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ANS Flashcards

1
Q

What is the ANS? What does it do? What does it consist of

A
  • Located in CNS and PNS
  • Coordinates and maintains steady state among the visceral organs
  • Neurons
    • preganglionic (myelinated)
    • postganglionic (unmyelinated)
  • 2 division classified anatomically
    • sympathetic
    • parasympathetic
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2
Q

Characteristics of SNS innervation?

A
  • Preganglionic neurons cell bodies located in T1-L2/3
    • INTERMEDIOLATERAL HORN OF GREY MATTER
  • Post ganglionic neuron cell bodies in ganglia
    • paravertebral chain
    • prevertebral ganglia (celiac, superior, inferior, mesenteric)
  • Short pre, long post
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3
Q

What is characteristics of PSNS?

A
  • Pre-ganglionic neurons arise from
    • cranio (medullary CN 3,7, 9. 10)
    • Sacral (spinal cord S2-S4) regions
  • Post ganglionic neuron cell bodies in
    • target organs
    • descrete ganglia in head/neck
  • LONG pre, short post
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4
Q

What is main role SNS?

A
  • Self preservation;: mst important function is maintenance of vasomotor tone
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5
Q

What is main function PSNS?

A

Rest for organism but excitatory visceral functions such as digestion

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6
Q

Many organs have innervation by SNS and PSNS. WHat are exceptions to the rule?

A
  • Only innervated by SNS
    • sweat glands
    • Blood vessels (however muscarinic are present at blood vessels)
  • Only innervated by PSNS
    • Ciliary muscle of the eye (accomodate eye for near vision)
    • bronchial smooth muscle (B2 receptors present though)

Receptros can be present in a tissue and NOT be innervated. In this case, receptor will only respond when something is circulating in blood

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7
Q

What is major role of SNS?

A
  • Amplicfication resposne with diffuse innervation
    • controls:
      • postural changes
      • excercie (world class marathon runner won’t want to take beta blocker)
      • Emergency massive response
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8
Q

PSNS exhibits ___ and ____ targeted resposnes

A

discrete; narrolwy targeted

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9
Q

Which baseline tones do both systems (SNS, PSNS) exhbiit at rest?

A

HR- Vagal predominance

Blood vessels- SNS tone

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10
Q

What is NT released/receptor at skeletal muscle?

A

ACh at nicotinic receptor (Nm)

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11
Q

Pre/post NT/receptor for blood vessels?

A
  • Pre ACh at Nic (Nn)
  • Post Norepinephrine @ adrenergic
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12
Q

Pre/post NT/receptor for sweat glands?

A
  • Pre: Ach at Nicotinic (Nn)
  • Post Ach at Muscarinic (exception to rule)
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13
Q

What is preganglionic for adrenal medulla?

A

Ach on nicotinic, adrenal medulla acts like post ganglionic

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14
Q

What is pre/post NT/receptor for parasympathetic system

A
  • Pre Ach at nicotinic
  • Post ach at muscarinic (salivary glands, etc)
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15
Q

What are receptors on cholinergic receptors?

A
  • Nicotinic Ach receptors
    • Nm and Nn<– selective drugs
  • Muscarinic Ach receptors
    • M1-M5 <– not as selective, more of a sledgehammer
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16
Q

What are adrenergic receptors?

A
  • alpha 1,2
  • Beta 1,2,3
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17
Q

What does adrenal medulla release?

A

Norepi 20%

Epi 80%

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18
Q

What are 3 major anomalies to SNS?

A
  • Adrenal medulla acts like ganglia but releases NE and Epi in 20/80 ratio
  • Sweat glands
    • sympathetic cholinergic fibers
    • Post ganglionic Ach onto muscarinic Ach receptor
  • Blood vessels
    • no innervation PSNS
    • there are muscarinic Ach on blood vessels, activate NO with eventual vasodilation if you had circulating Ach
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19
Q

M1?

Receptor, signal, 2nd messenger, physio response?

A
  • Receptor: Gαq
  • Signal: excitatory CNS, modulatory at ganglia
  • 2nd messenger:
      1. PLC activated
      1. IPC & DAG increase
      1. PKC and increased free Ca, decreased K conductance= contraction!
  • Physiologic response
    • CNS activity, modulation at ganglia
    • located CNS and stomach
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20
Q

M2

Receptor? Signal? 2nd messenger? Physiologic response?

A
  • Receptor Gαi
  • Signal: inhibitory cardiac
  • 2nd messenger:
      1. inhibit adenylate cyclase
      1. decrease cAMP
      1. increase K conductance
  • Physiologic effect
    • decreased cAMP slows HR and decreases contractility
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21
Q

M3?

Receptor, signal, 2nd messenger, physiologic?

A
  • Receptor: Gαq
  • Signal: excitatory smooth muscle, glands
  • 2nd messenger
      1. PLC activated
      1. IP3 and DAG increase
      1. PKC and increased free Ca
  • Physiologic response: smooth muscle contraction
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22
Q

Nn receptor?

Signal, 2nd messenger, physiologic response?

