front 1 A patient with open-angle glaucoma is treated with a muscarinic
stimulant applied directly to the cornea to reduce intraocular
pressure while limiting systemic bradycardia. This benefit is best
explained by: | back 1 B. Pharmacokinetic selectivity |
front 2 A medical student develops diaphoresis, miosis, and bronchospasm
after exposure to a cholinomimetic. The autonomic
neuroeffector–junction effects of acetylcholine and similar drugs are
best termed: | back 2 D. Parasympathomimetic effects |
front 3 A researcher classifies cholinoceptors by transmembrane signaling
mechanism. Which pairing is correct? | back 3 A. Muscarinic—G protein; Nicotinic—ion channel |
front 4 Which site is most consistent with muscarinic
receptor localization described in autonomic pharmacology? | back 4 C. Effector-cell plasma membrane |
front 5 What agents bind to and activate muscarinic or nicotinic receptors? Which produce their primary effects by inhibiting acetylcholinesterase? | back 5 Direct-acting |
front 6 Which produce their primary effects by inhibiting acetylcholinesterase? | back 6 Indirect-acting |
front 7 A pesticide exposure causes cholinergic excess by preventing
acetylcholine breakdown. The inhibited enzyme normally hydrolyzes
acetylcholine into: | back 7 B. Choline and acetic acid |
front 8 A quaternary choline ester shows minimal CNS effects even at high
doses. The most direct physicochemical explanation is that it is
relatively: | back 8 D. Insoluble in lipids |
front 9 Two enantiomers of bethanechol are compared in vitro. One is ~1000×
more potent at muscarinic receptors. Which configuration is more
potent? | back 9 C. (S)-bethanechol |
front 10 A clinician wants the longest duration among common choline esters
due to maximal resistance to cholinesterase. Which best fits? | back 10 B. Bethanechol |
front 11 A toxicology consult notes that certain natural cholinomimetic
alkaloids are well absorbed from most sites because they are tertiary
amines. List them: | back 11 A. pilocarpine, nicotine, lobeline |
front 12 Several people develop cholinergic toxicity after eating wild
mushrooms. Which agent is specifically noted as a quaternary amine
that can still enter the brain and be toxic when ingested? | back 12 C. Muscarine |
front 13 A patient ingests a tertiary-amine cholinomimetic. Which intervention
would accelerate clearance based on urinary handling? | back 13 D. Urine acidification |
front 14 A patient’s organ response to parasympathetic activation includes
both direct effector changes and reduced neurotransmitter release from
certain nerve terminals. The second mechanism is best described as
acetylcholine acting on muscarinic receptors to: | back 14 A. Inhibit transmitter release |
front 15 In a salivary gland acinar cell, a muscarinic agonist produces
increased secretion via a classic second-messenger cascade. Which
pathway is most consistent with M1/M3/M5 activation? | back 15 C. IP3/DAG signaling |
front 16 In classic studies of nicotinic receptors, which tool most directly
enabled receptor labeling and isolation because it binds very
tightly? | back 16 A. α-bungarotoxin |
front 17 Why were electric organs especially useful for detailed nicotinic
receptor studies? | back 17 D. Extremely high receptor density |
front 18 A patch-clamp experiment activates neuronal nicotinic receptors.
