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152 Cards in this Set

  • Front
  • Back
PC Clonidine is

A. Alpha 2 agonist centrally that acts presynaptically

B. Alpha 1 agonist

C. Alpha 2 antagonist

D. Alpha 1 antagonist

E. ?
ANSWER A
TMP-121 PC Levosemendin:

A. Increases contractility and myocardial oxygen consumption

B. Increases SVR

C. Binds to troponin C and induces a conformational change

D. Increases contractility by increasing calcium influx

E. Causes coronary vasodilation but NOT peripheral vasodilation
ANSWER C

LEVOSIMENDAN
-Calcium sensitizor used for inotropic support in acute severe decompensated cardiac failure.

Mode : binds to cardiac Troponin C in a calcium-dependent manner
-positive inotropic effect
-vasodilatory effect by opening ATP-sensitive K+ channels in vascular SM
-therefore decreasing preload and afterload

Contraindications
-renal impairment
-hepatic impairment
-hypotension
-tachycardia

Adverse effects
-tachyarrthymias
-myocardial ischemia
PZ. The active metabolite of ketamine is:
a. Hydroxyketamine

b. Hydroxynorketamine

c. Ketamine glucuronide

d. Ketamine sulphonamide

e. Norketamine
ANSWER E

norketamine Metabolites of ketamine are norketamine and dehydronorketamin
Thiopentone 2.5% precipitates with (when injected through the same cannula):

A. Pancuronium

B. d-Tubocurarine

C. Vecuronium

D. Suxamethonium

E. Alcuronium

F. All of the above
ANSWER F

Thiopentone (highly alkaline solution) is incompatible with the following drugs and MUST NOT be mixed with:

* Muscle relaxants
o succinylcholine
o pancuronium
o vecuronium

* Opioids
o codeine
o morphine
o pethidine
o alfentanil
o sufentanil
* Catecholamines
o metaraminol
o norepinephrine

* Others
o midazolam
o atropine
o amikacin
o dimenhydrinate
o diphenhydramine
o insulin
o penicillin G
Foetal thiopentone:

A. Peaks (?within 2 minutes/?at 10 mins) of intravenous administration to the mother

B. Effects are proportional to maternal peak level

C. Level is reduced if given during a contraction

D. Has an increased effect due to foetal BBB being more permeable
ANSWER C

A. FALSE : peaks within 30-45 seconds, fetal-maternal ration 0.40-1.0

B. FALSE effects are not proportional to maternal peak level. why?

C: TRUE levels are decreased during contraction

D: FALSE why?
PL03 ANZCA version [1986] [1988] [Mar93] [2004-Aug] Q40, [2005-Apr] Q74
The difference in duration of action of lignocaine and bupivacaine is most marked with:
A. Infiltration anaesthesia
B. Carbonated solutions
C. Peripheral nerve block
D. Extradural anaesthesia
E. Solutions containing adrenaline 1 in 200,000
ANSWER A
PL04
Adrenaline is an advantage in increasing the duration of action of anaesthesia when used with:
A. Bupivacaine
B. Etidocaine
C. Prilocaine
D. Lignocaine
E. Amethocaine
ANSWER ??

From Miller's, 6th edition, pp. 586,7:

Epinephrine will prolong the duration of infiltration anesthesia by all local anesthetics, although this effect is most pronounced when epinephrine is added to lidocaine
PL05 [Aug93] [Mar94]
Placental transfer of bupivacaine:
A. Lipid solubility
B. Low F/M ratio of bupivacaine
C. High F/M ratio of bupivacaine metabolites
D. Molecular weight ??
E. Detectable levels of bupivacaine & PPX in the neonate for several days
ANSWER B

Bupivacaine is 96% protein bound, so less free drug is available for transfer than with lidocaine (67% bound).

The mean F/M ratio for bupivacaine is approximately 0.3 and for lignocaine 0.5, confirming lignocaine's greater placental transfer
PL06
In 5 mls of 1% lignocaine with 1:200,000 adrenaline, the amount of adrenaline is:
A. 10 mcg
B. 25 mcg
C. 50 mcg
D. 100 mcg
ANSWER B
PL08

Bupivacaine ('Marcaine'):
A. Possesses an ester type chemical formula
B. Is unsuitable for paediatric caudal anaesthesia
C. Is biotransformed in the liver
D. Has poor plasma binding properties
E. Has a shelf-life of one year
ANSWER C

* Aminoamide local anaesthetic (NOT an ester)

* Higher toxicity so better to use something else for caudal. Small but significant risk of IV injection with caudal injection.

* Metabolised in the liver (as are all the amide LAs)

* Lipid soluble -> high plasma protein binding

Amides have a shelf life of up to 2 yrs
PL11a

Which of the following has the greatest cardiotoxic effect?
A. Amethocaine
B. Procaine
C. Dibucaine
D. Etidocaine
E. Prilocaine
ANSWER A

bupivacaine >tetracaine = etidocaine > lignocaine = chloroprocaine > mepivacaine = prilocaine >>>procaine
PL11b ANZCA Version [Jul06] Q109, [Apr07]

The local anaesthetic LEAST likely to cause cardiac toxicity after inadvertent
intravenous injection is

A. bupivacaine
B. etidocaine
C. levobupivacaine
D. lignocaine
E. ropivacaine
ANSWER D

bupivacaine >tetracaine = etidocaine > lignocaine = chloroprocaine > mepivacaine = prilocaine >>>procaine
PL24 ANZCA version [2003-Aug] Q133, [2004-Apr] Q4

The MOST correct statement concerning lignocaine toxicity is that
A. extremely high concentrations of lignocaine will produce persistent ventricular fibrillation
B. hypercarbia increases the convulsive threshold of the drug
C. the first sign of lignocaine toxicity is cardiovascular collapse
D. the initial treatment of lignocaine induced convulsions is phenytoin
E. tonic-clonic convulsions may be preceded by symptoms such as auditory disturbances
ANSWER E

* A - False. Miller, 6th ed. p 594: "Ventricular arrhythmias were rarely seen with lidocaine, mepivacaine, or tetracaine." and "Ventricular arrhythmias and fatal ventricular fibrillation may occur more often after rapid intravenous administration of a large dose of bupivacaine but far less frequently with lidocaine."
* B - False. "Hypercarbia can lower seizure threshold by several mechanisms: (1) Increased CBF with increased drug delivery to the CNS; (2) increased conversion of the drug base to the active cation in the presence of decreased intracellular pH; and (3) decreased plasma protein binding, which increases the amount of free drug available for diffusion into the brain." Goldfrank's toxicologic emergencies

(Caffeine: Think hypercarbia ie acidosis actually said to decrease seizure threshold: hyperventilation test as used in the past for dx petit-mal and diamox used as adjunct for Rx of intractable seizures by inducing acidaemia. Agree with increased blood flow delivering more drug to brain with hypercapnoea though. E best answer.)

* C - False. "Initial symptoms are subjective and include tinnitus, lightheadedness, circumoral numbness, disorientation, confusion, auditory- and visual disturbances and lethargy." Goldfrank's toxicologic emergencies
* D - False. "Treatment: supportive, with oxygenation / cardiovascular support as for CPR. Thiopental or diazepam / midazolam may be used for convulsions, although hypotension may be exacerbated." Yentis, 3rd ed., p 321.
* E - True. Sequence of: "Toxicity . . . tingling . . . unconsciousness and or convulsions." Yentis, 3rd ed., p 321.
PL25 ANZCA version [2005-Apr] Q114

Prilocaine is superior to lignocaine for intravenous regional anaesthesia because prilocaine

A. exhibits no cardiotoxicity
B. has a higher pKa
C. has a larger volume of distribution
D. is an ester, metabolised in the bloodstream
E. is more highly protein bound
ANSWER C

* A. exhibits no cardiotoxicity - false
* B. has a higher pKa
* C. has a larger volume of distribution - true
o Prilocaine: "Distribution: Vd: 0.7-4.4 L/kg; crosses blood-brain barrier"
o Lignocaine: "Distribution: Vd: 1.1-2.1 L/kg"
* D. is an ester, metabolised in the bloodstream - false: Prilocaine is an amide anaesthetic.
o "Prilocaine is a membrane stabilising agent and a local anaesthetic of the amide type" (Mims online)
* E. is more highly protein bound - false
o Prilocaine: "Protein binding: 55%" (uptodate)
o Lignocaine: "Protein binding: 60% to 80% to alpha1 acid glycoprotein" (Uptodate)
PL27 ANZCA version [2004-Apr] Q141

All of the following may be useful in the treatment of ventricular fibrillation due to bupivacaine
cardiotoxicity EXCEPT
A. adrenaline
B. diazepam
C. intralipid
D. propofol
E. vasopressin
ANSWER C
PL28 ANZCA version [2004-Apr] Q137, [2004-Aug] Q59, [Jul 06] Q41

Intra-nasal topical cocaine used in nasal surgery

A. has a duration of action of the order of 6 hours
B. is metabolised more quickly by the liver if the patient is using ecothiopate eye drops
C. is typically used in a dose of approximately 5 ml of 5% solution in an adult
D. may be metabolised more slowly in patients with liver disease
E. reaches a peak plasma concentration in 3 hours
ANSWER D

* A. has a duration of action of the order of 6 hours - false
o "There has been an increase in both IV administration and inhalation of pyrolyzed cocaine via smoking. Following intranasal administration, changes in mood and sensation are perceived within 3–5 min, and peak effects occur at 10–20 min. The effects rarely last more than 1 h. "(Harrisons Ch389)
o "Peak anesthetic effect following topical application of cocaine or lidocaine occurs within 2 to 5 minutes (3 to 8 minutes with tetracaine), and anesthesia lasts for 30 to 45 minutes (30 to 60 minutes with tetracaine)." (Goodman and Gilman)
o "Peak venous plasma concentrations of cocaine are achieved at approximately 30 to 40 minutes after intranasal administration... The duration of effects is approximately 60 minutes or longer after peak effects." (Stoelting p.178)
* B. is metabolised more quickly by the liver if the patient is using ecothiopate eye drops - false: "Demecarium, echothiophate, and isoflurophate are indirect-acting parasympathomimetic agents, which are also known as cholinesterase inhibitors and anticholinesterases. {37} {60} {63} {88} Cholinesterase inhibitors prolong the effect of acetylcholine, which is released at the neuroeffector junction of parasympathetic postganglion nerves, {37} by inactivating the cholinesterases that break it down" (http://www.drugs.com/mmx/ecothiopate-iodide.html)
* C. is typically used in a dose of approximately 5 ml of 5% solution in an adult - false: Beyond safe dose. Dose = 50mg/ml*5ml=250mg; "Maximal safe total dosages for topical anesthesia in a healthy 70-kg adult are 300 mg for lidocaine, 150 mg for cocaine, and 50 mg for tetracaine." (Goodman and Gilman Ch 14)
* D. may be metabolised more slowly in patients with liver disease - true: "Cocaine is metabolised by plasma and liver cholinesterases to water-soluble metabolites that are excreted in urine. Plasma choliesterase activity is decreased in parturients, neonates, the elderly, and patients with severe underlying hepatic disease." (Stoelting Pharmacology p 165)
* E. reaches a peak plasma concentration in 3 hours - false: See answer A
PL29 [Aug09]

Ventricular fibrillation (VF) following caudal anaesthesia in 20kg six year old child.
The recommended dose of of Intralipid 20% is:
A. 10mls
B. 20mls
C. 30mls
D. 40mls
E. 50mls
ANSWER C

Dose of Intralipid 20% is 1.5 ml/kg = 30ml

AAGBI guidelines 2010 - Immediately give iv 1.5ml/kg over 1 min and start and iv infulsion of 15 ml/kg/hr
PL30 [Mar10]

Maximum dose (with low risk of toxicity) of lignocaine (with adrenaline 1:100000)
for liposuction with tumescence technique:
A. 3 mg/kg
B. 7 mg/kg
C. 15 mg/kg
D. 25 mg/kg
E. 35 mg/kg
ANSWER E

Tumescent liposuction - Klein noted that the correct maximum safe dose of lidocaine was never investigated but rather extrapolated from procaine. He showed that infusion of lidocaine, by using the tumescent formula of 0.1% lidocaine with 1:1,000,000 epinephrine, into the subcutaneous tissues of a concentration of 35 mg/kg was safe.

The maximum plasma level that was reached at 11-15 hours postoperatively was 0.8-2.7 mcg/mL, well below the toxic level of 5 mcg/mL. Tumescent anesthetic produces a delay in achieving the peak serum lidocaine level and does not produce as high a level compared with conventional local anesthetic.
PL31 Aug10

Time to reach peak plasma concentration after injection of
2% lignocaine with adrenaline into epidural space

A. 20 min
B. 30 min
C. 40 min
D. 50 min
E. 60 min
ANSWER A

CJA. Between 20-30mins. Only took 2 samples though. Could have missed peak. Highest 4.4mcg/ml.

http://www.springerlink.com/content/12727258463u7q30/

Look at Fig 1 in

Anaes & Anal: 1979 58(5); 360-363
PN42b ANZCA Version [2006-Mar] Q125, [Jul06] Q69

When instructing ward staff on monitoring for respiratory depression in a patient
using PCA (patient controlled analgesia) you would advise that early respiratory
depression is best detected by monitoring

A. frequency of boluses on PCA machine
B. pulse oximetry
C. pupil size
D. respiratory rate
E. sedation scores
ANSWER E

These studies confirm that assessment of sedation is a more reliable way of detecting opioid induced respiratory depression, although monitoring respiratory rate is still important"
PC35 ANZCA version [Apr99] [2002-Aug] Q56, [2003-Apr] Q11, [2006-March] Q45, [Jul06] Q30

Side effects of digoxin are increased by

A. hyperthyroidism

B. hypocalcaemia

C. hyperkalaemia

D. hypermagnesaemia

E. hypothyroidism
ANSWER E

hypokalemia, hypomagnesemia, myocardial disease, old age, hypothyroidism, and a variety of other metabolic disturbances (hypoxemia, acid-base abnormalities, hypercalcemia, and hypernatremia
PI77b ANZCA Version [2006-Mar] Q121, [Jul06] Q67

Nitrous oxide anaesthesia may cause all of the following EXCEPT

A. an increased incidence of myocardial ischaemia
B. decreased leukocyte chemotactic response
C. elevation of plasma homocysteine levels
D. megaloblastic anaemia
E. reversible inhibition of methionine synthetase
ANSWER E

A. False

* The ENIGMA trial (currently underway) is out to answer this question

B. True

* "The chemotactic migration of neulrophils and monocytes...a significant depression...was observed with enflurane, halothane, methoxyflurane and nitrous oxide (p < 0.05)...severity of depression of migration was maximal with nitrous oxide" CJA 84(6);631-37

C. True

* Nitrous oxide anesthesia causes increased postoperative plasma homocysteine levels. Acute increases in plasma homocysteine are associated with impaired endothelial function and procoagulant effects. This nitrous oxide-induced plasma homocysteine increase may therefore affect the risk of perioperative cardiovascular events.

