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23 Cards in this Set
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PS01 [Mar96] [Jul98] [Jul01] [Jul02] Benzodiazepines:
A. Are all lipid soluble (OR: None are water-soluble) B. Are all renally excreted unchanged C. Causes retrograde amnesia D. Lorazepam is more lipophilic than midazolam E. Block GABA receptors F. Have high therapeutic index |
ANSWER A and F
A TRUE (lipid soluble at physiological pH - they all must be to have any central effects]) B false - some metabolised in liver (remember to beware abolutes such as "all" and "never") C false anterograde amnesia "Stored information (retrograde amnesia) is not altered by benzodiazepines" (Stoelting 3rd ed. p.126) D false(hence slower onset of Lorazepam into CNS) E false - they actually facilitate GABA binding at the GABAa receptor, increasing the frequency of chloride channel opening (Stoelting 3rd ed. p.127) F ?True - They have a "greater magin of safety after an overdose, and elicit fewer and less serious drug interactions" compared to barbiturates. (Stoelting 3rd ed. p.126) This is relative, not absolute... |
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PS02 [Mar97] [Jul97] [Jul99] [Mar03] Which is TRUE regarding monoamine oxidase inhibitors (MAOI)?
A. Should/must be ceased for two weeks prior to general anaesthesia B. Cause hypotension and sedation in combination with pethidine C. Inhibit activity of indirect sympathomimetics D. Ingested tyramine causes hypertension due to indirect effects E. Includes doxepin and amitriptyline |
ANSWER D
A - False. Old advice. Now considered risk is greater from rebound depression. Also unknown whether 2 weeks would be sufficient to restore MAO levels from irreversible block. B- False. Due to pethidine's inhibition of 5HT uptake, causes excitatory phenomena and hypertension with MAOIs. C- False, ephedrine and metaraminol activity enhanced. D- True. MAO in gut metabolises ingested bioactive amines such as tyramine which would otherwise cause hypertension via indirect sympathomimetic effects. E- False, these are TCAs. MAOIs include phenelzine, moclobamide and selegiline. |
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PS03 [Jul97] [Jul98] [Jul00] [Jul01] Neuroleptic malignant syndrome:
A. Occurs only with chronic use B. 80% (60%) mortality C. ?Treated /? not treated with dantrolene D. Can be caused by acute withdrawal of L-Dopa therapy E. Is treated with bromocriptine |
ANSWER CDE
NMS is a life threatening disorder (with 10% mortality) which is characterised by altered mental status, rigidity, fever and autonomic instability in response to the use of a neuroleptic agent. It usually occurs within the first two weeks of neuroleptic use but can be precipitated by a rapid rise in dose, parenteral therapy, or an acute illness. It can also occur on withdrawal or reduction of L-Dopa or Dopamine agonist therapy in patients with Parkinson's Disease. Excessive rapid postsynaptic dopamine receptor blockade is thought to be responsible. Investigations may reveal elevated CK (from muscle damage)and leukocytosis (acute stress). Treatment involves stopping the neuroleptic agent and immediate supportive care. Extrapyramidal symptoms can be treated with antiparkinsonian medications and muscle relaxation achieved with Diazepam. Dantrolene (a direct-acting skeletal muscle relaxant), and bromocriptine (a dopamine agonist) are also helpful. |
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PS04 [Jul97] Inhibitors of monoamine oxidase A
A. Allow tyramine to enter the circulation from the gut B. ? C. ? D. ? |
MAO enzymes come in two forms MAO-A and MAO-B which are distributed around the body. They are responsible for the metabolisation of neurotrnasmitters including serotonin, NAdr, Adr and dopamine thus MAO enzyme inhibition increases the synaptic concentrations of these neurotransmitters resulting in antidepressive effects.
