowadays under GA using volatiles, do you get
different ED95 values? Why? If I have a pt losing a lot of plasma protein, say nephrotic syndrome, which one’s elimination
rate is affected more? Atrac. Is it clinically significant? No, it’s not. What’s the receptor occupancy rate for a NMBD do you
start to see twitch depression? Can you draw me a graph of the twitch height vs occupancy? Bell rang………

1. Tramadol. MoA. Preparations. Doses. Effects of liver failure. Renal excretion and renal failure. Other patient factors altering
duration of action. Interaction with fluoxetine. codeine metabolism.

2. Stats. Shown normally distributed graph of weight. P values and confidence intervals. Statistical analysis. Difference
between statistical and clinical significance.

3. Washout curves of sevoflurane and isoflurane. Why do we use Fa/Fao. explanation of phases. Why rapid initially then slow.

4. Drug interaction. Classify and describe. Given information about methadone and asked to explain possible interactions. (I
was stumped by this one and struggled through...).

1. What is bioavailability? Define, drew graph. Now imagine this is a graph of IV versus IM adrenaline. How would it change?
Now, you give the adrenaline down the ETT, how would it change? What other factors affect bioavailability? Tell me about 1st
past metabolism? Tell me about hepatic extraction ratio? What are examples of high and low extraction ratio drugs? What else
could affect drug metabolism in the liver. Phase 1 and 2 reactions etc etc

2. Tell me about nicotine!!! (What is it, methods of delivery etc). Where does it act? Is it water soluble or lipid soluble? Tell
me about the nicotinic AcH receptor? Where found, diff types etc.... How is nicotine metabolised? What is its half life? How is
it cleared? What would be the effect of nicotine on someone who had it administered? (Diff effects for fist time user versus
chronic user). I spoke about chronic effects more, and mentioned dopamine reward pathway etc ..

3. Shown a drug ..... They said 'This is lignocaine' without even given me a chance to say what it was. Can you tell em about
the structure activity of this molecule? Diff parts .... Where would this molecule become ionised? How ionised is lignocaine?
Point to it .... What structural changes occur with bupivacaine? Why is bupivacaine so much more toxic? What levels of
lignocaine would you see when you get toxic effects .... What symptoms as levels increase? What is the CVS:CNS ratio?

4. Can you list for me the antiplatlet agents? Gave a list, straight away went to clopidogrel....... What is clopidogrel? What do
you mean its a prodrug? What is its MOA? Wanted a very detailed description... Tell me about its pharmocokinetics? Where is
it metabolised? CYT P450 2C19 .... Do you know anything that changes its efficacy .... (Spoke about aspirin, PPI's etc) ...

The examiners do try and help you, but be aware that some of them have good poker faces and give you nothing. You will be
so nervous when you get your first question, so try and calm down before you start talking. Deep breath. Good luck

Tuesday am

1. Opiods Opiods are commonly used in clinical practice, but have some important side effects. Could you tell us about some
opiod side effects? Went through them by systems. Could you tell us more about how opiods produce nausea and vomiting...is
it a dose related response? No. What other effects can high dose opiods have? I said muscle rigidity including truncal rigidity.
How does this pose a problem clinically? I said difficulty in ventilation, may require use of muscle relaxants, etc. They were
looking for something more but i didn't know exactly what they wanted and then they prompted: so how will this affect oxygen
consumption? I said increase due to increase aerobic/anaerobic metabolism. How does muscle rigidity affect the CVS system?
No direct effect on cardiac muscle, but due to incr oxygen demand, can produce tachycardia, risk of ischaemia. They seemed
happy.

2. Anti-cholinergics Have you ever used glycopyrrolate? What is glycopyrrolate? Where might we use glycopyrrolate? Where
else? Anti-sialogogue, for eg as a pre-med. How does glycopyrrolate differ from atropine? Doesn't cross BBB because of
structure, therefore no risk of sedation, central anticholinergic syndrome. What is this? Do you think that everyone will
experience the central effects of atropine? No, elderly at risk. Do you think this might happen, say at even 1200mcg? Seemed
like a loaded question, so i said no. Seemed happy. Where else can we use atropine? Not sure. I think they were looking for
organophosphorus poisoning. What are some of the other routes by which we can give atropine? I said oral but poor oral
bioavailability. So what is the bioavailability of atropine orally? I couldn't remember, said i wasnt sure but i think it's less than
50%, they seemed surprised. Actual answer is around 15%. Moral of the story: if you don't know, don't bs. I didn't mention
intra-tracheal, but that's what they might have been looking for. What effect does atropine have on cardiac output? I said can
incr due to incr HR (and upon seeing the examiners questionable looks), quickly added that if the tachycardia decr filling time
and therefore EDV and SV, then CO may be decreased.