A
  • Receptor: ligand gated ion channel
  • Signal: excitatory ganglia CNS
  • 2ND messenger: Na and K permeability
  • Physiologic resposne: depolarization
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23
Q

Nm

Receptor? Signal? 2nd messenger? Phsyiologic response?

A
  • Receptor: ligand gated ion channel
  • Signal: excitatory @ NMJ
  • 2nd messenger: increase Na and K permeability
  • Physiologic: depolarization
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24
Q

α1?

Receptor, signal, 2nd messenger, physiologic resonse?

A
  • Receptor: Gαq
  • Signal: Excitatory blood vessels
  • 2nd messenger:
      1. PLC acticated
      1. IP3 and DAG increased
      1. PKC and increased free Ca
  • physiologic response: smooth muscle vasoconstriction
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25
Q

α2

Receptor, signal, 2nd messenger, pysiologic reponse?

A
  • Receptor: Gαi
  • Signal: inhibitory BV @ pre, CNS @post
  • 2nd messenger:
      1. inhibit adenylate cyclase
      1. decrease cAMP
      1. Increase K conductance
  • Physiologic
    • decreased cAMP increases smooth muscle contraction (post)
    • hyperpolarization with increase K
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26
Q

B 1,2,3

Receptor, signal, 2nd messenger, physiologic?

A
  • Receptor: Gαs
  • Signal: excitatory or inhibitory depends on cAMP actions
  • 2nd messenger
      1. activate adnylate cyclase
      1. increase cAMP
  • Physiologic
    • increased cAMP causes smooth muscle relaxation
    • stimulates cardiac contractility and increases rate
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27
Q

Where are α1 found? Actions?

A
  • Most vascular smooth muscle (blood vessels, sphincters, bronchi)->>> causes contraction
  • Iris–> contraction, dilates pupils
  • pilomotor—> erects hair
  • prostate and uterus–> contracts
  • heart—> increases force of contraction (B1 more important though)

Remember, α1 causes activation PLC–> IP3 & DAG–> PKC and increased free Ca causing contraction!

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28
Q

Where are α2 receptors found? Actions?

A
  • platelets–> aggregation
  • adrenergic and cholincergic nerve terminals **presynaptic**–> inhibits transmitter release (decrease HR and BP)
  • Vascular smooth muscle–> contraction (post synaptic) and dilation (pre-synaptic, CNS)
  • GI tract–> relaxation (presynpatic)
  • CNS—> sedationa nd analgesia via decrease CNS outflw from brain stem

Remember, alpha 2 causes inhibition of adenylate cyclase–> decrase cAMP–> increase K conductance

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29
Q

Where are beta 1 receptors found? Actions?

A
  • Heart–> increase force and rate of contraction
  • Kidney–> stimulate renin release

Remember Beta 1 (all betas) is Gαs causing increase adenylate cyclase, increase cAMP, and causing smooth muscle relaxation

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30
Q

Where are B2 receptors found, actions?

A
  • Respriatory, uterine, vascular, GI, GU–> promotes smooth muscle relaxation
  • Mast cells–> decrease histamine release
  • Skeletal muscle–> potassium uptake, dilation of vascular beds, tremor, increase speed of contraction
  • Liver–> glycogenolysis
  • Pancrease–> increase insulin secretion
  • adrenergic nerve terminals –> increase release NE

Remember Beta 2 is Gαs causing increase adenylate cyclae, increase cAMP, and causing smooth muscle relaxation, but also cAMP increase force/rate of contraction in cardiac muscle.

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31
Q

Where are beta 3 receptors found? Action?

A

Fat cells–> activate lipolysis, thermogenesis

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32
Q

Where are D1 receptors found, actions?

A
  • Tissues- Post synaptic location: dilates renal, mesenteric, coronary, cerebral blood vessels
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33
Q

Where are D2 receptors found, actions?

A
  • Nerve endings- presynpatic: modulates transmitter release; nausea and vomiting
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34
Q

What are endogenous catecholamines?

A

Epi, Norepi, Dopamine

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35
Q

What are synthetic catecholamines?

A

Isoproterenol,

Dobutamine

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36
Q

What are synthetic non-catecholamines?

A
  • Indirect acting
    • ephedrine
    • mephentermine
    • amphetamines
  • Direct acting
    • phenylephrine
    • methoxamine
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37
Q

What are selective alpha-2 agonists

A

Clonidine

Dexmedetomidine

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38
Q

What are selective beta-2 adrenergic agonists?

A

Albuterol

Terbutaline

Ritodine

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39
Q

What are direct agonists?

A

Varied affinities for alpha 1, alpha 2, beta1, beta 2

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40
Q

What are indirect agonists?

A

Increase the release of neurotransmitters by stimulating nerve endings

Dnagerous to give long term, because you’re depleting nerve endings of neurotransmitters

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41
Q

How to choose right drug for right situation?

A
  • All sympathomimetics are not created equal, have differing affinities for various types of adrenergic receptors
  • need to consider all particular drug effects before giving it
  • example phenylephrine vs ephedrine
    • phenyl is direct
    • ephedrine indirect
      *
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42
Q

All sympathomimetics are ___

A

beta-phenylethylamine derivatives

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43
Q

What makes something a catecholamine?