Which immediate measurable change best supports successful activation
as described? | back 18 B. Ionic conductance change |
front 19 A pharmacologist focuses on neuronal nicotinic
receptors. Their subunit composition is best described as
containing: | back 19 C. α and β only |
front 20 A drug is desired to produce muscarinic effects with a higher
likelihood of systemic absorption from multiple administration sites
compared with quaternary choline esters. Which agent best fits that
property? | back 20 D. Nicotine |
front 21 A resident wants a cholinomimetic with poor CNS penetration due to
hydrophilicity and limited distribution. Which choice best
matches? | back 21 B. Bethanechol |
front 22 A patient receives a cholinesterase inhibitor and develops marked
muscarinic effects. The drug class responsible for the
primary pharmacologic effect is best characterized as
inhibiting: | back 22 A. Acetylcholinesterase |
front 23 A patient with open-angle glaucoma receives a muscarinic agonist
drop. Which ocular action most directly produces the key pupillary
change? | back 23 D. Iris sphincter contraction |
front 24 After the same drop, the patient can read fine print better. Which
mechanism explains this near-vision effect? | back 24 A. Ciliary muscle contraction |
front 25 A healthy volunteer receives a minimally effective IV acetylcholine
infusion (20–50 mcg/min). What pattern is most expected? | back 25 C. Hypotension with tachycardia |
front 26 With larger IV acetylcholine doses, which heart-rate response becomes
prominent from direct cardiac effects? | back 26 A. Bradycardia |
front 27 A patient on higher-dose IV acetylcholine develops hypotension. Which
additional finding best fits the same dose range? | back 27 D. Bradycardia with AV slowing |
front 28 In isolated atrial tissue, a muscarinic agonist directly reduces the
slow inward calcium current. Which current is decreased? | back 28 B. ICa |
front 29 A pacemaker-cell study shows slower phase 4 depolarization after a
muscarinic agonist. Which current is reduced? | back 29 C. If |
front 30 A patient has only mild net bradycardia after a muscarinic agonist
despite strong direct SA slowing. Best explanation? | back 30 A. Reflex sympathetic discharge |
front 31 In an artery-ring lab, endothelium is mechanically removed. Which
acetylcholine vascular response is most affected? | back 31 D. Endothelium-dependent vasodilation |
front 32 The receptor subtype responsible for acetylcholine-induced
vasodilation on intact endothelium is: | back 32 B. M3 |
front 33 A vasodilatory response to muscarinic stimulation depends on release
of endothelium-derived relaxing factor. The mediator is: | back 33 C. Nitric oxide |
front 34 A patient with asthma receives a systemic muscarinic agonist. Which
airway effect is most likely? | back 34 A. Bronchial smooth muscle contraction |
front 35 After cholinomimetic exposure, a patient develops cramping and
diarrhea. Which GI change best explains this? | back 35 D. Increased motility and secretion |
front 36 A muscarinic agonist is given for urinary retention. Which
coordinated bladder effect promotes voiding? | back 36 B. Detrusor contracts; sphincter relaxes |
front 37 A patient on a muscarinic agonist reports watery eyes, runny nose,
and heavy sweating. Which glands are directly stimulated? | back 37 C. Thermoregulatory sweat, lacrimal, nasal |
front 38 A cognition study targets the muscarinic subtype richly expressed in
brain regions involved in cognition. Which subtype is it? | back 38 D. M1 |
front 39 Despite fewer nicotinic than muscarinic receptors, nicotine and
lobeline strongly affect which CNS regions? | back 39 A. Brain stem and cortex |
front 40 In hippocampal circuits, acetylcholine regulates norepinephrine
release via which nicotinic receptor subtype? | back 40 C. α3β4 |
front 41 A presynaptic mechanism in hippocampus and cortex limits further
