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92 Cards in this Set
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++[Mar12][Aug12] You are asked by an Obstetrician to help relax a uterus in labour and deliver for manual removal of placenta. What is a safe and effective dose of IV GTN to be delivered?
a. 5 mcg b. 50 mcg c. 250 mcg (or 200mcg in Aug12) d. 400 mcg e. 500 mcg |
b. ?50mcg (safe) - tend to give in 50mcg boluses.
c. 200mcg? quoted dose sometimes is 100-200mcg ----------- |
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++Rpt: Lap chole on citalopram. What is NOT relatively contraindicated?
A. Omeprazole B. Clonidine C. Pethidine D. Tramadol E. ?Midazolam |
E. Midazolam (if it was an option!)
From: http://www.medscape.com/viewarticle/409573_4 Midazolam is metabolised by CYP3A4. Other SSRIs which inhibit CYP3A4 can increase concentration of midazolam. -- A. Given the risk of dose dependent QT prolongation, citalopram dosage should not exceed 20mg/day when prescribed in combination with CYP450 2C19 inhibitors such as OMEPRAZOLE (drug interaction website); also from MIMS - 'Citalopram may have its serum concentration increased by omeprazole'. B. BJA 2009, 102(4) 567-568 - Interaction between clonidine and escitalopram (similar interaction with citalopram): " This article showed that long-term treatment of rats with citalopram, among other antidepressants, caused a significant decrease in cerebral cortical binding of clonidine accompanied by a functional hyposensitivity of alpha2 adrenergic receptors. This led to attenuation of several central effects of clonidine such as hypothermia and sedation. This is the opposite of what we saw in our patient. It may be that there is a difference in the interaction of escitalopram with clonidine, as opposed to citalopram. Alternatively, this may represent an additive effect of the sedation seen with both drugs. Whatever the mechanism, caution is needed with all centrally acting drugs used in the critically ill. C. Citalopram has its toxicity increased by Pethidine (MIMS) D. Citalopram has its toxicity increased by Tramadol (MIMS) ----------- |
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[2001 Aug] Q144.
Ketamine causes 1. an increase in intracranial pressure 2. malignant hyperpyrexia in susceptible patients 3. an increase in heart rate 4. hypotension when given intrathecally |
1. an increase in intracranial pressure
3. an increase in heart rate ----------- |
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[May09] Rapid infusion of mannitol IV initially causes:
A. Raised ICP B. Reduced CBF C. Reduced K D. Reduced Na E. ? |
A. Raised ICP
The physical bolus of Mannitol causes an initially transient increase, then decreases as interstitial water is drawn out. ----------- |
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[May09][Oct09]
What antibiotics are required for bacterial endocarditis prophylaxis in a woman with MV prolapse for cholecystectomy. A. None B. gentamicin C. ampicillin and gentamicin D. ampicillin E. cephazolin |
A. None
- No antibiotics specifically for prolapse. However will receive cephazolin as part of standard prophylaxis. ----------- |
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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 |
E
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Antibiotics for SBE prophylaxis for a woman with MVP for lap chole
A. None B. Gent C. Amp and gent D. Amp E. Cefazolin |
A. None
Prophylaxis for Prosthetic valve or valve repair PH of BE Unrepaired or palliated cyanotic CHD Partially repaired cyanotic CHD Repaired CHD within 1st 6/12 Heart transplant with valvulopathy ----------- |
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AP43 [Apr 08][Oct08]
Antidepressants drugs are useful in the management of all of the following conditions EXCEPT: A. Chronic headache B. Chronic back pain C. Chronic pain after acute herpes zoster D. Trigeminal neuralgia E. Acute herpes zoster F. Chronic pain post mastectomy (Oct08 version) |
B. Chronic back pain
D. Trigeminal neuralgia F. Chronic pain post mastectomy See latest APMSE 3rd guideline -- - There is no good evidence that antidepressants are effective in the treatment of low back pain (Reversed) (Level 1 [Cochrane Review]) - TCAs are effective in the treatment of chronic headaches (U) and fibromyalgia (N) (Level 1) - Antidepressants reduce the incidence of chronic neuropathic pain after acute herpes zoster (U) (Level II) - Withdrawal of previous key message: Antidepressants reduce the incidence of chronic neuropathic pain after breast surgery - this has been deleted as the information and evidence supporting it has been withdrawn. - Latest guidelines endorse carbamazepine not TCAs for tx of trigeminal neuralgia. ----------- |
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Drug not used to treat intermittent porphyria
A. Morphine B. Phenytoin |
B. Phenytoin
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Elimination half life of tirofiban?
A. 2hrs B. 4hrs C. 6hrs D. 8hrs E. 10hrs |
A. 2hrs
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IV Paracetamol
A. Late plasma levels same as oral B. Highly protein bound C. 30% renally cleared D. Vd 10L/kg |
A. Late plasma levels same as oral
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MH59 [Mar10][Aug10]
70 year old post TKJR. On sub-cut heparin. Develops clinical DVT and platelets 40 (sounds like HITS type-II). Management A. Enoxaparin B. Fondoparinux C. Heparin by infusion D. Lepirudin E. Warfarin |
D. Lepirudin
- Management of HIT: First task is to discontinue unfractionated heparin from ALL sources (including heparin-coated lines, etc). LMWH can also cause HIT, therefore not suitable as a replacement. Fondaparinux is an indirect Factor-Xa inhibitor (synthetic pentasaccharide), and there are some reports of it being used in HIT successfully. Warfarin (Vit K antagonist) is contraindicated in acute HIT (or if suspected HIT), as it can cause skin necrosis or venous limb gangrene. Current recommendations are to treat with DTI's (lepirudin, argatroban, bivalirudin) or danaparoid. Although danaparoid is a LMW heparinoid, there is an extremely low cross-reactivity rate with HIT antibodies, and this is rarely clinically significant. As danaparoid is not an option, the best answer is therefore a direct thrombin inhibitor (DTI), and lepirudin is the only one listed, so answer is D. ----------- |
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Hydroxylethyl starch with intermediate volume replacement
A. 6%HES 130/0.4 |
A. 6%HES 130/0.4
- Voluven or tetrastarch HES is an non-ionic starch derivative or glucose polymer, avoid in RF, coagulopathy Duration >6hrs Halflife 12 hours ----------- |
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PZ07b ANZCA version
Moclobemide (Aurorix) is an antidepressant which A. reversibly blocks mono-amine oxidase (MAO) types A and B B. blocks MAO enzymes for 24-36 hours C. is safe to use with pethidine D. is safe with direct acting sympathomimetics E. is safe with indirect acting sympathomimetics |
D. is safe with direct acting sympathomimetics
- A. reversibly blocks mono-amine oxidase (MAO) types A and B – More selective for MAO A. B. blocks MAO enzymes for 24-36 hours – False. 12-18 hours. C. is safe to use with pethidine – False. May percipitate serotonin syndrome. D. is safe with direct acting sympathomimetics – Ref: Bryson et al. Patient selection in ambulatory anesthesia – An evidence-based review: part II. CAN J ANESTH 2004 / 51: 8 / pp 782–794. E. is safe with indirect acting sympathomimetics – Potentiates their effect. ----------- |