A
  • Amine group side chain
  • hydroxyl group on 3,4 carbon of benzene ring–> called catechol (maximal alpha nad b receptor activity)
  • thus names catechol-amines
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44
Q

What is doa of catecholamines vs non-catecholamines?

A

Catecholamines are very short DOA, more potent

Non- catecholamines are longer acting and may not be as potent as local agonists

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45
Q

What is pathway for creation of epinephrine?

A
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46
Q

What is mechanoism of action for sympathomimetics?

A
  • Activation of g-protein coupled receptr (D, beta, alpha)
    • indirect= drug increases endogenous NE release form post-ganglionic SNS nerves which then activates receptor
    • direct= directly stilumates the receptor and activates G-protein itself
  • G-protein will activate or inhibit an intracellular enzyme (adenylate cycale–> camp–> plc) or will open or close ion channel
  • Usually g-protein cascade has an eventual positive or negative effect on amount on intracellular ca= physiologic effect we see clinically
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47
Q

What does specific effect of sympathomimetics depend on?

A
  • Receptor stimulated
  • receptor density in a given tissue
  • what second messengers activate at a molecular level in the cell

Receptors will up or down regulate based upon plasma concentrations of sympathomimetic

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48
Q

How do we terminate effect of catecholamines?

A
  • Reuptake
    • uptake I- neuronal reuptake
    • upatke II- extraneuronal uptake
  • MAO
  • COMT
  • Lungs

Need infusion because it is short acting

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49
Q

How do we terminated effect of non-catecholamines?

A
  • MAO
  • Urinary excretion (unchanged)
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50
Q

What is it a bad idea to administer sympathomimetics to people taking MAOIs?

A
  • MAO is in presynpatic terminal in order to break down norepinephrine
  • If this is inhibited, then you aren’t metabolizing NE as much, and will have even more NE release with subsequent stimulation
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51
Q

What is selectivity of receptor for phenylephrine?

A

alpha 1> alpha 2>>>>> Beta

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52
Q

What is receptor selectivity of clinidine?

A

alpha 2> alpha 1>>>>>> B

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53
Q

What is receptor selectivity for norepinephrine?

A

alpha 1=alpha 2; B1>>>>>>>>>>> B2 (no clinical effect)

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54
Q

What is receptor selectivity for epinephrine?

A

alpha 1= alpha 2; b1=b2

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55
Q

Selectivity of B-agonist recpeotrs?

Dobutamine

Isoproteronol

Terbutaline/albuterol

A

Dobutamine B1>B2>>>>> alpha

Isoproterenol B1=B2>>>ALPHA

Terbutaline/albuteral B2>>B1>>>> ALPHA

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56
Q

What is receptor selectivity of dopamine agonists?

A

Dopamine D1=D2>>B>>ALPHA

Fenoldopam D1>>D2

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57
Q

Route, duration, dosages, indication for epinephrine?

A
  • Route: SQ (onset 5-10 min), IV (1-2 min onset)
  • Duration 5-10 min
  • Dosages
    • standard bolus dose 10 mcg/kg IV
    • Start 2-8 mcg/kg
    • 1-2 mcg/min IV- beta 2<<- low dose for anaphylaxis
    • 4-5 mcg/min IV- beta 1
    • 10-20 mcg/min IV- alpha and beta
  • Indication
    • bronchial asthma
    • acute allergic reaction
    • cardiac arrest, asystole
    • electromechanical dissociation
    • vfib unresponsive to intial defibriallation
  • Poorly lipid soluble- little CNS effect
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58
Q

CV effects epinephrine?

A
  • ALPHA 1:
    • vasoconstriction- Increase BP, Increase CVP, Increase cardiac work
    • skin, mucosa, hepatic, renal constriction
  • alpha 2: negative feedback (decreaes BP) keeps sympathetic tone in check
  • B1: Increased contractility, HR, CO, increae BP
  • B2:
    • peripheral vasodilation (decrease BP)
    • Skeletal muscle dilation, increase K uptake, increase glucose

With moderate epi dose, SBP increases (B1, Alpha 1) DBP tends to decrease (B2), map stays same

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59
Q

Cerebral effects epinephrine?

A
  • At clinically relevant doses, minimal vasoconstriction of artieroles in
    • cerebral vasculature
      • increase cerebral blood flow in general (even with normal BP secondary to redistribution of flow)
    • Coronary vasculature
    • pulmonary vasculature
60
Q

Ocular effects of epinephrine?

A
  • Acoomodation for far vision
    • alpha 1- mydriasis (dilation of eyes)
  • Regulation of ocular pressure
    • alpha 1, alpha 2- increase humoral outflow
    • B1- increase produciton of aqueous humor
61
Q

Respiratory effects of epinephrine?

A
  • Dilate smooht muscles of bronchial tree
    • B2
  • Decreased release of vasoactive mediators (histaomine) in bronchial vasculature
    • B2
  • Reduce mucosal secretion- decongestion
    • alpha 1<– give with nasal intubation
62
Q

GI effects of epinephrine?

A
  • Decreased digestive secretions
    • alpha 2
  • decreased peristalsis
    • alpha 2, b2- direct smooth muscle relaxation
  • decreased splanchnic blood flow
    • alpha 1- blood flow drasitcally reduced even if BP relatively normal
63
Q

GU effects of epinephrine?

