Pharmacology Reviewer: Answers and Rationales (one to fifty)
Pharmacology Reviewer: Answers and Rationales (one to fifty)
One. Primary neurotransmitter released by all preganglionic autonomic fibers
Answer: Acetylcholine
Rationale: All preganglionic neurons of both sympathetic and parasympathetic systems release acetylcholine. It acts on nicotinic receptors in autonomic ganglia.
Two. Propofol plus Nitrous oxide during surgery
Answer: It achieves anesthesia with lower doses
Rationale: Using multiple anesthetic agents produces additive or synergistic effects, allowing lower doses of each drug, reducing toxicity and adverse effects.
Three. Primary inhibitory neurotransmitter in spinal cord
Answer: Glycine
Rationale: Glycine is the major inhibitory neurotransmitter in the spinal cord, especially in motor control pathways.
Four. Low blood-gas partition coefficient anesthetic (Desflurane)
Answer: It reaches arterial equilibrium faster
Rationale: Low blood solubility leads to faster rise of alveolar concentration, faster brain equilibrium, rapid induction and recovery.
Five. "Craniosacral" division of ANS
Answer: Parasympathetic nervous system
Rationale: Parasympathetic outflow originates from cranial nerves three, seven, nine, ten and sacral segments two to four.
Six. ENS function after vagus nerve severed
Answer: It contains complete sensory and motor reflex arcs locally
Rationale: The enteric nervous system has intrinsic neurons capable of autonomous reflexes, allowing GI motility even without CNS input.
Seven. Significance of cotransmission in ANS
Answer: It modulates the primary transmitter's postsynaptic response
Rationale: Autonomic nerves may release multiple transmitters, such as ATP and neuropeptides, that modify the effect of the main transmitter.
Eight. Opioid inhibition of pain transmission
Answer: Closing presynaptic Calcium channels
Rationale: Opioids inhibit calcium influx, reducing release of pain neurotransmitters like substance P and glutamate.
Nine. Drug causing dissociative anesthesia
Answer: Ketamine
Rationale: Ketamine produces dissociative anesthesia characterized by analgesia, amnesia, and catalepsy via NMDA receptor blockade.
Ten. Cholinergic receptor at neuromuscular junction
Answer: Nicotinic muscle receptor
Rationale: Skeletal muscle contraction occurs when acetylcholine activates nicotinic muscle receptors.
Eleven. Phenylephrine cardiac response
Answer: Decrease in heart rate due to increased vagal nerve firing
Rationale: Phenylephrine causes al vasoconstriction, increased blood pressure, baroreceptor reflex, vagal stimulation, and reflex bradycardia.
Twelve. Why Pralidoxime must be given early
Answer: To regenerate the active enzyme at the neuromuscular junction sites
Rationale: Pralidoxime reactivates acetylcholinesterase before "aging" occurs in organophosphate poisoning.
Thirteen. Tachycardia after vasodilator
Answer: The baroreceptor reflex reduces the vagal inhibitory tone
Rationale: Vasodilation leads to decreased blood pressure, baroreceptor reflex, increased vagal tone, and increased sympathetic activity causing tachycardia.
Fourteen. Non-selective beta blocker during anaphylaxis
Answer: It prevents the beta-two mediated reduction in airway resistance
Rationale: Blocking beta-two receptors prevents bronchodilation, worsening bronchospasm during anaphylaxis.
Fifteen. NSAID that irreversibly inhibits enzyme
Answer: Aspirin
Rationale: Aspirin irreversibly acetylates COX enzymes, unlike other NSAIDs which inhibit reversibly.
Sixteen. Mechanism of morphine tolerance
Answer: Upregulation of the enzyme Adenylyl cyclase
Rationale:
Chronic opioid use causes compensatory increase in cAMP signaling, contributing to tolerance and dependence.
Seventeen. Muscarinic activation in iris
Answer: Miosis
Rationale: Muscarinic stimulation contracts circular iris muscle, causing pupil constriction.
Eighteen. Concept of dominant tone
Answer: The resting activity of one division exceeds the other
Rationale:
Most organs have baseline activity from one ANS division, which determines resting function.
Nineteen. Target enzyme of NSAIDs
Answer: Cyclooxygenase
Rationale: NSAIDs inhibit COX-one and COX-two, reducing prostaglandin synthesis.
Twenty. Effect of selective alpha-one agonist
Answer: Vasoconstriction
Rationale:
Activation of alpha-one receptors on vascular smooth muscle causes vasoconstriction, increasing blood pressure.
Twenty-one. Pilocarpine in glaucoma
Answer: It opens the trabecular meshwork by contracting the ciliary muscle
Rationale:
Muscarinic activation improves aqueous humor drainage, lowering intraocular pressure.
Twenty-two. Receptor causing bronchodilation
Answer: Beta-two receptor
Rationale: Beta-two activation relaxes bronchial smooth muscle, producing bronchodilation.
Twenty-three. Intrinsic GI nervous system
Answer: Enteric nervous system
Rationale: The ENS contains myenteric and submucosal plexuses controlling digestion.
Twenty-four. Beta-one selective blocker in asthma
Answer: It avoids blocking the receptors that cause bronchodilation
Rationale: Beta-one selective drugs avoid blocking beta-two receptors in lungs, preventing bronchospasm.