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PZ26
The antibiotic LEAST likely to be effective for the management of anaerobic peritonitis is A. carbenicillin B. cefoxitin C. cephalothin D. chloramphenicol E. clindamycin |
C. cephalothin
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PZ29
Each of the following drugs increases lower oesophageal sphincter tone EXCEPT A. metoclopramide B. domperidone C. prochlorperazine D. cyclizine E. atropine |
E. atropine
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PZ34a ANZCA version
Each of the following is a complication of loop diuretic treatment EXCEPT A. hypokalaemia B. hyponatraemia C. hypermagnesaemia D. irreversible sensori-neural deafness E. metabolic alkalosis |
C. hypermagnesaemia
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PZ45b ANZCA version
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 |
D. metoclopramide increases the lower oesophageal sphincter tone but relaxes the pyloric sphincter
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PZ48
Non-steroidal anti-inflammatory drugs (NSAIDs) are NOT A. known to cause reversible renal impairment B. known to cause a clinically significant increase in average operative blood loss C. recognised as a cause of renal papillary necrosis D. known to induce life-threatening asthma in atopic patients with aspirin sensitivity |
B. known to cause a clinically significant increase in average operative blood loss
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PZ53c ANZCA version
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 |
E. will reduce the venous admixture when administered in a concentration of 20 ppm
- 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 ----------- |
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PZ59b ANZCA version
All of the following have anti-emetic properties EXCEPT A. cannabinoid- 1 agonists B. dopamine-2 agonists C. 5-hydroxytryptamine- 1A agonists D. 5-hydroxytryptamine-3 antagonists E. neurokinin- 1 antagonists |
B. dopamine-2 agonists
Dopamine ANTagonists are anti-emetic ----------- |
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PZ65 [Apr07][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 |
A. 12 hours
or ?B. 1-2 days - The answer is either A or B, depending on the formulation used. I wonder what the examiners take for their post-exam hangover??? 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. ----------- |
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PZ68c ANZCA version
Heparin Induced Thrombocytopenia (HITS) A. is associated with antibodies to complexes of Antithrombin 3 (ATIII) and heparin B. is associated with a more rapid drop in platelet count if the patient has been exposed to heparin within the last three months C. is not associated with the use of low molecular weight heparins D. results in the maintenance of heparin-dependent antibody levels indefinitely after their development E. results in thrombotic complications in most patients |
B. is associated with a more rapid drop in platelet count if the patient has been exposed to heparin within the last three months
vs E. results in thrombotic complications in most patients - A. is associated with antibodies to complexes of anti-thrombin 3 (ATIII) and heparin - Clinically, there are two types of HIT that can result from heparin administration: HIT type I, a benign non-immune condition in which no heparin- dependent antibodies are present; and HIT type II, a immune-mediated syndrome caused by an antibody to the heparin-platelet factor 4 (PF4) complex. B - TRUE for HIT II. Thirty percent of patients present with ‘rapid- onset’ HIT type II. They show an abrupt drop in platelet count when heparin is administered. These patients have often received heparin within the last 3 months. C. is not associated with the use of low molecular weight heparins - Less binding to PF4 occurs with low molecular weight heparin (LMWH) and pentassacharide, and consequently, these are less antigenic and cause HIT less frequently. D. results in the maintenance of heparin-dependent antibodies indefintely after their development - HIT–IgG antibodies are transient and cannot be detected several weeks or months following the episode of HIT type II. HIT–IgG usually are not re-stimulated despite re-exposure to heparin. E. results in thrombotic complications in most patients – True for HIT II. Bleeding associated with thrombocytopenia is rare but thrombotic complications are common. Of the patients who develop HIT–IgG seroconversion, 30–50% will develop thrombocytopenia; and of these, 30–80% will demonstrate isolated thrombotic events, 0.01–0.1% of whom will experience multiple thromboses or ‘white clot syndrome’. - E. TRUE FOR HIT Type II • Immunogenic heparin-PF4 complexes which cause an immunologic response • Antibodies are generated resulting in a complex forming between antibodies, heparin, and PF4 (mediated through the FcyIIa portion of the platelet). This complex leads to further platelet activation resulting in formation of microparticles and thrombin generation. • Antibodies also recognize PF4 bound to heparin on the endothelial surface and this surface becomes activated leading to another route of thrombin production. ----------- |
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PZ68b ANZCA version [2002-Aug][2003-Apr][2004-Apr][2004-Aug][Mar06][Jul06][Oct08][Sep11]
Immunologically mediated heparin induced thrombocytopaenia is characterised by A. onset within a few days of first starting heparin B. intravascular thromboses C. platelet count rarely reduced below 100x10^9/L D. continuation of thrombocytopaenia after cessation of heparin E. presence of non-specific (heparin-independent) platelet antibodies |
B. intravascular thromboses
- From wiki: A. onset within a few days of first starting heparin - false: "A second form of HIT, HIT type II or immune-mediated HIT, demands more attention. In patients receiving heparin for more than 5 days, antibodies to the heparin-platelet factor 4 complex can form, which are capable of binding to platelet Fc receptors and inducing platelet activation and aggregation." (Stoelting Ch17) B. intravascular thromboses - true: "In vivo, this leads to both an increased clearance of platelets with resultant thrombocytopenia and venous and/or arterial thrombus formation, with the potential for severe organ damage (loss of limbs, stroke, myocardial infarction) as well as unusual sites of thrombosis (adrenal, portal vein, skin)." -- HIT Type II • Immunogenic heparin-PF4 complexes which cause an immunologic response • Antibodies are generated resulting in a complex forming between antibodies, heparin, and PF4 (mediated through the FcyIIa portion of the platelet). This complex leads to further platelet activation resulting in formation of microparticles and thrombin generation. • Antibodies also recognize PF4 bound to heparin on the endothelial surface and this surface becomes activated leading to another route of thrombin production. ----------- |
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PZ69b ANZCA version
Low molecular weight heparin A. has a similar ratio of antithrombotic to anticoagulant activity as normal heparin B. has a lower antifactor Xa activity than normal heparin C. has a higher antifactor IIa activity than normal heparin D. is prepared by fractionation of normal heparin E. anticoagulant effect can be monitored by activated clotting time and APPT |
D. is prepared by fractionation of normal heparin