cholinergic signaling. What effect is described? | back 41 B. Inhibited acetylcholine release |
front 42 The most abundant nicotinic receptor oligomer in the brain
is: | back 42 D. α4β2 |
front 43 Chronic nicotine exposure produces which sequence at nicotinic
receptors? | back 43 A. Depolarization then desensitization |
front 44 A patient ingests high-concentration nicotine and develops tremor and
emesis. What additional central effect best fits? | back 44 C. Respiratory center stimulation |
front 45 A drug-development team targets a nicotinic subtype linked to
cognition and pain perception. Which subtype matches? | back 45 B. α7 |
front 46 Proposed anti-inflammatory actions of α7 nicotinic receptors are
based on their presence on: | back 46 D. Immune nonneuronal cells |
front 47 Fast excitatory transmission in autonomic ganglia is primarily
mediated by which nicotinic subtype? | back 47 A. α3 |
front 48 In autonomic ganglia and adrenal medulla, heteromeric neuronal nAChRs
commonly include α3 plus: | back 48 C. β2 and β4 subunits |
front 49 Compared with skeletal muscle nAChRs, nicotine has somewhat greater
affinity for: | back 49 A. Neuronal nicotinic receptors |
front 50 Which best fits deficiency? Microcystis (inadequate development of
the urinary bladder), microcolon, and intestinal hypoperistalsis
syndrome; urinary incontinence, urinary bladder distention, and
mydriasis. | back 50 D. m3 |
front 51 A depolarizing nicotinic agonist that is not rapidly hydrolyzed
causes weakness after initial activation. The transmission block most
directly reflects: | back 51 A. Depolarization blockade |
front 52 Nicotinic agonist applied to an end plate by iontophoresis causes
immediate depolarization. The primary ionic basis is increased
permeability to: | back 52 B. Na+ and K+ |
front 53 A very brief-acting cholinesterase inhibitor is used diagnostically
because it is a simple alcohol with a quaternary ammonium. Which drug
fits? | back 53 D. Edrophonium |
front 54 Which agent is a carbamic acid ester cholinesterase inhibitor
(carbamate) used clinically? | back 54 A. Neostigmine |
front 55 Which drug is an organophosphate cholinesterase inhibitor used
clinically? | back 55 C. Echothiophate |
front 56 An insecticide is engineered for very high lipid solubility to speed
absorption into insects and rapid CNS distribution. Which is
typical? | back 56 B. Carbaryl |
front 57 A clinician prefers an organophosphate with very long duration but
improved stability in aqueous solution. Which agent best
matches? | back 57 B. Echothiophate |
front 58 A military exposure causes profound cholinergic crisis; the agent is
an extremely potent “nerve gas.” Which is most consistent? | back 58 A. Sarin |
front 59 A quaternary carbamate requires a much larger oral dose than
parenteral dosing. The best explanation is: | back 59 C. Permanent charge limits lipids |
front 60 An AChE inhibitor is well absorbed from all sites and can be used
topically in the eye. Which drug fits? | back 60 D. Physostigmine |
front 61 Most organophosphate cholinesterase inhibitors are dangerous to
humans because they are: | back 61 B. Well absorbed from mucosa |
front 62 Which organophosphate is noted as highly polar and more stable than
most others? | back 62 A. Echothiophate |
front 63 You want an AChE inhibitor lasting about 5–15 minutes. Which duration
matches best? | back 63 C. Edrophonium |
front 64 A postoperative patient needs an AChE inhibitor with 0.5–4 hour
action. Which agent best matches? | back 64 B. Neostigmine |
front 65 A patient needs sustained symptomatic coverage with an AChE inhibitor
lasting 4–6 hours. Which duration fits? | back 65 D. Pyridostigmine |
front 66 A clinician selects an AChE inhibitor with 0.5–2 hour duration and
good absorption from all sites. Which best fits? | back 66 A. Physostigmine |
front 67 A glaucoma regimen uses an AChE inhibitor with ~100-hour duration.
