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Pharmacology > pharm of autonomic nervous system > Flashcards

pharm of autonomic nervous system Flashcards

1
Q

Most important function of SNS is?

A

Preserve vasomotor Tone

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2
Q

Location of Sympathetic innervation pregang

A

Preganglionic neurons cell bodies located in (T1-L2-3) of spinal cord
Intermediolateral horn of grey matter

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3
Q

Location of Sympathetic Innervation postgang

A 
Post ganglionic neuron cell bodies are located in ganglia
Paravertebral chains (either side spinal column)
Prevertebral ganglia (i.e. celiac, superior, inferior mesenteric ganglia in abdomen)
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4
Q

Parasympathetic innervation preganglionic location

A

Cranial” (medullary CN 3,7, 9, 10)

“Sacral” (spinal cord S2-4) regions

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5
Q

Parasympathetic Innervation Postganglionic

A

Target organs

Discrete ganglia in the head and neck (i.e. ciliary ganglia)

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6
Q

Only Innerverted by PSNS

A

The ciliary muscle of the eye

Bronchial smooth muscle (B2 receptors present though)

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7
Q

Only innervated by the SNS

A 
Sweat glands…can be blocked by antimuscarinic
Blood vessels (Muscarinic receptors present though)
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8
Q

Both systems exhibit baseline tone at rest,they are?

A

Both systems exhibit“baseline tone” at rest
Heart rate – vagal predominance
Blood vessels- SNS tone

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9
Q

Sympathetic effector sites are?

A

Blood vessels, sweat glands, adrenal medulla

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10
Q

SYmpathetic should be ACH-N.E, whats the exception

A

ACh(Pre)-(post)ACh(muscarinic) per sweat glands

and (ACh) -(Post) Adrenal medulla(Epi 80%/N.E 20%)

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11
Q

Receptors In the PNS Include

A 
Cholinergic Receptors:
Nicotinic Ach receptors: Nm and Nn
Muscarinic Ach receptors: M1-5
Adrenergic receptors
ALpha (1,2)
 Beta (1, 2, 3)
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12
Q

G alpha q sends its signal to what location

A

CNS…increase Cns activity
, Smooth Muscles/glands..Contract
and Blood vessels(smooth muscles)…Vasoconstrict

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13
Q

Action of G alpha q is propagated by what process

A

Ip3-Plc-DaG—–ca release
Increase ca
decrease potassium conductance

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14
Q

G alpha i sends its signal to what location

A 
Cardiac---Slow HR, Slow Contractility(Increase potassium,Hyperpolarize cell)
Blood vessel(Pre)-Cns(Post) ....Blood vessel contract
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15
Q

Action of G alpha i is propagated by what process

A

Decrease Adenyl cyclate—decrease C-Amp–Increase potassium conductance…Constrict/contract

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16
Q

What tissue does alpha 1 act on and what are the effects on these Tissues per sympathetic response

A

Most vascular smooth muscle; (i.e blood vessels, sphincters & bronchi)…..Contraction

Iris (radial muscle)….Contraction which dilates pupil per sympathetic response

Pilomotor smooth muscle…Erects pilo

Prostate and Uterus …Contraction to maintain tone during sympathetic activity

Heart…Beats faster to pump blood fast

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17
Q

Alpha 2 acts on what tissue and whats the reaction

A

Platelets….Aggregation
Adrenergic & cholinergic nerve terminals *presynaptic…….Inhibits transmitter release causing low Hr and Low Bp

Vascular smooth muscle…Contraction (post-synaptic)OR Dilation (pre-synaptic, CNS)

GI tract…Relaxation

CNS…..Sedation and analgesia via ↓SNS outflow from the brain stem.

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18
Q

Beta 1 acts on what tissue and whats the reaction(Increase C-Amp)

A

Heart/Kidneys…Increases the force & rate of contraction,
Stimulation of renin release

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19
Q

Beta 2 acts on what tissue and whats the reaction(increase C-amp)

A

Respiratory, uterine, vascular, GI, GU (visceral smooth muscle)———Promotes smooth muscle relaxation(asthmatics)
Used per preterm labor.

