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N550 Pharm > ANS > Flashcards

ANS Flashcards

0
Q

Where are preganglionic and postganglionic neurons of SNS located?

A

Preganglionic: T1-L2/L3, intermediolateral horn of grey matter
Postganglionic: Paravertebral chains, prevertebral ganglia

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1
Q

Are preganglionic vs. postganglionic neurons myelinated or unmyelinated?

A

Preganglionic- myelinated

Postganglionic- unmyelinated

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2
Q

Where are PSNS preganglionic neurons and postganglionic neurons located?

A

Preganglionic: Cranial (CN 3,7,9,10) Sacral (S2-4)
Postganglionic: target organs, also ganglia in head and neck

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3
Q

Does SNS or PSNS have long preganglionic neurons and short postganglionic neurons?

A

PSNS

SNS has short pre and long post

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4
Q

Most organs are innervated by SNS and PSNS.
What are the innervations for the exceptions? (sweat glands, ciliary muscle of the eye, bronchial smooth muscle, and blood vessels)

A

SNS: sweat glands and blood vessels (muscarinic receptors present)
PSNS: ciliary muscle of the eye and bronchial smooth muscle (B2 receptors present)

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5
Q

Ach binds to _____ receptors, what are the types?

Epi, NE, and dopamine bind to _______ receptors, what are the types?

A

ACh binds to cholinergic receptors, which are nicotinic (ligand gated) or muscarinic (g-protein coupled)
Epi, NE, and dopamine bind to adrenergic receptors, which are alpha 1-2 and beta 1-3 (**NE does NOT stimulate beta-2)

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6
Q

The adrenal medulla releases ____% epi and _____% norepi

A

80% epi, 20% norepi

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7
Q

What receptors activate G-alpha-Q? What is the effect?

A

Alpha-1, M1, and M3

Increased calcium -> contraction/vasoconstriction

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8
Q

What receptors activate G-alpha-I? What are the effects?

A

Alpha-2, M2
Inhibits adenylate cyclase which DECREASES cAMP (post synaptic) -> contraction!
Presynaptic increases K conductance

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9
Q

What receptors activate G-alpha-S? What are the effects?

A

Beta 1,2,3
S=Stimulate the activation of adenylate cyclase increasing cAMP
Vasodilates, increases HR and contractility

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10
Q

Alpha-1 effects?

A 
Vascular smooth muscle CONTRACTION
Iris contracts, pupil dilates
Pilomotor smooth muscle erects hair
Prostate/uterus contraction
Heart increases force of contraction (not as mjuch as beta-1)
Think of Phenylephrine!
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11
Q

Alpha-2 effects?

A

Platelets aggregate
Presynaptic inhibition of adrenergic/cholinergic transmitter release (decrease BP/HR)
Presynaptic/CNS vasodilation, postsynaptic vasoconstriction
GI relaxation
CNS sedation and analgesia (via decreased SNS outflow from brain stem)
Think of Clonidine!

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12
Q

Beta-1 effects?

A

Heart- increase force and rate of contraction

Kidney- stimulate renin release (this will increase BP)

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13
Q

Beta-2 effects?

A

Respiratory, uterine, vascular, GI, GU- relaxation
Mast cells- decrease histamine release
Skeletal muscle- dilation, uptake of K, increased speed of contraction
Liver- glycogenolysis
Pancreas- increase insulin secretion (so you can use the glucose)
Adrenergic nerve- increase release of NE

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14
Q

Beta-3 effects?

A

Activates lipolysis, thermogenesis

worry about athrosclerosis

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15
Q

D-1 effects?

A

Smooth muscle- (postsynaptic) dilates renal, mesenteric, coronary, and cerebral blood vessels (decreased afterload)

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16
Q

D-2 effects?

A

Nerve endings- (presynaptic) modulates transmitter release, increases N/V

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17
Q

All sympathomimetics are derivatives of what?