3. Propofol PK Here is a graph of propofol plasma concentration over time given to an obese patient. Explain what is
happening. Where does it distribute to? Now how would this graph differ if the dose was calculated for lean body mass instead
if total body weight in this obese patient? I said peak dose would decr, the whole graph will shift downwards in a parallel
fashion. Wasn't too sure about the answer, sort of fumbled through it. Examiner started questioning me as I was explaining,
which made me doubt myself, and then went back on my answer, but then stuck to it at the end. How would you calculate the
clearance, Vd, half life and rate constant for elimination from this graph. Talked about and wrote out the various equations.

4. Amiodarone AF is a common condition, can you tell us some of the pharmacological therapy used for rapid AF? Started
mentioning that always correct electrolytes, but they quickly reiterated they wanted drug therapies. Digoxin, ca channel
blockers, b blockers, amiodarone. What is Amiodarone? How does it work? Draw for me a cardiac action potential from the
SA node and indicate how amiodarone alters it. Remember to label axes! Question caught me a little off-guard so was thinking
while drawing, and so was quite slow but they seemed to guide me through it. So what effect does amiodarone have on the
refractory period? Here is some data regarding amiodarone (showed me a piece of paper with half life, Vd and clearance
figures). What is a loading dose? Why do we use it? What problems are there with using a loading dose? I said possible
toxicity esp if low therapeutic ratio. How can you calculate the loading dose for amiodarone? I think the half life and clearance
figures were there as distractors. Didn't actually have to calculate it, just mention the principles. Amiodarone can have some
serious toxic side effects. If a patient took their year's worth of amiodarone in a month, and presented to hospital, how would
you manage them? ABC, supportive treatment of bradycardia and hypotension...BELL, END OF VIVA.

Time goes by extremely quickly. The examiners are there to give you as many marks as possible, so at times it seems like they
are rushing through the questions, which is a good thing. My examiners were quite helpful and not poker faced, but I guess
there would be some inter-examiner variability. Have a sip of water between questions. All the best!
1. Anticholinesterases. Classify and MOA. when can neostigmine be used to antagonise sux. compare and contrast neostigmine
and physostigmine (only interested in the fact that physo crosses BBB and neo doesnt)why does physo cross BBB. uses of
physo - mentioned central antichol synd and alzheimers

2. stats. given raw data. types of data. measures of central tendency. when can p>0.05 be a good thing? (when you want to
show that the two groups are actually similar) given another graph to interpret

3. asked to identify picture of noradrenaline. SAR of catecholamines. how do you increase B2 selectivity. How would you
formulate it if i want to administer the drug orally (lipid sol and resistant to MAO). can you give possible reasons as to why a
noradrenaline infusion given to a critically ill pt does not show clinical response?

4. LAs. MOA. lipid sol and implications. why is bupi > cardiotoxic. intralipid - give 2 possible MOA

Examiners were lovely and trying to help guide me along the right path throughout.

September 2011
Pharm viva 21/Sep/2011

1. DES Mac value How does MAC change with age? Give figures. How old are the subjects on your standard curve. Draw
dose response curve. Are there any other MAC?Superimpose MACaw and MACbar Define MAC, MACaw&MACbar Mark
ED95 on the curve. What is the Mac at ED95? What is the MAC if patient are given 1mcg/kg and 100mcg/kg fentanyl. Draw
desflurane wash in curve. At what time fa/Fi will reach 90%?

2. Define colloids Classify colloids. What is HES? What us commonly used. What is 6% meant? What is in the bag? Half life?
What is albumin? How is it made? What is in the bag? Half life? How is it metabolized ? What is the infection risk?

3. How are drugs handled by kidney? Which part of the kidney get involved? What factors influence this? Tell me about
ionization, protein binding, MW, solubility Give an example of drug that formulated in salt form to improve solubility. List
drugs that cause kidney impairment. How do you avoid gentamicin toxicity. You do not normally give gent for orthopedic
surgery, what do you normally use? How does cephazoline affect kidney?

