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