D. True

* exposure to nitrous causes megaloblastic changes in the bone marrow

E. FALSE

* the inhibition of methionine synthase is irreversible
PN46 ANZCA version [2006-Mar] Q128, [Jul06] Q83 (NB. PN43b = the same question)

Concerning opioids,

A. fentanyl is the agent of choice for patient controlled analgesia (PCA) in the opioid addicted patient presenting for surgery
B. morphine in therapeutic dosage is a common cause of postoperative confusion
C. pethidine is suitable for subcutaneous injection
D. sufentanil has a higher affinity for the mu receptor than morphine
E. the patient’s age is the best clinical indicator of opioid requirement in the perioperative period
ANSWER ?C

A. FALSE

B. FALSE: Morphine causes confusion in 14% of patients

C. TRUE: MIMs states pethidine can be given SC, most correct answer

D. TRUE: Sufentanil has a high affinity for the mu receptor, higher than any other opioid

E. TRUE: from latest pain book. But it is also dependent on the type of surgery
PN47 ANZCA version [2006-Mar] Q129, [Jul06] Q48

Correct statements concerning naloxone include each of the following EXCEPT

A. appropriate titration of naloxone will allow reversal of opioid induced respiratory depression
B. naloxone is a partial agonist
C. naloxone is most effective at blocking mu receptors
D. serious side effects such as arrhythmias and pulmonary oedema are rare
E. the elimination half-life of naloxone is approximately 60 minutes
ANSWER B

* A True, respiratory depression is mu effect
* B False (so correct answer) naloxone is competitive antagonist
* C True but also some action at delta and kappa
* D True rare, but reported
* E True 1.2 hours
PZ119 ANZCA VERSION [Mar06] Q144, [Apr07], [Jul07]

Fondaparinux Sodium (Arixtra)

A. activates platelet
B. cross reacts with sera from patients with heparin induced thrombocytopaenia
C. has a mechanism of action that is antithrombin (ATIII) dependent
D. is associated with thrombocytopaenia
E. can be safely used in patients with severe renal failure
ANSWER C

* A. activates platelet - false: "Fondaparinux does not inactivate thrombin (activated factor II) and has no effects on platelet aggregation."
* B. cross reacts with sera from patients with heparin induced thrombocytopaenia - false: "It does not cross react with sera from patients with heparin induced thrombocytopenia." (MIMS online)
* C. has a mechanism of action that is antithrombin (ATIII) dependent - true: "Fondaparinux is a synthetic and specific inhibitor of activated factor X (Xa) with no animal sourced components. The antithrombotic activity of fondaparinux is the result of antithrombin III (ATIII) mediated selective inhibition of factor Xa. By binding selectively to ATIII, fondaparinux potentiates (about 300 times) the innate neutralisation of factor Xa by antithrombin. Neutralisation of factor Xa interrupts the blood coagulation cascade and inhibits both thrombin formation and thrombus development." (MIMs Online)
* D. is associated with thrombocytopaenia - false: "To date a causal association between treatment with fondaparinux and the occurrence of HIT has not been established." (MIMS online)
* E. can be safely used in patients with severe renal failure - false: "Fondaparinux is almost completely excreted by the kidney as unchanged compound. The elimination half-life (t1/2) is about 17 hours in healthy young subjects and about 20 hours in healthy elderly subjects." Also "Arixtra is contraindicated in severe renal impairment" (Both from MIMS online)
PI76 ANZCA version [2005-Apr] Q138, [2005-Sep] Q4

When comparing propofol (induction and infusion for maintenance) with desflurane
(propofol induction only) anaesthesia for ambulatory surgery, which statement is INCORRECT?

A. anti-emetic use is higher with desflurane
B. incidence of postoperative nausea is higher with desflurane
C. time to eye opening in recovery is shorter with desflurane
D. time to home readiness is shorter with desflurane
E. time to obeying commands in recovery is shorter with desflurane
ANSWER D

Propofol Versus Desflurane There were 13 studies (2,5,8,25–34) with extractable data that were included in the meta-analysis (Table 2). Time to eye opening was significantly quicker with desflurane compared with propofol (1.3 min), as was the time to obey commands (1.3 min), with significant heterogeneity between the anesthetics (Table 5). No differences were found in home readiness or discharge between the anesthetics. The RR for postoperative complications including PON (NNT, 7) and POV (NNT, 10) was significantly greater with desflurane compared with propofol and the need for antiemetics was also increased with desflurane (RR, 3.9) (Table 5). No other differences were seen between the anesthetics.

Gupta (et al) Comparison of Recovery Profile After Ambulatory Anesthesia with Propofol, Isoflurane, Sevoflurane and Desflurane: A Systematic Review Anesth Analg 2004;98:632–41
PR04 [1985] [Mar95] [Apr97] [Jul97] [Apr98] [Jul98] [2002-Aug] Q11, [2003-Apr] Q39, [Jul05] [Mar06]

The percentage of the population which is heterozygous as regards pseudocholinesterase, thus having a dibucaine number between 30 and 80 is

A. 0.04%

B. 0.4%

C. 4%

D. 14%

E. 40%
ANSWER C

Heterozygous 4%

Homozygous 1:2500 = 0.04%

* "All possible combinations of heterozygotes exist – they constitute 3.8% of the population and remain apnoeic for approximately 10 minutes after receiving suxamethonium." Sasada & Smith, 3d ed., p.368.

* "U: Homozygote Usual (normal), frequency = 96%, UA: Heterozygote Usual/Atypical, frequency = 3%, A: Homozygote Atypical, frequency 1 in 3,000, US : Heterozygote Usual/Silent, frequency = 0.7%, S: Homozygote Silent, frequency 1 in 40,000, AS: Heterozygote Atypical/Silent, frequency 1 in 8,000 (0.0125%). Others rare." National reference laboratory : Pseudocholinesterase, Dibucaine Inhibition. [1]

* "In most Caucasian populations the frequency of occurence of heterozygotes for the normal and atypical genes is about 1 in 25, and the frequency of homozygotes for the atypical gene is about 1 in 2500. The atypical gene is rare in orientals and African blacks." Pantuck EJ: Plasma cholinesterase: Gene and variations. Anesth Analg 77:380-386, 1993

* "In addition, heterozygotes with one normal and one abnormal gene (5% of the population) with dibucaine number of 40-60 may show prolonged paralysis of about 10-20 min." Yentis, 3rd ed., p.117.
PR56 ANZCA version [March 2006] Q97

The duration of action of suxamethonium may be increased by
A. betamethasone
B. bleomycin
C. carvedilol
D. neostigmine
E. all of the above
ANSWER D

Increases phase II block.
PC35 ANZCA version [Apr99] [2002-Aug] Q56, [2003-Apr] Q11, [2006-March] Q45, [Jul06] Q30

Side effects of digoxin are increased by

A. hyperthyroidism
B. hypocalcaemia
C. hyperkalaemia
D. hypermagnesaemia
E. hypothyroidism
ANSWER E

UpToDate:

* Predispose to toxicity: advanced age, certain cardiac diseases (active ischemia, myocarditis, cardiomyopathy, cardiac amyloidosis, cor pulmonale) and metabolic factors (hypokalemia, hypomagnesemia, hypoxemia, hypernatremia, hypercalcemia, and acid-base disturbances)
* In acute cardiac glycoside toxicity, hyperkalemia is an ominous sign and a predictor of morbidity and mortality. Hyperkalemia means much more severe blockade of Na/K ATPase and K is extracellular.
PI80 ANZCA version [2005-Sep] Q109, [Mar06] Q83, [Apr07] Q26 [Jul07]

The MAC (Minimum Alveolar Concentration) of volatile anaesthetics is DECREASED by

A. hypercarbia (pCO2 55 mmHg)
B. hypernatraemia
C. hyperthermia
D. lithium
E. tricyclic antidepressants
ANSWER D

Decrease MAC
Nitrous oxide
Hypothyroid/myxoedema
Hypocapnia
Hypothermia-decrease is roughly linear
Hyponatraemia
Increasing age - (MAC Hal < 3 months ~ 1.1 % MAC Hal > 60 years ~ 0.64 %)
Hypoxaemia
Hypotension
Anaemia
Pregnancy
CNS depressant drugs - opioids, benzodiazepines, major tranquilizers, TCA's
Other drugs - lithium, lidocaine, magnesium, methyl dopa, clonidine
Acute alcohol abuse
IC77 ANZCA version [2005-Sep] Q115, [Apr07] Q84, [Jul07]

The signs of exposure to a nerve agent such as Sarin or VX include

A. bronchodilation
B. dry skin
C. muscle fasciculation
D. pupillary dilatation
E. tetany
ANSWER C

Inhibition of acetylchonlinesterase

Causing a cholinergic crisis

People exposed to a low or moderate dose of VX by inhalation, ingestion (swallowing), or skin
absorption may experience some or all of the following symptoms within seconds to hours of
exposure:
* Runny nose
* Watery eyes
* Small, pinpoint pupils
* Eye pain
* Blurred vision
* Drooling and excessive sweating
* Cough
* Chest tightness
* Rapid breathing
* Diarrhea
* Increased urination
* Confusion
* Drowsiness
* Weakness
* Headache
* Nausea, vomiting, and/or abdominal pain
* Slow or fast heart rate
* Abnormally low or high blood pressure
# Even a tiny drop of nerve agent on the skin can cause sweating and muscle twitching where the
agent touched the skin.
# Exposure to a large dose of VX by any route may result in these additional health effects:
* Loss of consciousness
* Convulsions
* Paralysis
* Respiratory failure possibly leading to death
PZ26 ANZCA version [1988] [Mar91] [2002-Aug] Q43, [2003-Aug] Q76, [2004-Apr] Q46, [Mar06], [Jul06] Q9

The antibiotic LEAST likely to be effective for the management of anaerobic
peritonitis is

A. carbenicillin
B. cefoxitin
C. cephalothin
D. chloramphenicol
E. clindamycin
ANSWER C - Cephalothin

Bacteroides fragilis and Clostridium perfringens are commonly implicated in anaerobic infections. Both these bugs are sensitive to cefoxitin, clindamycin and chloramphenicol and demonstrate some sensitivity to carbenicillin.

(B. fragilis is resistant to cephalothin and C. perfringens has variable sensitivity.)
PZ114 ANZCA version [2004-Aug] Q121, [2005-Jul] Q137 [2006-Mar] Q91

Regarding glycoprotein IIb/IIIa antagonists, which of the following statements is INCORRECT?

A. platelet dysfunction persists for over 48 hours after cessation of drug
B. their effects may be monitored by use of a platelet turbidometry aggregometer
C. they are known to cause severe thrombocytopaenia in some patients
D. they are used to treat acute coronary syndromes
E. they block fibrinogen binding to platelet glycoprotein IIb/IIIa receptors
ANSWER A

* A - False (THUS THE CORRECT ANSWER). With regard to abciximab: "ReoPro remains in the circulation for 15 days or more in a platelet bound state, although platelet function recovers over the course of 48 hours." AND "As patients receiving abciximab experience platelet dysfunction for 12–24 h after termination of the infusion, it would seem prudent that surgery should be delayed for at least 12–24 h after abciximab if the patient’s cardiac status permits. Surgery should be delayed for 4–6 h to reduce the risk for increased bleeding in patients who have received eptifibatide or tirofiban." Anesthesiology 2002; 96:1237–49 (P. Kam) BUT It has a plasma half-life of 20 minutes but remains bound in the circulation for up to 15 days with some residual activity." Peck, Hill & Williams, 2nd. ed., p.339 AND Table 27.6 in Stoelting 4th. ed., p.518 showing that abciximab has to be stopped 72 hours before surgery.
* B - True. "The pharmacological effects of GP IIb/IIIa antagonists can be assessed in a number of different ways. The most widely used method is turbidometric aggregometry..." Scarborough et al., GP IIB/IIIa Antagonists. Circulation 1999;100;437-444.
* C - True. "In 0.1–0.5% of patients, severe thrombocytopenia occurs after intravenous administration of glycoprotein IIb/IIIa inhibitors in the nonsurgical setting. Abciximab causes thrombocytopenia in 0.4–1.6% patients, and this can occur after a single dose. In trials with other glycoprotein IIb/IIIa antagonists, the incidence of thrombocytopenia is generally lower than 1%. Thrombocytopenia usually occurs within hours of exposure and resolves on discontinuation of the drug, rarely requiring platelet transfusion unless accompanied by active bleeding." Anesthesiology 2002; 96:1237–49 (P. Kam)
* D - True. "The efficacy of the glycoprotein IIb/IIIa antagonists in the treatment of acute coronary syndromes (unstable angina and non–Q wave MI), MI, and percutaneous coronary interventions has been demonstrated in several multicenter trials." Anesthesiology 2002; 96:1237–49 (P. Kam)
* E - True. "Eptifibatide (a smaller molecule compared with abciximab) binds to the glycoprotein IIb/IIIa receptor between the IIb and IIIa arms of the extracellular parts of the receptor and prevents binding of fibrinogen." AND "Tirofiban occupies a binding pocket on the glycoprotein IIb/IIIa receptor and competitively inhibits platelet aggregation mediated by fibrinogen and von Willebrand factor." Anesthesiology 2002; 96:1237–49 (P. Kam)
PZ45b ANZCA version [2001-Aug] Q5, [2003-Aug] Q34, [2004-Apr] Q30, [Mar06] Q17

When used to prevent aspiration pneumonitis

A. ranitidine has a similar onset time and a shorter duration of action than cimetidine
B. anticholinergic drugs increase gastric acidity and increase lower oesophageal sphincter tone
C. non-particulate antacids have a longer duration of action than particulate antacids
D. metoclopramide increases the lower oesophageal sphincter tone but relaxes the pyloric sphincter
E. suxamethonium reduces the barrier pressure in most adults
ANSWER D

For the ANZCA version, D is the best answer.

As regards the other options:

* A: Ranitidine has a LONGER duration (10-12hrs) than cimetidine (4-8hrs) although onset times are similar (1-2hs). (Morgan and Mikhail p244)
* B: Anticholinergic drugs DECREASE gastric acidity.
* C: Non-particulate antacids have a MORE rapid action and shorter duration than particulate antacids (Morgan & Mikhail pg 245)
* E: Suxamethonium increases LOP pressure AND intragastric pressure such that barrier pressure is little affected. (Peck & Williams)


LOS tone increased by:

* metoclopramide
* domperidone
* neostigmine
* pancuronium

and decreased by:

* anticholinergics
* opioids
* volatile anaesthetics
* most IV anaesthetics
* ganglion blocking drugs

and unaffected by:

* H2 receptor blockers

Suxamethonium increases intragastric pressure but also increases LOS tone so that barrier pressure is maintained

Ref: Yentis p322

* Cimetidine: onset 1-2hrs, duration 4-8hrs;
* Ranitidine: onset 1-2hrs, duration 10-12hrs (Morgan & Mikhail pg 244)

Non particulate antacids mix more rapidly with gastric contents and lose effectiveness within 30-60 minutes. (Morgan & Mikhail p245)

Maxolon increases the tone and amplitude of gastric (especially antral) contractions, relaxes the pyloric sphincter and the duodenal bulb, and increases peristalsis of the duodenum and jejunum resulting in accelerated gastric emptying and intestinal transit. It increases the resting tone of the lower oesophageal sphincter. It has little, if any effect on the motility of the colon or gall bladder. MIMS
PZ53c ANZCA version [Apr97] [Jul97] [Apr98] [Apr99] [Aug99][2001-Aug] Q11, [2002-Mar] Q5, [2003-Aug] Q5, [2004-Apr] Q25, [2005-Sep] Q12, [Mar06] Q10

Nitric oxide, when used as supportive treatment for adult respiratory distress syndrome,

A. potentiates the effect of the endothelial releasing factor in the lungs
B. must be given by inhalation as it is rapidly metabolised by leucocytes
C. may cause systemic hypotension when administered in a concentration of about 40 ppm
D. must be administered continuously as the effect lasts only about 30 minutes
E. will reduce the venous admixture when administered in a concentration of 20 ppm
ANSWER E

A. False. Nitric Oxide (NO) is EDRF. Potentiate means one drug increases the action of another

B. False. NO is metabolised by Oxy-Hb

C. False. Stuedal et al "pulmonary vasoldilatation in the absence of systemic vasodilatation has been confirmed in numerous subsequent studies" p1096 - also confirmed in Miller p2815.

