Pharma MCQ 2 Flashcards

1
Q

How many quaternary amines has succinylcholine?

A

2

It’s two acetylcholines joined via an acetyl group

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2
Q

How is succinylcholine broken down?

A

Rapidly hydrolysed by plasma cholinestrase in the plasma to succinic acid and choline.

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3
Q

What enzyme can prolong the action if succinylcholine?

A

Inhibitors of plasma and acetylcholinesterases

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4
Q

Elimination half life of succinylcholine

A

4-5 mins

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5
Q

Which the following do not inhibit COX:

Azapropazone 
Phenazocine
Benorylate 
Levorphanol 
Paracetamol
A

Azapropazone - NSAID derivative

Phenazocine - opioid agonist

Benorylate - ester of paracetamol and aspirin

Levorphanol - pure opioid agonist

Paracetamol - COX-3 and COX-1 inhibitor

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6
Q

Aspirin metabolised by?

A

Esterases in the intestinal mucosa and liver to acetic acid and salicylate

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7
Q

Aspirin protein binding?

A

80-90%

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8
Q

Aspirin pKa

Less ionised in plasma or stomach?

A

Aspirin is a weak acid
pKa 3.5
More unionised in stomach at pH1-2.
Therefore less ionised in the stomach.

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9
Q

How does morphine cause hypotension after an IV bolus?

A

Histamine release
Vagal stimulation
Arteriolar dilation- local vasc smooth muscle effects and inhibition CNS.
Decreased sympathetic activity

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10
Q

Pethidine:
Half life compared to morphine?

Lipid solubility compared to morphine?

A
  1. Longer terminal half life. Morphine: 2-3 hours
    Pethidine: 3-5 hours
  2. More lipid soluble than morphine
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11
Q

Pethidine:

  1. Relation to atropine?
  2. Metabolites? Active/ inactive?
  3. Relation to local anaesthetics?
A
  1. Atropine like chemical and has atropine like actions.
  2. Active metabolite- norpethidine
  3. Relation to local anaesthetic- LA membrane stabilising properties.
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12
Q

Which of these are MAO inhibitors?

Amitryptyline 
Tranylcypromine 
Diazepam 
Ephedrine 
Phenelzine
A

Tranylcypromine
Ephedrine
Phenelzine

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13
Q

Neostigmine:

Is orally well absorbed?

A

False, permanently charged quaternary amine, limited absorption.

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14
Q

Shortest duration of action: order of anticholinesterases?

A

Edrophonium
Neostigmine
Pyridostigmine

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15
Q

Neostigmine mechanism of action

A

Carbamylates acetylcholinesterase therefore increasing concentration of acetylcholine

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16
Q

How does dopexamine affect cardiac contractility?

A

Beta-adrenergic sympathomimetic

Increases contractility

17
Q

How does theophylline affect myocardial contractility? The

A

NON-specific phosphodiesterase inhibitor.

Increases cAMP.

Therefore increases Ca in myocytes.

Increases contractility.

18
Q

How does epinephrine influence myocardial contractility?

A

Increases contractility through B-agonist activity.

19
Q

How does glucagon affect myocardial contractility?

A

Through G-protein-coupled receptor.

Increases adenylate cyclase activity.

Increases cAMP.

Increases Ca in myocytes.

Increases contractility.

20
Q

How does Digoxin affect myocardial contractility?

A

Increases intracellular Na.

By inhibiting Na/K ATPase.

This increases Na/Ca exchanger activity.

Increases Ca in myocyte.

Increases contractility.

21
Q

Nifedipine effect on myocardial contractility?

A

Calcium channel blocker.

Reduces intracellular Ca, reduces myocardial contraction.

22
Q

Nifedipine effect on arteriolar dilation/ contraction?

A

Vasodilation - blocks Ca channel, reduced Ca in cell for contraction.

23
Q

Nifedipine is completely absorbed sublingually? T/F?

A

True- sublingual avoids first pass metabolism.

24
Q

Which is more effective in SVT: verapamil or nifedipine?

A

Verapamil.

Nifedipine (dihydropyridine) does not delay AV node conduction, Verapamil (phenylalkylamines) does.

25
Verapamil should not be given with b-blocker why?
Delays AV node conduction and will cause severe Brady.
26
What is disopyramide? And what is it used for?
Class 1a anti-arrhythmic Negative ionotropy and reduces BP, (prolongs PR interval and duration of action potential). No effect peripherally, only centrally.
27
What arrhythmias can disopyramide trigger?
VT, VF or torsades de pointes. No extrasystoles.