➮ higher antifactor Xa activity than normal heparin ➮ lower antifactor IIa activity than normal heparin ----------- |
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PZ76
The dose response relationship for non-steroidal anti-inflammatory drugs is characterised by A. a small variation in effective dose B. an effect that increases linearly as dose increases, reaching a maximum effect C. a minimal effective dose, and continuously increasing effect as dose increases D. no ceiling dose with no minimal effective dose E. a minimal effective dose and a bounded maximal effect |
E. a minimal effective dose and a bounded maximal effect
"In contrast to the dose-dependent analgesic effects of opioids, NSAIDs appear to exhibit a ceiling effect when used for postoperative analgesia" Stoelting NSAIDs have can have >50% variation in effective dose between individuals. Their effect increases exponentially to a maximum effect (when all COX blocked) and they have a minimum effective dose (blockage of sufficient COX to give effect). Katzung p540 ----------- |
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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 |
D. the elimination half life is 2 - 2.3 hours
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PZ79b ANZCA version [2003-Aug] Q105, [2004-Apr] Q69, [Jul06] Q54, [Apr07
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 administration |
D. a one hour delay between peak plasma concentration and maximum analgesia
- A - false - maximum is 90mg/kg/day up to 4g B - ----------- |
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PZ80e ANZCA version [2003-Aug]
Low molecular weight heparins A. are cleared principally by the liver B. are ineffective if only administered post-operatively C. cross the placenta D. have a dose-dependent half-life E. have a longer half-life than standard (unfractionated) heparin |
E. have a longer half-life than standard (unfractionated) heparin
LMW Heparin (cf. Unfractionated Heparin) • Higher bioavailability due to lower protein binding • Not fully reversible with protamine • Longer t1/2 (4-5hrs vs 1-2 hrs) and more predictable kinetics • Less HITS and less platelet function affect ----------- |
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PZ80d ANZCA version [2002-Aug] Q44, [2003-Apr] Q27, [Jul06]
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 |
B. 2 to 4 times that of unfractionated heparin
LMW Heparin (cf. Unfractionated Heparin) • Higher bioavailability due to lower protein binding • Not fully reversible with protamine • Longer t1/2 (4-5hrs vs 1-2 hrs) and more predictable kinetics • Less HITS and less platelet function affect ----------- |
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PZ81a [Jul07][Apr08]
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) |
D. sedation, dry mouth, orthostatic hypotension and cardiac conduction defects
"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 & clinical implications in anaesthesia & critical care medicine Kam, Peter, Anaesthesia 1997 Vol52 p982-988 ----------- |
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PZ83
Middle-aged man for cataract extraction & insertion IOL. He is for general anaesthesia because he cannot cooperate due to mental retardation. He has nasal speech and first degree heart block on ECG. Which group of drugs would you avoid? A. Barbiturate anaesthetic agents B. Synthetic opioids C. Muscle relaxants D. Volatiles E. Anticholinergics |
A. Barbiturate anaesthetic agents
Likely to have Myotonica Dystrophica ----------- |
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PZ84b ANZCA version [2002-Aug] Q101, [2003-Apr]
Thiazide diuretics may cause A. hypernatraemia B. precipitation of acute gout C. hypoglycaemia D. hyperkalaemia E. hepatic failure |
B. precipitation of acute gout
• decrease Na / K • increase Ca / glucose / urate "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. ----------- |
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PZ86a ANZCA version [2001-Apr] Q150
The herbal remedy, 1. St John's wort, a herbal antidepressant, may interact with serotonin uptake inhibitors 2. Ginko biloba interferes with the coagulation system, resulting in increased bleeding 3. Valerian root enhances the effect of sedative agents 4. Ephedra (ma huang) may produce hypotension |
1,2,3 - true
- 1. St John's wort, a herbal antidepressant, may interact with serotonin uptake inhibitors - true: "As St John's Wort increases serotonin levels, a serotonin syndrome may occur when it is taken with other serotoninergic drugs such as serotoninergic reuptake inhibitors and tricyclic antidepressants" (Anaesthesia Volume 57, Issue 11, 2002. Pages: 1083–1089) 2. Ginko baloba interferes with the coagulation system, resulting in increased bleeding - true: "Danshen, dong quai, jui, ginkgo biloba and garlic have anticoagulant effects and therefore increase the risk of bleeding during surgery." (Anaesthesia, Volume 57, Issue 11, 2002. Pages: 1083–1089) 3. Valerian root enhances the effect of sedative agents - true: "As valerian causes sedation, it is advised that it should not be combined with benzodiazepines, barbiturates and alcohol" (Anaesthesia Volume 57, Issue 9, 2002. Pages: 889–899) 4. Ephedra (ma huang) may produce hypotension - false ----------- |
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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 |
B. ginko
4G's (Ginko, Ginger, Garlic, Ginseng) + Vitamin E cause bleeding ----------- |
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PZ86c ANZCA version [2005-Apr]
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 |
B. ginseng and ephedra may produce cardiovascular complications during general anaesthesia
- ----------- |
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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 |
E. St Johns wort
4G's (Ginko, Ginger, Garlic, Ginseng) + Vitamin E cause bleeding ----------- |
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PZ86e [Aug10]
Serotonin syndrome has been reported following SSRI coadministration with: A. Gingko B. Garlic C. Ginger D. St John’s wort E. Vallerian [NB: PZ86 seems to be the same Q as it has same options, but is about bleeding not serotonin syndrome. Remembered wrongly here??] |
D. St John’s wort
- From UTD: Use of St. John's wort should be avoided in combination with other antidepressants until a definitive mechanism of action is elucidated to avoid the potential for the serotonin syndrome [77]. Several cases of serotonin excess (agitation, hyperthermia, diaphoresis, tachycardia, and neuromuscular disturbances including rigidity) also have been reported in elderly individuals taking St. John's wort and SSRIs together. ----------- |
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PZ87a ANZCA version [2001-Apr] Q90, [2003-Apr] Q83, [2003-Aug] Q17, [Apr07]
When compared with non-selective non-steroidal antiinflammatory drugs (NSAIDs), the COX-2 selective drugs A. are less likely to induce bronchospasm in aspirin sensitive patients B. cause significantly fewer adverse renal effects C. have less effect on platelet function D. have lower analgesic efficacy E. have a similar incidence of gastrointestinal side-effects |
A. are less likely to induce bronchospasm in aspirin sensitive patients
vs C. have less effect on platelet function A>>C - From APMSE 3rd ed - Coxibs do not appear to produce bronchospasm in individuals known to have aspirin‐ exacerbated respiratory disease (U) (Level I). Coxibs do not IMPAIR platelet function; this leads to reduced perioperative blood loss in comparison with non‐selective NSAIDs (S) (Level II). i.e. they still affect platelet function... |
