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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Carbachol in the eyes

A
  • Pupillary constriction
  • Aqueous humor production effected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A
  • Nicotine
  • *mix of PS and S effects
  • *muscle twitching=stimulates skeletal muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Dose effects in this course

A
  • Assume all effects are possible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Atropine moderate dose: what do you see?

A
  • Inhibits urination more
  • Reduced salivation significantly
  • Increased HR
  • Decreased accommodation of vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Atropine high dose: what do you see?

A
  • Complete inhibition of salivation
  • Max out HR
  • Max decrease of accommodation of vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Phenylephrine
- Predominantly vasoconstriction o Support BP in crashing animal OR decongestion - *alpha1>alpha2>>beta
26
Clonidine; xylazine
- Cause sedation - *alpha2>alpha1>>beta
27
Terbutaline, clenbuterol, salbutamol
- Beta 2 agonists - *bronchodilate (ASTHMA) - Too high dose=beta 1 receptors (monitor) - *beta 2>beta1>>alpha
28
Humans: beta-3 agonists are used for (ex. mirabegron)
- 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
Glaucoma (cause and effects of muscarinic and beta-adrenergic stimulation)
- 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
Alpha antagonists examples
- Prazosin - Phenoxybenzamine - Phentolamine - Tolazone, atipamezole
31
Prazosin
- Alpha COMPETITIVE antagonist - Alpha1>>>>>alpha2 o Old school ANTI-HYPERTENSIVE - *works too good so not used in human med anymore
32
Phenoxybenzamine
- Alpha IRREVERSIBLE antagonist - Alpha1>alpha2
33
Phentolamine
- Alpha antagonist - Alpha1=alpha2
34
Tolazine, atipamezole
- Alpha antagonist - Alpha2>>alpha1 - *used to REVERSE the alpha 2 agonists used for sedation
35
Mixed antagonists examples
- Labetalol, carvedilol - *less selective
36
Labetalol, carvediol
- 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
Beta antagonists examples
- Metoprolol, acebutolol, atenolol - Propranolol, timolol
38
Metoprolol, acebutolol, atenolol
- Beta antagonists - Beta1>>>beta2 o Heart: anti-arrhythmic (slow down heart) o Juxtaglomerular apparatus: prevent renin release - *anti-hypertensive
39
Propranolol, timolol
- 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
Give NE: effects on CV system
- *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
How can you have increased CO when HR is lower?
- Increased SV: due to strong beta1 stimulation in heart muscle cells o increased contractility
42
Give E: effects on CV system
- 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
Give Isoproterenol: effects on CV system
- 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
Give Dopamine (higher dose): effects on CV system
- 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