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MEDCHEM FINAL MCPHS EXAM QUESTIONS AND ANSWERS WITH COMPLETE SOLUTIONS VERIFIED LATEST UPDATE 2024/2025 $10.49   Add to cart

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MEDCHEM FINAL MCPHS EXAM QUESTIONS AND ANSWERS WITH COMPLETE SOLUTIONS VERIFIED LATEST UPDATE 2024/2025

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MEDCHEM FINAL MCPHS EXAM QUESTIONS AND ANSWERS WITH COMPLETE SOLUTIONS VERIFIED LATEST UPDATE 2024/2025 Quinidine cardioquin, dura-quin, quinora anti-arrythmic oral & injection (hospital only) Class 1a sodium channel blocker block phase 0 decrease max depolarization increase duration of a...

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  • November 2, 2024
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MEDCHEM FINAL MCPHS EXAM QUESTIONS AND

ANSWERS WITH COMPLETE SOLUTIONS VERIFIED

LATEST UPDATE 2024/2025


Quinidine

cardioquin, dura-quin, quinora

anti-arrythmic

oral & injection (hospital only)

Class 1a sodium channel blocker

block phase 0

decrease max depolarization

increase duration of action potential



Has a lipophilic area (aromatic rings), spacer and a nitrogen → may cause anticholinergic effects



"quin" - has quinolone in it



Natural product alkaloid(has basic N) produced from cinchona plant

Gives drug quinine - same chemistry but differs in 1 carbon stereochemistry

Used for anti-malaria and as rat poisoning

Quinidine has a chiral carbon which is the differentiation from quinine

,Quinidine and quinine are stereoisomers




since alkaloid - has basic N → administer as a salt (sulfate or gluconate)



orally = very lipophilic → oral absorption is good

Once in the liver, it will get metabolized by CYP (O-demethylation)

Very little direct phase 2 metabolism because of the steric hinderance

Albumin in our system binds to drugs in order to form a water soluble complex - which is why

lipophilic drugs bind well to plasma protein

Quinidine binds well to plasma proteins



cinchonism - whistling in ears - drug goes to ears = nerve problems


Procainamide

procan, rhythmin, pronestyl

anti-arrythmic

oral & injection

Class 1a sodium channel blocker

block phase 0

decrease max depolarization

increase duration of action potential



Has a lipophilic area (aromatic rings), spacer and a nitrogen → won't cause anticholinergic effects seen

In quinidine

, developed from procaine (local anesthetic - Dentist to numb gums)

procaine Has an ester group - cannot use it for arrhythmia because drug will not survive long enough

until reaching the cardiac tissue



Procainamide

Bioisosteric replacement (-O to -NH) =different functional group but same activity

Amidases are found in the liver, not in GIT

More stable than procaine

Used PO and injection

Has poor absorption and poorly binds to plasma protein

injection preferred

It won't cause anti-cholinergic effects as seen with quinidine

Metabolism - N-demethylation by CYP, Amidase,

NH2 will undergo phase 2 directly - polar

Metabolism is similar to Hydralazine - NAT puts an acetyl group on the N outside the ring → different

responses by patients → slow acetylators is in risk for developing arrhythmia


Disopyramide

norpace, rhythodan

anti-arrythmic



oral & injection

Class 1a sodium channel blocker

block phase 0

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