-
Aspirin is:
a) Something about ibuprofen
b) As potent as abciximab
c) Less efficacy than clopidogrel
- v
- v
- v
- v
- a) Something about ibuprofen
Aspirin is more potent than abciximab
More efficacy than clopidogrel
-
Elimination Coefficient units:
a) Mg/ml
b) Mcg/ml
-
Which of the following drugs has low first pass metabolism?
a) Aspirin
b) Midazolam
c) Lignocaine
d) Metoclopramide
e) Morphine
The others all have high first pass metabolism, Metoclopramide has variable first pass from ~ 40 - 80%
-
Which drug is optimally given as a racemic mixture?
a) Dexmetetomidine
b) Bupivacaine
c) Morphine
d) Methadone
e) Noradrenaline
- v
- v
- v
- v
- b) BupivacaineDexmetetomidine not racemic
- Morphine ? not racemic
- Methadone is racemic but one is better
- Norad not racemic?
-
All are secreted by the proximal tubule in the kidney except?
a) frusemide
b) penicillin
c) diazepam
d) probenicid
e) morphine
-
The second gas effect is seen with nitrous oxide because?
a) Larger volume
b) It is used in higher concentrations
c) It is taken up more rapidly than other agents
d) Faster equilibration
e) It has a low solubility
- v
- v
- v
- v
- b) It is used in higher concentrations
-
Isoflurane is?
a) a halogenated methyl ethyl ether
b) no odour
c) boiling point higher than sevo
d) requires thymol as a preservative
e) enantiomer of enflurane
a) a halogenated methyl ethyl ether
has odour, sevo has highest boiling point
-
The therapeutic index of modern volatiles is in the order of?
a) < 2
b) 2 - 4
c) 4 - 6
d) 6 - 8
e) >10
b) 2 - 4
-
Which volatile is metabolised least?
a) desflurane
b) enflurane
c) isoflurane
d) halothane
e) sevoflurane
a) desflurane
Des 0.02% - Iso 0.2%
- Enflu 2%
- Sevo 2%
- Halo 20%
-
Volatile metabolism?
a) Isoflurane metabolised 0.2% in the kidneys
b) Isoflurane 0.2% by CYP2E1
c) Other wrong options
b) Isoflurane 0.2% by CYP2E1
-
The addition of sodium carbonate to thiopentone is?
a) To reduce pain on injection
b) To make it bactericidal
c) To increase ionised portion
d) To increase pH
d) to increase pH
-
Comparing thiopentone to propofol?
a) Resistance to infection thio > prop
b) Elimination half life keo prop = thio
c) Effect site concentration thio fast than prop
d) Pain on injection prop > thio
a) resistance to infection thio > prop
-
Ketamine is not usually used as a sole TIVA agent because?
a) It causes profound analgesia but insufficient hypnosis for procedure
b) It causes emergence phenomena in up to 30% of patients when given as an infusion
c) It is too water soluble compared to propofol
d) Half life is 80 mins
b) It causes emergence phenomena in up to 30% of patients when given as an infusion
-
Bupivacaine has a pKa of 8.1, in acidotic tissue at pH 7.1, how much of the drug will be ionised?
a) 1%
b) 10%
c) 25%
d) 90%
e) 99%
d) 90%
-
Which of the following is an amide local anaesthetic agent?
a) cocaine
b) benzocaine
c) Prilocaine
d) Procaine
e) Tetracaine
c) Prilocaine
-
Cocaine:
a) increases uptake of noradrenaline
b) effect is due to central dopaminergic effect
c) direct sympathomimetic effect
c) direct sympathomimetic effect
-
Regarding iv magnesium sulphate?
a) The S enantiomer is the only active form
b) has high clearance ...?
c) Cardiac Output is preserved after admin despite decrease contractility due to its effects on vascular smooth muscle
d) The dose must be reduced in liver failure
e) It is ? metabolised by the liver
unsure which is the answer ? b or c
-
Which is not a serotonin receptor antagonist?
a) clozapine
b) sumatriptan
c) ketanserin
d) cyproheptadine
e) ondansetron
b) sumatriptan
-
When is the safest time to give a drug to a lactating mother?
a) 3 - 4 hours before breastfeeding
b) immediately before breastfeeding
c) 30 - 60 mins before breastfeeding
d) immediately after breastfeeding
e) Either A or D
d) immediately after breastfeeding
30 - 60 mins before breastfeeding is the worst possible time because thats when peak blood concentration occurs
-
Which drug reversibly inhibits platelet aggregation?
a) diclofenac
b) aspirin
c) clopidogrel
d) warfarin
e) heparin
a) diclofenac
Aspirin and clopidogrel both irreversibly bind platelets
-
Which is true for LD50?