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PZ87b ANZCA version [2002-Mar] Q65, [2002-Aug]
When compared with non-specific nonsteroidal anti-inflammatory drugs (NSAIDs), NSAIDs which are selective for the inducible cyclooxygenase- 2 (Cox-2) enzyme, A. induce significantly fewer cases of severe gastrointestinal bleeding with long-term use B. have less inhibitory effects on platelet aggregation because they do NOT block platelet thromboxane production C. are more protective of renal function D. are effective in chronic musculoskeletal pain but NOT acute postsurgical pain E. do NOT inhibit endothelial production of prostacyclin (PGI2) |
B. have less inhibitory effects on platelet aggregation because they do NOT block platelet thromboxane production
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PZ87c ANZCA version [2005-Apr]
Which of the following statements is INCORRECT? Selective cyclo-oxygenase-type 2 (COX-2) inhibitors A. are contraindicated in patients with ischaemic heart disease B. block the production of prostacyclin in diseased vessels C. block the synthesis of prostaglandins involved in renal salt and water homeostasis D. block thromboxane A2 synthesis in platelets E. do NOT block the synthesis of prostaglandins involved in gastric mucosal protection |
D. block thromboxane A2 synthesis in platelets
Platelet thromboxane A2 production is preserved (or even enhanced due to lower prostacyclin), hence platelet aggregation is unimpaired. - COX II inhibitors have an increased incidence of myocardial infarction in patients who have IHD - Prostacyclin synthesis is inhibited NEJM : COX II Inhibitor - Prostaglandin is involved in renal protection. COX II Inhibitors have an effect on reducing GFR. - Gastric mucosal production of prostaglandings is preserved. COX 1 and COX 2 both present in the stomach but ulcer rate not increased because COX 1 is not inhibited. ----------- |
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PZ88
Advantages of rofecoxib over an equi-analgesic dose of naproxen include A. a lower incidence of thrombo-embolic stroke B. greater safety in patients with renal impairment C. a longer duration of action D. less risk of bronchospasm E. less risk of fluid retention and hypertension |
D. less risk of bronchospasm
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PZ89
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 |
A. should NOT be given high doses of tramadol
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PZ91
The dose of phenylephrine in one drop (assume one drop = 0.05 ml) of 10% phenylephrine solution is A. 5 microgram B. 20 microgram C. 200 microgram D. 1 milligram E. 5 milligram |
E. 5 milligram
10% solution = 100mg/ml one drop = 0.05 ml = 0.05 x 100 = 5mg ----------- |
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PZ92
The herbal medicine most likely to be associated with cardiovascular instability in the peri-operative period is A. echinacea purpurea (echinacea) B. ephedra sinica (ma-huang) C. ginkgo biloba (ginkgo) D. hypericum perforatum (St. John's Wort) E. tanacetum parthenium (feverfew) |
B. ephedra sinica (ma-huang)
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PZ95
Correct statements regarding intravenous phenylephrine include all the following EXCEPT A. A reasonable bolus dose for hypotension is 250 micrograms. B. Associated reflex bradycardia should NOT be treated with atropine. C. It acts directly on alpha-adrenergic receptors. D. It increases systolic and diastolic pressures. E. It is metabolised by Monoamine Oxidase |
B. Associated reflex bradycardia should NOT be treated with atropine.
Usual dose would be 100 mcg ----------- |
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PZ97
In its pure form arnica (a herbal medication) can cause postoperative A. Angina B. Bleeding C. Prolonged sedation D. Oculogyric crises E. Vomiting |
B. Bleeding
- (previous grp said E. vomiting) ----------- |
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PZ98 [Mar12][Aug12]
Cephalothin has NO significant activity against A. escherichia coli B . proteus mirabilis C. pseudomonas aeruginosa D. staphylococcus aureus E. streptococcus pneumoniae |
C. pseudomonas aeruginosa
MIMS: The in vitro bactericidal action of cephalothin results from inhibition of cell wall synthesis. In general cephalothin has higher activity against Gram positive than Gram negative organisms. Gram negative organisms vary greatly in their sensitivity to the drug. Susceptibility testing is highly desirable because the range of antibiotic concentrations at which bacteria are inhibited may vary substantially according to the isolate. Cephalothin is usually active against the following organisms in vitro: beta-haemolytic and other Streptococci (most strains of Enterococci, e.g. Enterococcus faecalis, are resistant); Staphylococci (including coagulase positive, coagulase negative, and penicillinase producing strains; methicillin resistant Staphylococci are resistant); Streptococcus pneumoniae; Haemophilus influenzae; Escherichia coli; Klebsiella; Proteus mirabilis. ----------- |
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PZ99
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 |
E. a peak analgesic effect at 60 minutes
• 5-10 mins - pain relief • 30 mins - anti-pyretic effect • 60 mins - peak analgaesia Duration of analgaesia and anti-pyretic effect both 6 hrs ----------- |
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PZ101 [Mar06][Apr08]
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 the treatment |
D. the placebo effect can be eliminated by using active treatments in both study groups
- 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 Placebo - McQuay, More. Postgrad Med J. 2005 Mar;81(953):155-60 ----------- |
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PZ102 ANZCA version [2005-Sep] Q122, [Mar06]
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 |
D. inhibits ADP induced platelet activation
ADP receptor antagonist. Irreversible. P2 receptor binds ADP and activates platelets to expose GPIIb/IIIa and aggregate + degranulate. The IIb/IIIa complex functions as a receptor mainly for fibrinogen and vitronectin but also for fibronectin and von Willebrand factor. Activation of this receptor complex is the "final common pathway" for platelet aggregation. ~~ ----------- The thienopyridines, ticlopidine and clopidogrel, are antiplatelet drugs. They are prodrugs and are metabolised in the liver to active metabolites that are non-competitive antagonists of the platelet adenosine diphosphate receptor, P2Y12. Inhibition of platelet aggregation by these drugs is delayed until 24–48 h after administration, with maximal inhibition achieved after 3–5 days. Recovery of platelet function after drug withdrawal is slow (7–14 days). |
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PZ103 [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 |
E. results in similar late plasma concentrations as oral paracetamol