Which drug matches? | back 67 B. Echothiophate |
front 68 Beyond acetylcholinesterase, these inhibitors also inhibit which
enzyme? | back 68 B. Butyrylcholinesterase |
front 69 A child with α3-subunit deficiency is evaluated. Which combination
best matches the syndrome? | back 69 B. Microcystis and microcolon |
front 70 A pathologist samples adrenal medulla ganglion-like tissue. Which
nAChR subunit pattern is most expected there? | back 70 C. α3 with β2/β4 |
front 71 Quaternary agents reversibly bind _____ and by _____ bonds
to the active site, thus preventing access of acetylcholine. | back 71 A. electrostatically, hydrogen |
front 72 A new AChE inhibitor forms a covalent carbamoylated enzyme that is
slowly hydrolyzed, prolonging recovery for 30 minutes to 6
hours. This mechanism best fits: | back 72 D. Carbamate ester inhibitors |
front 73 Which pair are classic examples of carbamate ester AChE
inhibitors? | back 73 B. Neostigmine and physostigmine |
front 74 The most prominent pharmacologic effects of cholinesterase inhibitors
are most evident in: | back 74 A. CV, GI, eye, NMJ |
front 75 A lipid-soluble AChE inhibitor at low concentration produces diffuse
EEG activation and subjective alertness. This effect most directly
reflects: | back 75 D. Central cholinergic stimulation |
front 76 At high concentrations, lipid-soluble AChE inhibitors can cause
generalized convulsions followed by coma and: | back 76 B. Respiratory arrest |
front 77 A patient exposed to an AChE inhibitor shows increased autonomic
outflow. These drugs can increase activity in: | back 77 C. Both sympathetic and parasympathetic |
front 78 Edrophonium, neostigmine, and physostigmine most closely mimic which
physiologic input on the heart? | back 78 D. Vagal nerve activation |
front 79 Cholinesterase inhibitors have minimal effects by direct
action on vascular smooth muscle because: | back 79 A. Most beds lack cholinergic innervation |
front 80 Moderate doses of AChE inhibitors can raise blood pressure primarily
by increasing systemic: | back 80 C. Vascular resistance |
front 81 In quaternary nitrogen AChE inhibitors, the pressor response is
initiated mainly at: | back 81 B. Sympathetic ganglia |
front 82 In lipid-soluble AChE inhibitors, the pressor response can also be
initiated at: | back 82 A. Central sympathetic centers |
front 83 A patient given an AChE inhibitor develops increased BP and plasma
norepinephrine; atropine prevents both. This best implies atropine
acts: | back 83 D. In central and peripheral sites |
front 84 Net cardiovascular effects of moderate-dose AChE inhibitors most
often include: | back 84 B. Bradycardia with hypertension |
front 85 Low therapeutic AChE inhibitor doses primarily: | back 85 C. Prolong released ACh effects |
front 86 A patient has weakness after a curare-like blocker. An AChE inhibitor
improves strength mainly by increasing: | back 86 A. Contraction strength at NMJ |
front 87 A key clinical use category of cholinomimetics is treatment
of: | back 87 D. Alzheimer’s disease |
front 88 Muscarinic stimulants and AChE inhibitors reduce intraocular pressure
chiefly by: | back 88 C. Ciliary body contraction |
front 89 In depressed smooth muscle activity without obstruction,
cholinomimetics may be helpful. Before use, the clinician must
exclude: | back 89 B. Mechanical obstruction |
front 90 Among choline ester cholinomimetics, the most widely used for GI/GU
disorders is: | back 90 B. Bethanechol |
front 91 A patient with chronic xerostomia is treated with a long-used agent
to increase salivary secretion. Which fits? | back 91 A. Pilocarpine |
front 92 A patient with Sjögren syndrome and dry mouth is started on a newer
direct-acting muscarinic agonist. Which drug is intended? | back 92 B. Cevimeline |
front 93 In myasthenia gravis, antibodies target the main immunogenic region on which nicotinic receptor subunit? | back 93 α1 |
front 94 One MG mechanism reduces receptor number, accelerating
internalization and degradation. This is best described as: | back 94 C. Receptor cross-linking |
front 95 Another MG mechanism reduces transmission when antibodies bind the