D. False. The effect lasts seconds, not minutes

E. True. All kinds of doses have been tried but 20ppm will do it. Stuedal at al "Inhaling 18ppm NO for 40min reduced the shunt fraction by 5% and increased the PaO2/FiO2 ration by 30% in patients with ARDS" p1102


NITRIC OXIDE
* Synthesized from l-arginine by NOS.
* Increases cGMP leading to smooth muscle relaxation.
* t1/2 of 4-40 secs
* Combines with Hb to form MetHb

* Usual dose in adults 1-40ppm
* Hypotension is not usually a significant problem
* NO2 and MetHb are usually the dose limiting factors
* In the body, nitric oxide (the 'endothelium-derived relaxing factor', or 'EDRF') is synthesized from arginine and oxygen by various nitric oxide synthase (NOS) enzymes and by sequential reduction of inorganic nitrate. Arginine is converted to citrulline by NOS. NO is a free radical. Nitric oxide can contribute to reperfusion injury when excessive nitric oxide produced during reperfusion (following a period of ischemia) reacts with superoxide to produce the damaging free radical peroxynitrite.
PZ120 [Mar06] Q134

Gabapentin used for acute postoperative pain

A. has its analgesic effect reduced by concurrent use of COX-2 inhibitors
B. increases anxiety if administered preoperatively
C. may require high doses to be effective
D. reduces the incidence of dizziness when compared with opioids alone
E. works by binding at GABA receptors
ANSWER C

A - sounds like nonsense

B - incorrect, it is an anxiolytic.

C - Doses of 300mg reduced morphine consumption post-op in this study Acta Anesthesiogica Scandanavica Volume 48 Issue 3, Pages 322 - 327. However the same (and clearly the ref for this Q) BJA editorial states "Unfortunately, it may be that smaller doses are ineffective."

D - When used with PCEA in the BJA study (ref below) "There was a significant increase in the incidence of dizziness (35% vs 5%) and a non-significant increase in somnolence (25% vs 10%)". But no mention of PCA. Could it be the examiners did not read the article poperly?

E - BJA ref below says this is not its bag, "despite its name gabapentin does not bind at the GABAA or GABAB receptor."
PZ121 ANZCA Version [2006-Mar] Q114, [Jul06] Q68

In elderly patients each of the following statements is true EXCEPT

A. antagonism of neuromuscular blockade with aniticholinesterases is
less likely to be effective than in the younger patient
B. atropine produces a lesser heart rate response than in younger patients
C. ephedrine is less likely to be effective (at raising blood pressure)
than in the younger patient
D. MAC of all inhalational agents is reduced by 20 to 40%
E. time of onset of neuromuscular blockade is prolonged due to a reduction in cardiac output
ANSWER A

* A - Antagonism of neuromuscular blockade with anticholinesterase drugs tends to be similar to younger adults FALSE, hence is THE CORRECT ANSWER
* B - This relatively poor response to b-stimulation also results in the reduced heart rate response to atropine TRUE
* C - Ageing is associated with reduced b-receptor sensitivity, which results in a reduction in response to exogenous b-agonists TRUE
* D - The MAC value of all inhalational anaesthetic agents is reduced by 20–40% from young adult values TRUE
* E - regarding NDMR, time of onset ... prolonged because of a reduction in cardiac output TRUE
PZ122 ANZCA version [2006-Mar] Q132

Ginseng (Panax Ginseng) has been associated with an increased risk of each of the following EXCEPT

A. agitation with concurrent mono amine oxidase inhibitors
B. bleeding with concurrent aspirin
C. brochospasm
D. hypoglycaemia in fasting patients
E. Stevens-Johnson syndrome
ANSWER C

SIDE EFFECTS OF GINSENG
-Stevens Johnson
-Hypertension
-Hypoglycaemia
-Bleeding
-Mania with MAOI
PZ78b ANZCA version [2001-Apr] Q34, [2004-Aug] Q53, [2005-Apr] Q40, [Mar06]

When paracetamol is used in infants and children,

A. a dose of 10 mg.kg-I is more effective than placebo for relief of symptoms of tonsillitis
B. the bioavailability of rectal suppositories is less than 50% of that from an equivalent oral dose
C. a rectal loading dose of 45 mg.kg-I will reliably produce therapeutic plasma levels with a peak concentration after 1 hour
D. the elimination half life is 2 - 2.3 hours
E. a far greater proportion of unmetabolised paracetamol is excreted by the kidney, compared to adults
ANSWER D
PZ86d ANZCA Version [Mar06]Q96 | [Jul06]Q20 | Aug10

Each of the following herbal treatments is associated with an increased risk of
perioperative bleeding EXCEPT

A. garlic
B. ginger
C. ginko
D. ginseng
E. St John's Wort
ANSWER E

St John's wart NOT assoc with coagulopathy. Ginseng DOES increase risk of bleeding, so actually 4 G's do this - ginseng, gingko, ginger, garlic.
PZ86b ANZCA version [2004-Apr] Q129, [2004-Aug] Q13

The herbal medicine associated with enhanced bleeding is

A. echinacae
B. ginko
C. golden seal
D. kava-kava
E. St. John's wort
ANSWER B

* A. echinacae - false: "Echinacea appears to have a favourable adverse effects profile [9, 23]. Although echinacea preparations contains pyrrozolidine alkaloids [24], hepatotoxicity is unlikely because these alkaloids are structurally different from the pyrrozolidine alkaloids known to be hepatotoxic [12, 25]. Adverse effects include unpleasant taste, gastro-intestinal upset, headache and dizziness."
* B. ginko - true: "Danshen, dong quai, jui, ginkgo biloba and garlic have anticoagulant effects and therefore increase the risk of bleeding during surgery."
* C. golden seal - false: "Effects on Bleeding: None reported" (Uptodate: Golden seal (Hydrastis canadensis): Natural drug information)
* D. kava-kava - maybe: "The herb may also affect platelets in an antithrombotic manner by inhibiting cyclo-oxygenase" (Curr Opin Anaesthesiol. 2007 Aug;20(4):294-9.)
* E. St. John's wort - false: "In vitro studies have demonstrated that St John's Wort decreases the efficacy of warfarin by this mechanism [106]. A decreased anticoagulant effect of warfarin associated with concomitant use of St John's Wort has been recorded [103]. Therefore, INR should be closely monitored when starting or stopping St John's Wort" (Anaesthesia Volume 57, Issue 9, 2002. Pages: 889–899)
PZ86c ANZCA version [2005-Apr] Q109

Correct statements regarding complementary and alternative medications include

A. ginger is a superior antiemetic to metoclopramide
B. ginseng and ephedra may produce cardiovascular complications during general anaesthesia
C. ginseng and ephedra may potentiate the analgesic properties, but not the bleeding
side-effects, of the non-steroidal anti-inflammatory drugs (NSAIDS)
D. it is generally recommended that patients can continue these medications perioperatively
E. St. John's Wort is associated with acute tubular necrosis perioperatively
ANSWER B

* A. ginger is a superior antiemetic to metoclopramide - false:
o "Ernst and Pittler performed a systematic review of the evidence from six double-blind, randomised, placebocontrolled studies of the efficacy of ginger in preventing nausea and vomiting [87]. Of the three studies on PONV, two studies suggested that ginger is equally effective as metoclopramide, and is superior to placebo. However, the pooled absolute risk decrease for the incidence of PONV indicated that there was no significant difference between ginger and the placebo groups. A recent doubleblind, randomised, placebo-controlled trial, which was not included in Ernst’s systematic review, concluded that ginger was not effective in decreasing the incidence of PONV after day-case gynaecological laparoscopy" (Anaesthesia, 2002, 57, pages 889–899)
* B. ginseng and ephedra may produce cardiovascular complications during general anaesthesia - true:
o "Furthermore, because of ginseng’s association with hypertension and the deleterious outcomes linked to chronic hypertension, the anesthesiologist should be aware of whether and for how long patients may have been taking this herbal product. Many anesthetic agents can cause generalized vasodilation, and so hemodynamic lability may be observed." (Current Opinion in Anaesthesiology 2007, 20:294–299)
o "Ephedra contains alkaloids such as ephedrine, pseudoephedrine, methylephedrine and norpseudo-ephedrine, obtained from the roots and branches of a shrub native to central Asia [79]. Ephedrine is the predominant active component and is a non-catecholamine sympathomimetic agent that acts directly and indirectly at alpha- and betaadrenergic receptors, causing increased blood pressure and heart rate, relaxation of bronchial and gastrointestinal smooth muscle, central nervous system stimulation and mydriasis." (Anaesthesia, 2002, 57, pages 889–899)
* C. ginseng and ephedra may potentiate the analgesic properties, but not the bleeding side-effects, of the non-steroidal anti-inflammatory drugs (NSAIDS) - false
* D. it is generally recommended that patients can continue these medications perioperatively - false:
o "Currently, the American Society of Anaesthesiologists recommends that patients cease herbal medicines at least 2 weeks before surgery" (Anaesthesia, 2002, 57, pages 889–899)
* E. St. John's Wort is associated with acute tubular necrosis perioperatively - false
PZ101 ANZCA version Mar06 Q146

Regarding Placebos

A. for every intervention, a fixed fraction of the population responds to placebo, whatever the outcome
B. randomisation of different numbers of patients to active and placebo groups can affect the response to placebo
C. the more invasive the method of delivering a treatment, the higher the response to placebo
D. The placebo effect can be eliminated by using active treatments in both study groups
E. the placebo response is a fixed fraction of the maximum effect of treatment
ANSWER D

Common misconceptions about the response to placebo:

Misconception 1: for every intervention, a fixed fraction of the population, usually a third, responds to placebo, whatever the outcome

Misconception 2: the placebo response is a fixed fraction (about a third) of the maximum effect of treatment—the bigger the treatment effect the bigger the placebo response

Misconception 3: the more invasive the method of delivering a treatment, the higher will be the response to placebo—injection will give bigger response than tablets

Misconception 4: randomisation of different numbers of patients to active and placebo can affect the response to placebo
PZ102 ANZCA version [2005-Sep] Q122, [Mar06] Q27

Clopidogrel

A. acts via the glycoprotein IIb/IIIa receptors on platelets
B. binds reversibly to its receptor on the platelet
C. blocks thrombin mediated platelet activation
D. inhibits ADP induced platelet activation
E. is inhibited by concurrent aspirin usage
ANSWER D
PZ103 ANZCA version [2005-Sep] Q140, [Mar06] Q70 [Aug10]

Intravenous paracetamol

A. has a volume of distribution of 10 l.kg-1
B. is excreted 20% unchanged
C. is highly protein bound
D. is mainly excreted in the gut
E. results in similar late plasma concentrations as oral paracetamol
ANSWER E

Distribution 1L/kg
Metabolism liver via 2 major pathways glucuronic acid and sulfuric acid conjugation
-4% by cytochrome P450
-rapidly detoxified by reduced glutathione
Elimination mainly excreted in the urine
-60% as glucuronide
-20% sulfate conjugates
-<5% unchanged
-Plasma 1/2 life 2.7 hour
-Clearance 18L/hour
PZ107 [Mar06] Q149, [Jul06] Q96

In patients with renal impairment, doses of all of the following
may require adjustment EXCEPT

A. carbamazepine
B. gabapentin
C. hydromorphone
D. morphine
E. oxycodone
ANSWER B
PZ112 ANZCA version [2004-Apr] Q105, [Mar06] Q131, [Jul06] Q2

Hepatotoxicity from paracetamol overdose is enhanced in

A. chronic renal failure
B. concomitant ingestion of benzopdiazepines
C. conditions associated with glutathione deficiency
D. obese patients
E. patients with hepatitis C antibody
ANSWER C
PL26 ANZCA Version Jul06 Q111

In severe bupivacaine toxicity, drugs likely to improve the cardiac conduction abnormalities
include

A. clonidine
B. lignocaine
C. ketamine
D. metoprolol
E. propofol
ANSWER ?A

Outdated question

Management

* Oxygenation/ventilation and good CPR to prevent acidosis.
* Defibrillation, adrenaline or vasopressin (vasopressin better).
* Best option would be 1ml/kg intralipid 20% x 3 doses q3min + infusion of 0.25ml/kg/hr as per A&IC.
* Cardiopulmonary bypass or intraaortic ballon pump.
* Amiodarone forms part of the current ACLS guidelines and has a non-significant trend to improved survival in piggies.
* Lignocaine has been reported but I can't find a reference and Miller says not to.
* Propofol is useful in early toxicity as may prevent seizures, but should not be used for treatment of arrhythmia or in severe cv collapse because the amount of lipid in propofol is low and the total propofol dose required would cause severe CVS impairment. Better to give Intralipid as that is the therapeutically effective agent.
PL28 ANZCA version [2004-Apr] Q137, [2004-Aug] Q59, [Jul 06] Q41

Intra-nasal topical cocaine used in nasal surgery

A. has a duration of action of the order of 6 hours
B. is metabolised more quickly by the liver if the patient is using ecothiopate eye drops
C. is typically used in a dose of approximately 5 ml of 5% solution in an adult
D. may be metabolised more slowly in patients with liver disease
E. reaches a peak plasma concentration in 3 hours
ANSWER D

A. FALSE: Intranasal adminstration: onset in 3-5min, peak at 10-20min, rarely last >1 hour

B. FALSE: ecothiopate is a plasma cholinesterase inhibitor, cocaine is metabolised extensively by the liver, only 1% excreted unchanged in the urine

C. FALSE: max dose is 3mlkg (150mg is typical adult dose)

D. TRUE: Cocaine is metabolised by plasma and liver cholinesterases to water-soluble metabolites that are excreted in urine. Plasma choliesterase activity is decreased in parturients, neonates, the elderly, and patients with severe underlying hepatic disease.

E. FALSE: Peak venous plasma concentration in 30-40 minutes after IN adminstration
PZ65b ANZCA version [2003-Apr] Q113, [Jul06] Q52, [Apr07] Q113 Aug10

To normalise platelet function prior to surgery, chronic diclofenac therapy
should be ceased for at least

A. 12 hours
B. 1-2 days
C. 4 days
D. 7 days
E. 10 days
ANSWER A or B depending on the formulation

* A. would seem appropriate for rapidly absorbed formulations
* B. would seem appropriate for slow-release formulations


Elimination t1/2 of diclofenac ("Voltaren") is 1.1-1.8 hours therefore stop for 1-2 days preop is adequate.

* However, diclofenac is often taken as a 'SR' preparation which delays absorption significantly. It's effects last much longer than the plasma t1/2 in these people. --lovethedrugs 23:33, 17 Jun 2008 (EDT)

* The reason diclofenac has such a short half-life is its high hepatic metabolism. Other NSAIDs (except for aspirin) have low rates of hepatic metabolism.

* The other important point to make here is that the inhibition of cyclo-oxygenase (COX) by diclofenac is reversible. In contrast the inhibition of COX by aspirin is irreversible so even with its short half-life, you have to wait longer for the effect of aspirin to be reversed (ie needs production of sufficient amounts of new platelets with newly synthetised COX.
PZ79b ANZCA version [2003-Aug] Q105, [2004-Apr] Q69, [Jul06] Q54, [Apr07] Q105

Features of paracetamol administration in children include

A. limitation of the daily dose to a maximum of 150 mg.kg-1 because of the risk of hepatotoxicity
B. reliable absorption when administered rectally with most patients achieving a therapeutic
concentration with a loading dose of 20 mg.kg-1
C. peak blood levels being reached approximately 1 hour following rectal administration
D. a one hour delay between peak plasma concentration and maximum analgesia
E. a faster absorption of high dose rectal paracetamol compared to oral
ANSWER D

Rectal administration may be erratic and prolonged.

