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Cholinergics- Nicotinics Flashcards

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1
Q

Nicotinics

A

Actions similar to nicotine, corresponds to actions of ACh released at autonomic ganglia, neuromuscular junction of skeletal muscle, and adrenal medulla

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2
Q

Nicotinic receptors

A

Ligand-dependent ion channels, allows Na and K flux down concentration gradient, depolarization, ionotropic

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3
Q

Types of nicotinic receptors

A

Nn- neuronal type, found in autonomic ganglia, blocked by ganglionic blockers
Nm- muscle typefound in neuromuscular junction, blocked by skeletal muscle relaxants

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4
Q

Nicotinic alkaloids

A

Both nicotine and lobeline are tertiary cholinomimetic alkaloids and well absorbed, excreted mostly by the kidneys, acidification of urine accelerates their clearance (weak bases)

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5
Q

Nicotine

A

Lipid-soluble, can be absorbed across the skin, indicated for assistance to smoking cessation

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6
Q

Lobeline

A

Plant derivative similar to nicotine, no clinical indication

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7
Q

Nicotinic choline esters

A

High affinity for nicotinic receptors, resistant to AChE, induces muscle paralysis during surgery by depolarizing blockade

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8
Q

Normal conditions

A

Agonists like ACh binds to nicotinic receptors and opens channels, AChE rapidly metabolize ACh, channels close

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9
Q

Depolarizing blockade

A

Succinylcholine (agonist) binds to nicotinic receptors and channels open, succinylcholine is resistant to metabolism, sticks around, causing channels to become unresponsive, prolonged presence causes channels to become less receptive and stay unresponsive

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10
Q

Nicotinic effects in CNS

A

Presynaptic nicotinic receptors regulate release of neurotransmitters (glutamate, serotonin, GABA, dopamine, norepinephrine), high concentration induces tremors, emesis, respiratory center stimulation, higher concentrations may cause convulsions and fatal coma

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11
Q

Clinical uses of nicotine

A

Direct-acting alkaloid, used for smoking cessation

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12
Q

Clinical uses of succinylcholine

A

Direct-acting choline ester, used for neuromuscular blockade during surgery, rapid sequence intubation

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13
Q

Side effects of nicotinics

A

Central stimulant- convulsions that may progress to coma and respiratory arrest
Skeletal muscle end plate depolarization- depolarization blockade and respiratory paralysis
Cardiovascular- hypertension and cardiac arrhythmias

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14
Q

Fatal dose of nicotine

A

Amount of nicotine in two regular cigarettes, most is destroyed by burning or escaping through second hand smoke

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15
Q

Function of ganglion blocking agents

A

Competitively block nicotinic receptors of parasympathetic and sympathetic autonomic ganglia

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16
Q

Ganglion-blocking agents

A

Tetraethylammonium (TEA)- short duration of action, Hexamethonium (C6)- prototypical agent used experimentally, Decamethonium (C10)- analogue of hexamethonium, Mecamylamine, Trimethaphan

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17
Q

Mechanism of action of ganglion-blocking agents

A

Nondepolarizing competitive antagonists, hexamethonium binds directly to nicotinic ion channel, trimetaphan blocks the nicotinic receptor, not the channel pore

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18
Q

Effects of ganglion-blocking agents on the CNS

A

Mecamylamine crosses the BBB, causes sedation, temor, choreiform movements, mental aberrations, discontinued in 2009

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19
Q

Effects of ganglion-blocking agents in the eye

A

Cycloplegia with loss of accommodation because ciliary muscle receives primarily parasympathetic innervation, parasympathetic tone dominates the pupil, blockade causes moderate pupil dilation

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20
Q

Cardiovascular effects of ganglion-blocking agents

A

Blood vessels only innervated by sympathetics, blockade normally decreases arteriolar and venous tone, heart normally under parasympathetic innervation, blockade causes moderate tachycardia

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21
Q

Effects of ganglion-blocking agents on GI tract

A

Parasympathetic normally predominates, blockade reduces secretion, inhibits motility, causes constipation

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22
Q

Genitourinary effects of ganglion-blocking agents

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A

Blockade causes hesitancy in urination, may precipitate urinary retention in men with prostatic hyperplasia, sexual function impaired due to prevention of erection and ejaculation

23
Q

Cholinesterase (ChE)

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A

Terminates the action of ACh, located on the basement membrane of the synaptic cleft of cholinergic neurons

24
Q

Structure of cholinesterases

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A

Serine hydrolases, active site consists of: anionic site which binds choline group, esteratic site where acetyl group is transferred during catalytic hydrolysis- releasing choline