receptor and: | back 95 A. Inhibit receptor function |
front 96 A patient with generalized MG remains weak despite optimized
pyridostigmine. Which adjunct is most appropriate for more widespread
weakness? | back 96 A. Immunosuppressant therapy |
front 97 A bedside edrophonium test is planned for suspected MG. After
baseline strength is measured, what is the initial IV dose? | back 97 B. 2 mg |
front 98 No effect is seen 45 seconds after the initial edrophonium dose. What
additional dose may be administered? | back 98 C. 8 mg |
front 99 Following edrophonium in true MG, improvement in strength typically
lasts about: | back 99 D. 5 minutes |
front 100 Long-term symptomatic therapy for MG is most commonly maintained
with: | back 100 C. Pyridostigmine |
front 101 If pyridostigmine cannot be used for MG maintenance, the classic
alternative is: | back 101 A. Neostigmine |
front 102 Because AChE inhibitors are short-acting, pyridostigmine often
requires dosing about every: | back 102 C. 6 hours |
front 103 Neostigmine often requires dosing about every: | back 103 A. 4 hours |
front 104 After surgery, rapid reversal of nondepolarizing neuromuscular
blockade is commonly accomplished with: | back 104 A. Neostigmine or edrophonium |
front 105 Which toxidrome is potentially lethal in children and can cause
prolonged behavioral disturbance and arrhythmias in adults? | back 105 B. Atropine intoxication |
front 106 A suicidal ingestion causes severe muscarinic blockade and QRS
widening risk. Which drug class is classically implicated? | back 106 B. Tricyclic antidepressants |
front 107 The first drug used for mild-to-moderate Alzheimer’s disease with
anticholinesterase and other cholinomimetic actions was: | back 107 A. Tacrine |
front 108 Which set are newer, more selective AChE inhibitors with similar
marginal benefit but less toxicity than tacrine? | back 108 A. Donepezil, galantamine, rivastigmine |
front 109 Overdose of pilocarpine or choline esters most predictably
causes: | back 109 A. Muscarinic excess signs |
front 110 Which symptom set best matches muscarinic excess from cholinomimetic
overdose? | back 110 A. Urinary urgency and sweating |
front 111 The most dangerous toxic effect of large nicotine doses includes
central stimulation causing: | back 111 B. Convulsions |
front 112 Another dangerous nicotine toxicity mechanism is end-plate: | back 112 B. Depolarization |
front 113 Severe nicotine toxicity can also produce hypertension with
cardiac: | back 113 B. Arrhythmias |
front 114 The primary neurotransmitter of the parasympathetic nervous system
is: | back 114 C. Acetylcholine |
front 115 Muscarinic receptors are GPCRs with how many transmembrane domains? | back 115 7 |
front 116 The muscarinic receptor domain classically coupled to G proteins is
the: | back 116 D. 3rd cytoplasmic loop |
front 117 Nicotinic receptors are primarily found in which set of
locations? | back 117 A. Autonomic ganglia, skeletal NMJ, adrenal |
front 118 What agents bind to and activate muscarinic or nicotinic receptors? | back 118 Direct-acting |
front 119 M2 receptor—best matching location, G protein, and pathway: | back 119 A. Heart nodes; Gi; ↓cAMP |
front 120 M3 receptor—best matching location, G protein, and pathway: | back 120 C. Smooth muscle/glands; Gq; IP3/DAG |
front 121 M4 and M5 are CNS receptors. Which pairing is correct? | back 121 B. M4: Gi/↓cAMP; M5: Gq/IP3 |
front 122 In a healthy artery with intact endothelium, acetylcholine activates
M3 receptors. Net vascular effect is: | back 122 C. Vasodilation via NO release |
front 123 The key smooth-muscle second messenger that mediates NO-driven
relaxation is: | back 123 A. cGMP |
front 124 In an endothelium-denuded vessel ring, acetylcholine most likely
causes: | back 124 D. Vasoconstriction via IP3-Ca2+ |
front 125 A direct-acting cholinomimetic produces effects primarily by: | back 125 B. Activating M or N receptors |
front 126 Butyrylcholinesterase inhibition matters clinically because it can
act as a: | back 126 D. Biological scavenger enzyme |
front 127 Which list contains only choline ester direct
agonists? | back 127 B. ACh, methacholine, carbachol, bethanechol |
