parasympathetic nervous system Flashcards

cholinergic blockade: identify the consequences of cholinoceptor blockade and list the main clinical uses and unwanted effects of muscarinic cholinoceptor antagonists

1
Q

where are nictotinic receptors located, and significance

A

between pre and post ganglionic neurones in ANS (or between neurone and adrenal medulla in one SNS pathway); present throughout so can affect all aspects of ANS

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2
Q

what are nicotinic receptor antagonists also called

A

ganglion blocking drugs

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3
Q

what 2 things do nicotinic receptor antagonists block

A

block actual receptor, or act as ion channel blockers (e.g. preventing Na+ influx)

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4
Q

2 examples of nicotinic receptor antagonists

A

hexamethonium (blocks ion channel; anti-hypertensives), trimetaphan (blocks receptor; most common)

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5
Q

what is a use-dependent block and to what type of antagonist does it apply to

A

use-dependent block: blocks ion channel incompletely, not receptor; more open channels are, more effective drug is; receptor block: more agonist, less effective antagonist; ion channel block: more agonist, more effective antagonist

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6
Q

antagonist vs ion channel blocker affinity

A

antagonists have affinity to block receptor, but if in channel pore just physical blockade of pore

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7
Q

slide 13

A

slide 13

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8
Q

outcome of nicotinic recepor antagonist use

A

could block out all ANS; depends which system is dominant in that moment in time (if SNS dominant at time, that is the effect that is lost, and vice versa)

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9
Q

outcome of increased SNS activity (at rest = dominant PSNS) due to nicotinic receptor antagonist use

A

pupil, trachea and bronchiole dilation; glycogenolysis and gluconeogenesis; lipolysis; increased renin secretion; detrusor relaxation and constriction of trigone and sphincter; thick, viscous secretions; piloerection and increased sweating; increased heart rate and contractility (at rest PSNS has more effect so this effect is lost, increasing heart rate); decreased GI motility and tone with sphincter contraction; dilation of skeletal muscle blood vessels; constriction of blood vessels innervating skin, mucous membranes and splanchnic area

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10
Q

why do nicotinic receptor antagonists cause hypotension

A

heart, blood vessels, kidneys: heart rate will increase (PSNS dominant at rest), but dilation of blood vessels to GIT (SNS dominant at rest; decreased TPR) and stops renin secretion to kidney (SNS dominant at rest; reduced blood volume, Ang II and TPR)

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11
Q

effect of nicotinic receptor antagonists on smooth muscle at rest

A

pupil dilation, decreased GI tone, bladder dysfunction, bronchodilation

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12
Q

effect of nicotinic receptor antagonists on exocrine secretions

A

decrease secretions from salivary glands, GIT, skin and trachea and bronchioles

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13
Q

what nicotinic receptor antagonist was the first anti-hypertensive

A

hexamethonium

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14
Q

when is trimetaphan (nicotinic receptor antagonist) used

A

during surgery as an anti-hypertensive as short acting

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15
Q

how does a-bungarotoxin work

A

covalently binds to receptor and must be replaced to restore function; designed to target skeletal muscle as binds to somatic nervous system nicotinic receptor at NMJ

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16
Q

nicotinic receptor antagonists vs muscarinic receptor antagonists

A

nicotinic too messy and broad to be useful as effect all of autonomic function; muscarinic is more discrete so therapeutically more useful