Therapeutic plasma concentrations (>10mcg/mL) are rarely achieved with a rectal loading dose of 20mg/kg but more commonly achieved with a rectal loading dose of 40-60mg/kg.

Peak plasma levels following rectal administration are at 2.6hrs and following oral administration at 1.6-1.9 hrs.

Rectal absorption is thus slower than oral absorption.

Toxicity occurs with plasma levels greater than 120mg/ml.

The maximum daily dose of oral paracetamol is 90-100mg/kg because at 150mg/kg hepatotoxicity
has occurred. The maximum daily dose for rectal paracetamol has not been elucidated in children
PZ104 ANZCA Version [Jul06] Q37

Established Legionnaires disease is best treated with

A. Aminoglycosides
B. Cephalosporins
C. Chloramphenicol
D. Crystalline penicillin
E. Erythromycin
ANSWER E
PZ105 ANZCA Version [Jul06] Q117

In morbidly obese patients drugs can be administered on a per kilogram of total body weight (TBW)
or a per kilogram of ideal body weight (IBW) basis. It is correct to say,

A. atracurium should be administered on an IBW basis
B. induction dose of propofol should be administered on an IBW basis
C. induction dose of thiopentone should be administered on a TBW basis
D. suxamethonium should be administered on a TBW basis
E. vecuronium should be administered on a TBW basis
ANSWER D

HIGHLY LIPOPHILIC DRUGS :
↑ VD IN OBESE. DRUG DOSES CALCULATED ON THE BASIS OF PATIENT’S TOTAL BODY WEIGHT (TBW):
THIOPENTAL, PROPOFOL, BENZODIAZEPINES, FENTANY, SUFENTANYL, DEXMEDETOMIDINE, SUCCINYLCHOLINE, ATRACURIUM AND CISATRACURIUM

WEAKLY LIPOPHILIC OR LIPOPHOBIC DRUGS :

UNCHANGED VD. DRUGS DOSES ARE CALCULATED ON BASIS OF THE PATIENT’S LEAN BODY WEIGHT (LBW)
= IDEAL BODY WEIGHT (IBW) + 20% TO 40%
IBW: ALFENTANYL, KETAMINE, VECURONIUM,ROCURONIUM AND MORPHINE

EXCEPTION : LIPOPHILIC DRUGS WITH UNCHANGED VD:

REMIFENTANYL DOSES ACCORDING TO LBW
reference yao and artusiao-gb
PZ108 ANZCA Version [Jul06] Q138

A patient with bipolar disorder presents for elective laparoscopic cholecystectomy. She takes
lithium and has therapeutic blood levels. The lithium

A. may increase her requirement for volatile anaesthetic agents
B. may prolong the duration off depolarising muscle relaxants
C. may prolong the duration of non-depolarising muscle relaxants
D. may prolong the duration of both depolarising and non-depolarising muscle relaxants
E. should be ceased 2 weeks pre-operatively
ANSWER D

A. FALSE: reduced MAC

D. TRUE: most correct answer

E. FALSE: may precipitate rebound depression and should not be stopped perioperatively
PZ109 ANZCA Version [Jul06] Q134

When using NSAIDs (non-steroidal anti-inflammatory drugs) and COX-2 (cyclo-oxygenase 2) inhibitors
for postoperative analgesia,

A. COX-2 inhibitors are more effective analgesics than NSAIDs
B. COX-2 inhibitors have less effect on renal function than NSAIDs
C. COX-2 inhibitors impair platelet function
D. COX-2 inhibitors trigger aspirin induced respiratory disease with a similar likelihood to NSAIDs
E. NSAIDS increase the risk of peri-operative bleeding after some types of surgery
ANSWER E

* A - False. COX-2 inhibitors are as effective as NSAIDs for postop pain...NNT's comparable with those for conventional NSAIDs for the treatment of mod-severe acute pain (APMSE 2005 Section 4.2.3)--Anaestheasy Tiger 01:15, 27 Jun 2009 (EDT)
* B - False. "Renal and cardiovascular effects of COX-2 inhibitors are similar to conventional NSAIDs." Stoelting, 4th. ed., p.281.
* C - False. "These drugs (COX-2 inhibitors) lack effects on platelets at therapeutic doses and may be associated with decreased gastrointestinal side effects in patients with arthritis, compared with nonspecific NSAIDs." and "COX-2 inhibitors have no effect on platelet aggregation, bleeding time or postoperative blood loss." Stoelting, 4th. ed., p.277 & 281. Also "COX-2 inhibitors do not impair platelet function; this leads to reduced perioperative blood loss in comparison with NSAIDs (level II - APMSE 2007 update)
* D - False. "A history of asthma exacerbation on exposure to aspirin is a reason to avoid NSAIDs that inhibit COX-1 and COX-2. Nevertheless, the COX-2 inhibitor rofecoxib may be safe in aspirin-sensitive patients." Stoelting, 4th. ed., p.282.
* E - True. "Preoperative NSAID therapy significantly increases intraoperative and postoperative blood loss in children undergoing tonsillectomy."Stoelting, 4th. ed., p.281, and "aspirin and some NSAIDs increase the risk of perioperative bleeding after tonsillectomy, except in paediatric patients. (level I (Cochrane Review) - APMSE update 2007)
PZ111 ANZCA version [2003-Aug] Q28, [2004-Apr] Q36

Lower oesophageal sphincter tone is increased by
A. suxamethonium
B. pancuronium
C. metoclopramide
D. prochlorperazine
E. ergometrine
ANSWER A
PZ126 ANZCA Version [2006-Mar] Q133 [2006-Jul] Q6

Transient Neurological Syndrome

A. comprises pain localised to the back
B. diagnosis is confirmed by typical findings on neurological examination
C. is associated with consistent abnormalities on magnetic resonance imaging and
electrophysiological studies (EPS)
D. is associated with long term deficits in 5% of cases
E. may occur with lignocaine, bupivacaine, prilocaine and procaine
ANSWER E

* A. comprises pain localised to the back - false: "Follow-up of patients who received uncomplicated spinal anesthesia revealed that some of them developed pain in the lower extremities—transient neurologic symptoms (TNS)" (A & A June 2005 vol. 100 no. 6 1811-1816)
* B. diagnosis is confirmed by typical findings on neurological examination - false: "In contrast to the lower extremity weakness and bowel and bladder dysfunction observed with cauda equina syndrome (8), neurologic examination, magnetic resonance imaging, and electropathological testing show no abnormalities in patients with TNS"
* C. is associated with consistent abnormalities on magnetic resonance imaging and electrophysiological studies (EPS) - false: See B
* D. is associated with long term deficits in 5% of cases - false: "There was no evidence that this painful condition was associated with any neurologic pathology; in all patients, the symptoms disappeared spontaneously by the 10th postoperative day."
* E. may occur with lignocaine, bupivacaine, prilocaine and procaine - true: "The relative risk for developing TNS after spinal anesthesia with lidocaine was higher than with other local anesthetics (bupivacaine, prilocaine, procaine, and mepivacaine)"
PV13 [Mar93] [Aug96] [Aug99] [Mar00] [Jul00] [Apr07] [Jul07]

A ‘sleep dose’ of thiopentone in a healthy adult is likely to result in:
A. A fall in peripheral resistance followed by a rise in cardiac output
B. A fall in cardiac output followed by a rise in peripheral resistance
C. A fall in peripheral vascular resistance followed by a fall in cardiac output
D. A rise in peripheral vascular resistance followed by a fall in cardiac output
E. A fall in cardiac output followed by a fall in peripheral vascular resistance
ANSWER C

From Miller

The primary cardiovascular effect of barbiturate induction is peripheral vasodilation resulting in pooling of blood in the venous system.[344] A decrease in contractility is another effect and is related to reduced availability of calcium to myofibrils. In addition, the heart rate is increased.[343] Mechanisms for the decrease in cardiac output include (1) direct negative inotropic action, (2) decreased ventricular filling because of increased capacitance, and (3) transiently decreased sympathetic outflow from the CNS.[332][345] The increase in heart rate (10% to 36%) that accompanies thiopental administration probably results from baroreceptor-mediated sympathetic reflex stimulation of the heart in response to the drop in output and pressure. Thiopental produces dose-related negative inotropic effects that appear to result from a decrease in calcium influx into the cells with a resultant diminished amount of calcium at sarcolemma sites. The cardiac index is unchanged or reduced, and mean arterial pressure is maintained or slightly reduced. Thiopental infusions and lower doses tend to be accompanied by smaller hemodynamic changes than those noted with rapid bolus injections. In the dose ranges studied, no relationship between plasma thiopental level and hemodynamic effect has been found. A sympathetic discharge in response to intubation increases the heart rate and blood pressure and can be attenuated by the administration of fentanyl (1 to 3 µg/kg)."
PN22 [Apr99] [Aug99] [Apr07] Q34, [Jul07]

Norpethidine toxicity
A. Is only seen if renal function is abnormal
B. Develops because the half life of norpethidine is twice that of pethidine
C. Is not seen unless treatment is prolonged
D. only seen if dose of pethidine in excess of 1.2g/day
E. May manifest early as anxiety and mood changes
ANSWER E

* A. Is only seen if renal function is abnormal - false
* B. Develops because the half life of norpethidine is twice that of pethidine - maybe: "Although the elimination half-life of pethidine varies from 3 to 6 h, that of norpethidine is around 17 h in healthy patients, but it may be much longer if renal function is compromised."
* C. Is not seen unless treatment is prolonged - false: "Numerous cases of seizures have been reported in patients receiving pethidine over a period of days or in some cases only hours."
* D. only seen if dose of pethidine in excess of 1.2g/day - false
* E. May manifest early as anxiety and mood changes - true: "toxic side effects such as seizures, agitation, irritability, tremors, twitches and myoclonus"
PR43 [Mar93] [Apr07]

Plasma clearance of non-depolarising muscle relaxants in pregnant patients (when compared with matched non-pregnant controls) is:

A. reduced because the distribution half-life is prolonged due to the increased circulating blood volume in late pregnancy
B. reduced because the elimination half-life is prolonged due to delayed hepatic & renal clearance brought about by hormonal changes in pregnancy
C. increased because the distribution half-life is shortened due to changes in cardiac output in pregnancy
D. increased because the elimination half-life is shortened due to increased hepatic and renal clearance brought about by hormonal changes in pregnancy
E. increased because the distribution half-life is shortened due to the placental transfer of the relaxant to fetal & placental tissue.
ANSWER D
PZ81a ANZCA version [2001-Apr] Q48, [2004-Aug] Q71, [2005-Apr] Q32, [Jul07]

Expected adverse drug effects in a geriatric population receiving a high dose
of a selective serotonin reuptake inhibitor for depression would include all
of the following EXCEPT

A. hyponatraemia caused by inappropriate secretion of ADH
B. impairment of platelet aggregation caused by depletion of 5HT (serotonin) stores
C. withdrawal symptoms characterised by anxiety, agitation and increased sweating
D. sedation, dry mouth, orthostatic hypotension and cardiac conduction defects
E. gastro-intestinal effects (nausea, vomiting, diarrhoea)
ANSWER D

The SSRIs do NOT cause sedation, dry mouth, orthostatic hypotension and cardiac conduction defects, all of which are seen with the tricyclics." (Selective serotonin reuptake inhibitors Pharmacology and clinical implications in anaesthesia and critical care medicine in Anaesthesia Volume 52, Issue 10, Date: October 1997, Pages: 982-988)
PZ80d ANZCA version [2002-Aug] Q44, [2003-Apr] Q27, [Jul06] Q32

The plasma half-life of low molecular weight heparin is

A. increased in conditions with raised plasma proteins
B. 2 to 4 times that of unfractionated heparin
C. much less predictable than unfractionated heparin
D. dependent upon a saturatable mechanism for clearance
E. longer than unfractionated heparin because of a higher affinity for plasma protein
ANSWER B
PC43 [2004-Apr] Q122, [2004-Aug] Q67, [Jul07]
The peri-operative use of beta-adrenergic antagonists
A. exerts a cardioprotective effect entirely by reduction of heart rates
B. is best started intra-operatively
C. is contraindicated in patients with chronic airways limitation
D. is contraindicated in patients receiving angiotensin converting enzyme inhibiting drugs (ACE inhibitors)
E. is safe in patients with moderately impaired ventricular function
ANSWER E

* A. exerts a cardioprotective effect entirely by reduction of heart rates - probably false
* B. Is best started intra-operatively - false
* C. Is contraindicated in patients with chronic airways limitation - maybe false: definitely false if there is no reversible component to the COAD, but if there is, beta-2 receptors cause bronchodilation and their blockage is relatively contraindicated
* D. Is contraindicated in patients receiving ACEI - false
* E. Is safe in patients with moderately impaired ventricular function - maybe true: bisoprolol and carvedilol are both beta blockers and are used to treat heart failure; however also note that beta-1 receptors increase cardiac contractility.
o Beta-blockers and angiotension converting enzyme inhibitors should be used in all patients with a recent or remote history of MI regardless of EF or presence of HF (AHA guidelines)
PC41 [2001-Apr] Q52, [2002-Aug] Q6, [2004-Aug] Q20, [2005-Apr] Q13
At a late stage in severe septic shock
A. the myocardium becomes increasingly sensitive to catecholamines
B. adrenaline should not be infused as it is predominantly an alpha agonist at low doses
C. the infusion of endogenously occurring catecholamines is futile as blood levels are already too high
D. the infusion of dopamine is strongly recommended as it exerts its effects in high doses via different receptors than in low doses
E. inadequate catecholamine synthesis may contribute to the poor circulation
ANSWER E

Option A. False. With increasing time, the myocardial receptors become downregulated, hence actually become less sensitive.


Option B. False. Adrenaline has predominantly beta effects at low doses, not alpha effects.


Option C. False. Administration of catecholamines is necessary to maintain cardiovascular support.


Option D. False. Whilst dopamine is an inotrope, it stands as a relatively poor relative to adrenaline or noradrenaline in the use of sepsis. Previous theories that low dose dopamine preserved renal function have now been soundly discredited. Dopamine itself is a diuretic, and its action is to increase urine output rather than preserve GFR.


Option E. Correct. Endogenous catecholamine synthesis is often a factor in sepsis, hence the theory that supplementation with glucocorticoids can maintain or enhance production of catecholamines, leading to an improved outcome.
PI68 [2001-Apr] Q44, [Jul07]
Effects of volatile anaesthetic agents on the brain include
A. maintenance of cerebral blood flow when used with hypocapnia
B. uncoupling of autoregulation, with a consequent rise in intracranial pressure
C. reduction of cardiac output and cerebral blood volume when used at concentrations of 1.3 MAC
D. maintenance of cerebral metabolic rate, but reduction of cerebral electrical activity
E. equal depression of all neurons of the brain at 1.3 MAC concentration
ANSWER B

Option A - Incorrect. Cerebral blood flow is increased

Option B - Correct. Autoregulation is uncoupled with volatiles, leading to a rise in ICP despite lowering cerebral metabolic rate.

Option C - Incorrect. Cerebral blood volume icnreases.

Option D - Incorrect. Cerebral metabolic rate decreases.