Twenty-five. Why Bethanechol preferred over Acetylcholine
Answer: It is resistant to hydrolysis by Acetylcholinesterase
Rationale: Bethanechol lasts longer because acetylcholinesterase cannot easily break it down.
Twenty-six. Edrophonium test for cholinergic crisis
Answer: Worsening of the muscle weakness
Rationale: In cholinergic crisis, excess acetylcholine causes receptor overstimulation, leading to weakness that worsens after edrophonium.
Twenty-seven. Dopamine increase by opioids and cannabinoids
Answer: Disinhibition of the Dopamine-secreting neurons
Rationale: These drugs inhibit GABA interneurons, removing inhibition on dopamine neurons.
Twenty-eight. Enzyme terminating Acetylcholine action
Answer: Acetylcholinesterase
Rationale: Acetylcholinesterase rapidly hydrolyzes acetylcholine in the synaptic cleft.
Twenty-nine. Catecholamine released by adrenal medulla
Answer: Epinephrine
Rationale: Adrenal medulla secretes approximately eighty percent epinephrine during stress.
Thirty. First-line DMARD for rheumatoid arthritis
Answer: Methotrexate
Rationale:
Methotrexate is the cornerstone DMARD due to strong efficacy and long-term disease control.
Thirty-one. Receptor increasing heart rate and contractility
Answer: Beta-one receptor
Rationale: Beta-one receptors in the heart increase chronotropy and inotropy.
Thirty-two. Drug reversing opioid overdose
Answer: Naloxone
Rationale:
Naloxone is a pure opioid antagonist that rapidly reverses respiratory depression.
Thirty-three. Rapid relief asthma drug
Answer: Albuterol
Rationale: Albuterol is a short-acting beta-two agonist used for acute bronchospasm.
Thirty-four. Barrier restricting drug entry to brain
Answer: Blood-brain barrier
Rationale: Tight junctions in cerebral capillaries limit entry of polar drugs.
Thirty-five. Side effect of Bethanechol
Answer: Excessive sweating and salivation
Rationale: Muscarinic stimulation causes increased secretions, sweating, and GI activity.
Thirty-six. Short-acting Acetylcholinesterase inhibitor for MG diagnosis
Answer: Edrophonium
Rationale: Edrophonium has very short duration, making it useful diagnostically.
Thirty-seven. Methotrexate mechanism in RA
Answer: It increases the release of Adenosine
Rationale: Low-dose methotrexate increases anti-inflammatory adenosine signaling.
Thirty-eight. Measure comparing potency of inhaled anesthetics
Answer: Minimum Alveolar Concentration
Rationale: Minimum Alveolar Concentration is the concentration preventing movement in fifty percent of patients; lower minimum alveolar concentration equals higher potency.
Thirty-nine. Opioid receptor causing morphine effects
Answer: Mu receptor
Rationale: Mu receptors mediate analgesia, euphoria, respiratory depression, and dependence.
Forty. High dose epinephrine blood pressure effect
Answer: Alpha receptor activation overcomes beta-two vasodilation
Rationale: Low dose causes beta-two vasodilation; high dose causes alpha vasoconstriction dominates.
Forty-one. Fight-or-flight division
Answer: Sympathetic nervous system
Rationale: Sympathetic activation prepares body for stress and emergency responses.
Forty-two. Effect of AChE inhibition
Answer: Parasympathetic effects dominate
Rationale: ACh accumulation stimulates muscarinic receptors in parasympathetic organs.
Forty-three. Muscarinic agonist for urinary retention
Answer: Bethanechol
Rationale: Bethanechol stimulates bladder detrusor contraction.
Forty-four. Alpha-2 agonists in hypertension
Answer: They decrease the sympathetic outflow from the brainstem
Rationale: alpha-2 activation in CNS reduces sympathetic tone, lowering BP.
Forty-five. Primary excitatory neurotransmitter in CNS
Answer: Glutamate
Rationale: Glutamate activates NMDA and AMPA receptors, producing excitation.
Forty-six. Why atropine doesn't treat muscle weakness
Answer: It blocks Muscarinic but not Nicotinic receptors
Rationale: Muscle weakness comes from nicotinic receptor overstimulation at NMJ.
Forty-seven. Why COX-2 inhibitors reduce GI bleeding
Answer: They spare gastric mucosal protection
Rationale: COX-1 produces protective gastric prostaglandins; COX-2 inhibitors spare this.
Forty-eight. Parasympathetic cranial nerves
Answer: CN Three, Seven, Nine, Ten
Rationale: Parasympathetic cranial outflow originates from these four cranial nerves.
Forty-nine. Nicotine addiction mechanism
Answer: It reduces the inhibitory tone on the Dopamine neurons
Rationale: Nicotine desensitizes GABA interneurons, increasing dopamine release.
Fifty. Most critical epinephrine effect in anaphylactic shock
Answer: Constriction of the resistance vessels via alpha-1 receptors
Rationale:
alpha vasoconstriction restores blood pressure and reverses shock.
Third EXAM REVIEWER (PCOL) Pharmacology Reviewer (CNS, ANS, and Clinical Applications)
Third EXAM REVIEWER (PCOL) Pharmacology Reviewer (CNS, ANS, and Clinical Applications)
This reviewer summarizes key concepts, drugs, mechanisms, and rationales based on the fifty pharmacology questions discussed.