a) calculated from quantal dose response curves
b) mean lethal dose
c) calculated from graded dose response curves
d) A probit score of 5 means it is 5 SD away from the median
e) You keep giving animals a drug until they die
a) calculated form quantal dose response curves
-
Dibucaine number for a normal person is:
a) 20
b) 40
c) 60
d) 80
e) 100
d) 80
Eu:Eu is normal and number is 80 - Ea:Ea is abnormal and number is 20
- other phenotypes are somewhere in between
-
In pseudo cholinesterase deficiency which of these two drugs will have a prolonged effect?
a) Mivacurium and Esmolol
b) Suxamethonium and Procaine
c) Remifentanil and Esmolol
d) Suxamethonium and Esmolol
e) Remifentanil and Mivacurium
- Mivacurium - enzymatic hydrolysis by plasmaChE & hydrolysis by liver esterases
- Esmolol - red cell esterases not plasmaChE
- Suxamethonium - pseudochol
- Remifentanil - hydrolysis non specific plasma and tissue esterases
- Procaine - pseudochol
b) Suxamethonium and Procaine
-
A prolonged duration of neuromuscular blockade is seen following a vecuronium infusion. What is the possible cause?
a) accumulation of 3,17 dihydroxy-vec
b) Long term steroid use
c) Hyperthermia
d) Hypomagnesemia
e) Hyperkalaemia
-
a) accumulation of 3,17 dihydroxy-vec
- other things that prolong vec:
- hypermagnesemia, hypokalaemia, hypocalcaemia, hypoproteinemia, dehydration, acidosis, hypercapnia
-
Beta blocker with highest oral bioavailability?
A. Labetalol
B. Atenolol
C. Sotalol
D. Metoprolol
E. Carvedilol
- .
- .
- C. Sotalol (which has > 90 bioavail)
-
Carvedilol for CCF because
A. Decrease renin release due to action at beta 2 receptor
B. it has some intrinsic sympathomimetic activity
- .
- .
- Renin release is due to Beta 1
- Carvedilol has no intrinsic sympathomim act
-
Which is true of beta-blockers?
A. may mask hypoglycaemic symptoms
B. decrease Na+ and water retention due to effects on beta 1 adrenoceptors
- .
- .
- effects of beta 1 cause dec renin release, therefore B is correct.
- is A also correct?
-
Carvedilol
A. can decrease renin secretion
B. selective beta-blocker
C. useful in CCF to improve stroke volume by decreasing remodelling
- .
- .
- A. can decrease renin secretion Carvedilol is nonselective beta and alpha blocker
- ACEI decrease remodelling not Carvedilol
-
Beta adrenergic receptor antagonists
A. seldom causes inhibition of lipolysis
B. causes inhibition of gluconeogenesis caused by adrenergic stimulation following hypoglycaemia
C. Does not mask the signs of hypovolaemia
D. Sudden cessation is not associated with rebound effects
E. There is no evidence of cardiac protection for high risk patients pre-operatively
- .
- .
- Beta 3 effects are lipolysis
- B is correctdoes mask the signs of hypoglycaemia
- Sudden cessation does cause rebound
- There is evidence for cardiac protection
-
Labetalol
A. Beta and alpha antagonism with partial agonist activity at alpha 2 receptors
B. Beta and alpha 1 antagonist
C. Alpha agonist and beta 1 antagonist
- .
- .
- B beta and alpha 1 antagonist partial beta 2 agonist
-
Atenolol
A. has higher lipid solubility than propranolol
B. is a nonselective beta blocker
- .
- .
- Both are incorrect
- Propranolol has higher lipid solubility
-
Which of the following has the highest oral bioavailability
A. Metoprolol
B. Esmolol
C. Labetalol
D. Atenolol
E. Carvedilol
F. Propranolol
- .
- .
- Either
- A Metoprolol (50%) or
- D Atenolol (40 - 50%)
-
Esmolol and Sotalol both have
A. Are both class III anti-arrhythmics
B. Both have 90% bioavailability
C. Prolong QT causing torsades
D. Depress SA node and prolong AV
E. Decrease refractory period
F. Increase effective refractory period of AV node but increasing AP
- .
- .
- D. Depress SA node and prolong AV
- Sotalol has 90%, Esmolol 0% bioavail
- Sotalol prolongs QT causing torsades
- Beta blockers increase AVN refract period
- Prolonging effect refract period of AV is class III action
-
Most important contradication for beta blockers
A. Asthma
B. Stable Heart Failure
C. First Line treatment in phaechromocytoma
D. HTN in T2DM
E. Treat IHD in DM with PVD
- .
- .
- C. First line treatment in phaeo
-
The betablocker with the greatest bioavail
A. Atenolol
B. Metoprolol
C. Sotalol
D. Labetolol
-
Non-selective beta blockade causes
A. Increased muscle blood flow
B. Decreased uterine tone
C. Hyperglycaemia
D. Bronchodilatation
E. Mydriasis
- .