A

Beta-phenylethylamine
An amine side chain, hydroxyl group on 3,4 carbons of benzene ring (catechol)
Thus the name catecholamine

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18
Q

Sympathomimetics: MOA

A

Activation of G-protein couple receptor directly (drug binds to receptor) or indirectly (drug increase NE release from SNS nerves activating the receptor)
G-protein will have downstream effects, usually effecting the amount of intracellular Ca

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19
Q

How are catecholamines vs. non-catecholamines metabolized?

A

Catecholamines: Reuptake (neuronal, extraneuronal), MAO, COMT, lungs
Non-catecholamines: MAO, urinary excretion
**If someone is on MAOI’s, this will increase the availability of neurotransmitters in the CNS/PNS

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20
Q

What is the selectivity of Phenylephrine vs. Clonidine?

A

Phenylephrine α1>α2»»>β
Clonidine α2>α1»»>β
These are alpha agonists

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21
Q

What is the selectivity of Norepinephrine vs. Epinephrine?

A

Norepinephrine* α1=α2; β1»»»>β2
*B2 not innervated
Epinephrine α1=α2; β1=β2
These are mixed alpha/beta agonists

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22
Q

What is the selectivity of Dobutamine, Isoproterenol, and Terbutaline/albuterol?

A

Dobutamine β1>β2»»α
Isoproterenol β1=β2»»α
Terbutaline/albuterol β2»β1»»α
These are beta-agonists

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23
Q

What is the selectivity of Dopamine vs. Fenoldopam?

A

Dopamine D1=D2»β»α
Fenoldopam D1»D2
These are dopamine agonists

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24
Q

Epinephrine: route, onset, duration?

A

Route: subq or IV
Onset: subq 5-10 min, IV 1-2 min
Duration: 5-10 min

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25
Q

Epinephrine: indications?

A 
Bronchial asthma
Acute allergic reaction
Electromechanical dissociation
V fib unresponsive to defib
Infusion to increase myocardial contractility (low dose)
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26
Q

Epinephrine dosing?

A

Resuscitation: bolus dose 10 mcg/kg IV (can start w 2-8 mcg/kg)
Beta-2: 1-2 mcg/min IV
Beta-1: 4-5 mcg/min IV
Alpha and Beta: 10-20 mcg/min IV (over 20 is alpha)

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27
Q

CV effects of Epinephrine?

A

With moderate doses, SBP increases (B1, A1), DBP decreases (B2), MAP stays the same
α1 - vasoconstriction - ↑ BP, ↑ CVP, ↑ Cardiac work
α2 - negative feedback - ↓ BP
β1 - increased contractility, HR, CO – ↑ BP
β2 - peripheral vasodilation - ↓ BP

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28
Q

Cerebral effects of Epinephrine?

A

Minimal vasoconstriction of arterioles in cerebral vasculature (increase CBF), coronary vasculature, and pulmonary vasculature

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29
Q

Ocular effects of Epinephrine?

A

Alpha-1-mydriasis
Alpha 1/2- increase humoral outflow
Beta 1- increase production of aqueous humor (inc intraoccular pressure)

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30
Q

Respiratory effects of Epinephrine?

A

B2- dilate bronchial tree, decrease release of histamine
A1- reduce mucosal secretion-decongestion
(Note: beta blockers do the OPPOSITE which is why asthmatics can’t handle them)

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31
Q

GI effects of Epinephrine?

A

A2- decreased secretions
A/B2- decreased peristalsis
A1- blood flow reduced even if BP normal

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32
Q

GU effects of Epinephrine?

A

A1- renal blood flow REDUCED, contract urethral sphincter
B1-kidney increases renin release
B2- decreases UO, inhibits labor
The kidneys take a big hit! Consider giving a vasodilator

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33
Q

Metabolic effects of Epinephrine?

A

B2- Increased liver glycogenolysis and insulin release
B3- lipolysis
A2- minorly opposes B2, inhibits insulin release
End result: BG goes up

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34
Q

Prep and dosage of norepinephrine (Levophed)?

A

For hypotension: 4-16 mcg/min

Mix in 5% glucose solution (to prevent oxidation)

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35
Q

What are the effects of norepinephrine?