A
  • Renal vasculature
    • Alpha 1- renal blood flow drastically reduced even if BP relatively normal
      • 2-10x more potent than NE for decreasing renal vascular resistance
    • Beta 1- in kidney increaes renin release–> cause angiotensin II vasoconstriction as well
  • Bladder
    • alpha 1- contraction urethral spincter- urinary continence
    • Beta 2- decreases urinary output
  • Erectile tissue
    • alpha 1- facilitates ejacluation
  • Uterus
    • beta 2- relaxation- inhibits labor
64
Q

Metabolic effects of epinephrine

A
  • Increased liver glycogenolysis and promotion of insulin release
    • B2
  • Increased adipose tissue lipolysis
    • B3
  • Inhibition of insulin release (more minor effect because opposed by B2)
    • alpha 1
  • May also cause mild hypokalemia d/t activation of Na-K pump and transfer of K into cells
65
Q

Norepinephrine

Dose, effects?

A
  • Dose for hypotension 4-16 mcg
  • Peripheral IV admin dnagerous if IV infiltation
  • Potent alpha and beta effect, minimal beta 2
    • intense vasoconstriciton skeletal muscle, liver, kidney, cutaneous tissue (at risk for metabolic acidosis)
    • increased SBP, DBP, MAP
    • Baroreceptors activated
      • decreased HR (vagal induced effect, ach on sa node)
      • Decreased respiration
  • Decreased venous return, CO, HR (despite B1 effect) Make sure you look and see if baroreceptors would be involved to potentially change expected effect!!!!
    • ​CO decreases d/t intense vasoconstriction
      • also why venous return decreases
66
Q

Dopamine highlights? Dosing?

A
  • Endogenous precursor of NE
  • Stimulates all adrenergic receptors including dopamine receptors
  • Dangerous IV infiltrate
  • Concurrently, increases myocardial contractiliy, renal blood flow, UO gfr
  • increase endogenous NE release- dopa may not work as well with depleted catechol stores
  • synergistic with dobutamine to reduce afterload and improve CO
  • inhibitory at carotid bodies
  • increaed intraocular pressure
  • dosing guidelines
    • 1-3 mcg/kg/min- dopa 1 stimulation dominates (“renal dose”)
    • 3-10 mcg/kg/min- Beta 1 receptor dominate
    • >10 mcg/kg/min- alpha receptor dominate

D1=D2>>B>>A

67
Q

Isoproterenol highlights?

A

B1=B2>>>> alpha

  • Synsthetic catecholamine
  • Selective B1 and B2 agonist
  • increases HR, contractility with decreased SVR (increase SBP,. decrease DBP, decrease MAP)
  • “Chemical pacemaker”
    • 1-5 mcg/min for heart block and bradydysrhythmias
  • Rapid metabolism by COMT
  • What kind of patient is at risk with this drug?
    • CAD pt, increase demand, decreased supply, setting up for failure
68
Q

Dobutamine highlights?

A

B1>B2>>>> alpha

  • Synthetic catecholamine
  • Dose 2-10 mcg/kg/min
  • B1 selective <5 mcg/kg/min (weak activity at SA node)
  • Weak alpha 1 >5mcg/kg/min
    • very weak compared to dopamine
  • Improves CO without increasing HR or BP substantially (good for CHF)
  • Is coronary artery vasodilator (B2 effect)
69
Q

Highlights ephedrine?

A
  • Indirect acting non-catecholamine
    • Some direct agonist
  • Weak epinephrine (misleading, 10x longer laster)
  • Given PO, IM, IV
  • Dose 10-25 mg IV; 10-50 mg IM
  • Tachyphylaxis with repeated dosing
    • NE depletion at nerve terminals
    • Receptor occupation long 1/2 life- CV compensation
  • Excreted unchanged in urine (about 40%) and slowly metabolized by MAO and conjugated in liver; E 1/2 t 3 hours
70
Q

Phenylephrine highlights?

A

alpha 1> alpha 2>>>>>>> b

  • Direct acting non catecholamine
  • primarily alpha 1
  • venonconstricitons > arterial constriction
  • less potent and longer lasting than norepinephrine
  • dose
    • 50-200 mcg IV
    • infusion 20-50 ug/min
  • Increases MAP, SBP, DBP, SVR
  • Decreases HR, CO
71
Q

What’s the worst drug you could give to correct overdose phenyl/epi?

A

Beta blocker. You’ll loose contractility that you so despeartely need to combat increased BP

Give alpha antagonist instead!

72
Q

Actions of Selective Beta 2 Agonist

A
  • Relax bronchiole smooth muscle
  • relax uterine smooth muscles
  • sustained DOA d/t different placement of their hydroxyl groups on benzene ring
  • Routes : PO, inhalation, SQ, IV
  • Useful in premature labor, asthma, COPD
  • Side effects: tremor (B2 in skeletal muscle), reflex tachycardia (vasodilation and B2 in heart)
    • reflex tachycardia baroreceptor mediated d/t profound vasodilation
  • Hypokalemia
73
Q

Albuterol highlights?