front 128 Choline ester lipid insolubility is mainly due to: | back 128 D. Quaternary ammonium charge |
front 129 Which list contains only alkaloid direct agonists? | back 129 C. Muscarine, pilocarpine, nicotine, lobeline |
front 130 Which agent reliably activates both muscarinic and
nicotinic receptors? | back 130 A. Carbachol |
front 131 Neonicotinoid insecticides act primarily at: | back 131 C. Nicotinic receptors |
front 132 In the PLC pathway, DAG primarily: | back 132 D. Activates protein kinase C |
front 133 In the PLC pathway, IP3 primarily: | back 133 B. Releases Ca2+ from stores |
front 134 M2 and M4 receptor signaling most directly: | back 134 C. Inhibits adenylate cyclase |
front 135 In cardiac tissue, muscarinic stimulation most
characteristically: | back 135 A. Increases K+ flux |
front 136 In autonomic ganglia and many smooth muscles, muscarinic stimulation
tends to: | back 136 D. Decrease K+ flux |
front 137 With nicotinic receptors, binding both agonist
sites: | back 137 D. Greatly increases opening probability |
front 138 Binding only one nicotinic site typically: | back 138 C. Increases opening probability |
front 139 A glaucoma drop causes miosis and accommodation. These
changes: | back 139 B. Increase aqueous outflow |
front 140 The aqueous humor drainage structure most directly facilitated is
the: | back 140 A. Canal of Schlemm |
front 141 A muscarinic agonist slows the SA node primarily
by: | back 141 B. Decreasing firing rate |
front 142 At the AV node, muscarinic activation most
characteristically: | back 142 C. Slows conduction; ↑ refractory |
front 143 In the atria, muscarinic stimulation most
characteristically: | back 143 A. Decreases strength; ↓ refractory |
front 144 In the ventricles, muscarinic stimulation produces
a: | back 144 B. Small strength decrease |
front 145 Direct cardiac muscarinic effects include increasing
which current? | back 145 D. K current |
front 146 Direct cardiac muscarinic effects include decreasing
which current? | back 146 C. Slow inward Ca current |
front 147 Muscarinic slowing of diastolic depolarization includes
reducing: | back 147 A. Hyperpolarization-activated current |
front 148 Without intact endothelium, ACh can constrict vessels because M3 on
VSM triggers: | back 148 B. IP3-mediated Ca2+ rise |
front 149 A systemic muscarinic agonist most predictably causes: | back 149 A. Bronchoconstriction |
front 150 Typical GI effects of muscarinic stimulation include: | back 150 C. ↑ peristalsis; ↓ sphincters |
front 151 A notable exception to “sphincters relax” is the: | back 151 D. Gastroesophageal sphincter |
front 152 Relative abundance is best summarized as: | back 152 A. Brain muscarinic; spinal nicotinic |
front 153 M1 receptors are cognition-linked; M1 knockout is associated
with: | back 153 C. Impaired forebrain plasticity |
front 154 Hypothalamic M3 receptor knockout is associated with: | back 154 D. Reduced appetite and fat |
front 155 Regarding autonomic ganglia, nicotine’s action on sympathetic vs
parasympathetic is: | back 155 A. Same direction in both |
front 156 Nicotine’s cardiovascular effects are best described
as: | back 156 B. Sympathomimetic |
front 157 Nicotine’s GI and urinary effects are best described
as: | back 157 C. Parasympathomimetic |
front 158 Which agent is muscarinic-selective and a choline ester? | back 158 D. Bethanechol |
front 159 A pharmacology exam asks for two carbamate
indirect-acting cholinomimetics. Which pair is correct? | back 159 B. Neostigmine, physostigmine |
front 160 A farmer presents after insecticide exposure; you suspect an
organophosphate. Which set contains only
organophosphate examples from your notes? | back 160 A. Echothiophate, sarin, malathion |
front 161 Parathion and malathion are best characterized as: | back 161 C. Thiophosphate prodrugs |
front 162 You need a very short-acting alcohol AChE inhibitor
for bedside testing. Best choice? | back 162 A. Edrophonium |
front 163 Most organophosphates are highly lipid-soluble liquids. Which
exception is more aqueous-stable yet still
long-acting? | back 163 C. Echothiophate |
front 164 Which class is generally better absorbed and