Mast Cells—Use Beta-blockers with caution for asthmatics(Histamine release Give per allergic reaction)

Skeletal muscle…….Potassium uptake, dilation vascular beds, tremor, ↑speed contraction

Liver—Glycogenolysis
Pancreas—-Insulin secretion
Adrenergic Nerve Terminals—–↑release of NE

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20
Q

Beta 3 acts on what tissue and whats the effect

A

Fats cells-Activates lipolysis; thermogenesis

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21
Q

D1 acts on what tissue and whats the action

A

Smooth muscle—-Post-synaptic location; Dilates renal, mesenteric, coronary, cerebral blood vessels

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22
Q

D2 acts on what tissue and whats the action

A

Nerve endings—-Pre-synaptic - Modulates transmitter release; nausea and vomiting..

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23
Q

Endogenous Catecholamines are

A

Epi, Norepi, Dopamine

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24
Q

Synthetic catecholamines

A

Isoproterenol, Dobutamine

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25
Q

Synthetic non-catecholamines—Indirect acting—Increases release of Norepi

A

Ephedrine, mephentermine, amphetamines(Impact reuptake, metabolization)

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26
Q

Synthetic non-catecholamines—Direct acting

A

Phenylephrine, Methoxamine…more potent

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27
Q

Selective alpha 2 agonist

A

Clonidine, dexmedetomidine

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28
Q

Selective Beta-2 adrenergic agonists

A

Albuterol, terbutaline, ritodrine

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29
Q

whats the action of direct agonist?

A

Alpha 1, Alpha 2, Beta 1, Beta 2..(only EPI) Affinities

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30
Q

Indirect Agonist

A

↑ release of neurotransmitters

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31
Q

All sympathomimetics are?

A

Beta-phenylethylamine derivatives
An amine (NH2) group side chain
Hydroxyl group on the 3,4 carbons of benzene ringcatechol (Maximal alpha and beta receptor activity)Thus the name catechol-amine

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32
Q

Sympathomimetics: Mechanism of Action

A

Activation of G-protein coupled receptor (Delta,Beta or alpha)

Indirect = the drug increases endogenous norepinephrine release from post-ganglionic SNS nerves which then activates the receptor

Direct = the drug binds to the receptor and activates the G-protein itself

G-protein will activate or inhibit an intracellular enzyme (adenylate cyclase→cAMP, phospholipase C) or will open or close an ion channel

Usually, the G-protein “cascade” has an eventual positive or negative effect on the amount of intracellular Calcium = physiological effect we see clinically.

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33
Q

How does the stimulation of G-protein happen with different parts of the body and density of Gprotein

A

Different parts of the body have different types and densities of receptors (skeletal muscle VS venous smooth muscle VS myocardium VS bronchial smooth muscle etc.)

The specific effect depends on the type of receptor-stimulated, receptor density in a given tissue, and what the 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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34
Q

Termination of effect/Metabolism of Sympathomimetics

Catecholamines

A 
REUPTAKE I
Uptake I – neuronal reuptake
Uptake II – extraneuronal uptake
MAO
COMT
Lungs….uptake ..comes back in as the plasma level equilibrates
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35
Q

Termination of effect/Metabolism of Sympathomimetics

Non-catecholamines

A 
MAO
Urinary excretion (unchanged)
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36
Q

what are the alpha agonist

A

Phenylephrine alpha1> Alpha 2»»»>Beta

Clonidine alpha 2> Alpha 1»»»Beta

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37
Q

What are the mixed beta-agonist we have

A

Norepinephrine* alpha1=alpha2,Beta1»»>Beta2

Epinephrine alpha1=alpha2,Beta1=beta2

remember this is what is released by post-ganglionic nerves in the SNS – now does it make sense why B2 receptors are present in many tissues but NOT innervated…)