- .
- C. Hyperglycaemia
- Bronchoconstriction, dec musc b.f.
- Alpha 1 effect is mydriasis so not affected with Beta blockade
- beta 2 effect is uterine relax
-
Example of a beta-1 selective antagonist with a plasma half life of 6 - 7 hrs and renal elimination
A. propranolol
B. Metoprolol
C. Esmolol
D.
E. Atenolol
-
Which is NOT a side effect of non-selective beta blockade
A. urinary retention
B. bronchospasm
C. hyperglycaemia
D. hyperkalaemia
- .
- .
- bronchospasm, hyperglycaemia, urinary retention (all beta 2 blocking effects)
- B2 stim acts on Na/K ATPase pump to promote intracell movement of potassium???
-
Which one of the following selective beta blockers has a low extraction ratio and is predominantly excreted in urine?
A. Propranolol
B. Esmolol
C. Atenolol
D. Metoprolol
-
Regarding Esmolol
A. Is metabolised by red cell esterases
B. half life something
C. instrinsic sympathomimetic
D.
- .
- .
- A is metabolised by red cell esterases
-
Phentolamine
A. Selective alpha-1 antagonist
B. Causes bradycardia
C. Causes increased cardiac output
D. Selective alpha 2 antagonist
- .
- .
- C. causes increased cardiac output
- phentol is non selective
- causes reflex tachy
-
Esmolol
A. Active at beta-1 & beta 2 receptors
B. Half life < 2 mins
C. Has methanol as a metabolite
D. Is metabolised by (?acetyl/?plasma) cholinesterase
E. Is excreted unchanged in the urine
F. Is a non-selective beta-1 recept antagonist
- .
- .
- C. Has methanol as a metabolite
- esmolol is cardioselective beta 1
- half life 10 mins
- metab by red cell esterases
- extensively metab, < 1% excreted unchanged
-
Esmolol
A. Is a non-selective beta antagonist
B. Has intrinsic sympathomimetic activity
C. Does not have membrane stabilising activity
- .
- .
- C. Does not have membrane stabilising activity
- esmolol is selective beta 1
- does NOT have intrinsic sympathmimetic act
-
Labetolol
A. Alpha agonist & beta agonist
B. Alpha agonist & beta antagonist
C. Alpha antagonist & Beta antagonist
D. Is a more potent alpha blocker than phenoxybenzamine
E. alpha > beta effect
- .
- .
- C. Alpha antagonist & beta antagonist
- relative weak alpha blocking - selective alpha1
-
Of the effects of beta blockers, which is not true
A. Relax uterine muscle
B. Increased AV conduction
C. Decreased lipolysis
D. Increased SVR
E. Mask hypoglycaemia
F. Negative inotropy
G. Opposing effects of insulin
H. Lipolysis
- .
- .
- A relax uterine muscleB - true - prolonged AV conduction
- C - true - decreased lipolysis beta 3
- D - true - true with beta 2 blockade
- E - true - initial sign is tachy which is masked
- F - true - negative inotropy
- G - true - opposes effects of insulin
- H. False - inhibits lipolysis
-
A non-selective beta-blocker with low extraction ratio, long half life and Int sympathomimetic activity?
A. Atenolol
B. Propranolol
C. Metoprolol
D. Labetalol
E.
- .
- .
- Atenolol is selective, low extraction, no ISA
- Propranolol, no ISA, high first pass, non selective
- Metoprolol selective, no ISA 60% first pass metab
- Labetolol, high extract, non seletive, ISA!
- So answer must have been E?
-
Which ONE of the following is water soluble, half life 6 -8 hrs ("and something else")
A. Esmolol
B. Metoprolol
C. Propranolol
D.
E. Atenolol
- .
- .
- Esmolol low lipid solubility
- Metoprolol moderate lipid sol, t1/2 3 -4 hrs
- Propranolol high lipid sol, t1/2 2 -3 hrs
- E Atenolol
-
Sotalol
A. Non selective beta blocker
B. Contraindicated in long QT
C. Increases K+ conductance
D. Used in the treatment of torsades
E. Class II anti-arrhymic drug
F. Is a selective beta 1 antag
G. Blocks K+ channels
- .
- .
- A Non selective beta blocker
- B Contraindicated in long QT
causes blockage of K+ chans - Causes torsades, so not treatment of it
- E Class II anti-arrhythmic - predom class III but has class II action as well
- G. Blocks K+ channels
-
Which one of the following beta-blockers is selective for beta 1?
A. Atenolol
B. Labetalol
C. Propranolol
D. Sotalol
E. Metoprolol
F. Esmolol
- .
- .
