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PHARMACOLOGY - 2 > 14b - Autonomic NS > Flashcards

14b - Autonomic NS Flashcards

1
Q

Direct-acting cholinergic agonist: non-selective cholinergic (N=M) examples

A
  • Acetylcholine
  • Carbachol: more metabolically stable, don’t use systemically=danger in stopping the heart (ex. used in the eyes)
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2
Q

Carbachol in the eyes

A
  • Pupillary constriction
  • Aqueous humor production effected
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3
Q

Direct-acting cholinergic agonist: nicotinic selective (N»M) example

A
  • Nicotine
  • *mix of PS and S effects
  • *muscle twitching=stimulates skeletal muscle
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4
Q

Direct-acting cholinergic agonist: muscarinic selective (M»N) example

A
  • Muscarine
  • Bethanechol
  • Pilocarpine
  • *can still affect the heart (be careful if use systemically)
  • *ophthalmically OR systemically for stimulating urination
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5
Q

Indirect-acting IRREVERSIBLE agonist (AChE inhibitors) examples

A
  • Organophosphate/carbamate
  • Insecticides
  • *non-selective cholinergic (N=M)
  • *accumulation of ACh
  • **double stimulation in PS (ganglion and effector organs)
    o SLUD
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6
Q

Indirect-acting REVERSIBLE agonist (AChE inhibitors) examples

A
  • Edrophonium
  • Neostigmine
  • *non-selective cholinergic (N=M)
  • *used after a paralysis drug (specifically in skeletal muscle)
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7
Q

Cholinergic antagonists: muscarinic selective (M»N) examples

A
  • Atropine: competitive
  • Ipratropium
  • *need to add A LOT of it to get a N effect
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8
Q

Cholinergic antagonists: Nn, ganglionic blocker (Nn>Nm»MM) examples

A
  • Hexamethonium
  • Trimethaphan
    • don’t use in a conscious animal
  • *controlled HYPOTENSION: stops firing of S and PS system=stops baroreceptor reflex=HR will remain low
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9
Q

Cholinergic antagonists: Nm, neuromuscular blocker (Nm>Nn»M) examples

A
  • Tubocurarine
  • Pancuronium
  • Succinyl choline (initially an agonist, then antagonizes receptor)
    o Ex. rapidly intubate and animal
    *if add a lot of the drugs=will start to antagonize the next receptor
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10
Q

Dose effects in this course

A
  • Assume all effects are possible
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11
Q

Atropine low dose: what do you see?

A
    1. Salivation: reduced
    1. Minor effect on inhibiting urination
  • No HR increase or accommodation of vision
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12
Q

Atropine moderate dose: what do you see?

A
  • Inhibits urination more
  • Reduced salivation significantly
  • Increased HR
  • Decreased accommodation of vision
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13
Q

Atropine high dose: what do you see?

A
  • Complete inhibition of salivation
  • Max out HR
  • Max decrease of accommodation of vision
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14
Q

ACh low to moderate dose IV

A
  • No affect on activity at autonomic ganglia (nicotinic): not as highly perfused
  • Decrease in diastolic BP=vasodilation (muscarinic)
  • Decrease HR (muscarinic)
  • Increase GI motility(muscarinic)
  • *transient effects
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15
Q

Atropine given IV and then give ACh low to moderate dose again

A
  • Atropine acts for many hours!
    o Give it once and it persists
  • *muscarinic antagonists
  • No change in gut motility
  • Slight drop in diastolic BP (minor vasodilation)
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16
Q

10x dose of ACh: does atropine still antagonize?

A
  • Yes
    o Effect in gut
  • *autonomic ganglion=more firing (now seeing more prominent S effects)
    o Increase in HR
    o Increase in diastolic pressure (vasoconstriction) (atropine already reduced the vasodilation response)
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17
Q

Give alpha+beta blockers after atropine and then give high dose ACh: what would happen?

A
  • Beta receptors in heart: no HR change
  • Alpha receptors in arterials: no change in diastolic pressure
  • NO effect in gut
  • Autonomic ganglia stimulation is not effected (due to them being nicotinic)
    o Would need an Nn blocker (ex. hexamethonium)
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18
Q

Give hexamethonium after atropine and then give high dose ACh: what would happen?

A
  • No gut effect
  • No HR or blood pressure response
  • No increase in autonomic ganglion activity (maybe even below baseline firing)
19
Q

Adrenergic agonists: E receptor selectivity

A
  • Alpha 1 and 2
  • Beta 1 and 2
  • *EQUALLY
20
Q

Adrenergic agonists: NE receptor selectivity

A
  • Alpha 1 and 2
  • Beta 1 > beta 2
21
Q

Adrenergic agonists: Isopreterenol receptor selectivity

A
  • *cardiac support in an emergency
  • Beta 1=2&raquo_space;alpha
22
Q

Adrenergic agonists: dopamine

A
  • D1>beta1>beta2>alpha
  • NT but effects outside of CNS
  • Really high doses=loses selectivity (stimulates D1
23
Q

D1 receptors:

A
  • vasculature (especially renal vasculature)
  • stimulated=dilates
    Ex. use in a shocked animal to prevent irreversible kidney damage due to lack of blood flow
24
Q