A

Potent alpha and beta-1, but minimal beta-2, leading to intense vasoconstriction (increased BP/MAP), baroreceptors are activated decreasing HR/respiration
Decreased venous return/CO/HR, preload is going up
Bottom line: good for shock/hemorrhaging, but will do a lot of damage if the problem isn’t fixed

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36
Q

How does dopamine work? What is the dose?

A 
Works on all adrenergic receptors (a,b,d)
D1 dominates ("renal dose" for peeing more, misleading) 1-3 mcg/kg/min
B1 dominates 3-10 mcg/kg/min
Alpha dominates over 10 mcg/kg/min
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37
Q

Why is dopamine not as useful with depleted catecholamine stores?

A

Increases endogenous norepinephrine release

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38
Q

If dopamine PIV infiltrates, dangerous
Inhibitory at carotid bodies, pt may have altered response to hypoxia
Increased intraocular pressure

A

Yup

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39
Q

Isoproterenol: what are the effects?

A

B1 and B2 agonists
Increases HR and contractility, decreases SVR
(inc SBP, dec DBP, dec MAP)

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40
Q

Who do you NOT give isoproterenol to?

A

Someone with a high HR, we decrease O2 delivery and increase demand, therefore setting them up for an MI

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41
Q

What is the dosage of isoproterenol?

A

1-5 mcg/min for heart block and bradydysrhythmias

Rapid metabolism by COMT so you need to give it as an infusion

42
Q

Dobutamine is used for what? What is it?

A

Its a good coronary artery vasodilator, improves CO without increase HR/BP, good for CHF
B1 selective drug (agonist)

43
Q

Dobutamine dose?

A

2-10 mcg/kg/min
B1 selective <5mcg/kg/min
Weak A1 stimulation over 5

44
Q

How does ephedrine work?

A

Indirect and direct agents of alpha and beta
“weak epi”, lasts 10x longer
Used frequently in surgery to increase BP (increases HR too)

45
Q

Ephedrine route and dosage?

A

PO, IM, IV

10-25 mg IV, 10-50 mg IM

46
Q

Ephedrine caution?

A

Tachyphylaxis with repeated dosing, NE depletion, receptor occupation long 1/2 life, CV compensation
Excreted in urine, slowly metabolized by MAO, conjugated in the liver
E1/2t 3 hours

47
Q

How does phenylephrine (neo-synephrine) work?

A

Primarily A1 stimulant, direct acting
VENOCONSTRICTION more than arterial constricts (improving preload)
Less potent and longer lasting than norepinephrine
Used in surgery to increase BP/SVR (decreases HR/CO)

48
Q

Phenylephrine dosage?

A

50-200 mcg IV or infusion 20-50 mcg/min

49
Q

If your pt gets an overdose of phenylephrine/epinephrine, what should you give?

A

Give an alpha-1 antagonist
They have massive alpha 1 stimulation
The absolute wrong answer here is a beta blocker, this will kill them because nothing will be left to balance out the alpha

50
Q

What effects do Beta-2 agonists have?

A

Relax bronchiole and uterine smooth muscle
Sustained duration of action
Useful in premature labor, asthma, COPD
Side effects: tremor (B2 in skeletal muscle), reflex tachycardia (vasodilation and B2 in heart)

51
Q

What is the preferred choice for bronchospasm due to asthma?

A

Albuterol - B2 agonist

To prevent, have them use this before surgery

52
Q

Albuterol dose? Side effects?

A

MDI: 100 ug/puff, 2 puffs q4-6h, max 16-20 puffs
Neb: 15 mg/h for 2 hours
Side effects: large doses can cause tachycardia and hypokalemia

53
Q

What are terutaline and salmeterol used for?

A

These are B2 agonists
Terbutaline for asthma/premature labor
Salmeterol has longer DOA than albuterol (clinically similar to albuterol)

54
Q

What is Ritordine used for? What are side effects?

A

Premature labor
Has some B1 so increase HR/CO
Can cause pulmonary edema

55
Q

What are these drugs? Midodrine (ProAmatine), oxymetazoline, tetrahydrozoline, xylometazoline?