The pharmacokinetics of oral paracetamol (500 mg) and intravenous propacetamol (1 g) were compared in a randomised, double blind, two period crossover study in 12 healthy male subjects. As expected, plasma concentrations of intravenous propacetamol were significantly higher and obtained earlier, compared to oral administration, however after the first hour and up to 24 hours the plasma concentrations remained similar. • Distribution The volume of distribution of paracetamol is approximately 1 L/kg. Paracetamol is not extensively bound to plasma proteins. • Metabolism Paracetamol is metabolised mainly in the liver following two major hepatic pathways: glucuronic acid conjugation and sulfuric acid conjugation. The latter route is rapidly saturable at doses that exceed the therapeutic doses. A small fraction (less than 4%) is metabolised by cytochrome P450 to a reactive intermediate (N-acetyl benzoquinone imine) which, under normal conditions of use, is rapidly detoxified by reduced glutathione and eliminated in the urine after conjugation with cysteine and mercapturic acid. However, during massive poisoning, the quantity of this toxic metabolite is increased. • Elimination The metabolites of paracetamol are mainly excreted in the urine. 90% of the dose administered is excreted in 24 hours, mainly as glucuronide (60 to 80%) and sulfate (20 to 30%) conjugates. Less than 5% is eliminated unchanged. Plasma half-life is 2.7 hours and total body clearance is 18 L/hour. ----------- |
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PZ103 ANZCA version [2005-Sep] Q140, [Mar06] Q70[Mar10] [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 |
E. results in similar late plasma concentrations as oral paracetamol
- ----------- |
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PZ104 [Oct08]
Established Legionnaires disease is treated with A. Aminoglycosides B. Cephalosporins C. Chloramphenicol D. Crystalline penicillin E. Erythromycin |
E. Erythromycin
From eMedicine: Standard antibiotic susceptibility tests are not reliable in Legionnaires disease. Erythromycin, with or without rifampin, is the drug of choice for Legionnaires disease, but the combined GI manifestations of the disease added to the GI effects of erythromycin may be problematic. For this reason, some specialists prefer to start with doxycycline. Other drugs include cotrimoxazole, tetracycline, and ciprofloxacin. The new fluoroquinolone and macrolide drugs may be indicated, but their efficacy has not been established. ----------- |
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PZ105 [Jul06][Apr08][Oct08]
When dealing with morbidly obese patients, there are two weight measures used to calculate drug doses, the Ideal Body Weight (IBW) and the Total Body Weight (TBW). Which ONE of the following is true? A. The dose of atracurium should be based on IBW B. The dose of propofol should be based on ?IBW C. The dose of thiopentone should be based on ?TBW D. The dose of suxamethonium should be based on TBW E. The dose of vecuronium should be based on TBW |
D. The dose of suxamethonium should be based on TBW
OR B. The dose of proposal shoold be based on IBW - CEACCP article 2004 Pharmacokinetics in obese patients Propofol - induction: IBW, Maintenance: TBW or IBW + (0.4x excess wt) TBW Suxamethonium - TBW; >140kg. Maximum 120 - 140mg. ----------- |
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PZ106
Patient with severe depressive episode unresponsive to medications. On tranylcypramine (Parnate). How do you manage him for ECT? A. Cancel the case. Do the ECT after he has been off his tranylcypramine for 2 weeks then proceed B. refer to tertiary centre C. use your normal drugs but proceed with caution D. use midazolam and thiopentone (or: induce with midazolam and remifentanil) E. give a small dose of esmolol then proceed. |
C. use your normal drugs but proceed with caution
- tranylpypramine is a MAOI - quote from Morgan and Mikhail Ch 27, this would appear to suggest that other than an exaggerated response to drugs that "The practice of discontinuing MAO inhibitors at least 2 weeks prior to elective surgery is no longer recommended. With the exception of tranylcypromine, these agents produce irreversible enzyme inhibition; the 2-week delay allows sufficient regeneration of new enzyme. Studies suggest that patients may be safely anesthetized, at least for ECT, without this waiting period. Phenelzine can decrease plasma cholinesterase activity and prolong the duration of succinylcholine. Opioids should generally be used with caution in patients receiving MAO inhibitors, as rare but serious reactions to opioids have been reported. Most serious reactions are associated with meperidine, resulting in hyperthermia, seizures, and coma. As with tricyclic antidepressants, exaggerated responses to vasopressors and sympathetic stimulation should be expected. If a vasopressor is necessary, a direct-acting agent in small doses should be employed. Drugs that enhance sympathetic activity such as ketamine, pancuronium, and epinephrine (in local anesthetic solutions) should be avoided." ----------- |
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PZ107 [Apr08]
In patients with renal impairment, doses of all the following drugs may require adjustment EXCEPT A. carbamazepine B . gabapentin C. hydromorphone D. morphine E. oxycodone |
E. Oxycodone
- see APMSE 3rd ed. ----------- |
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PZ108
A patient with well controlled bipolar disorder on lithium is booked for an elective laparoscopic cholecystectomy. Regarding lithium A. it increases requirements for volatile anesthetics B. potentiates non-depolarising muscle relaxants C. potentiates suxamethonium D. potentiates both depolarising and non-depolarising muscle relaxants E. should stop lithium for 2 weeks before elective surgery |
D. potentiates both depolarising and non-depolarising muscle relaxants
Prolongation of neuromuscular block was reported in patient receiving lithium carbonate and both depolarising and nondepolarising neuromuscular blockers. Only one report did not demonstrate prolongation of recovery from succinylcholine in pts receiving lithium. ----------- |
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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 |
E. NSAIDS may increase the risk of bleeding after some surgical procedures
• COX-2 causes prostaglandin inhibition with unopposed Thromboxane A2 (TXA2) activity resulting in a PROcoagulant state. - 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. ----------- |
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PZ110 [Mar10]
All the following prolong QT interval except A. volatiles B. suxamethonium C. magnesium sulfate D ?raised intrathoracic pressure E ? |
C. magnesium sulfate
Anesthesia for Patients with Congenital Long QT Syndrome Anesthesiology. Volume 102(1), January 2005, pp 204-210 Prolonged QT = impaired ventricular repolarisation • Although ALL Volatiles prolong the QT interval to some extent, they have been successfully used in patients with c-LQTS receiving beta blocker therapy. • Succinylcholine prolongs the QT interval in patients with c-LQTS unless pretreatment with a priming dose of tubocurarine is used. • Vecuronium and atracurium have no effect on QT • Hypomagnesaemia causes prolonged QT • Atropine can precipitate Torsades, Glycopyrrolate prolongs QT • Combined anticholinergic medications (glycopyrrolate or atropine) plus anticholinesterases (neostigmine or edrophonium) has been shown to prolong the QT • Sympathetic stimulation prolongs QT (ie. physical activity emotional stress, anxiety, or fear) • Fentanyl and morphine have been used without adverse effects in patients with c-LQTS ~~ ----------- Magnesium sulfate is the treatment of choice for prevention of recurrence in patients with drug-induced TdP even with normal magnesium concentrations. Furthermore, there appears to be no contraindication to its use in patients with c-LQTS. |
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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 |
All of them increase tone.