A
  • Prototype for selective Beta 2 agonist
  • preferred choice for bronchospasm due to asthma
  • Dose
    • MDI 100 mcg/puff, 2 puffs q 4-6 hours
    • max 16-20 puffs
    • Nebulization for life threatensing asthma 15 mg/hr for 2 hours
  • Tachycardia and hypokalemia with large doses
74
Q

Terbuatline?

A

Oral, SC (0.25 mg) or puffs

For premature labor or asthma

75
Q

Salmeterol?

A
  • MDI, DOA >12 HOURS
  • otherwise, similar ot albuterol
  • lots of attention lately for causing sudden death in asthmatics
76
Q

Ritordine?

A
  • FOr treatmnet of premature labor
  • some beta 1 activity, thus increase HR and CO
  • Can cause pulm edema d/t decreased excretion of Na, K and h2o
77
Q

Direct acting, non catecholamines your patient may be taking that are alpha agonists?

A
  • Midodrine- postural hypotension
  • Oxymetazoline (afrin),Tetrahydrozoline, xylometazoline
    • all nasal and ocular decongestants
78
Q

Alpha 2 agonists your patient might be taking?

A
  • Clonidine (partial)D
  • Dexmedetomidine (full agonist)
  • methyldopa (BP in pregnant women)
  • Decreased SNS output from CNS
    • decreases BP
    • sedation and analgesia
79
Q

Indirect-acting sympathomimetics your patient might be taking?

A
  • Amphetamine
    • increase release NE, 5HT, dopamine
    • blocks reuptake
    • blocks vesicular transport
    • inhibitor MAO
  • Methamphetamine
    • similar to amphetamine but higher CNS effects
  • Methylphenidate (Ritaline)
  • Pemoline (Cylert)
  • Amphetamine variants- ADHD
80
Q

What are the actions of amphetamines?

A
  • increase release NE, 5HT, dopamine
  • blocks reuptake
  • blocks vesicular transport
  • inhibitor MAO
81
Q

Which drugs are inhibitors of catecholamine storage and reuptake?

A
  • Reserpine (originalyl developed as anti HTN)
    • vesicles lose ability to store NE, 5HT, dopamine
    • MAO breaks down excess except in high doses
      • hypotension and psych depression common
  • Cocaine
    • prevents reuptake of catechols (NE, DA, 5HT)
    • Interferes with catecholamine transport
82
Q

Which drugs are our alpha antagonists?

A
  • Prazosin, terazosin, doxazosin
    • alpha 1>>>> alpha 2
  • Phentolamine
    • alpha 2= alpha 1
  • Yohimbine, tolazoline
    • alpha 2>> alpha 1
83
Q

Which drugs are mixed alopha and beta antagonist?

A
  • Labetalol, carvedilol
    • B1=B2>alpha 1> alpha 2
84
Q

Which drugs are mixed B antagonist?

A
  • Metoprolol, atenolol, esmolol
    • B1>>> B2
  • Propanolol, nadolol, timolol
    • B1=B2
  • Butoxamine
    • B2>>> B1
85
Q

What are CV effects of alpha-1 antagonism?

A
  • Decreases PVR and lowers BP
    • also causes tachycardia via baroreceptor mediated reaction
  • Postural hypotension due to failure of venous vasoconstriction upon standing
86
Q

What are effects of alpha 2 antagonism?

A
  • Increases NE release from nerve terminals
  • Blocking the negative feedback mechanism
87
Q

Non-selective alpha agonists ___ blood pressure ___ significantly

A

drop; more

88
Q

GU , eye effects, nasal effects of alpha antagonists?

A
  • GU effects
    • blockade in prostate and bladder cause muscle relaxation and ease micturation
  • Miosis
    • pupillary constriction
  • Increased nasal congestion (generally a negative)
89
Q

MOA of alpha antagonist?

A
  • Bind selectively to alpha receptors and interfere with ability of catecholamine to cause reposne
    • some competitive
      • phentolamine, prazosin, yohimibine
    • others bind covalently and are non competitive
      • phenoxybenazmine
90
Q

What is phentolamine?

Causes? Dose? Uses?

A
  • Nonselective alpha blocker
  • causes: vasodilation, decrease BP, increase HR and CO
  • Used in:
    • hypertensive emergencies
      • pheochromocytoma or autnomic dysreflexia
      • nice drug for correcting immediate vasoconstrictions. very short acting
  • Dose:
    • 30-70 mcg/kg IV
    • Onset 2 min
    • DOA 10-15 min
  • Local infiltation also for accidental extravascular admin of sympathomimetics
    • 2.5-5mg in 10 mL
91
Q

What is phenoxybenazmine?

A
  • Binds covalently<– means it lasts forever and not good for saving in OR
    • will be stuck with this decision
  • Alpha 1 activity >alpha 2
    • decrease SVR, vasodilation
  • Pro-drug with 1 hour onset time; long acting (E1/2t of 24 hours)
  • Preop for pts with pheochormocytoma, can be used for pts with raynaud’s dx
92
Q

Prazosin?