A

A1 agonists
Midodrine for postural hypotension
Oxymetazoline, tetrahydrozoline, xylometazoline for nasal/ocular decongestants

56
Q

What are clonidine, dexmedetomidine, and methyldopa?

A

A2 agonists
Decreased SNS output from CNS, decreases BP and causes sedation and analgesia
Clonidine- partial agonist
Dexmedetomidine- full agonist

57
Q

How does amphetamine and methamphetamine work?

Note: methylphenidate (ritalin) and pemoline (cylert) are for ADHD and are amphetamine variants

A

Amphetamine increases release of NE, 5HT, and dopamine, blocks repute and vesicular transport and inhibits MAO
Methamphetamine is similar but has more CNS effects
These drugs are impossible to predict how a pt will react

58
Q

How do reserpine and cocaine work?

*Note that Cocaine can be used as a LA by working on Na channels to provide analgesia to the area

A

These are inhibitors of catecholamine storage and reuptake
Reserpine- vesicles lose ability to store NE, 5HT, and dopamine and MAO breaks down excess, causes hypotension and depression
Cocaine- prevents reuptake of catecholamines (NE,5HT,DA) and interferes with transport

59
Q

What are the selectivity of these drugs? What is the class? Prazosin, terazosin, doxazosin, phentolamine, yohimbine, tolazoline?

A

Prazosin, terazosin, doxazosin α1»»α2
Phentolamine α2=α1
Yohimbine, tolazoline α2»α1
These are alpha antagonists

60
Q

What are the selectivity of these drugs? What is the class? Labetalol and carvedilol?

A

Labetalol, carvedilol β1=β2>α1>α2

These are mixed alpha and beta antagonists

61
Q

What are the selectivity of these drugs? What is the class? Metoprolol, atenolol, esmolol, propranolol, nodal, timolol, butoxamine?

A

Metoprolol, atenolol, esmolol β1»>β2
Propanolol, nadolol, timolol β1=β2
Butoxamine β2»>β1
These are beta-antagonists

62
Q

What happens when we block alpha-1?

A

If we block alpha-1 we get rebound tachycardia because we will have vasodilation, decreased BP/PVR, then the baroreceptors kick in to increase HR (we also get postural hypotension)

63
Q

What happens when we block alpha-2?

A

If we block alpha-2 we are blocking the negative feedback so we will have more NE available (alpha-2 inhibits neurotransmitter release, so when we block, it is not being inhibited anymore)

64
Q

What are general alpha-antagonist effects with GU, eyes, and nasal?

A

Blockade in prostate/bladder causes muscle relaxation, eases micturation
Miosis (constricted pupil)
Increased nasal congestion (secretions)

65
Q

What is phentolamine?

A

Nonselective alpha blocker

Causes dec BP and inc HR/CO

66
Q

What doses are given for phentolamine for hypertensive emergencies vs. local infiltration (ex. dopamine)?

A 
Hypertensive emergency (pheochromocytoma or autonomic dysreflexia): 30-70 mcg/kg IV, onset 2 min, DOA 10-15 min (works fast, stops working fast)
Local infiltration dose: 2.5-5 mg in 10ml
67
Q

What is phenoxybenzamine used for? How long is the onset and E1/2t?

A 
Binds covalently meaning it will have a long acting drug
Onset: 1 hr, E1/2t: 24 hours!!
Works on alpha-1 more than alpha-2
Decreases SVR, vasodilation
Used for pheochromocytoma and raynaud's
68
Q

Why might your patients be taking prazosin or yohimibine?

A

Prazosin for pheochromocytoma, blocks A1, has less reflexive tachycardia
Yohimibine is a A2 blocker, increases NE release, used for orthostatic hypotension and impotence

69
Q

Why might your patients be taking tarazosin and tamulosin?

A

Long acting A1-agonist effective in prostatic smooth muscle relaxation
Helpful for BPH

70
Q

Why would we avoid Beta (b2 specifically) blockers in asthma patients?

A

If we block b2 they will be more likely to have a bronchospasm, asthma pt need the b2 for bronchodilation effects
Note, when giving beta-1 antagonists, the drug can lose selectivity and still cause bronchospasm, so be careful!