4. Compare and contrast fentanyl and alfentanyl. I m interested in physical chemical properties. Tell me why alfentanyl has
quicker onset? What would lipid solubility affect clinically if infusion is used. Define CSHT. Draw CSHT for both. How
fentanyl redistributed after iv bolus? What is the role of lung? Which drug has the highest lipid solubility in phenylpiperidine
opioidgroup? You mentioned fentanyl patch, why alfentanyl does not have topical formulation?

Monday pm Pharm:

1. Local anaesthetic toxicity: What to do? Cardiac and CNS effects at differing levels? Why is Bupivacaine worse than
lignocaine wrt CVS? Treatment - what is in intralipid? What antiarrthymic to use?

2. Vecuronium: Draw log concentration versus %, what is ED95 of Vec? Why is the shape of the graph steep? What happens
when you add Neostigmine? What is the antagonist to NDNMB?

3.Inotropes: Classify inotropes. What is the main MOA of inotropes? What are the mechanisms of action of digoxin? Digoxin
therapeutic index and levels of toxicity? Treatment of toxicity? Other inotropes discussed: Noradrenalin, PDE-inhibitors
(named 4 - discussed mostly aminophylline), calcium.

4. Stats: What is statistics? Define: p-value, Ho and H1, alpha value, type 1 and 2 error, confidence intervals. Then a discussion
on the use of p values versus confidence intervals.

My viva:
1. Fentanyl: What is fentanyl? Draw the plasma conc-time graph. What is a normal peak plasma concentration? How would it
differ in the elderly? Why? Where is the apnoeic threshold? Is it the same in everyone? Why not? (I said tolerance). How can
tolerance be reversed? ( I said time, and ketamine. They seemed happy with this).

2. Insulin: What is insulin? Can you compare the time to peak effect and duration of action of neutral insulin given
intravenously v subcut. Why the difference? How is it metabolised? What effects the metabolism? What are the effects of
insulin? What is glucagon. How does it work? Does glucagon always work in an anaesthetic setting? (This was a bit confusing;
I started talking about glucagon receptors in cardiac muscle, then moved on to the requirement for glycogen to be present for
glucagon to be effective, which I think is what they wanted.)

3. Sevoflurane/ Fa/Fi: What is sevoflurane? How does it differ from other volatiles (wanted information on the carbon
structure, and also the type of halogen substitutions). Draw the Fa/Fi curve for sevo. What affects Fa/Fi? How about in
neonates? What is the second gas effect? Is N2O really a highly soluble gas? Compared to sevo? What about washout curves?
What is the effect of cardiac output on washout?

4. Isomers: What is an isomer. Define and classify them, with examples. Why are some drugs presented as racemic mixtures,
and some as enantiopure preparations? What is a chiral centre? I was shown a diagram of L-DOPA. Where is the chiral centre?
What is R-DOPA? Discuss the structure-function relationships of this molecule. What are the effects of orally ingested L-
DOPA? What other drugs are used to treat parkinson's disease?

Monday am Room 1:

1. NSAIDs. What are they? Uses? Went through side effects by system. Why do they cause bronchoconstriction? Which
patients are at risk?

2. IV fluids. Name crystalloids, what's in normal saline? Why 154mmol/L of Na+ isn't this much higher than physioligical?
What problems can result from too much N/saline? what's in Hartmann's? What happens to lactate. What are colloids? Name
them. Does gelofusine or HES last longer? Why? What's the MW of HES? of Gelofusine?

3. Antiemetics. Classes and examples. Tell me about droperidol. What else is it used for? What side effects? Tell me about
metoclopramide. What side effects? If you're called to recovery and your patient is vomiting would you give dexamethasone?
How does dexamethasone work?

4. Vasopressors. Similarities and differences between ephedrine, metaraminol and phenlephrine. He drew a line on the paper
and asked for the 3 drugs to be placed along spectrum of indirect <--> direct action. Could you give these drugs orally? Why?
Something about tachyphylaxis. Do you know any problems with use of these 3 agents in pregnant women? If there is
hypotension unresponsive to repeated doses of these vasopressors would you give vasopressin? Would it work? Why?