Option E - Incorrect. Not all volatiles depress equally e.g. enflurane is capable of producing excitation and seizures.
PI79 [2005-Sep] Q112
What percentage of the total greenhouse gas effect is due to the use of volatile anaesthetic agents?
A. 0%
B. less than 1%
C. 2%
D. 5%
E. 10%
ANSWER B
PN44 [Jul07] Naltrexone
A. given as a single usual dose antagonises the effects of opioids for approximately 8 hours
B. mainly renally metabolised
C. no hepatic side effects even at high doses
D. is mixed opioid agonist-antagonist
E. used for alcohol abuse
ANSWER E

A. FALSE: duration of oral naltrexone is 72-108 hours

B. FALSE: hepatic metabolism

C. FALSE hepatocellular injury when given in excessive doses

D. FALSE: opioid anatgonist

E. TRUE: used for alcohol and opiate dependence
PZ116 ANZCA version [2005-Sep] Q147

Serotonin syndrome may be appropriately managed with each of the following EXCEPT

A. bromocryptine
B. chlorpromazine
C. cyproheptadine
D. diazepam
E. non-depolarizing neuromuscular blockers
ANSWER A

As per A&IC article "Serotonin Syndrome and the Anaesthetist" April 2005 (local rag with perfect timing for Jul05 exam), drugs useful inclde:

* cryproheptidine (5HT2 antagonist)
* chlorpromazine (70% as potent as cryproheptidine)- antipsychotic.
* diazepine (to treat neuromuscular abnormalities)
* neuromuscular paralysis ie NDMR (aims to counter myoclonus to prevent rhavdomyolysis)

Bromocriptine is a dopamine receptor agonist, so should not have a role in serotonin syndrome
PZ124 [Jul07]

Which of the following is NOT associated with serotonin syndrome
A. phenelzine
B. pethidine
C. ondansetron
D. chlorpromazine
E. sumatriptan
ANSWER D
MM21 ANZCA version [Apr08] Q122

Serotonin syndrome

A. delays clinical treatment (sic)
B. has the specific antidote promethazine
C. has signs and symptoms which are difficult to distinguish from neuroleptic malignant syndrome, but the distinction between the two syndromes is unnecessary for clinical management
D. is self-limiting
E. may be contributed to by pethidine
ANSWER E

* No direct antidote
* Cyproheptadine and chlorpromazine potentially antagonize serotonin in the CNS, but there are no controlled trials of these agents...chlorpromazine may be contraindicated in neuroleptic malignant syndrome because of its antidopaminergic properties (important as they are hard to distinguish)...Current Critical Care, 2008
* Benzodiazepines generally are considered useful for the serotonin syndrome. They are anticonvulsants, are not associated with serotonin release, and are anxiolytic and sedating. Dantrolene uncouples excitation-contract in skeletal muscles and has been used in malignant hyperthermia, neuroleptic malignant syndrome, and serotonin syndrome. There are case reports of benefit from dantrolene in serotonin syndrome but no controlled trials.

* Meperidine-induced serotonin syndrome in a susceptible patient, Br. J. Anaesth., September 2009; 103: 369 - 370.
* Tramadol, pethidine, fentani(y)l (and congeners), methadone, dextromethorphan, dextropropoxyphene, pentazocine...all possible
ANZCA Version [Jul07]

An adult male patient requires general anaesthesia. He admits to long-standing
substance abuse with central nervous system (CNS) stimulants. Compared with a
patient who is not a substance abuser, he is likely to require an
A. increased dose of induction agent and increased dose of opioid
B. increased dose of induction agent and reduced dose of opioid
C. increased dose of induction agent and unchanged dose of opioid
D. unchanged dose of induction agent and increased dose of opioid
E. unchanged dose of induction agent and unchanged dose of opioid
ANSWER C

CEACCP (2002) says "the main effects of stimulant drugs will be an increased MAC for anaesthetic agents and cardiovascular instability. Generous premedication and good analgesia may help to obtund major changes in heart rate and blood pressure in response to surgical pain" - suggests to me an increased dose of induction agent and increased or unchanged opiate. Combined with ANZCA pain book "these drugs do not exhibit any cross-tolerance with opioids" and "no data from the clinical setting of any difference in opioid requirements compared from patients who do not use these drugs"
PR48 [Apr98] [Jul98] [Apr99] [Jul07]
With regard to non-depolarising muscle relaxants:
A. NDMR actions are increased with hyperkalemia
B. Vecuronium exclusively (or primarily) undergoes renal elimination
C. Mivacurium half-life 10 minutes
D. Cisatracurium is metabolised to laudanosine by the liver
E. May require larger doses if treated with phenytoin and theophylline
ANSWER E

* A - False. (Hypokalaemia prolongs action, not hyperkalaemia)
* B - False. Vecuronium undergoes elimination also by the liver (ie non-exclusive elimination)
* C - False. (about 2 min)
* D - False. Cisatracurium undergoes spontaneous metabolism to produce laudanosine, not organ dependent.
* E - True. In Sasada and Smith under "Phenytoin" ... "it appears to increase the dose requirements of all of the non-depolarising relaxants (with the exception of atracurium) by 60-80%. No entry for Theophylline, but under "Aminophylline" says "in high concentrations, the drug will antagonise non-depolarising neuromuscular blockade caused by pancuronium or tubocurarine"
PN45 ANZCA Version [Jul07] Q126

Which one of the following statements concerning Tramadol is FALSE?

A. It has an active metabolite
B. It inhibits serotonin and noradrenaline reuptake
C. It is LESS likely (at normal doses) to cause respiratory depression than other opioid agonists
D. It is metabolised in the liver and excreted in the kidneys
E. It structurally resembles codeine
ANSWER E

* A. It has an active metabolite TRUE, THEREFORE NOT THE ANSWER = O desmethyltramadol
* B. It inhibits serotonin and noradrenaline reuptake TRUE AND THEREFORE NOT THE ANSWER [2]
* C. It is less likely to (at normal doses) to cause respiratory depression than other opioid agonists TRUE AND THEREFORE NOT THE ANSWER. APMS third edition 2010 page 63.
* D. It is metabolised in the liver and excreted in the kidneys TRUE AND THEREFORE NOT THE ANSWER [3]
* E. It structurally resembles codeine FALSE AND THEREFORE THE ANSWER.
ANZCA Version [Jul07]

Regarding chemotherapy agents,
A. azathioprrne is a cholinesterase inhibitor and may interact with suxamethonium
B. bleomycin may have an idiosyncratic (i.e. not dose related) association with progressive respiratory fibrosis
C. cyclophosphamide has NO known interactions with neuromuscular blocking agents
D. high cumulative doses of doxorubicin are associated with cardiomyopathy
E. nonsteroidal anti-inflammatory drugs (NSAIDs) do NOT interact with methotrexate
ANSWER D

A - False: Azathioprine is a purine analog, main interaction is with Allopurinol

B - Maybe true: Blue Book 2007 says "potential for idiosyncratic reactions such as pneumonitis from Bleomycin has drawn interest." Later also says risk factors for pneumonitis include... total cumulative dose." Doses <450mg have 3% chance, whereas doses 450-550mg have 15% chance. 2 questions here: 1 - is "pneumonitis" different enough to "progressive pulmonary fibrosis", and 2 - is this a predictable dose-related effect or an unpredictable idiosyncratic reaction?

C - False: Cyclophosphamide inhibits pseudocholinesterase activity, so it would effect suxamethonium and mivacurium

D - True and possibly best answer: Doxorubicin - "chronic use causes dose-dependent cardiomyopathy"

E - False: NSAID's when used with Methotrexate reduce methotrexate clearance and enhance methotrexate-related toxicity
TMP-121 [Apr08] [Aug08]

Levosimendan:
A. Increases contractility and myocardial oxygen consumption
B. Increases SVR
C. Binds to troponin C and induces a conformational change
D. Increases contractility by increasing calcium influx
E. Causes coronary vasodilation but NOT peripheral vasodilation
ANSWER C

Levosimendan is a calcium sensitiser that can be administered intravenously (IV) to patients with acute decompensated congestive heart failure (CHF). At therapeutic dosages levosimendan enhances myocardial contractility without increasing oxygen requirements, and causes coronary and systemic vasodilation.---medscape

The drug works via a dual mechanism of action which enhances cardiac contractility and vasodilatation without affecting intracellular free calcium, and so should have reduced proarrhythmic potential. It can be administered intravenously (IV) which makes it a therapeutic option for acute decompensated CHF.[----medscape
PZ68b [2002-Aug] Q93, [2003-Apr] Q58, [2004-Apr] Q49, [2004-Aug] Q80
Immunologically mediated heparin-induced thrombocytopaenia is characterised by
A. onset within a few days of first starting heparin therapy
B. intravascular thromboses
C. platelet count rarely reduced below 100 x 109.1-I
D. continuation of thrombocytopaenia after cessation of heparin
E. presence of non-specific (heparin-independent) platelet antibodies
ANSWER B
PZ. The active metabolite of ketamine is:
a. Hydroxyketamine
b. Hydroxynorketamine
c. Ketamine glucuronide
d. Ketamine sulphonamide
e. Norketamine
ANSWER E
PZ19. Antidepressants are not effective/recommended for
a. Chronic headache
b. Chronic back pain
c. Chronic pain post mastectomy
d. Chronic pain post acute herpes zoster
e. Trigeminal neuralgia
ANSWER B
PZ115 ANZCA version [2005-Sep] Q123

Correct statements regarding fondaparinux include each of the following EXCEPT

A. it has a structure unrelated to heparin
B. it is administered once daily
C. it is a synthetic, selective Factor Xa inhibitor
D. it is recommended for DVT prophylaxis in major orthopaedic surgery
E. the dosage does NOT need to be adjusted for age and sex
ANSWER A

* A - derived from the factor Xa-binding moeity of unfractionated heparain (FALSE, hence ANSWER)
* B - single daily dose (TRUE)
* C - "It is a synthetic and specific inhibitor of activated Factor X (Xa)" [1] (TRUE)
* D - only licensed for DVT prophylaxis in orthopaedic surgery (TRUE)
* E - implies standard dose for all (TRUE)
PN40 ANZCA version [2004-Apr] Q106, [2004-Aug] Q86

Codeine phosphate
A. is converted by the liver to its active metabolite, oxycodone
B. is not associated with tolerance on chronic use
C. is not effective as an analgesic in approximately 20% of Causcasians
D. is poorly absorbed from the gastrointestinal tract
E. when given orally has approximately 5% of the analgesic potency of intramuscular morphine
ANSWER E

# A - False, most to codeine-6-glucuronide, some to norcodeine, morphine, normorphine and hydrocodone.
# B - False, tolerance does occur therefore oxycodone a better choice.
# C - False,CYP2D6 exhibits genetic polymorphism in 9% UK and 30% Hong Kong population.
# D - False, oral bioavailability of at least 50%.
# E - True, see above or consider 60mg codeine oral goes to 30mg with first pass and then 10% metabolised to morphine is 3mg - 5% if you put oral codeine vs IM morphine.
PC44 ANZCA version [2005-Apr] Q148 [?Aug08]

In clinically used doses levosimendan, a novel inotrope used in heart failure,

A. acts by increasing levels of intracellular cyclic AMP
B. increases myocardial intracellular calcium
C. increases myocardial oxygen consumption
D. increases the rate of fatal ventricular arrhythmias
E. increases the sensitivity of intracellular contractile proteins to calcium
ANSWER E
PN: A man on PCA controlled with 2 mg morphine bolus is having a lot of pruritus. You decide to switch him to fentanyl. Which dose is the most appropriate bolus to be equi-analgesic with morphine 2mg:
A. 10mcg
B. 20mcg
C. 40mcg
D. 60mcg
E. 80mcg
ANSWER C
A patient with chronic pain using morphine PCA after lower limb orthopaedic surgery. Daily usage of IV morphine works out at about 400mg/day. What dose of oral methadone would you start him on to replace the morphine?
A. 60mg/day
B. 120mg/day
C. 400mg/day
D. 600mg/day
E: 1200mg/day
ANSWER A

Methadone replacement depends on dose of oral morphine
Daily Dose : Conversion Ratio
<100mg 3:1
100 - 300mg 5:1
300 - 600mg 10:1
600mg - 800mg 12:1
800mg - 1000mg 15:1
>1000mg 20:1
400mg IV = 1200mg oral. 20:1 conversion so 60mg of methadone per day = A
44.
Aneursym clipping, Best monitor of depth of block during this is ?

A. TOFR
B. TOFC
B. DBS
C. PTC
ANSWER C
45.
Closed circuit anaesthesia with 70%N2O,70kg man (low flow i think) what is the uptake of N2O after 90 mins anaesthesia:

A. less than 50ml/min
B. 100ml/min
C. 200ml/min
D. 500ml/min
E. 1000 ml/minut
ANSWER B

uptake is 1000 divided by the square root of the time administered in minutes (which works out roughtly to be B
Rapid infusion of mannitol IV initially causes:
A. Raised ICP
B. Reduced CBF
C. Reduced K
D. Reduced Na
E. ?
ANSWER A

The physical bolus of Mannitol causes an initially transient increase, then decreases as interstitial water is drawn out.
TMP-129 [Aug09] Methylene blue given intravenously has the effect:

A. Pulse oximetry goes down
B. Blood Gas Pa02 decrease
C. Hypotension
D. Metabolic acidosis
E. Increased heart rate
ANSWER A
24. (NEW) Rate of phenytoin administration:
a. 50 mg/min
b. 70 mg/min
c. 100 mg/min
d. Over 5 minutes
e. As fast as possible
ANSWER A

Admin by slow IVI (max 50 mg/min) into large vein via catheter
25. EV08 Hypothetical anaesthetic agent. Flows 2 L oxygen and 2L nitrous. Copper kettle vaporiser flow 0.5 L. Volatile with SVP 380 mmHg. Inspired volatile concentration (no numbers were exactly correct)
a. 2%
b. 5%
c. 10%
d. 11%
3. 15%
ANSWER C

Reading the explanation in Morgan and Mikhail, if 0.5L of gas enters the vapouriser, 1L exits, with a volatile concentration of 50%. This is diluted by 4L of FGF, so you have a total of 5L of gas. 500mL in 5L is 10%. Doesn't make sense? A copper kettle has a dedicated flow meter which is dialed up separately. To make your 0.5L of gas flow fully saturated with vapour at an SVP of 380mmHg, you need to double it (ie 380mmHg of vapour in 380mmHg of gas). This is mixed with the FGF which is separate; thus giving 500mL of vapour, 500mL of gas which went into the copper kettle, 2L of oxygen and 2L of nitrous.
27. (NEW) As per ANZCA Acute Pain Guidelines (2nd ed update), after a prophylactic subcutaneous dose of heparin, minimum time before you can remove epidural catheter is
a. 2 hours
b. 4 hours
c. 6 hours
d. 8 hours
e. 10 hours
ANSWER C

From update guidelines "Thromboprophylaxis with SC heparin is not a contraindication to neuraxial blockade. To identify heparin-induced thrombocytopenia, a platelet count should be done prior to removal of an epidural catheter in patients who have had more than 4 days of heparin therapy. Epidural catheters should be removed a minimum of 6 hours after the last heparin dose and not less than 2 hours before the next dose."
30. (NEW) Drug LEAST likely to cause hypoxia in ARDS
a. Noradrenaline
b. Milrinone
c. Isoprenaline
d. Isoflurane
e. SNP
ANSWER A
31. PI82 (NEW) Pulmonary hypertension, which will affect PVR the most
a. Isoflurane
b. Sevoflurane
c. Desflurane
d. Propofol
e. Remifentanil
ANSWER B
TMP-134

A Hetastarch of intermediate plasma expansion and intermediate plasma duration is;
A. 10% HES 250/0.6
B. 10% HES 200/0.5
C. 6% HES 450/0.7
D. 6% HES 130/0.4
E. 3% HES 200/0.5
ANSWER D
TMP-133 [Aug09]

Hetastarch 130/0.4.
The 0.4 means:
A. 40 mg/l
B. 40 g/l
C. 4 hydroxylations of every 10 glucose residues
D. every 4th glucose is hydroxyethylated
E. ?
ANSWER C

The 130 is the molecular weight of the starch

0.4 is the MS (molar substitution) is the ratio of hydroxyethyl groups to glucose residues
105.(NEW) Which drug is an example of a specific PDE III inhibitor:
a. Aminophyline
b. Sildenafil
c. Milrinone
d. Dipyridamole
e. ?
ANSWER C
47. Mechanism of action of antiepileptics in chronic pain, which is false?
a. Phenytoin workes at Na channels
b. Gabapentin increases gaba in cns
c. Carbamazepine works at Na channels
d. Valproate increases GABA in the CNS
e. lamotrogine acts at Ca channel
ANSWER B and E
71. PI81 Which volatile has the minimum effect on ICP at 1 MAC
A. Isoflurane
B. Sevoflurane
C. Desflurane
D. Enflurane
E. Halothane
ANSWER B
88. Central anticholinergic syndrome, which is NOT true:
A. Will improve with neostigmine
B. Peripheral anticholinergic symptoms
C. Caused by Anti-Parkinson drugs
D. CNS depression
E. Associated with agitation, delirium, and ???
ANSWER A

Central anticholinergic syndrome

Historically, anticholinergic syndrome was a commonly encountered sequel to anaesthesia. Nowadays, less anticholinergic medications are used. Symptoms range from cerebral irritation with delirium and agitation to CNS depression with stupor and coma. These accompany peripheral anticholinergic effects that is tachycardia, blurred vision, dry mouth and urinary retention. The symptoms are rapidly reversed by physostigmine (an acetylcholinesterase inhibitor), but may recur when its effect terminates. Anti-Parkinsonian, antidepressant and antihistamine drugs can cause central anticholinergic syndrome.