A
  • Contorl BP in pheochromocytome
  • selective alpha 1 blocker
  • minimal alpha 2
  • less reflex tachycardia (remember alpha 2 is inhibitory to NE releae)
93
Q

What is yohimibine?

A
  • Alpha 2 selective blocker
  • increases the release of NE form post-synaptic neuron
    • inhibits + feedback so more NE present
  • used with orthostatic hypotension, impotence
94
Q

WHat are terazosin and tamulosin?

A

Long acting selective alpha-1a particularly effective in prostatic smooth muscle relaxation

95
Q

How do beta-adrenergic antagonists work, effects?

A
  • Prevent sympathomimetic (via competitive antagonism) from provoking a beta response on:
    • heart
      • improve O2 supply and demand balance
    • Airway
      • can provoke bronchospasm
    • blood vessels
      • vasoconstriction in skeletal muscle
      • PVD symptoms increae
    • Juxtaglomerular cells
      • decreae renin release- indirect way of decreasing BP
    • Pancreas
      • decreased stimulation of insulin release by epi/NE at b2 and then masked symptoms of hypoglycemia B1
        *
96
Q

MOA of beta adrenergic receptor antagonist?

A
  • Slective binding to beta receptors (influence inotropy, chornotropy)
  • Competitive and reversible inhibiton- large doses of agonists will completely overcome antagonism
  • chronic use is associated with increase in # receptors (up-regulation)
    • cannot stop these suddenly. will make patients have profound increase HR and contractility
97
Q

Beta adrenergic receptor antagonists are all derivatives of ____

A

isoproterenol

some may act more like partial agonist

98
Q

Classifications of beta adrenergic receptors?

A
  • Non selective (beta 1&2)
    • propranolol, nadaolol, timolol, pindolol
    • beta-2 is nearly always negative
  • Cardioselective (beta 1 only)
    • metoprolol, atenolol, acebutolol, betaxolol, esmolol
    • large doses lose selectivity
      • this occus in all meds
99
Q

What is propranolol?

A
  • Non selective
    • equal B1 and B2
  • Lacks sympathomimetic activity thus it is a pure antagonist (no partial agonist present)
  • Administered in stepwise manner until goal of 55-60 achieved
100
Q

Cardiac effects of propranolol?

A
  • Decreased HR (more with exercise, not so much resting HR), Contractility, decreased CO
    • Above effects especially prominent during exercise and sympathetic outflow
  • Blockade of B2
    • increased PVR, increased coronary vascular resistance
  • However due to decreased HR and CO, oxygen demand is lowered opposing the above effects
  • Sodium retention due to renal system respone to drop in CO
101
Q

Pharmacokinetics of propranolol?

Dose?

Metabolized?

Significance r/t LA? Opioids?

A
  • Goes through significant first pass effect (90-95%)
    • oral dose much larger than IV dose
    • 0.05 mg/kg IV or 1-10mg (give slowly q 5 min)
  • Protein bound (90-95%)
    • unique amoung beta blockers
  • Metabolized in liver
    • e1/2 t= 2-3 hours
      • prolonged in low hepatic blood flow states
  • Decreases clearance of amide LA due to drop in hepatic blood flow/metabolism inhibition
  • decrease pulmonary first pass effect of fentanyl
    • more fent will be in system, increasing effects
102
Q

What is timolol?

A
  • Non-selective beta blocker
  • used to tx glaucoma- decreases intraocular pressure by decreasing production of aqueous humor
  • eye drops can cause decerase BP, HR and increase airway resistance
103
Q

What is nadolol?

A
  • Non selective beta blocker
  • no significant metabolism (renal/biliary elimination)
    • excreted unchanged
  • E1/2 t of 20-40 hrs taking 1x dialy
    • longer lasting
104
Q

What is metoprolol?

A
  • Selective beta 1 blockers
  • prevents inotropy and chronotropy
  • selectivity is dose related
  • about 60% goes through first pass effect
    • po 50-400 mg
    • IV 1-15 mg
  • E1/2 t of 3-4 hours
    • extensive hepatic metabolism
    • crosses BBB easily b/c lipid solubility
      • CNS depression
      • lethargy/fatigue
105
Q

What is atenolol?

A
  • Most selective beta 1 antagonist and thought to have least CNS effects
  • E1/2 t= 6-7 hours
  • Not metabolized in liver, excreted via renal system, therefore E1/2T is increased markedly in pts with renal dx
  • very useful in cardiac pt with CAD
106
Q

What is betaxalol?

A
  • Cardioselective beta 1 blocker
  • e1/2 t 11-22 hours
    • slightly less concernign if patient doesn’t take in AM
  • Single dose daily for HTN
  • Topically for glaucoma
  • less risk of bronchospasm as seen with timolol, so good alternative choice in asthmatics with glaucoma
107
Q

What is esmolol?

A
  • Selective beta 1 antagonist
  • rapid onset, short acting
  • typical dose of 0.5 mg/kg IV (10-180 mg IV)
    • DOA <15 min
    • infusion 50-300 mcg/kg/min
  • Effects HR without decreasing BP sig in small doses
    • great for blunting short lived noxious stimuli in OR or for controlled hypotension
    • be careful of admin if patient has profound sympathetic mediated vasoconstriciton b/c can precipitate CV collapse
    • great for young pt where you want HR control or cardiac pt who needs lower HR to allow filling time
  • In doses used, it does not occupy sufficient beta receptors to cause negative inotropy
108
Q

E 1/2t of esmolol? Metabolized by?