71
Q

Beta antagonist effects?

A

Heart: improve oxygen supply and demand balance
Lungs: provokes bronchospasm
Vessels: vasoconstriction in skeletal muscle, PVD worsen symptoms
Kidney: decrease renin release, decreasing BP
Pancreas: B2 release insulin, B1 mask symptoms of hypoglycemia

72
Q

Beta agonist MOA?

A

Selective binding to beta receptors, competitive and REVERSIBLE inhibition (large doses of agents will overcome antagonists)
Chronic use will upregulate receptors

73
Q

What happens intra-op if the pt doesn’t get their beta-blocker?

A

Higher incidence of intra-op MI if they don’t get their beta blocker

74
Q

What is propranolol?

A

Pure antagonist, equally blocking B1 and B2 (nonselective)

75
Q

CV effects of propranolol?

A

Decrease HR, contractility, CO (especially during exercise and SNS outflow)
B2-Increase PVR, increase coronary vasc resistance
Sodium retention (bc renal is responding to CO drop)

76
Q

Propranolol pharmacokinetics? (Protein bound? E1/2t? Clearance?)

A 
Highly protein bound
Significant first pass effect (need large po dose compared to IV dose)
Metabolized in liver, E1/2t 2-3h 
Can decrease clearance of LAs
Decreases first pass effect of fentanyl
77
Q

Timolol uses?

A

Non selective b-blocker
Tx glaucoma, decreases intraocular pressure by decreasing production of aqueous humor
Eye drops can cause systemic absorption, decreases BP/HR and increasing airway resistance

78
Q

What is nadolol’s E1/2t?

A

Non selective b-blocker with no significant metabolism (renal/biliary elimination)
E1/2t 20-40 hours!

79
Q

Metoprolol uses? Dose? E1/2t?

A

Selective B1 blocker, prevents inotropy and chronotropy
PO 50-400 mg (60% first pass effect)
IV 1-15 mg
E1/2t 3-4h

80
Q

Atenolol uses? E1/2t?

A

Most selective b1-blocker. Has least CNS effects, doesn’t cross BBB, so useful with people that have trouble with CNS side effects, also useful for CAD (prevents MI intra-op). NOT good for someone with renal disease bc it is not metabolized in the liver, excreted renal
E1/2t 6-7h (longer in renal disease)

81
Q

Why might someone be on betaxolol?

A

Selective b1 blocker. E1/2t 11-22h
Taken for HTN
Taken topical for glaucoma, especially asthmatics (less risk of bronchospasm)

82
Q

Esmolol uses and dose? DOA?

A 
B1 antagonist
Rapid onset, short acting, used for dec HR without significant BP drop, can be used at the end of a case
IV 0.5 mg/kg (10-180mg)
Infusion 50-300 mcg/kg/min
DOA less than 15 min
83
Q

Esmolol E1/2t? metabolism?

A

E1/2t 9 min!

Rapidly hydrolyzed by plasma esterase’s (not the same as sux, no effect on that)

84
Q

B-blocker side effects?

A

CV: dec HR/contractility/BP, exacerbate PVD
Lungs: bronchospasm, airway resistance
Metabolism: alter and mask hypoglycemia symptoms (the HR will not increase like usual)
Inhibit uptake of K into skeletal muscle
CNS: fatigue, lethargy
GI: N/V/D

85
Q

RELATIVE contraindications of B-blockers?

A

Pre-existing AV heart block or heart failure
Asthma
DM
Hypovolemia

86
Q

B-blocker use?

A

hypertension treatment, angina management, decrease mortality in tx of post-MI, suppress tachyarrythmias, prevent SNS activity

87
Q

What is labetalol used for? What are the cautions and side effects?

A

Selective A1,B1,B2 blocker (more B, 7:1)
Decrease BP, SVR, HR (CO unaffected)
Caution in renal pt, metabolize glucuronic acid, in urine
Side effects orthostatic hypotension, bronchospasm, heart block, CHF, bradycardia

88
Q

Labetalol dose and E1/2t?