Emedicine

Physostigmine is the only reversible acetylcholinesterase inhibitor capable of directly antagonizing the CNS manifestations of anticholinergic toxicity; it is an uncharged tertiary amine that efficiently crosses the blood brain barrier
PL30 [Mar10]

Maximum dose (with low risk of toxicity) of lignocaine (with adrenaline 1:100000)
for liposuction with tumescence technique:
A. 3 mg/kg
B. 7 mg/kg
C. 15 mg/kg
D. 25 mg/kg
E. 35 mg/kg
ANSWER E

Tumescent liposuction - Klein noted that the correct maximum safe dose of lidocaine was never investigated but rather extrapolated from procaine. He showed that infusion of lidocaine, by using the tumescent formula of 0.1% lidocaine with 1:1,000,000 epinephrine, into the subcutaneous tissues of a concentration of 35 mg/kg was safe.

The maximum plasma level that was reached at 11-15 hours postoperatively was 0.8-2.7 mcg/mL, well below the toxic level of 5 mcg/mL. Tumescent anesthetic produces a delay in achieving the peak serum lidocaine level and does not produce as high a level compared with conventional local anesthetic.
TMP-100 [Mar10] [Aug10]

Compared to lignocaine, bupivacaine is:

A. Twice as potent
B. Three times as potent
C. Four times as potent
D. Five times as potent
E. Same potency
ANSWER C
TMP-114 [Mar10]

Paralysed with atracurium. TOF is 1(25%). You give a dose of 0.1 mg/kg mivacurium to close the abdomen. When will you be back to TOF 1(25%)?

A. 5 min
B. 10 min
C. 30 min
D. 60 min
E. 90 min
ANSWER C

A study by Naguib et. al. showed that after an initial intubating dose of atracurium, and spontaneous recovery of the first twitch (T1) to 10% of its control height, a maintenance dose of 0.1mg/kg of mivacurium resulted in a time of 25 minutes to regain T1=10%. My guess would be the answer is C, but it's still a guess
TMP-113 [Mar10] [Aug10]

The BEST agent to decrease gastric volume AND increase gastric pH before semi-urgent procedure

A. Omeprazole
B. Cimetidine
C. Ranitidine
D. Sodium citrate
E. ?
ANSWER C

From the ANZCA Obstetric SIG
Ranitidine has been the most extensively studied (Escolano et al 1996, Level II; Lin et al 1996, Level II; Rout et al 1992, Level II).
To date, no other agent has been consistently demonstrated to be more effective than ranitidine and most are more expensive.
A number of studies have been done in the non-obstetric elective surgery setting. Maltby et al (1990, Level II) showed that 150 mg
of oral rantitidine when given two to three hours before surgery resulted in a mean gastric pH of 5.86 (+/- 1.73) and with only one
out of 49 patients having an ‘at risk’ combination of pH <2.5 plus gastric volume of >25 mL.

According Stoelting's Co-exisiting disease - p281 rantitidine is the most potent agent for reducing volume and increasing pH within the time span, ie 1-1.5 hours. Omeprazole needs to be given the night before. There are other PPI than can be give immediately prior to surgery, but this was not an option.
PC50 [Mar10] [Aug10]

Elimination Half life of tirofiban
A. 2hrs
B. 8hrs
C. 12hrs
D. 24hrs
E. 15 minutes
ANSWER A
67.Regarding anticholinesterases:
A. pyridostigmine has slow onset of effect
B. physostigmine does not rely on renal metabolism/excretion
C. neostigmine cannot reverse centrally acting cholinergics
D. edrophonium is less reliable in reversal?
ANSWER ABC

Is this an “EXCEPT” question?

A. True. Has a slower onset of action than neostigmine and its duration of action is longer.
B. True. “Physostigmine is hydrolysed at its ester linkage and renal excretion is of minor importance” (Stoelting)
C. True. It contains “a quaternary ammonium group… poorly lipid soluble and thus do not easily penetrate lipid cell membranes barriers such as… blood brain barrier” (Stoelting)
D. False. Edrophonium produces “reversible inhibition of acetylcholinesterase through its electrostatic attachment to the anionic site on the enzyme…further stabilized by hydrogen bonding on the esteratic site on the enzyme… duration of action considered to be brief, reflecting its reversible binding” (Stoelting)
TMP-Jul10-007 Anaphylaxis to rocuronium. Which is most likely to cause coss-reactivity ?

A. Vecuronium
B. Pancuronium
C. Atracurium
D. Cisatracurium
E. None of the above -cross reactivity too variable to predict
ANSWER E

From Allergy 2007; 62: 471-487 Review Article: Anaphylaxis during anaesthesia:diagnostic approach "Cross Reactivity between NMBA is said to be common because of ubiquitous ammonium groups in these drugs. The estimated prevalence of cross-reactivity between NMBA is about 65% by skin tests and 80% by radioimmuno assay inhibition tests. While some pairings are common, the patterns of cross-reactivity vary considerably between patients." This was given to me in its paper form by our department allergy specialist. The fact that cross reactivity is unpredictable was also highlighted in the recent Allergy Podcast on the college website and that you cannot predict, without skin testing, which other NMBA you can use clinicall
TMP-Jul10-008 Hypotension post propofol induction in elderly patient. More pronounced / profound than in younger patient. Reason ?

A. Concentric LVH associated with ageing and therefore preload dependent
B. Because of increased lean body mass
C. Decreased cardiac output with ageing
D. Increased sensiticity to all anaesthetic agents, thus relative overdose is common
E. Decreased liver blood flow with ageing, decrease drug clearance and increased drug concentration
ANSWER A

IV propofol causes hypotension in many patients. An incidence of 25-40% is quoted for typical induction doses. The incidence is highest in:
* the elderly
* those with pre-existing hypotension (an obvious clinical indication there)
* patients at ASA >= III

The main reason for the hypotension is venodilatation, and this is more pronounced with propofol than thiopentone

A = ? True
* The reduction in preload is the main contributor to hypotension according to Fundamentals of Anaesthesia, p576

B = False
* Reduced

C = False
* The statement is true, but this is not the main mechanism of hypotension

D = ? False
* A true statement in terms of loss of consciousness, but not necesscarily the cause of hypotension

E = ? False
* For the same reasons as D
TMP-Jul10-034 Liposuction. Infiltration of lignocaine with 1:200,000 adrenaline. Peak plasma concentration of lignocaine occurs at:

A. 1 hour
B. 3 hours
C. 18 hours
D. 24 hours
E. 30 mins
ANSWER C

5. Tumescent anesthesia: This is a technique of local anesthesia which involves the subcutaneous injection of large volumes of dilute LA in combination with epinephrine and other agents. It is used for dermabrasion, skin grafting, rhinophyma correction, liposuction and hair transplant procedures. The injection consists of 1000 ml of normal saline, 50 ml of 1% lidocaine, 1 ml of 1:1000 adrenaline and 12.5 ml of sodium bicarbonate (1 mEq/L). Total doses of lidocaine range between 35-55 mg/kg, and the plasma concentrations may peak more than 8-12 hours after infusion.[13] Clinicians are advised to exercise great caution in administering additional local anesthesia by infiltration or other routes for at least 12-18 hours following the use of this technique.

Burk RW 3rd, Guzman-Stein G, Vasconez LO. Tumescent anesthesia with a lidocaine dose of 55 mg/kg is safe for liposuction. Dermatol Surg 1996:22:921 Back to cited text no. 13
TMP-Jul10-013 Timing of peak respiratory depression post intrathecal 300 mcg morphine:

A. < 3.5 hours (think it was one hour)
B. 3.5 – 7.5 hours (then three hours)
C. 7 - 12.5 hours (then 7.5 - 12.5 hrs)
D. 12.5 -18 hours
E. > 18 hours
ANSWER B

ANZCA Acute Pain: Scientific Evidence 3rd ed p195:

"Respiratory depression occurs in up to 1.2% to 7.6% of patients (Meylan et al, 2009 Level I) given intrathecal morphine. When measured in opioid-naive volunteers, respiratory depression
peaked at 3.5 to 7.5 hours following intrathecal morphine at 200 to 600 mcg doses (Bailey et al, 1993 Level IV). Volunteers given 600 mcg had significant depression of the ventilatory response to carbon dioxide up to 19.5 hours later.
TMP-Jul10-004 Exponential decline / definition of time constant (with various options)

A. time for exponential process to reach log(e) of its initial value
B. Time until exponential process reaches zero
C. Time to reach 37% of initial value
D. Time to reach half if its initial value
E. 69% of half life
ANSWER C
TMP-Jul10-040 Salicylate poisoning:

A. Respiratory acidosis
B. Metabolic acidosis (/ don’t think this was an option - ak )(yep i think it was- mm)
C. Increased CO2 (production)
D. High output renal failure
E. Hyperthermia (/ pretty sure this option was HYPOthermia - too late)
ANSWER B

In high doses, leads to toxicity a. uncoupling of oxidative phosphorylation (mainly in skeletal muscle) increases oxygen consumption, and carbon dioxide production, thus decreasing PaO2 & increasing PaCO2 b. hyperventilation via direct effect, and increased PaCO2, leads to respiratory alkalosis, with renal compensation c. with even larger doses, - depress respiratory centre, causing further CO2 accumulation, resulting in uncompensated respiratory acidosis - metabolic acidosis with accumulation of pyruvic, lactic and aceto-acetic acid, and absorption of salicylic acid - hyperpyrexia due to increased metabolic rate - initial CNS stimulation, then later coma
PZ86d Serotonin syndrome has been reported following SSRI coadministration with:

A. Gingko
B. Garlic
C. Ginger
D. St John’s wort
E. Vallerian
ANSWER E
PL31 Aug10

Time to reach peak plasma concentration after injection of
2% lignocaine with adrenaline into epidural space

A. 20 min
B. 30 min
C. 40 min
D. 50 min
E. 60 min
ANSWER A
22. NEW. Anaesthetising an obese patient. Acelerometer on TOF 0.9. Could dose suxamethonium on ideal body weight or total body weight. With respect to 1mg/kg IBW vs. TBW you will see:

A: shorter onset and faster twitch recovery
B: shorter onset and similar twitch recovery
C: shorter onset and slower twitch recovery
D: similar speed of onset with similar speed of twitch recovery
E: similar onset and longer recovery
ANSWER E

A & A February 2006 vol. 102 no. 2 438-442

The appropriate dose of succinylcholine (SCH) in morbidly obese patients is unknown. We studied 45 morbidly obese (body mass index >40 kg/m2) adults scheduled for gastric bypass surgery. The response to ulnar nerve stimulation of the adductor pollicis muscle at the wrist was recorded using the TOF-Watch SX® acceleromyograph. In a randomized double-blind fashion, patients were assigned to one of three study groups. In Group I, patients received SCH 1 mg/kg ideal body weight, in Group II 1 mg/kg lean body weight, and in Group III 1 mg/kg total body weight. After SCH administration, endotracheal intubating conditions were scored. The recovery from neuromuscular block was recorded for 20 min. There was no difference in the onset time of maximum neuromuscular blockade among groups, but maximum block was significantly less in Group I. The recovery intervals were significantly shorter in Groups I and II. In one third of the patients in Group I, intubating conditions were rated poor, whereas no patient in Group III had poor intubating conditions. Our study demonstrates that for complete neuromuscular paralysis and predictable laryngoscopy conditions, SCH 1 mg/kg total body weight is recommended.
23. NEW: The half life of the active metabolite of levosimendan (OR-1896) is:

A: 1hr
B: 8hr
C: 24hr
D: 3 days
E: 7 days
ANSWER D

Clin Pharmacokinet. 2007;46(7):535-52.