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38
Q

what are beta-agonists we have

A

Dobutamine Beta 1>Beta 2»»>alpha
Isoproterenol Beta1=Beta2»»»alpha
Terbutaline/albuterol Beta 2»>B1»»alpha

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39
Q

What are the dopamine agonist we have

A

Dopamine D1=D2»»B»>ALpha

Fenoldopam D1»D2

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40
Q

Epinephrine dose, onset, and mech of action

A 
Most potent activator alpha receptors
Routes: SQ or IV
Very poorly lipid soluble = little CNS effect
Onset:  (SQ) 5-10 min (IV) 1-2 min 
Duration: 5-10 min
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41
Q

Epinephrine indication

A

Indications:
Bronchial asthma
Acute allergic reaction
Cardiac arrest, asystole
Electromechanical dissociation
V.fib. unresponsive to initial defibrillation
Infusion to increase myocardial contractility

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42
Q

Epinephrine dose

A

standard bolus dose for resuscitation is 10mcg/kg IV

Can start with 2-8mcg/kg

Need infusion – with single bolus dose CV effects dissipate after 1-5min.

1-2mcg/minute IV = Beta-2

4-5mcg/min IV = Beta-1

10-20mcg/min IV = Alpha & Beta

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43
Q

Cardiovascular Effects of Epinephrine

A

Epinephrine stimulates all adrenoreceptors
Major role - BP regulation
A1 - vasoconstriction - ↑ BP, ↑ CVP, ↑ Cardiac work
A2 - negative feedback - ↓ BP
B1 - increased contractility, HR, CO – ↑ BP
B2 - peripheral vasodilation - ↓ BP
With moderate epinephrine doses SBP tends to increase B1, A1 DBP tends to decrease B2, & MAP stays the same
A1 - skin, mucosa, hepatic, renal
B2 - skeletal muscle

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44
Q

What are the cerebral effects of epinephrine

A

At clinically relevant doses minimal vasoconstriction of arterioles in:
Cerebral vasculature
↑ cerebral blood flow in general (even with normal BP secondary to redistribution of blood flow)
Coronary vasculature
Pulmonary vasculature

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45
Q

Ocular Effects of Epinephrine

A 
Accommodation for far vision
AlPHA 1 - mydriasis
Regulation of intraocular pressure
A1 and A2 - increase humoral outflow
B1- - increase the production of aqueous humor
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46
Q

Resp effects of epinephrine

A

Dilate smooth muscles of bronchial tree Beta 2

Decreased release of vasoactive mediators (histamine) in bronchial vasculature
Beta 2

Reduce mucosal secretion - decongestion
alpha1

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47
Q

GI effects of epinephrine

A

Decreased digestive secretions–A2
Decreased peristalsis
A and B2 - direct smooth muscle relaxation
Decreased splanchnic blood flow
A1 –blood flow drastically reduced even if BP relatively normal

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48
Q

Gu effects of epi

A

Renal Vasculature –(hint: Important!!!!!)
A1 – renal blood flow drastically reduced even if BP relatively normal
B1 - in kidney increase renin release
Hint: think about why beta blockers might decrease BP…
Bladder
A1 - contraction of urethral sphincter - urinary continence
B2 - relaxation - decreases urinary output
Erectile tissue
A1 - facilitates ejaculation
Uterus
B2 - relaxation - inhibits labor

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49
Q

Metabolic effects of Epi

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 )….A2

Low dose epi can also cause a mild hypokalemia secondary to activation of the Na-K pump transfer of K into cells.