PHARMACOLOGY

Examiner 1

Can you classify IV induction agents? Tell me about Ketamine? I started saying it's a phencyclidine, NMDA antagonist, clear
colourless solution... & I got stopped quite quickly and asked can you tell me what's in an ampoule of Ketamine? What does
racemic mean? What is an enantiomer? Why is being racemic important for ketamine? Which enatiomer of ketamine has
which effects? What is the mechanism of action of ketamine? Can you describe the NMDA receptor? Why would ketamine be
beneficial to use in a trauma patient who has sustained large blood loss? Would it always increase the BP and HR? Why not?
List other drugs that act at NMDA receptors.

What are measures of central tendency? Describe in more detail the mean, median and mode? If I had a set of data about
patient ASA scores, which measure of central tendency would be best to use? Why? What sort of data are pain scores? Which
tests could you use to analyse the data and how would you choose which one to use? What does parametric mean? Can you
draw a normal distribution curve? How is this different from a standard normal curve? I started talking about Z-transformation
and he cut me off to hand over to the next examiner...
Examiner 2

List for me different situations when you would use rocuronium? What are the side effects of rocuronium? How do these
compare with the side effects of suxamethonium? In what situations would rocuronium be preferable to suxamethonium for a
rapid sequence induction? When would you not use rocuronium for a rapid sequence? How can we clinically speed the onset of
rocuronium? What do you mean by ED95? What is the ED95 for rocuronium? For Sux? In what multiples of this are our usual
doses given? Why does giving multiples of ED95 speed the onset of a muscle relaxant? If we gave cis-atracurium in multiples
of its ED95 would it also speed the onset for this drug? What else will speed the onset of a muscle relaxant?

How can we manipulate gastric acidity? Give examples of drugs that reduce gastric volume and pH? How do antacids work?
What is the benefit to using a non-particulate preparation? Can you write the chemical equation for the reaction between
sodium citrate and gastic acid? I said I wasn't sure of the formula for citrate, and she said ok then use sodium bicarbonate
instead.... so I wrote that and figured out it would form H2CO3 What are the problems with the formation of H2CO3 in large
amounts, for example if a patient takes regular doses of an antacid? I said it would dissociate to form CO2 which in large
amounts would cause high gastric pressures And what will the patient do? I said they might reflux or burp, then the bell rang :)

ONE How do you choose a volatile. They wanted the answer as broad as possible – physical, PK, PD, interactions, cost,
neurosurgery, interaction with CO2 absorber.

TWO • Non-opioid options for post-operative pain • Further detail on NSAIDS. Is the lack of antiplatelet activity of selective
COX2 inhibitors an advantage or disadvantage in acute post-op period. • Why don’t we use aspirin for analgesia

THREE • Local anaesthetics • Structure and function relationships • Metabolism • Differential block • Maximum dosage of
drugs.

FOUR • Showed a picture of adrenaline, asked me “what drug is this” • Describe structure-function relationships of
sympathomimetics • Asked how salbutamol looks. (Told them I have no idea). • How can catecholamines be classified. (I got a
bit thrown because they asked specifically for catecholamines, not sympathomimetics). • Volume of distribution of
noradrenaline. (That was just plain weird).

All the best guys! I know other people have said this, but I'll reiterate. If you don't know something, just say so and don't waste
time. The examiners are actually on your side! Also, don't forget the basics - speak clearly, confidently, and take a deep breath
before answering the more complicated questions.

'''Pharmac''' 1. What drug would you give to treat hypotension, bradycardia post SAB ephedrine or phenylephrine, can you
draw basic structure of these agents, catecholamine skeleton, modification at each position how does it affect the activity
/metabolism basically SAR , didn’t do too well in this part. Tell me about metaraminol. Straight forward pharmac question

2. Differences between fentanyl, remif and alfent. Onset and off set, why is there a difference. Basically diff in Vd, pka,
ionisation Define CSHT draw graph of the three opiods, I think I did pretty well in this section since it was straightforward
core drug topic.

3. What are anticholinesterases I divided into 3 groups and the mech of axn uses, differences between neostigmine and
edrophonium, adverse effects. Anticholinergics glycopyrolate and atropine. Adv effects, compare with onset with neostigmine.