A

Dose 0.1-0.5 mg/kg
Give 5mg at a time for HTN, wait to redose, BP will drop in 5-10 after IV administration
E1/2t 5-8h, prolonged in liver disease

89
Q

Why should we call anticholinergics the name “antimuscarinics” instead?

A

These drugs don’t work on Ach, they work on the muscarinic receptors. The name is misleading. They competitively antagonize Ach at the muscarinic receptors only. This is REVERSIBLE.
This allows SNS response to dominate (blocks PSNS)

90
Q

Atropine effects

A

Sedation, nausea +
Inc HR +++
Relax smooth muscle ++
Anti-sialagogue +

91
Q

Scopalamine effects

A

Sedation, nausea +++
Inc HR +
Relax smooth muscle +
Anti-sialagogue +++

92
Q

Glycopyrrolate

A

Sedation, nausea 0! (Doesn’t cross BBB)
Inc HR ++
Relax smooth muscle ++
Anti-sialagogue ++

93
Q

Which antimuscarinics are tertiary amines (alkaloids of belladonna plants)? Which are quaternary ammonium derivatives?

A

Tertiary amines: Atropine and scopalamine

Quaternary ammonium derivative: glycopyrrolate (robinal)

94
Q

Compare onsets, duration of action and E1/2t of IV atropine and IV glycopyrrolate

A

Atropine onset 1 min, DOA 30-60 min, E1/2t 2h (18% unchanged in urine)
Glycopyrrolate onset 2-3 min, DOA 30-60 min, E1/2t 1.25h (80% unchanged in urine)
Scopolamine extensively metabolized with only 1% unchanged in urine

95
Q

Why do CRNAs use antimuscarinics?

A

Pre-op: antisialagogue, sedation, nausea prevention
Anytime: treat bradycardia (esp vagal, note: young have high tone= more tacky; old have less tone= less tacky), bronchodilation, mydriasis and cycloplegia for ophtho cases (don’t give for glaucoma bc it increases IOP), reduce biliary and ureteral spasm with opioids
ALWAYS give with anticholinesterase drugs to antagonize NMB

96
Q

Ipratropium uses and dose?

A

Use: bronchodilation, given in asthmatics, COPD, and smokers before surgery
MDI 40-80 mcg/2 puffs
0.25-0.5 mg neb
Onset 30-90 min

97
Q

Dose of scopolamine?

A

Preop IM: 0.3-0.5 mg or 5mcg/kg

Transdermal 1.5 mg (5mcg/h x 72h)

98
Q

Dose of atropine?

A

IV pre-op: 0.2-0.4 mg
IV brady: 0.4-1 mg
Neb: 2 mg in 5 mL NS (bronchodilate)

99
Q

Dose of glycopyrrolate?

A

0.1-0.2 mg IV for pre-op or bradycardia

100
Q

What is central anticholinergic syndrome? How is it treated?

A

Caused by scopalamine or atropine (unlikely with glycopyrrolate as it doesn’t cross BBB)
Restlessness, hallucination, somnolence, unconscousness, delayed recovery in PACU
Treat with physostigmine 15-60 mcg/kg IV repeat q1-2h prn

101
Q

Why might your patient be on ipratropium (atrovent) or tiotropium (spiriva)

A

Muscarinic antagonist that has bronchodilator effects for COPD

102
Q

Why might your patient be on oxybutynin (ditropan), tolterodine (detrol), darifenacin (enablex), or solifenacin (vesicare)?

A

Muscarinic antagonists good for overactive bladder
Oxybutynin and tolterodine are nonspecific muscarinic antagonists
Darifenacin and solifenacin are M3 specific

103
Q

Where are M1-5 receptors, where are Nm and Nn receptors?

A

M1: CNS stomach
M2: cardiac, CNS, airway smooth muscle
M3: airway smooth muscle, glandular tissues
M4/5: CNS
Nm: skeletal muscle at NMJ
Nn: autonomic ganglia, adrenal medulla, CNS

N550 Pharm (14 decks)

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