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50
Q

Norepi Dose and effects

A

Dose for hypotension 4-16 mcg/min

Peripheral IV administration dangerous if IV infiltrates
Potent alpha and beta-1 effects

Minimal beta-2 effects
Intense vasoconstriction skeletal muscles, liver, kidneys, cutaneous tissue (at risk for metabolic acidosis)
Increased SBP, DBP, MAP

Baroreceptors activated
Decreased HR
Decreased respiration
Decreased venous return, CO, HR (despite B1 effect)

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51
Q

Dopamine dose

A

Endogenous precursor of norepinephrine
Stimulates all adrenergic receptors including dopamine receptors
Dosing guidelines*
1-3 mcg/kg/min – Dopamine 1 receptor stimulation dominate (“renal dose dopamine” – misleading term )
3-10 mcg/kg/min – Beta 1 receptor stimulation dominate
>10 mcg/kg/min – Alpha receptor stimulation dominate

  • Just because one receptor is dominate at a dosage range does not mean other effects will not occur; dosage ranges are not reliable predictors of expected plasma concentration
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52
Q

Dopamine Effects

A

Peripheral IV administration dangerous if IV infiltrates

Concurrently, increases myocardial contractility, renal blood flow, urine output, GFR

Also increases endogenous norepinephrine release = why dopamine not as useful with depleted catecholamine stores

Synergistic with dobutamine to reduce afterload & improve cardiac output

Inhibitory at carotid bodies – a patient may have altered response to hypoxia
Increased intraocular pressure

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53
Q

Isoproterenol dose and effects

A

Selective B-1 and B-2 agonists
Increases HR, contractility with decreased SVR (↑SBP, ↓DBP, ↓MAP)
The “chemical pacemaker”
1-5 mcg/min for heart block & bradydysrhythmias
Rapid metabolism by COMT (need infusion)

54
Q

Dobutamine dose and effects

A

Dose is 2-10mcg/kg/min
B-1 selective at < 5mcg/kg/min (weak activity at the SA node)
Weak Alpha-1 stimulation at >5mcg/kg/min (2 stereo-isomers are antagonistic at alpha receptors)
Improves CO without increasing HR or BP substantially (good in CHF)
Is a coronary artery vasodilator

55
Q

Ephedrine dose and effects

A

Indirect and direct agonist at alpha and beta receptors
“Weak Epinephrine” (term a little misleading) lasts 10X longer
Given PO, IM, IV
Used frequently during anesthesia to correct hypotension (increases HR also)
Dose 10-25mg IV; 10-50mg IM
Tachyphylaxis with repeated dosing
Norepi depletion
Receptor occupation long ½ life – CV compensation
Excreted unchanged in urine (about 40%) & slowly metabolized by MAO and conjugated in liver; E1/2 life 3 hours

56
Q

Phenylephrine dose and effects

A

Primarily A1-adrenergic receptor stimulant
Mostly direct acting
Venoconstriction>arterial constriction
Less potent & longer lasting than norepinephrine
Dose: 50-200mcg IV or infusion (20-50 mcg/min)
Used frequently during anesthesia to correct hypotension (decreases HR)
MAP, SBP, DBP, SVR; HR, CO
Use in OB anesthesia being reconsidered
Drug Error Alert (sounds like neostigmine – don’t call it “neo”)

57
Q

Selective beta 2 agonist characteristics are

A

Relax bronchiole smooth muscles
Relax uterine smooth muscles
Sustained duration of action due to different placements of their hydroxyl groups on the benzene ring
Routes of administration: PO, inhalation, SQ or IV
Useful in premature labor, asthma, COPD

Table 12-2 Stoelting useful for comparison among agents….Review now

Side Effects: tremor (B2 in skeletal muscle), reflex tachycardia (vasodilation and B2 in heart),

58
Q

Albuterol dose and effects

A

Prototype for selective Beta-2 agonists
The preferred choice for bronchospasm due to asthma.
MDI: 100ug per puff, 2 puffs q 4-6hrs, max 16-20 puffs.
Nebulization for life-threatening asthma: 15mg/hr for 2 hrs.
Can cause tachycardia and hypokalemia with large doses

59
Q

Terbutaline dose,effects and route

A

Oral, SC (0.25 mg), or puffs. For asthma or premature labor

60
Q

Salmeterol dose effects

A

MDI, Duration of action > 12 hours; otherwise similar clinical effect as albuterol

61
Q

Ritordine dose and effects .