4. What are the new updates in CPR I talked about the AHA 2010 update. Role of adrenaline and atropine just went straight
into the axns of each.defibrillator biphasic and monophasic difference and advantage. I didn’t know much about this just
guessed about smaller current and less adv effects , any other drugs you would like to use mentioned anti arrhythmic which
they didn’t seem to be too excited about..prob they wanted vasopressin. They did go into a bit about amiodarone though.

April 2011
My viva:

 What is rocuronium?

 When do you use it?

 Why would you choose roc over other agents?

 Discussed inverse relationship between potency and onset

o She asked about the affinity of drug for the receptor

 Draw dose response curve and show more potent drug

 What advantage does roc have over atracurium? – histamine

 I didn’t mention suggamadex but should have

 Ways to pharmacologically reduce gastric acid

 Tell me about particulate antacids

o Draw the equation

 Disadvantages of long term use of eg Mylanta

o Iron absorption

o Immune

o Protein digestion

o Metabolic alkalosis

 Inducing 5 yr old with sevo – what factors speed onset?

 Why does FGF make a difference?

 Size of circuit? Paed vs normal

 Wash-in curve 70%N20, then 9% desflurane – what is blood-gas partition coefficient? Why are curves different?
Where would N20 curve be if it was given at 9%?

 Systematic review vs meta-analysis?

 SR – what do they do once they have all the studies? How do they weight them? Does a well designed small trial
carry the same weight as a well designed large trial? – apparently yes.

 How do trials reporting comparisons between treatments normally report the findings – as a risk ratio
  How do meta-analyses often graph their results? What is the null hypothesis –

If I give someone an intubatiing dose of Rocuronium, how do I know that they are paralysed? (needed to eventually say muscle
stimulator)

 How do peripheral nerve stimulators work?

(I said they deliver a supra-maximal stimulus)

 What is a supra-maximal stimulus?

(They kept me here for ages wanting a good definition)

 If we gave a single twitch, what will the response be?

(lots more questions probably coming but I had wasted a lot of time on the definition of supra-maximal stimulus

What drugs are used to treat pulmonary hypertension? (I had hardly any idea - I said calcium channel blockers, NO donors,
beta 2 agonists)

 Do you know what Milrinone is?

 How does it work?

(I wasted time talking about it inotropic effects instead of smooth muscle effects)

 What are the peripheral effects of milrinone?

 How does this occur?

(wanted info about 2nd messenger systems)

 Name another 2nd messenger system

(I said phopholipase C, they were happy with that)

 Are there any anaesthetic induction drugs that you would avoid in pulmonary HT?

(they wanted ketamine)

Draw a FA/FI curve for Desflurane

 What is happening here at the shoulder?

 Why does sevoflurane have differences at the start and right at the end (The examiners drew a curve just below mine,
with a gap near the begining and end)

 What is a partition coefficient?

  If a patient is at equilibrium with 5% des, and the blood:gas partition coefficient is 0.42, and the gas concetration is 1
ng/mL, what is the blood concentration? (I was flipping out at this point and my recollection of the question and
figures may need some straightening)

 If the brain:gas coefficient is 0.53, what is the brain concentration?

Tell me about clopidogrel (I didn't get far before they cut me off)

 What is its mechanism of action?

 What makes it a pro-drug?

 What can reduce its effectiveness, starting from the point of administration?

 What is it's duration of action?

What is MAC?

 draw a curve of dose response curve for MAC

 can you find MAC for an individual?
 what is the effect of body temp and atm pressure on MAC?

Placental drug transfer

 what are the factors

 talk about ionization/ ion trapping/ Fick's law

How do you treat anaphylaxis?

 adrenaline, antihistamine, steroid

 what receptors do each drugs act on?
 what other effect does antihistamine have

Tell me about nicotine

 routes of administration
 nicotinic receptors, what types are there? neuronal, ganglian, neuromuscular.
 effect of nicotine on naive patient vs chronic smokers: concept of tolerance.

April 2009
PK's and PD's of local anaesthetic injected intrathecally - Didn't seem interested in PK's though, despite the question

 Where does it go? Effect site? Mechanism of action of LA's?

