Procaine MCQs With Answer

Procaine MCQs With Answer

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Procaine MCQs With Answer is a focused set of practice questions tailored for B. Pharm students to master procaine’s pharmacology. This guide emphasizes key concepts: procaine as an ester local anesthetic, mechanism of action (voltage-gated Na+ channel blockade), metabolism by plasma (pseudo)cholinesterase to PABA, pKa and onset, short duration, clinical uses in infiltration/dental anesthesia, common adverse effects, allergic reactions, and management of systemic toxicity. Questions probe deeper into structure–activity relationships, drug interactions, and practical considerations such as vasoconstrictor effects and contraindications. Clear answers reinforce learning and exam readiness. Now let’s test your knowledge with 30 MCQs on this topic.

Q1. Which best describes the primary mechanism of action of procaine?

  • Inhibition of cyclooxygenase enzymes
  • Blockade of voltage-gated sodium channels on nerve membranes
  • Activation of GABA-A receptors
  • Antagonism of NMDA receptors

Correct Answer: Blockade of voltage-gated sodium channels on nerve membranes

Q2. Procaine belongs to which chemical class of local anesthetics?

  • Amide-type local anesthetic
  • Ester-type local anesthetic
  • Steroid local anesthetic
  • Ketone local anesthetic

Correct Answer: Ester-type local anesthetic

Q3. The primary metabolite responsible for allergic reactions to procaine is:

  • Benzoic acid
  • Para-aminobenzoic acid (PABA)
  • Monoethylglycine
  • Para-hydroxybenzoate

Correct Answer: Para-aminobenzoic acid (PABA)

Q4. Compared with lidocaine, procaine typically has a:

  • Faster onset of action
  • Slower onset of action
  • Longer duration of action
  • Greater lipophilicity

Correct Answer: Slower onset of action

Q5. Which statement best describes the clinical duration of action of procaine when used for infiltration?

  • Ultra-short acting (minutes)
  • Short acting (approximately 30–60 minutes)
  • Intermediate acting (2–4 hours)
  • Long acting (6–12 hours)

Correct Answer: Short acting (approximately 30–60 minutes)

Q6. Addition of adrenaline (epinephrine) to procaine solutions typically results in:

  • Faster metabolism of procaine
  • Increased systemic absorption and toxicity
  • Prolonged local anesthetic duration and reduced systemic absorption
  • Conversion of procaine into an amide-type anesthetic

Correct Answer: Prolonged local anesthetic duration and reduced systemic absorption

Q7. The approximate pKa of procaine, which influences its onset, is:

  • 7.4
  • 8.9
  • 6.0
  • 5.5

Correct Answer: 8.9

Q8. Procaine is most commonly used clinically for which of the following?

  • General anesthesia induction
  • Dental and infiltration anesthesia
  • Long-term epidural analgesia for labor
  • Topical mucosal anesthesia for bronchoscopy

Correct Answer: Dental and infiltration anesthesia

Q9. An allergic reaction to procaine is most likely due to:

  • The parent procaine molecule directly
  • The ester linkage itself
  • Formation of para-aminobenzoic acid (PABA) metabolite
  • Contaminants in injectable water

Correct Answer: Formation of para-aminobenzoic acid (PABA) metabolite

Q10. Procaine is relatively contraindicated in patients with a known deficiency of which enzyme?

  • Monoamine oxidase
  • Plasma cholinesterase (pseudocholinesterase)
  • CYP3A4
  • Acetaldehyde dehydrogenase

Correct Answer: Plasma cholinesterase (pseudocholinesterase)

Q11. Which enzyme primarily metabolizes procaine in the body?

  • Liver microsomal CYP450 enzymes
  • Plasma cholinesterase (pseudocholinesterase)
  • Monoamine oxidase
  • Renal dehydrogenase

Correct Answer: Plasma cholinesterase (pseudocholinesterase)

Q12. A distinguishing structural feature of procaine compared to amide local anesthetics is:

  • An amide bond linking aromatic and amine groups
  • An ester linkage susceptible to plasma hydrolysis
  • A tertiary amine that prevents hydrolysis
  • A steroid backbone

Correct Answer: An ester linkage susceptible to plasma hydrolysis

Q13. The typical pattern of CNS toxicity with increasing systemic procaine levels is:

  • Depression-first without excitation
  • Initial excitation (tremor/seizures) followed by depression and respiratory arrest
  • Isolated peripheral neuropathy without CNS signs
  • Purely cardiotoxic effects without CNS involvement

Correct Answer: Initial excitation (tremor/seizures) followed by depression and respiratory arrest

Q14. In severe systemic toxicity from a local anesthetic like procaine with cardiovascular collapse, which therapy is recommended as part of resuscitation?

  • Oral activated charcoal
  • Intravenous lipid emulsion therapy
  • High-dose aspirin
  • Subcutaneous epinephrine only

Correct Answer: Intravenous lipid emulsion therapy

Q15. Compared with potent amide local anesthetics such as bupivacaine, procaine is generally:

  • More cardiotoxic and longer acting
  • Less potent and shorter acting
  • More lipophilic and longer acting
  • Biotransformed primarily by hepatic CYP enzymes

Correct Answer: Less potent and shorter acting

Q16. How does procaine’s high pKa affect its clinical onset at physiological pH?