See wiki. And see Stan's MCQ. Ref: Ng et al. Gastroesophageal Reflux and Aspiration of Gastric Contents in Anesthetic Practice. Anesth Analg 2001;93:494 –513. ----------- |
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PZ112 [2004-Apr] Q105, [Mar06]
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 |
C. conditions associated with glutathione deficiency
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PZ113 ANZCA version [2004-Aug] Q110, [Mar06]
Following acute subarachnoid haemorrhage, the use of antifibrinolytic agents is associated with decreased A. incidence of hydrocephalus B. incidence of rebleeding C. incidence of pulmonary embolus D. mortality from all causes E. mortality from ischaemic neurological events |
B. Incidence of rebleeding
- The Lancet Volume 369, Issue 9558, 27 January 2007-2, Pages 306-318 Seminar-Subarachnoid haemorrhage. "Antifibrinolytic drugs prevent rebleeding after aneurysmal rupture, but because they increase the risk of cerebral ischaemia, they have no useful effect on overall outcome." ----------- |
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PZ114 [2004-Aug] Q121, [Jul05][Oct08]
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 |
A. platelet dysfunction persists for over 48 hours after cessation of drug
- 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) [edit] ----------- |
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PZ115 ANZCA Version [Oct08][Mar11]
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 |
A. it has a structure unrelated to heparin
- As per Yentis pg 214 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) - ➭ Fondaparinux is a synthetic pentasaccharide selective Factor Xa inhibitor ➭ the antithrombotic activity is the result of antithrombin III—mediated (ATIII-mediated) selective inhibition of Factor Xa (MIMS) ➭ Fondaparinux is a novel anti-coagulant with anti-Xa and anti-IXa activity which does not cross react with HIT antibodies. Its usefulness for the treatment of HIT type II has not been established." 'Heparin-induced thrombocytopenia' C.L. Thong, P.C.A. Kam Current Anaesthesia & Critical Care (2005) 16, 143–150 ➭ ARIXTRA is contraindicated in patients with severe renal impairment (creatinine clearance <30 mL/min) - renally excreted ➭ Thrombocytopenia. Until further experience with fondaparinux sodium is gained, platelet monitoring is recommended at baseline and at the end of treatment. ➭ Heparin-Induced Thrombocytopenia Associated with Fondaparinux http://content.nejm.org/cgi/content/short/356/25/2653 http://www.arixtra.com/ & MIMS ----------- |
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PZ116 [Jul05]
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 |
A. bromocripitine
false so answer to choose. i hate these double negatives. - Bromocriptine is a dopamine receptor agonist, so should not have a role in serotonin syndrome - it is used in the treatment of NEUROLEPTIC MALIGNANT SYNDROME. B. chlorpromazine - true: "Second, chlorpromazine has been advocated as a potential therapy for the serotonin syndrome" C. cyproheptadine - true: "The most widely prescribed 5-HT antagonist is cyproheptadine, which can only be given orally or via nasogastric tube. Cyproheptadine acts primarily on 5-HT2 receptors, and produces rapid (within one hour) resolution of symptoms, particularly of the CNS effects" D. diazepam - true: "The mainstay of managing increased muscle tone is neuromuscular paralysis and benzodiazepine infusions." E. non-depolarizing neuromuscular blockers - true: See above ----------- |
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PZ117 [Jul05]
Which of the following herbal treatments is most likely to cause central serotonin syndrome when combined with a serotonin reuptake inhibitor? A. echinacea B. ginko C. ginseng D. St John’s Wort E. valerian |
D. St John’s wort
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PZ118 [Jul05] [Mar06] [Apr07] Q80, [Jul07] [?Aug12]
In patients with renal failure each of the following drugs has prolonged clearance or has active metabolites with prolonged clearance EXCEPT A. aspirin B. buprenorphine C. codeine D. pethidine E. tramadol |
B. buprenorphine
Of the opioids, buprenorphine poses the least risk to patients with renal failure as the metabolites are virtually inactive and if accumulation does occur it is of no significance. Update in Anaesthesia Issue 7 (1997) Article 2: Page 5 of 7 The Management of Postoperative Pain "Morphine and codeine are avoided in renal failure/ dialysis pts; Hydromorphone and oxycodone are used with caution and close monitoring; and that methadone and fentanyl/sufentanil appear to be safe to use". also stated "insufficient data to make recommendation" on use of oxycodone in renal failure, also stated "use of oxycodone best avoided in dialysis pts". Opioids in Renal Failure and Dialysis Pts Journal of Pain and Sx Mx" Vol 28. No5, Nov 2004. ----------- |
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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 |
C. has a mechanism of action that is antithrombin (ATIII) dependent
- ➭ Fondaparinux is a synthetic pentasaccharide selective Factor Xa inhibitor ➭ the antithrombotic activity is the result of antithrombin III—mediated (ATIII-mediated) selective inhibition of Factor Xa (MIMS) ➭ Fondaparinux is a novel anti-coagulant with anti-Xa and anti-IXa activity which does not cross react with HIT antibodies. Its usefulness for the treatment of HIT type II has not been established." 'Heparin-induced thrombocytopenia' C.L. Thong, P.C.A. Kam Current Anaesthesia & Critical Care (2005) 16, 143–150 ➭ ARIXTRA is contraindicated in patients with severe renal impairment (creatinine clearance <30 mL/min) - renally excreted ➭ Thrombocytopenia. Until further experience with fondaparinux sodium is gained, platelet monitoring is recommended at baseline and at the end of treatment. ➭ Heparin-Induced Thrombocytopenia Associated with Fondaparinux http://content.nejm.org/cgi/content/short/356/25/2653 http://www.arixtra.com/ & MIMS -- 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) ----------- |
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PZ120 [Mar06]
Gabapentin used for acute postoperative pain A. has it 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 opiates alone E. works by binding at GABA receptors |
C. may require high doses to be effective
- A. has it analgesic effect reduced by concurrent use of COX-2 inhibitors – False. B. increases anxiety if administered preoperatively – False. Anxiolytic. C. may require high doses to be effective - Day 1, 300 mg od; day 2, 300 mg bd; day 3, 300 mg tds, increasing up to 800 mg tds. D. reduces the incidence of dizziness when compared with opiates alone – False. Increases. E. works by binding at GABA receptors – False. It appears to have an inhibitory action at voltage-gated calcium channels where it blocks the a2δ subunit. Ref: Ryder et al. Treatment of chronic pain: antidepressant, antiepileptic and antiarrhythmic drugs. CEACCP 2005. 5:1:18-21. - does not act via GABA receptors Gabapentin was initially synthesized to mimic the chemical structure of the neurotransmitter gamma-aminobutyric acid (GABA), but is not believed to act on the same brain receptors. Its exact mechanism of action is unknown, but its therapeutic action on neuropathic pain is thought to involve voltage-gated N-type calcium ion channels. It is thought to bind to the α2δ subunit of the voltage-dependent calcium channel in the central nervous system. - reported doseages of 1200mg pre-op -"the incidence of dizziness was significantly increased and the authors commented that this may be a problem in the context of day-case surgery" Editorial II: Gabapentin: a new drug for postoperative pain? British Journal of Anaesthesia 2006 96(2):152-155 ----------- |
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PZ121 [Mar06][May09]
In elderly patients each of the following statements is true EXCEPT A. antagonism of neuromuscular blockade with anticholinesterases 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 Which statement regarding pharmacology in elderly patients is NOT TRUE? A. Anticholinesterase drugs may not reverse muscle relaxants as well as in younger patients B. Atropine has less effect on the heart rate compared to younger patients C. The MAC of volatile agents is 20 - 40% less D. Ephedrine is not as reliable at correcting hypotension E. Non depolarising muscle relaxants are slower in onset because of a lower cardiac output |
A. antagonism of neuromuscular blockade with anticholinesterases is less likely to be effective than in the younger patient