A
  • E1/2 t= 9 min
  • rapidly hydrolyzed by plasma esterases
  • not same esterases as cholinesterases responsbile for metabolism of sux, therefore no effect on sux metabolism
109
Q

Side effects of beta-blockers

A
  • CV system- decreases HR, contractility, BP
  • Exacerbation of peripheral vascular disease
    • block beta2- vasodilation
  • airway resistance- bronchospasm
  • metabolism- alter carb and fat metabolism
    • masks hypoglycemia increase in HR
  • distrubtion of ECF potassium
    • inhibits uptake of potassium into skeletal muscle
  • interaction with anesthetics- may have decrease BP with IAs
  • nervous systm- fatigue, lethargy
  • nausea, vomiting, diarrhea
110
Q

What are relative contraindications of beta-blockers?

A
  • Pre-existing AV heart block or cardiac failure (acute only)
  • Reactive airway dx
  • diabetes mellitus (without BS monitoring)
  • hypovolemia
111
Q

Clinical uses of beta blockers?

A
  • Treatment of HTN
  • Management of angina (oxygen supply/demand issue in heart)
  • decrease mortality in treatment of post MI pts
    • slows remodeling process
  • used periop and preop for pt at risk for MI
  • Suppresion of tachyarrthmias
  • prevention of excessive sympathetic nervous system activity
112
Q

What is labetalol?

Selectivity? Metabolism?

E 1/2 T

Dose?

Can cause…

A
  • Selective at alpha 1 and beta 1 and 2
    • IV beta to alpha 7:1 ratio
  • Metabolism conjugation of glucuronic acid <5% in urine
  • E1/2 t 5-8 hours, prolonged in liver dx
    • max drop in BP 5-10 min after IV<– lil more alpha blockade
  • Dose
    • 0.1-0.5 mg/kg
    • usually 5 mg at a time for mild hypertension in OR
  • Can cause orthostatic hypotension, bronchospasm, heart blcok, CHF, bradycardia
113
Q

Anticholingergic drugs are more appropriately called _______ drugs

A

Anti-muscarinic

114
Q

Where can ACh act on synapse?

A
  • Nicotnic ACh receptor post synapse
  • nicotinic ACh receptor pre synpatically
  • Muscarinic ACh (M1-M5) post synaptically
  • Muscarinic (m2, m5) pre synaptic
    • don’t have meds that really specifically target pre-synaptically
    • you’ll block pretty much all muscarinic receptors
115
Q

What are cholinergic receptor subtypes?

A
  • Nicotinic receptors
    • pentameric (5 subunit ) structures
    • funciton as ligand-gated ion channels
  • Muscarinic receptors
    • G protein coupled
      • M1, M3 M5, inositol phosphate pathway Gαq pathway
      • M2, M4, inhibit adenylyl cyclase reduce cAMP–> Gαi
116
Q

Where are each of the cholinergic receptors located?

A
  • M1- CNS, stomach
  • M2- cardiac muscle, CNS, airway smooth muscle (anitcholinergics cause dilation here)
  • M3- airway smooth muscle, glandular tissue
  • M4- CNS
  • M5- CNS
  • Nm- skeletal muscle at NMJ
  • Nn- autonomic ganglia, adrenal medulla, CNS
    • sledgehammer, fallen out of favor
117
Q

MOA and structure of antimuscarinic drugs?

A
  • Competitively antagonize ACh at muscarinic receptors only
  • Cation portion of the drug ifts into ACh place on anticholinergic receptor and reversibly inhibits ACH binding
  • Allow sympathetic response to predominate
  • competitive inhibition can be reversed if [ACh] increases
  • Natural antimuscarinics (atropine and scopolamine) are tertiary amines
    • alkaloids of belladonna plant
    • crosses BBB
  • Semi-synthetic (glyco/Robinal) are quaternary ammonium derivatives
    • does not cross BBB
118
Q

What is atropine’s largest effect?

A
  • Mainly increase HR(+++)
  • Slight relax in smooth muscle(++)
  • some confusion and anti-sialogogue (+)
    • can occasionally cause patient to wake up confused
119
Q

Scopolmain comparative effects?

A
  • Sedation, mydriasis and motion induced nausea, as well as anti-sialagogue
    • (+++)
  • Minimal effect HR and relax smooth muscle (+)
120
Q

Gylcopyrrolate comparative effects?

A
  • Equal (++) on HR, Relax smooth muscle, and antisialagogue
  • 0 on sedation, mydriasis, and motion induced nausea
121
Q

What can scopalamine also be used for when patient unstable?

A
  • Also a sedative that decreases risk of recall when you can’t utilize anesthesia gases
  • doesn’t have huge impact on hemodynamic status
122
Q

If HR is <40 and BP not great, which would be best antimuscarinic to use?

If HR is around 40s and BP tolerating, which would be a better drug?

A

Atropine (need that HR up quick!)

