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Pharmacology Basics > Pharma MCQ 2 > Flashcards

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
Q

Verapamil should not be given with b-blocker why?

A

Delays AV node conduction and will cause severe Brady.

26
Q

What is disopyramide? And what is it used for?

A

Class 1a anti-arrhythmic

Negative ionotropy and reduces BP,

(prolongs PR interval and duration of action potential).

No effect peripherally, only centrally.

27
Q

What arrhythmias can disopyramide trigger?

A

VT, VF or torsades de pointes. No extrasystoles.

Pharmacology Basics (25 decks)

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