- CEACCP 2004, perioperative care of the elderly And from wiki: A. antagonism of neuromuscular blockade with aniticholinesterases is less likely to be effective than in the younger patient - false and answer to choose: "Antagonism of neuromuscular blockade with anticholinesterase drugs tends to be similar to younger adults." (Perioperative care of the elderly Murray and Dodds Contin Educ Anaesth Crit Care Pain. 2004;4:193-196) B. atropine produces a lesser heart rate response than in younger patients: true - "Ageing is associated with reduced b-receptor sensitivity, which results in a reduction in response to exogenous b-agonists. However, the response to alpha-agonists is comparable to that seen in younger patients. This relatively poor response to beta-stimulation also results in the reduced heart rate response to atropine." C. ephedrine is less likely to be effective (at raising blood pressure) than in the younger patient - true: "Ephedrine is likely to be ineffective in the elderly; alpha-agonists such as metaraminol or phenylephrine should be used in preference." D. MAC of all inhalational agents is reduced by 20 to 40% - true: "The MAC value of all inhalational anaesthetic agents is reduced by 20–40% from young adult values." E. time of onset of neuromuscular blockade is prolonged due to a reduction in cardiac output - true: "However, the time of onset and the duration of action are both prolonged because of a reduction in cardiac output and reduced metabolism, respectively" ----------- |
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PZ122 [Mar06]
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. bronchospasm D . hypoglycaemia in fasting patients E. Stevens-Johnson syndrome |
C. bronchospasm
- From Kaye et al. Pharmacology of herbals and their impact in anesthesia. Current Opinion in Anaesthesiology 2007, 20:294–299. A. With regard to ginseng’s interaction with antidepressants such as monoamine oxidase inhibitors, concurrent use of ginseng with phenelzine sulfate should be avoided because manic episodes have been reported with routine use of both [79,80]. B. Typically, ginseng is well tolerated, but side effects such as bleeding abnormalities secondary to antiplatelet effects, headache, vomiting, Stevens – Johnson syndrome, epistaxis, and hypertension have been reported [68 – 74]. C. no increased risk - answer to choose. D. Finally, because of ginseng’s poten- tial to cause decreased blood glucose levels, it should be used cautiously in diabetic patients receiving insulin or other oral hypoglycemic agents, and blood glucose levels should be monitored. E. see A. ----------- |
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PZ123 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 |
D. high cumulative doses of doxorubicin are associated with cardiomyopathy
- A. false - There is clinical evidence that azathioprine antagonises the effect of NMDRs and potentiates the neuromuscular block caused by suxamethonium via a phosphodiesterase effect. B. false - dose dependent C. cyclophosphamide has pseudocholinesterase inhibitor properties that persist for 3-4 weeks after the last dose. This can reduce the breakdown of suxamethonium, resulting in protracted postoperative apnoea. D. True. E. false - NSAID's when used with Methotrexate reduce methotrexate clearance and enhance methotrexate-related toxicity . ----------- |
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PZ124 [Jul07]
Which of the following is NOT associated with serotonin syndrome A. phenelzine B. pethidine C. ondansetron D. chlorpromazine E. sumatriptan |
D. chlorpromazine
Serotonin = 5-hydroxytryptamine, or 5-HT ➭ phenylzine is a MAO inhibitor - Serum serotonin levels are tightly regulated and controlled by endothelial monoamine oxidase inactivation and cellular uptake. Usually any excess serotonin is cleared by the pulmonary or hepatic endothelium or absorbed by the platelets. (http://psy.psychiatryonline.org/cgi/reprint/42/3/258.pdf) ➭ The phenylpiperidine series opioids, pethidine (meperidine), tramadol, methadone and dextromethorphan and propoxyphene, appear to be weak serotonin re-uptake inhibitors and have all been involved in serotonin toxicity reactions with MAOIs (including some fatalities). ➭ Ondansetron is 5-HT3 receptor antagonist - Canadian Adverse Reaction Newsletter: 'Symptoms of serotonin syndrome have also been reported with the concomitant use of 5-HT3 receptor antagonists (e.g., dolasetron, granisetron, ondansetron) - Perhaps blocking one type of serotonin receptor and functionally increasing systemic and CNS levels of serotonin simultaneously, hence presenting excessive serotonin to other receptors, increases the risk for serotoninsyndrome ➭ chlorpromazine is a is a phenothiazine antipsychotic - has minimal effects on the serotonergic pathways ➭ sumatriptan is structurally similar to serotonin, and is a 5-HT (types 5-HT1D and 5-HT1B[1]) agonist Serotonin Syndrome ----------------- The syndrome is characterized by a triad of altered mental status, neuromuscular abnormalities, and autonomic dysfunction. Symptoms are variable and have included the following: confusion, hypomania, agitation, myoclonus, hyperreflexia, diaphoresis, incoordination, seizures, paresthesias, rhabdomyolysis, myoglobinuric renal failure, diarrhea, nausea, abdominal pain, dyspnea, changes in blood pressure, arrhythmias, disseminated intravascular coagulopathy, thrombocytopenia and leukopenia. ----------- |
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PZ125 ANZCA Version [Jul07][Apr08]
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 |
E. unchanged dose of induction agent and unchanged dose of opioid
- (Stan says E also) From the ANZCA pain book - there is no pharmacologcal reason for the use of a higher than usual initial opiod dose. (10.9.2. CNS Stimulant drugs. pg 262) ACUTE use is likely to be associated with a higher induction agent requirement and MAC. CHRONIC use may deplete catecholamines in nerve endings making hypotension and haemodynamic instabilty more likely, (need to use direct acting sympathomimetics). ----------- |
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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 |
E. may occur with lignocaine, bupivacaine, prilocaine and procaine
- 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)" ----------- |
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PZ127 ANZCA Version [2006-Mar] Q136
Nonsteroidal anti-inflammatory drugs given during pregnancy, have been associated with all of the following EXCEPT: A. foetal cardiac complications if given in late pregnancy B. foetal renal complications if given in late pregnancy C. increased production of amniotic fluid D. increased risk of miscarriage E. persistent neonatal pulmonary hypertension |
C. increased production of amniotic fluid
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PZ128 Jul07
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 that of unfractionated heparin D. Dependent upon a saturatable mechanism for clearance E. Longer than unfractionated heparin because of a higher affinity for plasma proteins |
B. 2-4 times unfractionated heparin
- A - False No effect B - True The pharmacokinetics of enoxaparin (Clexane) and unfractionated heparin were compared by crossover study in healthy volunteers, using three different assays. After intravenous administration, unfractionated heparin was cleared with a half-life of 35 min, irrespective of assay methods. However, the concentration of enoxaparin, measured by competitive binding assay, declined with the longer half-life of 60 min, and its anti-Factor IIa and anti-Factor Xa activities had half-lives of 40 and 275 min, respectively....Comparison of the pharmacokinetics of enoxaparin (Clexane) and unfractionated heparin; Dawes J. (Heart Research Institute, NSW, Australia); Acta Chir Scand Suppl. 1990;556:68-74. C- False More predictable D - False Elimination appears monophasic...Enoxaparin sodium is primarily metabolised in the liver by desulfation and/or depolymerisation to lower molecular weight species with much reduced biological potency. Renal clearance of active fragments represents about 10% of the administered dose and total renal excretion of active and non-active fragments 40% of the dose Clexane Data Sheet E - False It has a lower affinity ----------- |
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PZ129 Sep11
Patient on cisapride. Which drug NOT to give in recovery? A. Tramadol B. ? C. ? |
Cisapride (prepulsid) has been withdrawn from the australian market over 10 years ago, I am not sure of it's availability in New Zealand. Its use was restricted due to risk of QT prolongation and death from torsades de pointes.