Inhibition of GIT MAO-A prevents the sympathomimetic tyramine (contained in aged cheeses and other foods) from being metabolized and thus allows it to be absorbed into circulation resulting in a hypertensive crisis called the "Cheese Reaction". |
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PS05 [Jul97] [Feb00] Benzodiazepines:
A. Have no analgesic effect B. Have an antanalgesic effect C. Have an analgesic effect D. Have dose-related analgesic and antanalgesic effects |
Unsure
Various studies have been done 1. addition of midazalam to intrathecal cocktails has resulted in analgesia in chronic pain 2. |
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PS06 [Jul98] [Jul99] [Mar03] [Jul04] The benzodiazepine with the longest elimination half-life is:
A. Diazepam B. Oxazepam C. Temazepam D. Midazolam E. Lorazepam F. Flunitrazepam |
ANSWER A
Elimination Half lifes: Diazepam 20-80 hours Oxazepam 10-20 hours Temazepam 10-40 hours Midazolam 2-4 hours Lorazepam 10-20 hours Flunitrazepam 20-30 hours |
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PS07 [Jul98] Fluoxetine:
A. Inhibits noradrenaline & adrenaline uptake in nerve terminals B. Inhibits serotonin uptake in the central nervous system C. Has a half life of 4-16 days and is excreted predominately using renal mechanisms D. Is metabolised to norfluoxetine using CTY2D6 E. Is excreted hepatically |
ANSWER D
Fluoxetine (prodrug), metabolised to norfluoxetine Absorption: 72% oral bioavailability Distribution: 95% PB Metabolism: hepatic CTY2D6, inhibitor of cytochrome P450 isoenzymes T1/2 1-3 days (increased to 4-6 days with chronic use) Active metabolite norfluoexetine with a T1/2 4-16 days Excretion: 80% renal Onset of action is slow. SSRI used mainly as anti-depressant Slow onset of anti-depressant effect CI with MAOI, pimozide, thioridazine Serotonin syndrome can be induced if used with tramadol Small increase in risk of suicide in patients aged < 25 years Norfluoxetine is a selective inhibitor of the reuptake of serotonin in nerve terminals |
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PS08 [Mar99] [Jul00] Flumazenil:
A. Formulated In propylene glycol in commercial preparation B. Inverse agonist C: Is slowly metabolised making resedation unlikely D. Reliably reverses the sedating effects of benzodiazepines but marked respiratory depression still can occur E. Is a partial agonist at mu opioid receptors |
ANSWER D
Mims states: Active. Flumazenil. Inactive. Disodium edetate, acetic acid, sodium chloride, sodium hydroxide in water for injections adjusted to pH 4.0. Peck & Williams says that flumazenil acts as: 1. Competitive BZ antagonist. 2. Some agonist activity (weak intrinsic activity) 3. Inverse agonist activity. |
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PS09 [Mar99] Diazepam:
A. Half-life of 5 to 10 hours B. Metabolised to mainly oxazepam & temazepam C. Has an elimition half life which increases with age D. Has an onset of action as rapid as that of thiopentone E. inhibits the action of vecuronium D. ? |
ANSWER C
A. FALSE: T1/2 20-100 hours B. FALSE : Two principal metabolites are oxazepam and desmethyldiazepam and a lesser amount is metabolised to temazepam. C. TRUE: As age advances, hepatic microsomal enzymes become less active and so the half-lives of drugs metabolised by this route increase. This is particularly true for oxidative reactions (demethylation is the first step in metabolising diazepam). The effect is potentially as much as a fourfold increase in half-life from the age of 20 to 70. D. FALSE: Most benzodiazepines (including diazepam) are of slower onset than Thiopentone which has an onset of about one arm-to-brain time E. FALSE: Prolongs the action of vecuronium by inhibiting the hepatic metabolism of vecuronium |
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PS10 [Mar99] [Jul99] Droperidol:
A. Substituted phenothiazine B. Reliably produces mental tranquility C. Does not act (directly) on CTZ D. Alpha-blockade with hypotension is not a problem with 2mg dose E. Slows alpha rhythm on EEG |
ANSWER E
A - Like haloperidol, it is a butyrophenone (and NOT a phenothiazine) B - "are less effective against anxiety" (Stoelting 3rd Ed. p.373) C - Very effective anti-emetic acts on dopamine receptors in CTZ D - Hypotension with larger doses E - Miller: Alpha rhythm persists with a reduced frequency |
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PS11 [Mar99] Monoamine oxidase inhibitors (MAOI):
A. Moclobemide is a reversible Type B inhibitor B. Interacts with tyramine to cause hypertension C. Interacts with pethidine to cause hypothermia D. ? |
A. FALSE: moclobemide is a reversible inhibitor of monoamine oxidase A
B. FALSE - inhibits metabolism of tyramine --> hypertensive crisis C. FALSE - causes hyperthermia |
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PS12 [Jul99] [Apr01] Metabolites of diazepam, all EXCEPT:
A. Temazepam B. Oxazepam C. Desmethyldiazepam D. Lorazepam |
ANSWER D
The main metabolic pathway for diazepam is diazepam -> desmethyldiazepam (active with long half-life) -> oxazepam (active) -> glucuronide conjugate (inactive, excreted). There is also a minor pathway diazepam -> temazepam (active, short half-life) -> glucuronide conjugate (inactive, excreted). Lorazepam is NOT a metabolite of diazepam. |
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PS13 [Jul00] With respect to action of midazolam:
A. Acts on GABA-B receptors B. increases duration of opening of Cl – channels C. ? competes with barbiturates for receptor site on GABA receptor D. Metabolism is decreased by cimetidine E. Decreases chloride conductance F. Interacts with the B1 subunit of GABA |
ANSWER D
A - wrong; GABA A receptor B - wrong; increases frequency of opening C - wrong; barbiturates and BZDs have separate binding sites D - correct; cimetidine inhibits cytochrome p450 E - wrong; increases chloride conductance F - wrong; acts at the alpha subunit |
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Whic one of the following is a partial opioid agonist with a low intrinsic activity?