Gylcopyyrolate (will give that little HR booster that you need)

123
Q

What might be an undesired effect of glycopyyrolate?

A

Can prevent elderly pt c BPH from urinaring.

124
Q

We can also use glycopyrrolate in

A

Bronchospasm

125
Q

Pharmacokinetics of IV atropine?

A
  • Onset 1 minutes
  • DOA 30-60 min
  • E1/2 t= 2.3 hours
    • 18% unchanged via urine, the rest undergoes hydrolysis
126
Q

Pharmacokinetics of glycopyrrolate

A
  • Onset 2-3 minutes
  • DOA 30-60 min
  • E1/2 t= 1.25 hours
  • 80% unchanged in urine
    • quaternary ammonia- caution in renal disease
127
Q

Pharmacokinetics scopolamine?

A
  • Extensively metabolized with 1% excreted unchanged in urine
    • very lipid soluble
128
Q

When might we use antimuscarinics?

A
  • Pre-op: Dry out mouth, sedation, nausea prevention
  • Treatment of bradycardia (especially vagally stimulated)
    • magnitude of effect dpeends on vaseline vagal tone
      • young pt= high tone= more tachycardia
      • elderly pt= less tone= less pronounced tachycardia
  • With anticholinesterase drugs always give antagonizing NMB
  • Promoting amnesia in unstable pt (scopolamine)
  • Bronchodilation (Ipratropium)
    • Ideally before sx
    • Dose MDI 40-80 2 PUFFS
    • 0.24-0.5mg via neb
    • Onset 30-90 min
    • Consider in asthmatics, COPD, and smokers prior to airway instrumentation
  • Mydriasis and cycloplegia (optho)
    • anticholinergics may be dangerous in pt with glaucoma
  • Reduce biliary and ureteral spasms r/t opioids
129
Q

Dose scopalamine?

A
  • 0.3-0.5 mg or 5 mcg/kg IM (preop)
  • 1.5 mg transdermal patch
    • 5mcg/hr x 72 hours for nausea
130
Q

Atropine doses?

A
  • 0.2-0.4 mg IV preop
  • 0.4-1 mg IV bradycardia
  • 2 mg in 5 mL NS via nebulizer
    • bronchodilator
131
Q

Glycopyrrolate doses?

A

0.1-0.2 mg IV (preop and bradycardia)

132
Q

What is central anticholinergic syndrome? What can we give to treat it?

A
  • Mainly scopolamine and atropine
  • Restlessness, hallucination
  • Somnolence and unconsciousness
  • Delayed emergence/recovery in PACU
  • Physostigmine 15-60 mcg/kg IV repeated as needed q 1-2 hours
    • this is an antichoinesterase, so allows more ACh to stay in synapse
    • crosses BBB
133
Q

What med to you have to give with phsyostigmine?

A

Atropine, some kind of anticholinergic

Otherwise, we’ll get excessive bradycardia, peristalsis etc

134
Q

What does ipratropium, tiotropium do?

A

Bronchodilator for COPD

135
Q

What are oxybutynin (ditropan), tolterodine (detrol)

A

for overactive bladder

nonspecific M-receptor

136
Q

What is darifenacin (enablex), solifenancin (vesicare) for?

A

Overactive bladder

M3 specific

137
Q

What do acetylcholinesterase inhibitors do?

A
  • Elevate concentraiton of endogenously released ACh in synapse by decreasing metabolism
    • increases transmission at Nm junction (reverses competitive NMB)
    • Increases parasympathetic tone
    • increases central cholinergic activity
      • only for those crossing BBB
138
Q

What are the indications of AChE inhibitors?

A
  • Useful in diseases of the Nm junction
    • myasthenia gravis- pyridostimgmine, neostigmine
  • Glaucoma
    • increases outflow of aqueous humor- physostigmine
  • Abdominal distention
    • increaes smooth muscle motility- neostigmine
  • AD and other forms of cognitiv dysfunction (first type of tranmission to fail in brain is ACh)
    • Tacrine (Cognex)
    • Donepezil (Aricept)
    • rivastigmine (exelon)
    • galantamine (razadyne)
139
Q

Adverse effects of ACHE?

A
  • Peripheral ACh effets on GI tract
    • n/v/d, anorexia, flatulence, abdominal cramping
    • dose dependent
140
Q

ACHe inhibitor contraindications?

A
  • Unstable or severe cardiac dx
  • uncontrolled epilepsy
    • placing more ACh in synapse can provoke sz prone area
  • active PUD
    • increases peristalsis
141
Q

What is methacholine?

A

Used in dx of asthma

142
Q

What is carbachol?

A

Decreases intraocular pressure, cause miosis

143
Q

What is bethanechol

A

GI and urinary tract motility- postop and postpartum urinary retention, neurogenic bladder

144
Q

What is succinylcholine

A

Continuous activation of nicotinic receptor channels result in depolarization blockade (depolarizing MR)

145
Q

What are non-depolarizing muscle relaxants?

A
  • Prevent endogenous ACh binding to nicotinic receptors an subsequent muscle cell depolarization
  • ex- pancuronium, cev, roc

Pharm Test 3 (5 decks)

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