A

For treatment of premature labor
Has some beta 1 activity, thus  HR and CO.
Can cause pulmonary edema due to decreased excretion of sodium, potassium and H2O.

62
Q

Direct-acting Sympathomimetics: Non-Catecholamines

Alpha1 AGonist

A

Alpha 1-agonists
Midodrine (ProAmatine) - postural hypotension

Oxymetazoline tetrahydrozoline, xylometazoline -nasal and ocular decongestants

63
Q

name the ALpha-2 selective adrenoreceptor agonist meds and effects

A

Decreased SNS output from CNS
Decreases BP,

Sedation and analgesia,

Clonidine (partial agonist)

Dexmedetomidine (full agonist)-Presynaptic

methyldopa

64
Q

Name the Indirect -acting sympathomimetics and their effects

A

Amphetamine
increases release of norepinephrine, 5HT and dopamine
Blocks reuptake
Blocks vesicular transport
Inhibits MAO….do not give indirect agent..give direct as Norepi.

Methamphetamine
similar to amphetamine but higher CNS effects

Methylphenidate (Ritalin), pemoline (Cylert) - amphetamine variants - ADHD

65
Q

Inhibitors of Cathecolamine Storage and reuptake

A

Inhibitors of Reserpine
Vesicles lose ability to store norepinephrine, 5HT and dopamine
MAO breaks down excess except in high doses
Hypotension and psychiatric depression common

Cocaine:
Prevents reuptake of catecholamines (NE, DA, 5HT)
Interferes with catecholamine transport

66
Q

NAme the alpha antagonist

A

Prazosin, terazosin, doxazosin ——alpha1»»alpha2
Phentolamine alpha2=alpha1
Yohimbine, tolazoline …alpha 2»alpha1

67
Q

Name the mixed alpha and beta antagonist

A

Labetalol, carvedilol

B1=B2>alpha1>alpha2

68
Q

Name the Beta-antagonist

A

Metoprolol, atenolol, esmolol …………B1»>B2

Propranolol, nadolol, timolol ….B1=B2

Butoxamine…..B2»>B1

69
Q

State the cardio effects of Alpha 1 antagonism

A

Decreases PVR and lowers BP

Postural hypotension due to failure of venous vasoconstriction upon standing

70
Q

State the cardio effects of Alpha 2 antagonism

A

Increases norepinephrine release from nerve terminals

Blocking the negative feedback mechanism

Alpha helps maintain tone(b/p) when position change…
Tarchycardia happens on both ..but worse with nonselective

71
Q

ALpha antagonist GU effects

A

Blockade in prostate and bladder cause muscle relaxation and ease micturation

72
Q

Mechanism of action of ALpha antagonist and Other General effects of alpha antagonist

A

Bind selectively to alpha receptors and interfere with the ability of catecholamines to cause a response.

causes Miosis
Increased nasal congestion

73
Q

Name the competetive antagonist

A

Phentolamine, Prazosin, Yohimibine(can be reversed by outcompeting it)

74
Q

name the none competive antagonist

A

Phenoxybenzamine

they bind covalently

75
Q

Phentolamine dose and effects

A

Nonselective alpha blocker
Causes: vasodilation, decrease BP,increase HR, and CO.