- A. Atenolol
- E. Metoprolol
- F. Esmolol
-
The beta blocker with greatest oral bioavailability is
A. Atenolol
B. Metoprolol
C. Sotalol
D. Labetalol
E. Carvedilol
-
Beta adrenergic receptor antagonists
A. Seldom causes inhibition of lipolysis
B. Causes inhibition of gluconeogenesis caused by adrenergic stimulation following hypoglycaemia
C. Does not mask the signs of hypoglycaemia
D. Sudden cessation is not associated with rebound effects
E. There is no evidence of cardiac protection for high risk patients pre-op
- .
- .
- B. causes inhibition of gluconeogenesis caused by adrenergic stimulation following hypoglycaemia
-
Labetalol
A. Beta and alpha antagonism with partial agonist activity at alpha 2 receptors
B. Beta and alpha 1 antagonist
C. Alpha agonist and beta 1 antagonist
- .
- .
- B. Beta and alpha 1 antagonist
-
Digoxin toxicity
A. shorten PR interval
B. visual disturbance
C. prolong QT interval
D. ventricular extrasystoles
E. > 1ng/ml
- .
- .
- B. visual disturbance
- dig prolongs PR interval in therapeutic doses
- shortens QT interval in therap doses
- Ventricular extrasystoles could be right, as it is a S/E
- toxicity > 2.5mcg/L (same as ng/ml)
- decreases slope of phase 0
- sharpens slope of phase 3
-
Digoxin
A. Inhibit Na-K ATPase by binding to K protein
B. Inhibits Na+/Ca2+ exchange
C. has a central effect on vagal nuclei
D. Increases atrial refractoriness
- .
- .
- C. has a central effect on vagal nuclei - increases PNS effects due to sensitisation & activation of vagal nuclei & no dose ganglion in CNS
-
ECG changes associated with digoxin at therapeutic levels
A. shortened PR interval
B. prolonged PR interval
C. ST segment changes
- .
- .
- B. prolonged PR interval
- C - also correct ST segement changes
-
Digoxin:
A. decreases ventricular response due to vagal stimulation in AF
B. Decreases myocardial oxygen consumption
C. Increases the R-T interval
D. decreases AV conduction
- .
- .
- A decreases ventricular response due to vagal stimulation in AF. also has direct mACh activity
- B - incorrect
- C - incorrect - shortens RT interval
- D - decreases AV conduction (most correct)
-
The most likely ECG changes with digoxin toxicity is:
A. increased PR interval
B. increased QT interval
C. peaked T waves
D. ST elevation
E. Ventricular extrasystoles
- .
- .
- increased PR happens normally (?)
- Dig tox tends to shorten QT interval
- tends to flatten or invert T waves
- ST depression.... so
- E is correct
-
Digoxin toxicity
A. inverted t waves
B. prolonged PR interval
C. Xanthopsia - yellow vision
D. Prolonged PT interval
- .
- .
- C. Xanthopsia is correct.
- all the others happen at therapeutic doses
-
Regarding Desflurane, Isoflurane and Sevoflurane:
A. All 3 inhibit ATPase K+ channels in mitochondria
B. All 3 are degraded into Carbon Monoxide
C. Desflurane is not metabolised to fluoride ions
- .
- .
- All 3 ACTIVATE K-ATPase in mitochondria which without oxygen/ATP causes hyperpolarisation
- ? Sevo doesn't b/down to CO. Millers says it does.
- Des IS metabolised to fluoride ions
-
With regards to the ratio of anaesthetic concentration at awareness to anaesthetic concentration required to prevent response to surgical stimulus
A. Ratio for nitrous oxide is higher than other volatiles
B. Ratio for nitrous oxide is the same as for other volatiles
C. Propofol has a higher ratio compared with volatiles
- .
- .
- A is correct
- 0.4MAC of iso prevents recall and responses to command, where nitrous requires higher than 0.5 or 0.6MAC
-
Toxic effects of inhalationals
A. Compound A not toxic to humans
B. All inhalational agents form CO in soda lime
- .
- .
- Compound A never been shown to cause human toxicity - causes glycosuria, proteinuria
- not all agents form CO in soda lime
-
Nitrous oxide:
A. Oxidises cobalt atom in B12
B. Triggers MH
C. oxidises methionine
- Nitrous oxide inhibits methionine synthase by oxidising cobalamin
- triggers for MH are halo, sevo,des, iso, enf. Other suspects include ketamine, catechols, phenothiazines. Rarely nitrous is suspected
- best answer? A. oxidises cobalt atom in B12
-
Most to least potent local anaesthetic when given intrathecally
A. lignocaine>
B. lignocaine>
C. ropivacaine>bupivacaine>levobupivacaine>ligno
D. levobupiv=bupiv>ropiv>ligno
E. bupiv>levo>ropiv>lignocine
- .
- .
- D. levobupiv = bupiv> ropivacaine > lignocaine
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