Contraindicated with - substances which inhibit cytochrome p450 3A4: macrolide antibiotics (eg erythromycin, clarithromycin), azole antifungals (eg fluconazole), protease inhibitors (ritonavir, indinavir), nefazodone and grapefruit juice. - with other agents which prolong the QT interval: quinine, terfenadine, some antiarrhythmic meds (amiodarone, quinidine, flecainide, sotalol), TCAs and some antipsychotics (phenothizaines, haloperidol, risperidone) - in patients with predisposing factors for arrhythmia or pre-existing QT-prolongation - in patients with hepatic failure I could not find anything regarding cisapride and tramadol ----------- |
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PZ130 [Sep11][Mar12]
Which drugs below does not need dose adjustment in renal failure patient A. Buprenorphine B. Morphine C. Tramadol D. ? E. ? |
A. Buprenorphine
- From APMSE 3e 2010: Analgesics that exhibit the safest pharmacological profile in patients with renal impairment are alfentanil, buprenorphine, fentanyl, ketamine, paracetamol (except with compound analgesics) and sufentanil. -- nb according to table 11.5 paracetamol - may need to increase dose interval in severe impairment; alfentanil - no dose adjustment unless renal failure is severe. ----------- |
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Rate of phenytoin administration
A. 50mg/min B. 70mg/min C. 100mg/min D. Over 5 mins E. Over 10mins |
A. 50mg/min
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TMP-113 [Mar10][Aug10][Aug12?]
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. Cisapride |
C. Ranitidine
- From wiki debate: 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. Therefore C in best answer. Na citrate increases volume. ----------- |
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TMP-133 [Oct09]
Hetastarch 130/0.4, the 0.4 means A. 40mg/L B. 40g/l C. 4 hydroxylation for every 10 glucose molecules |
C. 4 hydroxylation for every 10 glucose molecules
The 130 is the MW of the starch/0.4 is the substitution ratio ----------- |
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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 |
D. 6% HES 130/0.4
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TMP-143 [Apr08] Q111
Clonidine A. inhibits postsynaptic alpha-2-receptors B. inhibits presynaptic alpha-2-receptors peripherally C. is an alpha-1-adrenergic agonist D. is an alpha-2-adrenergic antagonist E. stimulates presynaptic alpha-2-receptors centrally |
E. stimulates presynaptic alpha-2-receptors centrally
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TMP-Jul10-040
Salicylate toxicity: A. Respiratory acidosis B. Metabolic acidosis (/ don’t think this was an option - ak) C. Increased pCO2 D. High output renal failure E. Hyperthermia (Alt: pretty sure this option was HYPOthermia - too late) |
B. Metabolic acidosis
- A. false - respiratory ALKALOSIS. Due to direct stimulation of respiratory centre as well as due to increased CO2 production (due to uncoupling of oxidative phosphorylation which increases O2 consumption and CO2 production). B. C. false - see A - ?net decrease in CO2. There IS an INCREASE in CO2 PRODUCTION D - E. Causes HYPERTHERMIA. ----------- |
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TMP-Mar11-023
The half life of the active metabolite of levosimendan (OR-1896) is: A: 1hr B: 8hr C: 24hr D: 3 days E: 7 days |
D: 3 days
- Levosimenden is primarily metabolised by conjugation to cyclic or N-acetylated cysteinylglycine and cysteine conjugates. Approx 5% of the dose is metabolised in the intestine by reduction to aminophenylpyridazinone (OR-1855), which after re-absorption is metabolised by N-acetyltransferase to the active metabolite OR-1896. The acetylation level is genetically determined. In rapid acetylators, the concentrations of the metabolite OR-1896 are slightly higher than in slow acetylators. However this has no implication for the clinical haemodynamic effect at recommended doses. … The prolonged haemodynamic effects (lasting up to 7-9 days after discontinuation of a 24hour levosimendan infusion are attributed to these metabolites. .. The circulating metabolites OR-1855 and OR-1896 are formed and eliminated slowly. Peak plasma concentration is reached about 2 days after termination of a levosimendan infusion. HALF-LIVES OF THE METABOLITES ARE ABOUT 75-80 HOURS. ----------- |
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TMP-Mar11-040
What makes tramadol less effective? A: ondansetron B: prochlorperazine C: metoclopramide |
A: ondansetron
- A: true - Anesth Analg 2002 Jun;94(6):1553-7 - "Ondansetron inhibits the analgesic effects of tramadol: a possible 5-HT(3) spinal receptor involvement in acute pain in humans" B: false - prochlorperazine is a dopamine D2 receptor antagonist that belongs to the phenothiazine class of antipsychotic agents that are used for the antiemetic treatment of nausea and vertigo. It is also a highly potent typical antipsychotic. There is an increased risk of SEIZURE when given with tramadol (www.drugs.com) C: false - metoclopramide is a D2 receptor antagonist and a mixed 5-HT3 receptor antagonist/5-HT4 agonists. Its antiemetic action is due to activity at D2 receptors in the CTZ in the CNS. At higher doses, 5HT3 antagonist activity may also contribute to the antiemetic effect. The gastroprokinetic activity of metoclopramide is mediated by muscarinic activity, D2 receptor antagonist activity and 5-HT4 agonist activity. There is a risk of SEIZURE with tramadol and sedation. see also PN30 ----------- |
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TMP-Mar12-002
[?Aug12] Which of the following is NOT a side effect of cyclosporine a. Alopecia b. Hypertension c. Renal impairment d. Gum hyperplasia |
A. Alopecia
- from www.rheumatology.org.au. Most common side effects - increase and darkening of body hair - bleeding, tender or enlarged gums - pins and needles in hands and feet. Slight tremor of hands though these tend to lessen after a few weeks - renal impairment - hypertension ----------- |
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TMP-Mar12-012
What colour is the label for subcutaneously administered drugs or Ketamine a. Pink b. Yellow c. Brown d. Red e. Blue |
c. brown for s/c (though strictly speaking beige - see below)
B. yellow for ketamine -- From National recommendations for user applied labelling of injectible medicines, fluids and lines Aug 2010: Subcutaneous tissue - beige 723 (pantone matching system) Neural tissue - Pantone yellow Intravenous - blue 2985 Intraarterial - red 1787 Misc (other routes) - pink 806 -- From Australian/New Zealand Standard – 'User-applied labels for use on syringes containing drugs used during anaesthesia,' 2001. Narcotics - blue Tranquilisers - orange Anticholinergics - green Major Tranquilisers and Antiemetics - salmon Induction agents - yellow All other classifications - white ----------- |
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TMP-Oct09-047
Mechanism of antiepileptics in chronic pain, which is false? A. Phenytoin works at Na channels B. Gabapentin increases GABA in the CNS C. Carbamazepine works at Na channels D. Valproate increases GABA E. Lamotrigine acts at a Ca channel |
E. Lamotrigine acts at a Ca channel
Acts at Na channel ----------- |
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TMP-Oct09-067
Ketamine for acute pain relief A. An appropriate dose is 0.5-1mg/kg B. Midazolam does not reduce unpleasant dreams C. Morphine is contraindicated D. Hallucinations are common E. Subcutaneous is better than intravenous |
D. Hallucinations are common
- wiki: A. FALSE Usual dose is 0.1 - 0.3mg/kg/hour (or as an initial bolus) B. FALSE Midazolam is useful C. FALSE Need an opioid for best effect D. TRUE Don't know about it being common, but... E. FALSE S/c is not better than; but can be used instead of IV. -- Ketamine 0.25-0.5mg/kg analgesic dose cf 1.5-2mg/kg anaesthetic dose ----------- |