25
Cholinesterase inhibitors (ChEI)
Reduce choline metabolism and increase endogenous choline conentration- cholinomimetic
26
Classes of ChEI
Simple alcohols- quaternary ammonium group (edrophonium) Carbamic acid esters of alcohol- quaternary or tertiary ammonium groups (neostigmine, physostigmine) Organic derivatives of phosphoric acid- organophosphates (isoflurophate)
27
Short acting ChEI
Edrophonium, binds to anionic site of cholinesterase and forms hydrogen bond to prevent ACh binding, reversible
28
Intermediate acting ChEI
Neostigmine, pyridostigmine, physostigmine, carbamyl group binds to AChE, breaking the carbamyl enzyme group is slower than the acetyl group, reversible
29
Long acting ChEI
Echothiophate, other organophosphates, organic group is released upon binding, leaving phosphorus covalently bound in AChE
30
Organophosphates and aging
Covalent binding stable, aging occurs when there is a loss of an alkyl group (makes phosphorylated enzyme more stable), hydration still occurs, rate is slow and "irreversible", new enzymes must be synthesized for activity
31
CNS effects of ChEI
High concentrations, lipid soluble ChEI causes generalized convulsions that can lead to coma and respiratory arrest
32
Effects of ChEI in the eye, respiratory tract, GI tract, urinary tract
Similar to direct-acting cholinomimetics- miosis, bronchoconstriction, urination, GI motility, secretion, defecation
33
Effects of ChEI on glands
Secretion in sweat, lacrimal, salivary, nasopharyngeal glands
34
Effects of ChEI in the heart
Parasympathetic effect predominates, moderate doses reduce heart rate
35
Effects of ChEI in vasculature
No parasympathetic innervation, sympathetic effect predominates, due to quaternary agents at autonomic ganglion and lipid soluble agents at central sympathetic centers
36
Net cardiovascular effect of ChEI
Moderate dose- modest bradycardia and increased vascular resistance, increased blood pressure High dose- bradycardia and hypotension
37
Effects of low doses of ChEI at neuromuscular junction
Moderately prolong and intensity actions of ACh, increase strength of contraction especially in weakened muscles (myasthenia gravis)
38
Effects of high doses of ChEI at neuromuscular junction
Result in muscle fiber fibrillation, antidromic firing (backward axon conduction toward soma) resulting in fasciculations of entire motor unit, depolarizing neuromuscular blockade followed by nondepolarizing blockade
39
Myasthenia gravis
Autoimmune disorder where circulating antibodies block ACh action at the postsynaptic neuromuscular junction, causing fluctating muscle weakness and fatigue, symptoms are ptosis, diplopia, difficulty speaking and swallowing, extremity weakness
40
Mechanism of antibodies in myasthenia gravis
Cross-link receptors and stimulate receptor internalization and degradation, cause lysis of postsynaptic membrane, bind to and inhibit nicotinic receptors
41
Edrophonium
Short-acting ChEI, used in diagnosis of myasthenia gravis, nondepolarizing reversal of neuromuscular blockade, improves muscle strength for about 5 minutes, not used for long term treatment
42
Neostigmine
Intermediate-acting ChEI, nondepolarizing reversal of neuromuscular blockade, urinary retention, myasthenia gravis, additional direct nicotinic agonist activity
43
Pyridostigmine
Intermediate-acting ChEI, used for reversal of neuromuscular blockade, myasthenia gravis (drug of choice), prophylaxis for organophosphate poisoning, slower onset but longer duration of action than pyridostigmine
44
Physostigmine
Intermediate-acting ChEI, used for glaucoma, reversal of anticholinergic toxicity, crosses the BBB
45
Echotiophate
Long-acting ChEI, used for glaucoma, esotropia with accommodative compensation, long duration can lead to acquired cholinesterase deficiency and prolonged block from neuromuscular blocking drugs
46
ChEI side effects
Muscarinic side effects initially predominate, central side effects follow rapidly (cognitive disturbances, convulsions, coma), followed by peripheral nicotinic effects (depolarizing neuromuscular blockade)
47
Cholinergic poisoning
Severe cholinergic excess is medical emergency, caused by insecticides, wild mushrooms, chemical warfare (nerve gases- sarin, VX, soman), nicotinic and muscarinic effects can be life-threatening, no treatment for nicotinic poisoning
48
Treatment options for cholinergic poisoning- reverse muscarinic effects
Tertiary amine drug must be used to treat CNS effects as well as peripheral effects of organophosphate inhibitors, atropine
49
Treatment options for cholinergic poisoning- cholinesterase regenerator compounds
Contain substituted oximes, not recommended for reversal of inhibition by carbamate inhibitors, pralidoxime- ineffective for reversing central effects of organophosphate poisoning due to charged quaternary ammonium groups
50
Cholinesterase regenerator
Organophosphates cause phosphorylation of serine OH group at active site of cholinesterase, oxime group has high affinity for phosphorus atom and competes with serine OH of cholinesterase
51
Pralidoxime
Cholinesterase regenerator, can hydrolyze phosphorylated enzyme and regenerate cholinesterase if the organophosphorus-cholinesterase complex has not aged
52
Treatment options for cholinergic poisoning- pretreatment with reversible enzyme inhibitor
Prevents binding of irreversible organophosphate inhibitor, reserved for situations in which possible lethal poisoning is anticipated, simultaneous use of atropine required to control muscarinic excess
53
Mushroom poisoning
Rapid onset, IV atropine for muscarininc excess, A. muscarina ingestion can cause atropine poisoning

Pharmacology (15 decks)

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