 What we see clinically - ie, bockade of autonomic nerves, sensory/pain fibres, motor block
 Duration of action factors? What effect does pKa have?
 Metabolism

Therapeutic Index

 Definition. Other indices of adverse effects

 Why is it not clinically important? Interindividual variability, idiosyncratic reactions such as MH
  Shown graph of Gentamicin plasma monitoring nomogram - why do we measure it at these time points? (I said that
peak may not be as important, also initially due to redistribution rather than clearance - seemed to accept that as what
he wanted)

Beta-blockers

 Classification - gave cardioselective, non-selective, Intrinsic sympathomimetic activity, membrane-stabilising activity,

and combined alpha-beta activity - He still wanted more!!
 Wanted to talk about lipid soluble vs water soluble, different agents, how does it affect PK's, duration of action, el 1/2
t
 Is labetalol 1:1 alpha:beta blocking? How is it different?

COX

 What is it? What are the different types? What is constituitive? What does COX do?
 Why COX2 inhibitors? Are they better? Talked about slightly lower incidence of GI issues, but increased thrombosis
- similar renal failure, asthma, etc
 Who wouldn't I give NSAIDs to? Renal impairment, ACEI, Pregnant women, aspirin to children, allergic
 How does aspirin work? low dose vs high dose - what is the difference?

Other people got - CVS effects of propofol, suxamethonium, CVS effects of volatiles, Diagnostic tests - 2x2 table,
sensitivity/specificity, screening tests, etc, analgesics to treat post-operative pain, what is good about alfentanil?

April 2009
1.Antihypertensive agents used to drop blood pressure intraoperatively

 Esmolol
 Durations of action – why?
 Hydralazine - Cardiovascular effects, Mechanism of action, Pregnancy Class C drugs – what does that mean?

2.N2O 70% with Sevoflurane – what effect does the N2O have

 Concentration effect, 2nd gas effect

 Factors affecting up take of sevoflurane
 Respiratory effects of sevoflurane
 Changes in alveolar ventilation
 mechanism

3.What type of drug is Suxamethonium

 Mechanism of action
 Why does it last longer than the natural agonist
 Phase II Block
 Draw a dose-response curve for sux (paper given with axes of response against dose – NOT log dose – I added Log!
 Why do we log it – EC50
 What is EC50
 What affects EC50

4.Pharmacokinetics of drugs in Hepatic Failure and Cardiac Failure

 Dose adjustments for Propofol

Sept 2008
Q1: IV drug options available to treat severe pain in post op pt. Tramadol MoA, SE (particularly of rapid push, does it cause
resp depression), interactions, contraindications

Q2: Incidence vs prevalence, types of data and examples of each including discreet/continuous/ratio/interval, 2x2 table- sens,
spec, PPV, NPV, effects of prevalence

Q3: About to start anaesthetic, have equipotent doses alfentanil, fentanyl, morphine. Which acts fastest, why? Why does
fentanyl have faster onset than morph. Considerations when swapping IV morphine to oral morphine post op on ward
(examiner focus was on bioavailability&quick discussion about BA). Pharmacology of oxycodone vs codeine, does codeine
have intrinsic mu receptor agonism

Q4: Local anaesthetic toxicity. Local vs systemic. What are transient neurological symptoms? Which drug classically caused
this? Isobaric or hyperbaric? Features of systemic toxicity, lignocaine plasma concn vs effects. Specifically cardiac toxicity,
what ECG changes, clinical effects. Contrast lignocaine and bupivacaine Re cardiac toxicity, affinity for Na channels.

 Drugs for VT/VF arrest. Talk about amiodarone: class(es), effect on QTc.

 Drugs for anaphylaxis.

 Thiopentone... dose adjustment in acidaemia.

 Draw suxamethonium...

April 2008 Pharm

 DOSE REPONSE CURVES

Presented with a series of graphs relating to unnamed non depolarising muscle relaxants, which looked like they'd been lifted
out of Stoelting.

What do they mean? What is semilogarithmic transformation and why is it used? What is a quantal response? ED95 vs ED50.
ED50 vs LD50 vs TD50.

 PHARMACOKINETICS

"If you inject a typical adult with 100mcg fentanyl, show me how the plasma conc varies with time"

"now superimpose how brain conc varies with time"

"now superimpose how peripheral concs vary with time"

Essentially lots of questions which could equally apply to propofol TCI kinetics, but using a drug which isn't usually studied in
that depth-therefore testing understanding of underlying principles.

 ANTIARRHYTHMICS

"You go and see a patient on the ward for a preoperative assessment. He starts to feel unwell, you attach an ECG monitor and
he's in fast AF. What are your pharmacological treatment options?" Mentioned digoxin and amiodarone.

