Cholinergic Physiology & Receptors
This neurotransmitter is released by all preganglionic sympathetic and parasympathetic neurons, postganglionic parasympathetic neurons, and somatic motor neurons.
What is acetylcholine (ACh)?
The lecture identifies acetylcholine as the neurotransmitter at all preganglionic autonomic neurons, postganglionic parasympathetic neurons, and the neuromuscular junction.
These drugs mimic acetylcholine by binding directly to cholinergic receptors.
What are direct-acting cholinoceptor stimulants?
Direct-acting agents activate muscarinic or nicotinic receptors themselves, just as acetylcholine does.
This mnemonic describes the classic symptoms of organophosphate toxicity.
What is SLUDGE?
The lecture states that organophosphate poisoning produces the SLUDGE syndrome: salivation, lacrimation, urination, defecation (or diarrhea), GI upset/cramps, and emesis.
This cardiac side effect of succinylcholine is worse after repeat doses and in pediatric patients.
What is bradycardia?
The lecture attributes succinylcholine-induced bradycardia to muscarinic stimulation and notes it is more common after subsequent doses and in children.
Unlike succinylcholine, NDMRs act as this type of drug at nicotinic receptors.
What is a competitive antagonist?
The lecture states that NDMRs competitively antagonize nicotinic receptors without intrinsic activity, preventing acetylcholine from binding.
These are the two major types of cholinergic receptors.
What are muscarinic and nicotinic receptors?
The lecture explains that physiologic responses depend on whether muscarinic or nicotinic receptors are activated and where they are located.
These drugs increase acetylcholine concentrations by inhibiting acetylcholinesterase.
What are indirect-acting cholinoceptor stimulants?
Indirect-acting agents inhibit acetylcholinesterase, preventing breakdown of acetylcholine and increasing its concentration.
This indirect-acting cholinoceptor stimulant is an example of reversible inhibition without a carbamyl group.What is edrophonium?
What is edrophonium?
Edrophonium reversibly inhibits acetylcholinesterase by electrostatic and hydrogen bond attachment rather than forming a covalent bond.
Hyperkalemia after succinylcholine is thought to result from proliferation of these receptors.
What are extrajunctional cholinergic (nicotinic) receptors?
Proliferation of extrajunctional receptors in denervated or injured muscle allows greater potassium efflux during depolarization.
These are the two structural classes of NDMRs.
What are benzylisoquinoliniums and aminosteroids?
NDMRs are classified structurally into benzylisoquinolinium compounds and aminosteroid compounds.
This nicotinic receptor subtype is found on skeletal muscle end plates.
What is Nm (N1)?
Nm receptors are located at the neuromuscular junction and mediate skeletal muscle contraction.
This direct-acting choline ester is rapidly hydrolyzed by acetylcholinesterase.
What is acetylcholine?
Acetylcholine is rapidly broken down by acetylcholinesterase, explaining its extremely short duration of action.
These three drugs form carbamyl esters when inhibiting acetylcholinesterase.
What are neostigmine, pyridostigmine, and physostigmine?
These agents form carbamyl ester complexes at the enzyme's esteratic site, preventing acetylcholine hydrolysis until the bond dissociates
The initial recommended IV dose of dantrolene for malignant hyperthermia is this amount.
What is 2.5 mg/kg IV?
The lecture recommends starting dantrolene at 2.5 mg/kg IV and repeating doses every 5–10 minutes until symptoms are controlled.
These two major drug classes commonly enhance the effects of NDMRs.
What are volatile anesthetics and aminoglycoside antibiotics?
The lecture lists several medications that potentiate NDMRs, including volatile anesthetics and aminoglycosides.
This nicotinic receptor subtype is found in autonomic ganglia.
What is Nn (N2)?
The lecture differentiates Nm receptors at skeletal muscle from Nn receptors located within autonomic ganglia.
This choline ester is approximately three times more resistant to acetylcholinesterase than acetylcholine.
What is methacholine?
Methacholine is more resistant to acetylcholinesterase degradation, giving it a longer duration than acetylcholine.
Compared with quaternary carbamates, these compounds are more lipid soluble and enter the CNS more readily.
What are tertiary amines?
The lecture notes that tertiary amines such as physostigmine are well absorbed and readily distributed into the CNS because of greater lipid solubility.
Succinylcholine transiently increases this pressure for approximately 5–10 minutes.
What is intraocular pressure?
The lecture notes a temporary increase in intraocular pressure lasting approximately 5–10 minutes after administration.
This electrolyte enhances neuromuscular blockade when its serum concentration is increased.
What is magnesium?
Magnesium is listed among the drugs and physiologic factors that intensify the effects of nondepolarizing neuromuscular blockers.
Acetylcholine is synthesized from these two molecules.
What are acetyl-CoA and choline?
The first step of cholinergic transmission is synthesis of acetylcholine from acetyl-CoA and choline.
This tertiary alkaloid is sufficiently lipid soluble to be absorbed through the skin.
What is nicotine?
Nicotine is lipid soluble enough to be administered transdermally, unlike many quaternary compounds.
Organophosphates inhibit acetylcholinesterase by forming this type of bond.
What is an irreversible bond?
Organophosphates irreversibly inactivate acetylcholinesterase, and recovery requires synthesis of new enzyme.
Name four manifestations of malignant hyperthermia described in this lecture.
What are tachycardia, increased ETCO₂, muscular rigidity, decreased oxygen saturation, increased body temperature, hyperkalemia, or acidosis?
The lecture lists these hallmark findings of an MH crisis resulting from uncontrolled skeletal muscle hypermetabolism. Any four receive full credit.
This disease is specifically listed as a neuromuscular disorder that enhances the effects of NDMRs.
What is myasthenia gravis?
The lecture notes that myasthenia gravis reduces receptor availability, making patients more sensitive to nondepolarizing blockers.