Levosimendan has been developed for the treatment of decompensated heart failure and is used intravenously when patients with heart failure require immediate initiation of drug therapy. It increases cardiac contractility and induces vasodilatation. The pharmacokinetics of levosimendan are linear at the therapeutic dose range of 0.05-0.2 microg/kg/minute. The short half-life (about 1 hour) of the parent drug, levosimendan, enables fast onset of drug action, although the effects are long-lasting due to the active metabolite OR-1896, which has an elimination half-life of 70-80 hours in patients with heart failure (New York Heart Association functional class III-IV). Although levosimendan is administered intravenously, it is excreted into the small intestine and reduced by intestinal bacteria to an amino phenolpyridazinone metabolite (OR-1855). This metabolite is further metabolised by acetylation to N-acetylated conjugate (OR-1896). The circulating metabolites OR-1855 and OR-1896 are formed slowly, and their maximum concentrations are seen on average 2 days after stopping a 24-hour infusion. The haemodynamic effects after levosimendan seem to be similar between fast and slow acetylators despite the fact that the enzyme N-acetyltransferase-2, which is responsible for the metabolism of OR-1855 to OR-1896, is polymorphically distributed in the population. Levosimendan reduces peripheral vascular resistance and has direct contractility-enhancing effects on the failing left ventricle. It also improves indices of diastolic function and seems to improve the function of stunned myocardium. Despite an improvement in ventricular function, levosimendan does not increase myocardial oxygen uptake significantly. An increase in coronary blood flow and a reduction in coronary vascular resistance have been observed. Levosimendan reduces plasma brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) levels substantially, and a decrease in plasma endothelin-1 has been observed. Levosimendan also exerts beneficial effects on proinflammatory cytokines and apoptosis mediators. The effects of a 24-hour levosimendan infusion on filling pressure, ventricular function and BNP, as well as NT-proBNP, last for at least 7 days.
PC49 [Apr07] Q121
The action of which drug is unchanged in a recipient following cardiac transplantation
A. Adenosine
B. Adrenaline
C. Atropine
D. Digoxin
E. Isoprenaline
ANSWER E
PC48 ANZCA version [2005-Sep] Q17

A dopamine infusion of 3 mcg/kg/min is likely to

A. increased myocardial contractility
B. increased renal blood flow
C. increased heart rate
D. increased systemic vascular resistance
E. all of the above
ANSWER B

Low dose infusion = renal dose

"Dopamine has significant adverse effects that should limit its use. Low-dose dopamine has been clearly shown not to be beneficial. Dopamine is predominantly a beta agonist in doses of 5 to 10 g/kg per minute; at doses exceeding 10 g/kg per minute, dopamine is an alpha agonist and therefore increases arterial resistance. Dopamine increases Pms and, hence, venous return increases, resulting in increased left ventricular filling pressures. The increased afterload at large doses and increased filling pressures associated with dopamine are often undesirable in treating decreased contractility." (Principles of Critical Care)
PC46 ANZCA version [2002-Aug] Q126, [2003-Apr] Q14

When the calcium antagonists diltiazem, verapamil or nifedipine are used in patients with cardiovascular disease
A. diltiazem causes the greatest depression of atrioventricular nodal conduction
B. nifedipine is the most likely to increase the heart rate
C. nifedipine causes the least systemic vasodilation
D. diltiazem causes the greatest depression of myocardial contractility
E. verapamil is the most likely to cause lower limb oedema
ANSWER B

Verapamil has most effect on the heart, nifedipine most on the blood vessels; diltiazem in between

A. Probably Verapamil

B. True - reflex tachy - Nifedipine incr; dil no change; ver dec

C. False - most

D. False - veramamil

E. False - nifedipine
PC45 ANZCA version [2003-Aug] Q127

Milrinone
A. prolongs conduction in Purkinje fibres
B. is contraindicated with ACE (angiotensin converting enzyme) inhibitors
C. inhibits a phosphodiesterase iso-enzyme
D. causes nodal tachycardia
E. increases systemic and pulmonary vascular resistance
ANSWER C

YENTIS

A: Faster conduction

B: Caution as can cause hypotension, but not contraindicated

C: True

D: Generally no change in HR, Ventricular and SV arrythmias can occur

E: Reduces SVR
PC44 ANZCA version [2005-Apr] Q148 [?Aug08]

In clinically used doses levosimendan, a novel inotrope used in heart failure,

A. acts by increasing levels of intracellular cyclic AMP
B. increases myocardial intracellular calcium
C. increases myocardial oxygen consumption
D. increases the rate of fatal ventricular arrhythmias
E. increases the sensitivity of intracellular contractile proteins to calcium
ANSWER E

Levosimendan, through its calcium-dependent binding to cardiac troponin C, exerts a positive inotropic effect on the myocardium. It also induces vasodilation by acting as an opener of ATP-dependent K-channels in vascular smooth muscle. Levosimendan itself has a short half-life, approximately 1 hour. Active metabolites of levosimendan that have longer half-lives have been identified.
PI83 [Mar10]
Desflurane vaporiser, heated because of
A. High SVP
B. High boiling point
C. Low SVP
D. High MAC
E. Low MAC
ANSWER A

Desflurane's SVP is so HIGH (~700mmHg). The other reason why a Tec-6 vaporiser is used with Desflurane is b/c of it's LOW boiling point (not HIGH boiling point - as per possible answers). As mentioned above, at 23C, that ambient temperature may cause the liquid to boil, causing significant variation in the vapour concentration. Read 'Understanding Vapourizers - CEACCP article
PI74 ANZCA version [2005-Apr] Q105

The MAC (Minimum Alveolar Concentration) of desflurane in infants less than one year of age is

A. less than 6%
B. 6 to 7%
C. 7 to 8%
D. 8 to 9%
E. greater than 9%
ANSWER E

Oxford Paediatric Anaesthesia says infant = 9.4%, neonate = 9.1%
PI71 ANZCA version [2003-Apr] Q101

The use of Xenon in anaesthesia is limited because it
A. has a blood/gas solubility coefficient similar to that of ether
B. is a myocardial depressant
C. is less potent than nitrous oxide
D. is expensive to extract
E. lacks analgesic properties
ANSWER D

Xenon: A little more detail on the drug, just to tempt us! Despite the high cost of xenon, xenon anaesthesia will become possible at a reasonable cost. The hourly uptake of xenon decreases rapidly and with full recycling of the gas during closed circuit anaesthesia, xenon anaesthesia will be economically viable.

* Physical properties
o Colourless, odourless, tasteless.
o Monatomic gas, atomic number = 54, molecular weight = 131,3
o Gas under normal temperature and pressure
o 9 stable isotopes.
o Freezing point -111,9oC, Boiling point -108,1oC.
o 4 times more dense than air.
o Nonflammable and will not support combustion.
o Diffuses freely through rubber and silicone components.
o Manufactured by separation from liquid air, often as a by product of steel making.

* Anaesthetic agent
o First used in 1951 by Cullen on an 81yr old man having an orchidectomy..
o Very close to the ‘ideal agent’
o The very large electron shell of xenon ca be distorted and polarised by nearby molecules, creating a dipole.
o Xenon inhibits the plasma membrane Ca2+ pump, altering excitability. It inhibits the nociceptive responsiveness of spinal dorsal horn neurons.
o MAC = 71%. (With more widespread usage the Russians have noticed the MAC to be closer to 60%)
o Minimal haemodynamic effects.
o Lowest blood/gas partition coefficient = 0,115 of currently available inhalational agents.
o Low oil/water partition co-efficient of 20.
o Rapid induction and eduction regardless of duration of administration
o Progressively decreasing xenon requirements during closed circuit anaesthesia makes it an economic viability.
o 4 stages of anaesthesia noted with 70% Xenon/ 30% oxygen.

i. Whole body paraesthesia & hypo-algesia.

ii. Euphoria & increased psychomotor activity.

iii. Analgesia with partial amnesia (after 3-4min).

iv. Surgical anaesthesia with a degree of muscle relaxation.

* Equivalent analgesia when compared with equipotent doses of N2O
* The analgesia produced by both gases is not reversible by naloxone.
* The analgesic action of nitrous oxide involves the descending inhibitory system from the brainstem. Xenon probably has a direct suppressive action on spinal dorsal horn neurons
* No occupational/ environmental disadvantages.

* Specific effects on the body
o Respiratory
+ Central depression causes a decrease in respiratory rate with a compensatory increase in tidal volume and can progress to apnoea
+ Higher density and viscosity (compared with oxygen, air and N2O) theoretically makes xenon more likely to increase airway resistance. Clinically the airway resistance is slightly less than that seen with N2O and it can be used safely in lung disease
+ Diffusion hypoxia is very mild as the blood/gas partition of Nitrogen (0.014) is only almost 10 times less than that of Xenon (0.115) as opposed to the almost 40 times less than Nitrous Oxide (0.47)
o Cardiovascular
+ No inhibitory effects on cardiac ion channels i.e. calcium, sodium and inward potassium channels.
+ No significant change in contractility, blood pressure and systemic resistance.
+ No sensitisation of the myocardium to adrenaline
+ May attenuate the myocardial depressant effects of isoflurane.
+ In an animal study, xenon anaesthesia produced the highest regional blood flow to brain, liver, kidneys and GIT. The control groups were 1% halothane in Nitrous oxide and thiopentone with fentanyl.
o Central nervous system
+ Xenon does not alter regional cerebral blood flow and autoregulation (Fink H, Blobner M, Bogdanski R, et al. Effects of xenon on cerebral blood flow and autoregulation: an experimental study in pigs. Br J Anaesth 2000; 84:221-225)
+ Inhaled xenon when used as a tracer for the measurement of cerebral blood flow increases cerebral blood flow, increases intracranial pressure and decreases cerebral perfusion pressure in acute head injury patients. This is not associated with cerebral oligaemia or ischaemia. This increase in cerebral blood flow is reversed by mild hyperventilation and so might have been a result of poorly controlled physiological variables. Hypercarbic induced vasodilatation induced by the sedative effects of the inhaled xenon, and the stress effect of breathing a dense gas mixture.
+ At present its use in neurosurgery is controversial
o Renal
+ No data available.
o Endocrine/neurohumoral
+ Attenuates surgical stress due to analgesia. Does not have any short or long term cortisol suppression effects.
o Toxicity
+ Platelet aggregation potentiated at 2atm (relevant to deep-sea divers).
+ No reported haematological toxicity.
+ Halted Cell Division
+ Mitosis is blocked at the metaphase-anaphase stage. This is reversible on withdrawing xenon and administering calcium to the cell.
+ The most likely site for inhibition is the enzyme complex called Ca MK II
o Malignant hyperthermia
+ Seems not to trigger malignant hyperthermia.
o Metabolism and elimination
+ Unlikely to be involved in any biochemical events in the body.
+ Eliminated via the lungs.

Why Xenon is going to become a potential volatile anaesthetic.

*
o Decreasing manufacturing costs.
+ All new liquid air production plants have xenon extraction apparatus fitted
+ Loss of xenon from the atmosphere from satellite engines will cease from next year
+ SASOL has completed a very large production facility in South Africa
o Use in a fully closed breathing system
+ A computer controlled closed circuit machine is now commercially available - The Draeger/Physio partnership Physioflex machine
+ The ability of xenon to alter the speed of sound allows an reasonably accurate measurement
+ Measurement is generally difficult as
# Xenon diamagnetic and does not absorb infrared radiation
# Low reactivity precludes the use of specific fuel cell or electrode-type device
# Mass spectrometry is expensive
# Rotating vane meters are available to measure gas flow
# Xenon causes Pitot tube and the variable orifice flowmeters to under - read
# Hot-wired anemometers under-read.
o Medical license
+ Russian Federation in November 1999
+ German is expected in 2001

Practical usage

1. Nitrogen must be washed out by giving a high flow of pure oxygen for at least 5 minutes
2. Normal induction and muscle relaxation
3. After intubation connect the patient to an appropriate anaesthesia delivery system
4. The hypnotic concentration of 40-45% is achieved after 1.5min
5. The anaesthetic concentration of 60-70% takes approximately 8 minutes.

Summary

* Colourless and odourless gas with no irritation to the respiratory tract. Well tolerated with gas induction
* Low blood/gas and oil/water partition co-efficients allowing rapid induction and eduction
* The central nervous system effects are readily reversibly and there is no stimulant activity.
* Produces unconsciousness with analgesia and a degree of muscle relaxation
* MAC of 60-70% allows a reasonable inspired oxygen concentration
* It does cause respiratory depression, to the point of apnoea.
* It is cardiac stable.
* Not metabolised in the body and is eliminated rapidly and completely via the lungs.
* It is non toxic, has inherent molecular stability and does not form flammable mixtures.
* Has no long-term adverse effects with chronic exposure at low dose.
* Stable in storage, no interaction with anaesthesia circuits or soda lime. Should not be used with rubber anaesthesia circuits as there is a high loss through the rubber
* Expensive - Routine usage will only be possible with a closed circuit delivery system that recycles xenon.

Owing to environmental concerns there may be no alternative but to use xenon even if it incurs an increase in cost.
PI69 ANZCA version [2001-Aug] Q64

The MAC (minimal alveolar concentration) and blood/gas partition coefficient of desflurane are
A. 2% and 0.47 respectively
B. 4% and 0.47 respectively
C. 6% and 0.67 respectively
D. 6% and 0.42 respectively
E. 8% and 1.4 respectively
ANSWER D
PI68 ANZCA version [2001-Apr] Q44, [Jul07]

Effects of volatile anaesthetic agents on the brain include
A. maintenance of cerebral blood flow when used with hypocapnia
B. uncoupling of autoregulation, with a consequent rise in intracranial pressure
C. reduction of cardiac output and cerebral blood volume when used at concentrations of 1.3 MAC
D. maintenance of cerebral metabolic rate, but reduction of cerebral electrical activity
E. equal depression of all neurons of the brain at 1.3 MAC concentration
ANSWER B

Option A - Incorrect. Cerebral blood flow is increased

Option B - Correct. Autoregulation is uncoupled with volatiles, leading to a rise in ICP despite lowering cerebral metabolic rate.

Option C - Incorrect. Cerebral blood volume icnreases.

Option D - Incorrect. Cerebral metabolic rate decreases.

Option E - Incorrect. Not all volatiles depress equally e.g. enflurane is capable of producing excitation and seizures.
PI64 ANZCA version [2001-Apr] Q85, [2001-Aug] Q42, [2003-Aug] Q22

The MAC (minimum alveolar concentration) and blood:gas partition coefficient of Xenon are
A. 71% and 0.14 respectively
B. 45% and 0.24 respectively
C. 101% and 0.24 respectively
D. 45% and 0.42 respectively
E. 71% and 0.47 respectively
ANSWER A
PI63 ANZCA version [Jul00] [2002-Mar] Q46, [2002-Aug] Q28, [2004-Aug] Q6, [2005-Apr] Q6

Xenon concentration can be measured by each of the following EXCEPT

A. piezoelectric adsorption
B. infra-red absorption spectrometry
C. mass spectrometry
D. thermal conductivity
E. ultrasound techniques
ANSWER B

The measurement of xenon is difficult because it is diamagnetic and does not absorb infrared radiation. Its low reactivity precludes the use of specific fuel cell or electrode-type devices. Mass spectrometry works but is expensive. Physical properties such as its high thermal conductivity have also been used. Because of its density and atomic mass, xenon alters the speed of sound such that when an ultrasonic beam is passed through a sample, an estimation of the percentage of xenon can be made. A recent study [6] has demonstrated the accuracy of such a device, with a maximum difference between readings of 1.22% when compared with a reference method of laser refractometry.
PI62 [Apr98] (type A)

MAC of halothane in children compared to adult:
A. Higher in neonate
B. Lower at 2 months
C. Lower at 6 months
D. Higher in 2 yr old
E. Unchanged <5 years old regardless of age
ANSWER D

n general - neonatal MAC = Adult MAC

* Prems are less
* Peaks at age 1 ~ 1.5 Adult MAC
* Falls back after this to puberty and adult values

MAC is higher in neonates than 40 year olds.
PI55b ANZCA version [2001-Apr] Q23, [2004-Aug] Q5, [2005-Apr] Q9

Desflurane

A. has a boiling point of 29.2º C at 1 atmosphere
B. has a blood:gas partition coefficient higher than isoflurane
C. has been reported as a triggering agent for malignant hyperthermia
D. is associated with a low incidence of reflex airway responses when used
for gaseous induction
E. increases cerebral blood flow at 1 MAC
ANSWER C
PL29 [Aug09]

Ventricular fibrillation (VF) following caudal anaesthesia in 20kg six year old child.
The recommended dose of of Intralipid 20% is:
A. 10mls
B. 20mls
C. 30mls
D. 40mls
E. 50mls
ANSWER C

* Weight = (Age(y) + 4) x 2 which is 20kg
* Dose of Intralipid 20% is 1.5 ml/kg = 30ml
PL27 ANZCA version [2004-Apr] Q141
All of the following may be useful in the treatment of ventricular fibrillation due to bupivacaine cardiotoxicity EXCEPT
A. adrenaline
B. diazepam
C. intralipid
D. propofol
E. vasopressin
ANSWER D
PL24 ANZCA version [2003-Aug] Q133, [2004-Apr] Q4