Dobutatmine

A
  • Less peripheral dilation
  • More pure cardiac stimulation
  • *beta1>beta2>alpha
25
Q

Phenylephrine

A
  • Predominantly vasoconstriction
    o Support BP in crashing animal OR decongestion
  • *alpha1>alpha2»beta
26
Q

Clonidine; xylazine

A
  • Cause sedation
  • *alpha2>alpha1»beta
27
Q

Terbutaline, clenbuterol, salbutamol

A
  • Beta 2 agonists
  • *bronchodilate (ASTHMA)
  • Too high dose=beta 1 receptors (monitor)
  • *beta 2>beta1»alpha
28
Q

Humans: beta-3 agonists are used for (ex. mirabegron)

A
  • Overactive bladder treatment
  • Target detrusor muscle=relaxes it=less likely to urinate
  • *selection for beta-3 may not actually be that good (still needs improvement!)
29
Q

Glaucoma (cause and effects of muscarinic and beta-adrenergic stimulation)

A
  • High intraocular pressure
    o Too much aqueous humor production
    o Impair aqueous humour outflow
  • Muscarinic receptor stimulation increases aqueous humour outflow
  • Beta-adrenergic stimulation increases aqueous humour production
30
Q

Alpha antagonists examples

A
  • Prazosin
  • Phenoxybenzamine
  • Phentolamine
  • Tolazone, atipamezole
31
Q

Prazosin

A
  • Alpha COMPETITIVE antagonist
  • Alpha1»»>alpha2
    o Old school ANTI-HYPERTENSIVE
  • *works too good so not used in human med anymore
32
Q

Phenoxybenzamine

A
  • Alpha IRREVERSIBLE antagonist
  • Alpha1>alpha2
33
Q

Phentolamine

A
  • Alpha antagonist
  • Alpha1=alpha2
34
Q

Tolazine, atipamezole

A
  • Alpha antagonist
  • Alpha2»alpha1
  • *used to REVERSE the alpha 2 agonists used for sedation
35
Q

Mixed antagonists examples

A
  • Labetalol, carvedilol
  • *less selective
36
Q

Labetalol, carvediol

A
  • Mixed antagonist
  • Beta1=beta2>alpha1>alpha2
  • *for HEART FAILURE
    o Beta1 antagonism: lower HR
    o Beta 2 antagonism: tolerated
    o Alpha 1 antagonism: reverse excess vasoconstriction
37
Q

Beta antagonists examples

A
  • Metoprolol, acebutolol, atenolol
  • Propranolol, timolol
38
Q

Metoprolol, acebutolol, atenolol

A
  • Beta antagonists
  • Beta1»>beta2
    o Heart: anti-arrhythmic (slow down heart)
    o Juxtaglomerular apparatus: prevent renin release
  • *anti-hypertensive
39
Q

Propranolol, timolol

A
  • Beta antagonists
  • Beta1=beta2
    o non-selective
  • *preferred beta blocker to use ophthalmic (to control aqueous humour production)
  • Can be a problem in asthmatics (would want to use a beta1 selective antagonist to reduce risk of triggering an asthma attack)
40
Q

Give NE: effects on CV system

A
  • *alpha1, alpha2, beta 1
  • HR: increase stretch increases firing of baroreceptors=cause decrease in S firing, and increase in vagal firing=decrease HR (*due to large increase in TPR)
    o *still increase in cardiac output (increased pulse pressure!)
  • BP: increase in TPR, increases diastolic P
  • TPR: pure alpha2 response=vasoconstriction=LARGE increase in TPR
  • CRASHING ANIMAL: if give NE=increased TPR could slow the heart down
    o Maybe if really high dose of NE=override the baroreceptors and get increased HR
41
Q

How can you have increased CO when HR is lower?

A
  • Increased SV: due to strong beta1 stimulation in heart muscle cells
    o increased contractility
42
Q

Give E: effects on CV system

A
  • Alpha1, alpha2, beta1, beta2
  • CRASHING ANIMAL: E preferred
  • HR: less stretch of baroreceptor=stimulate S and inhibit PS=NET effect is to increase HR (NOT fighting the direct stimulation of E on the heart=further support stimulator effect)
    o HR and SV increased=CO increased!
  • BP: diastolic P decreased due to decreased TPR
  • TPR: beta2=vasodilate=decrease slightly
43
Q

Give Isoproterenol: effects on CV system

A
  • Beta1=beta 2, little to no alpha stimulation
  • HR: increased (CO increased!)
  • BP: more decreased diastolic pressure
  • TPR: large decreased due to beta2=vasodilation (add to stimulator effects on the pacemakers, baroreceptor not firing as much)
44
Q

Give Dopamine (higher dose): effects on CV system

A
  • D1>beta1>beta2>alpha
  • Renal vascular dilation
  • HR: increased (decreased stretch and the beta1 effects)
  • BP: slight decrease in diastolic and increase in systolic
  • TPR: slight decrease vasodilation (not as high receptor affinity for beta2)
    o Dilation in renal vasculature
    o Minor dilation in peripheral skeletal muscle vascular beds
  • *VERY DESIRABLE IN AN EMERGENCY

PHARMACOLOGY - 2 (6 decks)

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