"Tell me about the pharmacology of amiodarone". How does it work, what effects does it have on ion conductances. How is
this manifest on the ECG. How do you commence treatment? Does it require loading? Why? Would you stop amiodarone
before anaesthesia if it had been running for 12 hours? What if the patient had been on it for 2 months? How does amiodarone
interact with other anaesthetic agents?
  VOLATILE AGENTS

Washin/washout curves. Factors affecting these curves. Role of nitrous oxide.

Define a partition coefficient.

Then presented with a series of unfamiliar figures (something like muscle-fat partition coefficients).

If the partial pressure in muscle is x mmHg and the concentration of volatile is y mg/ml, what are the corresponding figures in
fat at equilibrium? ANSWER-partial pressure the same, concentration is different. Not expected to know the obscure figures,
but expected to be able to apply them in unfamiliar settings.

September 2008
 DESFLURANE/MAC

What is the MAC of desflurane. what factors affect MAC? what other types of MAC are there? draw a dose response curve for
desflurane. superimpose sevoflurane. tell me about partition coeffients.

 STATS

probability-limitations. alpha and beta error. calculation of p value. confidence intervals. calculate variance. absolute vs
relative risk.

 DRUGS USED TO TREAT NEUROPATHIC PAIN

Classify with examples, mechanism, adverse effects.

 PHARMACOKINETICS

for a single IV bolus of a drug in a 3 compartment model, represent the plasma conc vs time on a graph. what data can be
derived (Vd, Cl). what is the equation for the curve. what is the value at time zero? how does this relate to TCIs? how would
the initial curve change if oral or SC administration?

August 2007 ANZCA

 Ampoule of thio - what's in it, what are they for. Draw graph of %ionized vs pH for thio. Ampoule of 1% lignocaine -
same questions, same graph. Then propofol - what additives, what for. But wait, there's more...Vec, Perfalgan,
Dantrolene, he had a whole stash under the desk! Wanted to know what the additives were and what their role was.
What is pKa - as in what is the Ka, what is the p.

 Factors affecting onset of volatiles. How do we tell if the volatile is working? MAC - definition. How does lack of
movement to surgical stimulus help us to know if it's working? (blathered about MACawake). Dose-response curve
for volatile vs benzodiazepine.

 Vecuronium compare and contrast with Rocuronium. ED95 definition, relation to intubating dose. Problems with
less potent drugs. Neuromuscular monitoring - TOF, PTC, DBS.

 Tell me about Tramadol. Stopped when I mentioned SS/SNRI. What other drugs act on the serotonergic system?
Can you give tramadol to someone on MAOI? Serotonin syndrome - what is it? What does tramadol do to seizure
threshold? How do the 5HT3 antagonists work? Do you think Tramadol would increase nausea and vomiting? What
about SSRI? Do you know any other drugs which are NAdr-reuptake inhibitors? Bell.
  What is volatile "potency"? What is MAC? What factors change MAC?
 What are the mechanisms of transfer of substances across the placental barrier? What is the effect of protein binding,
specifically in reference to Warfarin.
 What is tolerance? Draw dose-response curves, and the effect of tolerance. What are the mechanisms of tolerance?
Give examples.
 What are the kinetics of fentanyl? Compare Alfentanil and Fentanyl. I volunteered the graph of CSHT vs Duration.

August 2007 Day 3

Examiner 1
 What influences the uptake of inhalational agents? How do you assess the depth of anaesthesia - how do you know
whether the person you are giving an anaesthetic to is not aware? Discussed MAC, MAC_BAR, MAC awake, what is
the sensitivity and specificity of MAC? Ideally what would it be, would you rather MAC be more sensitive or more
specific?

 Can you classify antiarrhythmics? Gave Vaughan-Williams and "others". Lets talk about others - discussion of
adenosine (where are adenosine receptors, what is its half life, how does it work, SE), digoxin and then amiodarone
(specifically what is amiodarones half life, how long does it take for a drug to reach steady state, how long does it take
amiodarone to reach steady state, how does it fit into V-W classification?

Examiner 2

 Fentanyl vs alfentanil as above, which would you use as an infusion and why - kinetics of both and explain the
effects clinically. Draw CSHT vs time for both and explain differeces.