therefore more dangerous to humans (and effective
insecticides)? | back 164 D. Organophosphates |
front 165 Which group typically has poor absorption because of
permanent charge, requiring larger oral doses? | back 165 B. Quaternary carbamates |
front 166 Carbamate and organophosphate AChE inhibitors share a key step: after
binding AChE, the ____ portion leaves rapidly. | back 166 C. Alcohol portion |
front 167 In that same shared mechanism, the ____ remains bound and is released
slowly. | back 167 A. Acidic portion |
front 168 The functional result of carbamate/organophosphate AChE inhibition is
best summarized as: | back 168 D. Blocked ACh hydrolysis |
front 169 Rank duration (longest → shortest): edrophonium, carbamates,
organophosphates. | back 169 B. Organophosphates > carbamates > edrophonium |
front 170 A student asks what is most prescribed now for
chronic glaucoma (instead of cholinomimetics). Best answer? | back 170 C. PG analogs and topical β-blockers |
front 171 Acute angle-closure glaucoma is a medical emergency. Initial medical
therapy commonly includes: | back 171 A. Pilocarpine |
front 172 After IOP control in angle-closure glaucoma, definitive correction is
typically: | back 172 D. Laser iridotomy |
front 173 A 5-year-old with hyperopia develops strabismus triggered by focusing
effort. This fits: | back 173 B. Accommodative esotropia |
front 174 Non-obstructive GI dysmotility (eg, post-op ileus): which drug is
usually used? | back 174 D. Bethanechol |
front 175 Bethanechol’s clinical profile is best described as: | back 175 A. Increases GI/GU motility, secretions |
front 176 Another MG mechanism reduces transmission via: | back 176 C. Postsynaptic membrane lysis |
front 177 MG antibodies can also bind the receptor and: | back 177 B. Inhibit receptor function |
front 178 A patient has ptosis and fatigable proximal weakness. Which bedside
diagnostic drug is used IV? | back 178 D. Edrophonium |
front 179 MG patients are notably sensitive to which agents during
anesthesia? | back 179 A. Curariform blockers |
front 180 A nondepolarizing neuromuscular relaxant listed as an anesthesia
adjunct is: | back 180 A. Pancuronium |
front 181 Immediate reversal of pharmacologic nondepolarizing paralysis post-op
commonly uses: | back 181 C. Neostigmine and edrophonium |
front 182 Which finding is least consistent with classic AChE
inhibitor toxicity (DUMBBELS)? | back 182 D. Mydriasis |
front 183 Flaccid paralysis in severe AChE inhibitor poisoning is most directly
due to: | back 183 A. NMJ AChR overactivation |
front 184 A patient eats Inocybe mushrooms and develops salivation, diarrhea,
bronchospasm. Best antidote? | back 184 C. Atropine |
front 185 Nicotine replacement with varenicline works because it is a partial
agonist at: | back 185 B. α4β2 nAChR |
front 186 Varenicline reduces nicotine reinforcement mainly by reducing
presynaptic: | back 186 D. Dopamine release |
front 187 The major cause of acute cholinergic toxicity worldwide is exposure
to: | back 187 A. Organophosphate insecticides |
front 188 In organophosphate poisoning, which drug restores AChE activity at
muscarinic/nicotinic sites but not CNS? | back 188 C. Pralidoxime |
front 189 In organophosphate poisoning, which drug reverses central and
peripheral muscarinic toxicity but not flaccid
paralysis? | back 189 B. Atropine |
front 190 Chronic cholinesterase inhibitor exposure can cause delayed
neuropathy via NTE inhibition. Prototype agent? | back 190 D. Triorthocresyl phosphate |
front 191 Which cholinomimetic is used for asthma challenge testing due to
bronchoconstriction? | back 191 B. Methacholine |
front 192 Varenicline use may be limited by which adverse-effect
cluster? | back 192 D. Nausea, insomnia, psychiatric worsening |
front 193 Typical severe organophosphate poisoning progression is best
described as: | back 193 B. Muscarinic → CNS → nicotinic |
front 194 Pralidoxime’s limitation in organophosphate poisoning is that
it: | back 194 A. Cannot enter CNS |
front 195 Parathion and malathion insecticides are “inactive” because they
require conversion to: | back 195 C. Phosphate derivatives |