A. Naloxone B. Naltrexone C. Methadone D. Buprenorphine E. None of the above |
ANSWER D
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On administration of an unknown dose of a new anti-physchotic, a 55 year old man developed extra pyramidal symptoms. The dose at which this effect appears would be established in which phase of clinical trials?
A. Phase 1 B. Phase 2 C. Preclinical Phase D. Phase 3 E Phase 4. |
ANSWER A
Preclinical phase: test on animals to determine mutagenicity, carcinogenicity and organ system toxicity Phase 1: first human clinical trials to determine, safety, toxicity, side effects and pharmacokinetics Phase 2: comparison to placebo to determine efficacy Phase 3: large blind RCT Phase 4: post marketing surveillance |
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PS15 [Jul00] [Mar03] [Jul04] Tricyclic antidepressants:
A. Do not cause sedation B. Formed from modification of the phenothiazine ring C. Avoid anti-cholinergic effects compared to other anti-depressants D. Does not decrease reuptake of 5HT ?at 5HT3 R E. Decrease CNS amine levels |
ANSWER B
A: False. Sedation is one of the most common side effects. B. True: Tricyclic antidepressants are closely related in structure to phenothiazines. They differ from phenothiazines due to the incorporation of an extra atom into the central ring. C. False. Tricyclic cause anticholinergic effects such as dry mouth, blurred vision, constipation and urinary retention. D. False. Mechanism of action is block the amine (noradrenalinse or serotonin) reuptake pumps which terminate amine neurotransmission. E. False. Mechanism of action is to block uptake of amines by nerve terminals hence increasing amine levels. |
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PS16 [Jul00] Diazepam 0.1 mg/kg given orally, the percent absorption is:
A. 100% B. 94% C. 74% D. 50% E. 15% |
ANSWER A
Goodman & Gilman Ch. 17 The benzodiazepines are absorbed completely |
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PS17 [Feb04] Clinical uses of Diazepam include:
A. Anticonvulsant B. Skeletal muscle relaxation C. Treatment of Delerium Tremens D. Induction of anaesthesia E. All of the above |
ANSWER E
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Which one of the following antidepressants can block the neuronal uptake of tyramine and potentially reduce the risk of tyramine-MAOI interaction?
A. SSRIs B. Moclobemide C. L-typtophan D. Tricyclic antidepressants E. Levothyroxine |
ANSWER D
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Which one of the following mood stabilizers can potentiate GABA transmission by increasing GABA release, reducing GABA metabolism and increasing GABA receptor density?
A. Lithium B. Carbamazepine C. Lamotrigine D. Valproate E. Vigabatrin |
ANSWER D
A. FALSE: lithium's mechanism of action remains speculative B. FALSE: prolongs sodium channel activation, leading to secondary increase in Ca channel inactivation C. FALSE: Lamotrigine is a membrane stabilizer D. TRUE E. FALSE: Vigabatrin is a GABA transaminase inhihibtor |
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The mechanism of action of St John's Wort is
A. Serotonin anatagonism B. Norepinephrine agonism C. MAO inhibition D. Multiple reuptake inhibition E. Membrane stabilization |
ANSWER D
St John's Wort is effective in mild to moderate depression. Acts by inhibiting reuptake of multiple monoamines including serotonin, norepinephrine and dopamine; and GABA and glutamate |
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A 30 year old known heroin user is brought to A&E after an overdose of heroin, with a GCS of 3, a respiratory rate of 4 breaths per minute, and pinpoint pupils. On adminstration of naloxone he developed running nose, diarrhoea and profuse sweating and multiple joint aches. The most likely explanation is
A. Residual symptoms of toxicity B. Allergic reaction to naloxone C. Effect of coadministered cocaine D. Precipitated opioid withdrawal E. None of the above. |
ANSWER D
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The mechanism of action of opioids in producing an analgesic effect is
A. Blockade of sodium channels on the neuronal membrane B. Increased production of cAMP in a neurone C. Reduction in intracellular calcium in a neurone D. Stimulation of Gs-protein coupled receptors in a neurone E. Direct action on nuclear transcription factors |
ANSWER C
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