 Lets talk about drugs that act on the uterus - talked about oxytocin/syntometrine/prostaglandins/misoprostol and
tocolytics. Discuss oxytocin - MOA, SE, "say a surgeon asks you to give 15U oxytocin as a push, what are you likely
to see", discuss the ergots, discuss GTN how does it work?

April 2007
 Tell me about drugs that are used to treat status epilepticus
 Shown a picture of nitric oxide - Tell me about the pharmacology of nitric oxide General discussion of
pharmaceutics, pharmacokinetics, pharmacodynamics with particular emphasis on side effects and how to get around
those
 Discuss diuretics Classified diuretics as per site of action at nephron and discussed
 Tell me about the drugs a patient with Myaesthenia Gravis might be treated on Discussion about cholinesterase
inhibitors, impact on pharmacokinetics and pharmacodynamics of NMBD.

ANZCA- March/May 2006

Examiner 1
 How do you classify beta blockers?
 Tell me about drugs that affect gastric pH?

Examiner 2

 You have a patient with myasthenia gravis who needs a rapid sequence induction, what are your pharmacological
concerns?
 Intranasal cocaine is being administered to a patient undergoing sinus surgery, what are the toxic potentials and what
patient factors may increase.
August/Sept 2006
Examiner 1
 What are the effects of a 15ml o.5% bupivacaine bolus in a pregnant woman?
 Ropivacaine vs bupivacaine: why different toxic effects? What other different effects?
 What treatment for hypertension intra-operatively?
 Metoprolol vs esmolol

Examiner 2

 Difference between anaphylactic/anaphylactoid?

 What common drugs trigger anaphylactic/oid reactions in anaesthesia?
 Treatment of anaphylactic/oid reactons? Why adrenaline?
 Midazolam: use as a pre-med, and pharmacodynamics.
 Fentanyl: use as a premed, pharmacodynamics, and synergy with midzolam.
 Pharmacodynamics of propofol

FRCA (UK) Pharmacology Primary Viva - May 2005

 A drug company is manufacturing a new IV anaesthetic agent, what features would you like?
 How would I improve propofol, what are the problems with its use? Which causes more hypotension on induction,
propofol or thiopentone, and why?
 You swallow an aspirin. Describe its course. They stopped me when the aspirin got to the systemic circulation.
 Define volume of distribution.
 Define bioavailability.
 Name a drug that is well absorbed across the gastric mucosa.
 Name a drug that is not well absorbed across the gastrointestinal wall.
 Discuss metabolism in the liver.
 Describe the Vaughan-Williams classification – write down the classes and name a drug in each one and say what
they were used for.

ANZCA- August/Sept 2005

Examiner 1

 Define Bioavailability.
 Draw conc vs time curve for oral dose.
 Define significant parts of curve.
 Difference between o/iv conc time curve.
 Define Hepatic extraction ratio.
 What is HER for morphine.
 How do you convert iv to oral morphine dose?
 Describe CVS effects of IV induction agents (STP vs propofol vs Ketamine).
 Compare with CVS effects of volatile agents (Sevo vs Des vs Halo).
 What is the cause of tachycardia associated with desflurane?

Examiner 2
 What are the advantages/disadvantages with Nitrous oxide?
 What are the possible side effects?
 Specifics about methionine synthetase and methionine deficiency.
 What's in a bag of Hartmann's, 0.9%NaCl, 5% Dextrose.
  Osmolalities of same bags.
 Which compartments do they go to and in what proportions?
 What hormones are involved in the elimination of these fluids?

ANZCA- April 2005

 Nitrous Oxide - Physicochemical characteristics, Side Effects, Production
 Statistics - Phases of a Trial, Power, Size of trial
 Lignocaine - Structure activity of LAs.Blood levels with toxicity, CC:CNS Ratio, CVS effects, Mechanism of cardiac
dysryhtmia
 Paracetamol - Identify structure,Metabolism, Pharamacokinetics, toxicity
 Bioavailabilty with panadol as example, Adult/paediatrc dosing

ANZCA- September 2003

 Phenytoin - Pharmacokinetics, Mechanism of action, Therapeutic levels
 Benzodiazepines - Mechanism of action
 Diuretics - Draw a nephron, Classes / site of action, Mode of action, Frusemide as example
 Propofol - Target levels with TCI, Effect site concentration/time curves
 MAC Awake
 Statistics - Study size, Alpha/beta error, p value definitions, etc