Week 4 Flashcards

1
Q

Depolarizing Block

A

ex. ACh+anticholinesterase or succinyl choline
Phase 1 block: Muscle is depolarized near E(ACh), ACh receptors are occupied, voltage-dependent sodium channels are inactivated at end plate
Phase 2 block: Voltage-dependent sodium channels at end plate are no longer inactivated. ACh receptor is still occupied by Sux and it is desensitized so no current is produced

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2
Q

Uses of neuromuscular blockade in anesthetized patients

A

Safe facilitation, orthopaedic manipulations, endotracheal intubations, diagnostic scopy’s

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3
Q

Tubocurarine

A

Obsolete, releases histamine, ganglionic block, hypotension, renal clearance

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4
Q

Pancuronium

A

steroid, duration of action is 1 hour, does not release histamine, ganglionic blocakde minmal, tachycardia due to vagus nerve block, renal clearance

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5
Q

Vecuronium

A

intermediate duration of action, no tachycarida, no histamine release, no cardiovascular effects, biliary excretion

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6
Q

Atracurium

A

benzylisoquinolinium, intermediate duration of action, Hoffman elimation or via plasma esterases, neither hepatic nor renal clearance, no vagal or ganglionic block, some histamine release, seizures

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7
Q

Cisatracurium

A

better version of Atracurium

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8
Q

Sux

A

Uses- intubation
Side effects- bradycardia, tachy cardia, malignant hyperthermia
Contraindications- Burn patients, cardiac arrhythmias, ChE deficiency, myalgia

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9
Q

End-plate potentials lead to muscle contraction

A

depolarization at the end point will reach t-tubule that is responsible for bringing action potential into the muscle fiber stimulating calcium release from the sarcoplasmic reticulum

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10
Q

Cholinesterase inhibitors

A

Neostigmine- used to treat myasthenia gravis by increasing the amount of ACh available
Edrophonium- an anticholinesterase that is rapidly hydrolyzed used to diagnose MG

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11
Q

Principle of synergy

A

When two blockers act at different sites along this chain then their effects are multiplicative and may be profound

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12
Q

Loci of muscarinic and nicotinic receptors in the ANS

A

Muscarinic- autonomic neuroeffectors

Ionotropic- autonomic ganglia, skeletal neuromuscular junction

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13
Q

Treatment of anticholinesterase toxicity

A

decontaminate, atropine (heroic amounts), artificial respiration, reactivation of enzyme via 2-PAM, pyridostigmine pretreatmnet, anticonvulsants

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14
Q

Indications of muscarinic blockade toxicity and treatment

A

Indications: decreased secretions, urinary retention, vasodilation, decreased sweating, mydriasis, CNS deficit
Treatment- emesis, gastric lavage, activated charcoal, physostigmine

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15
Q

Identify the differences between adrenergic and cholinergic transmission

A

Ne action is terminated by upake not by destruction like Ach

Presynaptic receptors for Ne (alpha 2)

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16
Q

Catecholamine synthesis

A

Tyrosine–> Dopa–>Dopamine–> NE–> Epi

hydroyxlation, decarboxylation, hydroxylation, methylation

17
Q

Adrenergic uptake

A

Uptake 1- on nerve terminal membrane, major route for NE inactiviation due to closeness of neuro and effector, high affinity, low capacity
Uptake 2- OCT or ENT transporter, found on effector membrane, relied upon when neuro and effector far, low affinity, high capacity

18
Q

Metabolism

A

MAO (phase 1 non-cyp), COMT (Phase 2)
Peripheral (due to aldehyde dehyrogenase) VMA
CNS (due to aldehyde reductase)- MHPG

19
Q

Rocuronium

A

popular for intubation, rapid onset, 100% biliary excretion

20
Q

Dantrolene

A

used to treat malignant hyperthermia, prevents huge amounts of calcium release caused by SUX

21
Q

Contraindications

A

burn patients, cardiac arryhthmia, genetic ChE deficiency, myalgia

22
Q

Brain barostatic reflex

A

Increase in blood pressure- Nerves 9 and 10 go NTS to vagal nerve (bradycardia)
Decrease in blood pressure- Decrease in baroreceptor firing increases NE release to increase vasomotor tone and increase heart rate