The MOST correct statement concerning lignocaine toxicity is that
A. extremely high concentrations of lignocaine will produce persistent ventricular fibrillation
B. hypercarbia increases the convulsive threshold of the drug
C. the first sign of lignocaine toxicity is cardiovascular collapse
D. the initial treatment of lignocaine induced convulsions is phenytoin
E. tonic-clonic convulsions may be preceded by symptoms such as auditory disturbances
ANSWER E
PL25 ANZCA version [2005-Apr] Q114

Prilocaine is superior to lignocaine for intravenous regional anaesthesia because prilocaine

A. exhibits no cardiotoxicity
B. has a higher pKa
C. has a larger volume of distribution
D. is an ester, metabolised in the bloodstream
E. is more highly protein bound
ANSWER C

* A. exhibits no cardiotoxicity - false
* B. has a higher pKa
* C. has a larger volume of distribution - true
o Prilocaine: "Distribution: Vd: 0.7-4.4 L/kg; crosses blood-brain barrier"
o Lignocaine: "Distribution: Vd: 1.1-2.1 L/kg"
* D. is an ester, metabolised in the bloodstream - false: Prilocaine is an amide anaesthetic.
o "Prilocaine is a membrane stabilising agent and a local anaesthetic of the amide type" (Mims online)
* E. is more highly protein bound - false
o Prilocaine: "Protein binding: 55%" (uptodate)
o Lignocaine: "Protein binding: 60% to 80% to alpha1 acid glycoprotein" (Uptodate)
PL18 [Aug92]

Which local anaesthetic vasoconstricts skin blood vessels:
A. Mepivacaine
B. Bupivacaine
C. Lignocaine
D. Ropivacaine
E. Prilocaine
ANSWER D
PL02

The toxic level of lignocaine is:
A. 1 mcg/ml
B. 2 mcg percent
C. 5 mcg/ml
D. 3 mcg percent
E. 10 mcg/ml
F. 10 mcg percent
ANSWER C

Local Anaesthetic Toxic plasma concentration
(mcg/ml)
Lignocaine >5
Prilocaine >5
Bupivacaine >1.5
Ropivacaine >4

Lignocaine: 5-10: excitatory 10-15: seizures, 15-25 coma >25 cvs collapse.
PN48 [Mar10] [Aug10]

Why is codeine not used in paediatrics?
A. Poor taste
B. High inter-individual pharmacokinetic variability
C. Not licensed for children < 10 years old
D. Not as effective as adult when given in ?weight adjusted dose?
E. ?
ANSWER B
PN39 ANZCA version [2004-Apr] Q118

A patient is requiring 70 mg per day of morphine by continuous subcutaneous infusion, for the
treatment of cancer pain. You are asked to change the patient to oral morphine. An appropriate
initial order for slow release oral morphine would be
A. 35 mg twice a day
B. 70 mg twice a day
C. 100 mg twice a day
D. 200 mg twice a day
E. 300 mg once a day
ANSWER C

Parental or oral morphine conversion is 3:1
PN38 ANZCA version [2003-Aug] Q141, [2004-Apr] Q35

Which drug is contra-indicated in a patient with chronic renal failure
presenting with a fractured femur?
A. fentanyl
B. morphine
C. paracetamol
D. pethidine
E. oxycodone
ANSWER D

Acute Pain Scientific Evidence

* Fentanyl - no dose adjustment required
* Oxycodone - no dose adjustment required
* Morphine - reduced dose, alternative agent if high doses anticipated
* Pethidine - dose reduction, altenative agent recoomended as norpethidine accumulation

None contra-indicated but Pethidine best avoided
PN37 ANZCA version [2003-Apr] Q135

Characteristics of remifentanil include all of the following EXCEPT
A. a weakly active metabolite
B. high potency
C. metabolism by pseudocholinesterase
D. muscle rigidity following rapid bolusing
E. very short context-sensitive half-life
ANSWER C
PN36 ANZCA version [2002-Mar] Q94, [2002-Aug] Q36

Tramadol
A. may be used with caution in patients receiving monoamine oxidase inhibitors (MAOI)
B. is useful in the treatment of narcotic withdrawal
C. has no clinically significant effect on heart rate, left ventricular function or cardiac index
at usual therapeutic doses
D. use in patients on selective serotonin reuptake inhibitors has NOT been associated with
signs of serotonin syndrome
E. needs to be given in reduced doses to patients with severe hepatic disease, but not to patients
with impaired renal function
ANSWER C
PN32 ANZCA version [2001-Aug] Q81

Remifentanil is
A. metabolised by non-specific esterases in the liver
B. metabolised by plasma cholinesterase
C. rapidly metabolised with a context sensitive half life of around 3 minutes
regardless of infusion duration
D. rapidly metabolised with a context sensitive half life of around 3 minutes
after a one hour infusion and around 7 minutes after a 6 hour infusion
E. metabolised by non-specific esterases in the kidney and liver
ANSWER C
PN24 [Mar00] (type A)
Known adverse effects of intrathecal pethidine include:
A. Hypertension
B. Hypotension
C. Tachycardia
D. Sedation
E. Increased sweating
ANSWER B and D

* A. False.
* B. True. "Following a dose of 0.5 mg/kg, the reported incidence of hypotension ranged from 0 - 17% . . ."
* C. False. "Bradycardia after intrathecal pethidine has been observed in a number of other reports."
* D. True. "Other adverse effects that are associated with intrathecal pethidine include nausea and vomiting, pruritus, sedation and respiratory depression."
* E. False.
PN23b ANZCA version [2003-Apr] Q82

Adverse effects of a remifentanil infusion for surgery under
general anaesthesia include:
A. 10% incidence of PONV
B. Delayed respiratory depression after prolonged infusion
C. Increased sensitivity to morphine postoperatively
D. Muscle rigidity with an infusion rate 0.5 mcg/kg/min
E. Pain on bolus injection
ANSWER D

"Skeletal muscle rigidity can be caused by remifentanil and is related to the dose and speed of administration. Remifentanil may cause chest wall rigidity (inability to ventilate) after single doses of > 1 microgram/kg administered over 30 to 60 seconds or infusion rates > 0.1 microgram/kg/minute. Administration of doses < 1 microgram/kg may cause chest wall rigidity when given concurrently with a continuous infusion of remifentanil."
PN13b ANZCA version [2002-Mar] Q7, [2002-Aug] Q20, [2005-Apr] Q39, [2005-Sep] Q6

The use of epidural opioids for analgesia after caesarean section is NOT associated with

A. respiratory depression
B. activation of herpetic lesions
C. facial pruritis
D. a higher incidence of nausea and vomiting than occurs with other techniques of administration
E. an increased incidence of urinary retention
ANSWER D
PR55 ANZCA version [2004-Aug] Q107
In patients with advanced liver disease who receive muscle relaxants
A. decreased plasma clearance of vecuronium and rocuronium leading to prolonged blockade is a consistent feature
B. duration of action of mivacurium is NOT affected
C. initial doses should be reduced as volume of distribution is decreased
D. plasma clearance of atracurium and cisatracurium is increased
E. when the desired level of block is achieved with the initial dose, subsequent recovery is comparable to patients without liver disease
ANSWER A

* A. decreased plasma clearance of vecuronium and rocuronium leading to prolonged blockade is a consistent feature - best answer:
o " Vecuronium and rocuronium, both steroid-based NMBs, have a prolonged elimination phase in severe liver disease." (doi:10.1093/bjaceaccp/mkp040 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 10 Number 1 2010)
* B. duration of action of mivacurium is NOT affected - false:
o "The metabolism of succinylcholine may be slowed because of reduced pseudocholinesterase concentrations, but in practice this gives few problems."
o "the duration of action of mivacurium is prolonged in those patients in whom liver disease was associated with decreased plasma cholinesterase activity" (Stoelting p.217 3rd Ed)
* C. initial doses should be reduced as volume of distribution is decreased - false:
o "There is an apparent resistance to non- depolarizing neuromuscular blockers (NMBs) in patients with liver disease, which may be due to an increased volume of distribution or to altered protein binding."
* D. plasma clearance of atracurium and cisatracurium is increased - false: Why should clearance be increased? If anything will be decreased, but Hoffman elimination buffers this.
o "Atracurium and cisatracurium are suitable NMBs as they do not rely on hepatic excretion. After prolonged administration, concentrations of laudanosine (a metabolite of both atracurium and cisatracurium with potential to cause seizures) are lower with cisatracurium than atracurium due to the higher potency of cisatracurium, although this is unlikely to be of clinical significance."
* E. when the desired level of block is achieved with the initial dose, subsequent recovery is comparable to patients without liver disease
PR54 ANZCA version [2003-Apr] Q129
In the management of exposure to toxic nerve agents (highly potent anticholinesterases)
A. early treatment with glycopyrolate is more effective than atropine
B. ketamine is contra-indicated for endotracheal intubation
C. oximes (eg.pralidoxime) in normal doses have no endogenous anticholinergic effects
D. oximes reactivate AChE by cleavage of phosphorylated active sites
E. pre-treatment with pyridostigmine prevents the effects of these agents
ANSWER D

* A: False. "Atropine and oximes are effective antidotes if administered early after exposure. Atropine antagonizes muscarinic side-effects and is more beneficial than glycopyrrolate, which has a shorter half-life and does not cross the blood-brain barrier."

* B: False. "Ketamine may be beneficial for intubation. But there is an increase in salivation.

* C: False. "They (oximes) in normal doses have an endogenous anticholinergic effect."

* D: True. "Administered early, oximes reactivate AChE by cleavage of phosphorylated active sites."

* E: False. Does not prevent the effects. "Pyridostigmine bromide may be used as a pretreatment . . . (though it is not a true pretreatment, which would protect against nerve agents, but an "antidote enhancer") . . . The rationale of pyridostigmine pretreatment is that pyridostigmine carbamylation of AChE binding sites produces a reservoir of temporarily inactivated AChE. After exposure, nerve agents are unable to bind to the carbamylated enzyme. Later dissociation of pyridostigmine reactivates AChE, which, by hydrolysing acetylcholine, reduces the incidence of cholinergic crisis (in conjunction with atropine and pralidoxime).
PV18 ANZCA version [2001-Apr] Q88

When ketamine is used for management of acute post-operative pain
A. analgesia is usually accompanied by hallucinations
B. a starting dose of 0.05 to 0.1 mg.kg-1.hour-1 is appropriate
C. benzodiazepines are ineffective in decreasing dysphoric reactions
D. morphine is contraindicated as respiratory depressant effects are additive
E. the intravenous route is recommended because absorption is more reliable than via the subcutaneous route
ANSWER B
PV16b ANZCA version [2002-Mar] Q72, [2002-Aug] Q55

Propofol
A. is contra-indicated in all patients who give a history of egg allergy
B. requires a higher dose, when given slowly for induction of anaesthesia
C. may be diluted with 5% dextrose solution
D. causes no pain on injection if 20 mg of lignocaine is pre-mixed with
200mg prior to intravenous injection
E. has a metabolic half-life of 8 minutes
ANSWER C

A False
B False
C True - according to PI
D False - pain on injection occurs in <10% of patients and the incidence can be decreased by potent short acting opioid or lignocaine 1%
E False - elimination t1/2 is 0.5-1.5 hours
PZ98 ANZCA version [2005-Apr] Q143, [2005-Sep] Q51
Cephalothin has NO significant activity against
A. escherichia coli
B. proteus mirabilis
C. pseudomonas aeruginosa
D. staphylococcus aureus
E. streptococcus pneumoniae
ANSWER C

Cephalothin :

* 1st generation cephalosporin
* Good activity against Gram-positive organisms
* Poor activity against Enterococci and Gram-negative organisms
* good activity against all except P. Aeruginosa (MIMS online)
PZ97 ANZCA version [2004-Aug] Q133
In its pure form, arnica (a herbal medicine), can cause postoperative
A. angina
B. bleeding
C. prolonged sedation
D. oculogyric crises
E. vomiting
ANSWER B

# "Two sesquiterpene lactones of Arnica montana, helenalin and 11, 13-dihydrohelenal have been shown to inhibit collagen-induced platelet aggregation, thromboxane formation, and 5-hydroxytryptamine secretion." (Uptodate)
# "Use with caution in individuals with a history of bleeding, hemostatic disorders, or drug-related hemostatic problems. Use with caution in individuals taking anticoagulant medications, including warfarin, aspirin, aspirin-containing products, NSAIDs, or antiplatelet agents (eg, ticlopidine, clopidogrel, dipyridamole). Discontinue use prior to dental or surgical procedures (generally at least 14 days before)." (
PZ99 ANZCA version [2005-Apr] Q124

Intravenous paracetamol has

A. a duration of antipyretic effect of 4 hours
B. an antipyretic effect within 10 minutes
C. an onset of analgesic effect at 30 minutes
D. a peak analgesic effect at 30 minutes
E. a peak analgesic effect at 60 minutes
ANSWER E

* A - False - lasts at least 6 hours
* B - False - ↓ fever within 30 minutes
* C - False - Onset within 5-10 minutes
* D - False - peak effect in one hour
* E - True
PZ89 ANZCA version [2002-Mar] Q73, [2002-Aug] Q21

Patients taking a selective serotonin reuptake inhibitor (SSRI e.g. fluoxetine):
A. should NOT be given high doses of tramadol
B. can have their SSRI medication ceased without risk of withdrawal symptoms
C. will have potentiation of the effect of direct acting adrenergic agonists
D. are less sensitive to benzodiazepines than the general population
E. will have the majority of active drug cleared from the body within
36 hours following discontinuation
ANSWER A

* A : True : Seizures and serotonin syndrome have been reported in patients using tramadol. Some medications, including fluoxetine, are known to reduce the seizure threshold. The risk of seizures and serotonin syndrome may be enhanced when fluoxetine and tramadol therapy are combined (Prod Info Ultram(R), 2001).
* B : False : Numerous case reports and several controlled studies document a withdrawal syndrome following discontinuation of selective serotonin reuptake inhibitors (SSRIs).
* C : False: MAOI's potentiate effect of direct acting adrenergic agonsists
* D : False
* E : False : Elimination Half-Life (Fluoxetine) : 4 to 6 days, chronic administration
PZ84b ANZCA version [2002-Aug] Q101, [2003-Apr] Q8

Thiazide diuretics may cause
A. hypernatraemia
B. precipitation of acute gout
C. hypoglycaemia
D. hyperkalaemia
E. hepatic failure
ANSWER B

* A - False. "Side effects include hypokalaemia, hyponatraemia, hyperuricaemia, hypomagnesaemia, hypochloraemic alkalosis, hyperglycaemia, hypercholesterolaemia, exacerbation of renal and hepatic impairment, impotence, and rarely rashes and thrombocytopaenia." Yentis, 3rd. ed., p.507.
* B - True. "Thiazides and uric acid are secreted by the same mechanism within the renal tubules. This competition leads to reduced uric acid excretion and a rise in plasma levels which may precipitate gout."Peck, Hill & Williams, 2nd ed., p.304.
* C - False. See quote at A.
* D - False. See quote at A.
* E - False. "Borderline renal or hepatic function may deteriorate further during treatment with thiazide diuretics, presumably reflecting drug-induced decreases in blood flow to these organs." Stoelting, 4th ed., p. 487-488. AND "Impaired hepatic function. Thiazides should be used with caution in patients with impaired hepatic function or progressive liver disease, since minor alterations of fluid and electrolyte balance may precipitate hepatic coma." Mims Online.