  • High pKa increases non-ionized fraction and speeds onset
  • High pKa reduces non-ionized fraction at pH 7.4, slowing onset
  • pKa has no effect on onset of local anesthetics
  • High pKa increases metabolism rate

Correct Answer: High pKa reduces non-ionized fraction at pH 7.4, slowing onset

Q17. The primary clinical benefit of adding a vasoconstrictor to procaine is to:

  • Neutralize PABA to prevent allergy
  • Increase systemic absorption for faster action
  • Prolong local effect and decrease bleeding at the site
  • Transform procaine into an amide anesthetic

Correct Answer: Prolong local effect and decrease bleeding at the site

Q18. Which adverse effect is NOT commonly associated with procaine use?

  • Immediate hypersensitivity due to PABA
  • Methemoglobinemia as a frequent complication
  • Transient CNS excitation at high plasma levels
  • Short duration anesthetic effect requiring repeat dosing

Correct Answer: Methemoglobinemia as a frequent complication

Q19. Cross-reactivity in allergic patients is most likely between procaine and which group of local anesthetics?

  • Amide local anesthetics (e.g., lidocaine)
  • Other ester local anesthetics (e.g., benzocaine)
  • All opioid analgesics
  • Corticosteroids

Correct Answer: Other ester local anesthetics (e.g., benzocaine)

Q20. Where does the primary hydrolysis of procaine occur?

  • In microsomal liver enzymes
  • In plasma by pseudocholinesterase
  • In renal tubular cells
  • In the gastrointestinal tract

Correct Answer: In plasma by pseudocholinesterase

Q21. Typical onset time for procaine when used for infiltration anesthesia is approximately:

  • 30–60 seconds
  • 2–5 minutes
  • 20–30 minutes
  • 1–2 hours

Correct Answer: 2–5 minutes

Q22. Which of the following is an amide local anesthetic (not an ester)?

  • Procaine
  • Tetracaine
  • Benzocaine
  • Lidocaine

Correct Answer: Lidocaine

Q23. Relative to bupivacaine, procaine’s cardiotoxic potential is generally:

  • Higher than bupivacaine
  • Lower than bupivacaine
  • Identical to bupivacaine
  • Unrelated to class of anesthetic

Correct Answer: Lower than bupivacaine

Q24. Which statement about procaine’s plasma protein binding is correct?

  • Procaine has very high protein binding (>90%)
  • Procaine has low plasma protein binding, contributing to short duration
  • Procaine irreversibly binds to albumin leading to accumulation
  • Protein binding is the main route of procaine elimination

Correct Answer: Procaine has low plasma protein binding, contributing to short duration

Q25. Which factor most increases the risk of systemic toxicity following a procaine injection?

  • Slow subcutaneous injection with aspiration
  • Inadvertent intravascular injection or rapid IV bolus
  • Adding a vasoconstrictor like epinephrine
  • Using very dilute procaine solutions

Correct Answer: Inadvertent intravascular injection or rapid IV bolus

Q26. The chemical name of procaine is best described as:

  • 2-(diethylamino)ethyl 4-aminobenzoate
  • 2-chloroethyl 4-aminobenzoate
  • 4-(diethylamino)butyl benzamide
  • N-(2,6-dimethylphenyl)propanamide

Correct Answer: 2-(diethylamino)ethyl 4-aminobenzoate

Q27. Individuals with pseudocholinesterase deficiency are at increased risk of prolonged effects from which drug, making screening relevant before certain anesthetic procedures?

  • Procaine topical gel
  • Succinylcholine (depolarizing neuromuscular blocker)
  • Lidocaine patch
  • Fentanyl infusion

Correct Answer: Succinylcholine (depolarizing neuromuscular blocker)

Q28. Which statement about hypersensitivity to procaine is correct?

  • Immediate IgE-mediated reactions are most commonly due to the parent procaine molecule
  • Most allergic reactions are due to PABA metabolites rather than procaine itself
  • All patients allergic to procaine will also be allergic to amide anesthetics
  • Allergic reactions are completely eliminated by adding epinephrine

Correct Answer: Most allergic reactions are due to PABA metabolites rather than procaine itself

Q29. The primary route of excretion for procaine metabolites is:

  • Biliary excretion unchanged
  • Renal excretion of hydrolysis products
  • Exhalation via lungs
  • Sequestration in adipose tissue

Correct Answer: Renal excretion of hydrolysis products

Q30. Which drug interaction is likely to prolong the duration of action of procaine?

  • Coadministration with a cholinesterase inhibitor (e.g., neostigmine)
  • Coadministration with an inducer of hepatic CYP enzymes
  • Concurrent use of activated charcoal
  • Topical antacid application

Correct Answer: Coadministration with a cholinesterase inhibitor (e.g., neostigmine)

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