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
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