Used in:
Hypertensive emergencies, usually in pheocromocytoma or autonomic dysreflexia

30-70 mcg/kg IV

Onset 2 minutes; DOA

Local infiltration for accidental extravascular administration of sympathomimetics
2.5-5.0 mg in 10ml

76
Q

Phenoxybenzamine

dose and effects

A

Binds covalently
Alpha 1 activity > alpha 2.
decrease SVR, vasodilation

Pro-drug w/ 1 hr onset time; Long acting (E1/2t of 24hrs)

Preop for pts with pheochromocytoma, can be used for pts with Raynaud’s disease

77
Q

Prazosin effects

A

Control BP in pheochromocytoma
Selective alpha 1 blocker (minimal alpha 2)
Less reflexive tachycardia (remember alpha 2 is inhibitory to NE release)

78
Q

Yohimibe effects

A

Alpha 2 selective blocker
Increases the release of Norepi from post-synaptic neuron
Used w/orthostatic hypotension, impotence

79
Q

Terazosin and Tamulosin

effects

A

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

Alpha Antagonists for BPH

80
Q

Effects of Beta-adrenergic receptor antagonists

A 
Prevent sympathomimetics (via competitive antagonism) from provoking a beta response on the:
Heart

Improve O2 supply and demand balance(beta 1 blocked)

Airway (beta 2 blocked)
Can provoke bronchospasm

Blood vessels
Vasoconstriction in skeletal muscles; PVD symptoms ↑

Juxtaglomerular cells
↓ renin release – indirect way of ↓BP

Pancreas
Decreased stimulation of insulin release by epi/norepi at B2 and then masked symptoms of hypoglycemia B1

81
Q

Mechanism of action for Beta adrenergic receptor ANtagonism

A

Selective binding to beta receptors (influence inotropy, chronotropy) B1 blocked

Competitive and reversible inhibition-large doses of agonists will completely overcome antagonism

Chronic use is associated with increase in the # of receptors (up-regulation)…if discontinued…the rebound effect will be profound

Derivatives of the beta agonist isoproterenol thus possessing some sympathomimetic effects
Substitution on the benzene ring

82
Q

What are the classess of the Beta-adrenergic receptor antagonists

A 
Non selective (beta 1 &amp; 2) 
propranolol, nadalol, timolol(glaucoma), pindolol (PPNT)

Cardio-selective (beta 1 only)
metoprolol, atenolol, acebutolol, betaxolol, esmolol..short half life.
(Beaam)
*Large doses lose selectivity

Beta 2 is always negative…try not to block it.

83
Q

Propranalol cardiac effects

A

Non selective
Lacks sympathomimetic activity, thus a pure antagonist
Equal at B1 and B2
Administered in a stepwise manner until goal of 55-60 bpm is achieved

Decreased HR, contractility, decreased CO
The above effects are especially prominent during exercise and sympathetic outflow

Blockade of B2 receptors-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 response to drop in CO

84
Q

Propranalol dose pharmacokinetics

A

Goes thru significant first-pass effect (90-95%)

Oral dose much larger than IV dose
0.05mg/kg IV or 1-10mg (give slowly 1mg q 5 min)

Protein bound (90-95%)

Metabolized in liver,
E1/2t of 2-3hrs (will be ↑in low hepatic blood flow states)

Decreases clearance of amide LAs due to a drop in hepatic blood flow/ metabolism inhibition
↓the pulmonary fist pass effect of fentanyl

85
Q

Beta adrenergic receptor antagonist

Timolol Effects and action

A

Non selective beta blocker
Used to tx glaucoma-decreases intraocular pressure by ↓ production of aqueous humor
Eye drops can cause ↓BP, ↓HR and ↑ airway resistance

86
Q

Beta adrenergic receptor antagonist

Nadolol effects and action

A

Non selective beta blocker
No significant metabolism (renal/biliary elimination)
E1/2t of 20-40hrs take 1X daily

87
Q

Metoprolol dose and effects

A 
Selective beta 1 blocker
Lipid soluble..crosses BBB
Prevents inotropy and chronotropy
Selectivity is dose related
About 60% goes thru first pass effect
PO 50-400mg
IV 1-15 mg
E1/2t of 3-4hrs
88
Q

Atenolol dose and effects

A

Most selective beta 1 antagonist and thought to have the least CNS effects
Less lipid soluble
E1/2t is 6-7hrs
Not metabolized in liver, excreted via renal system, therefore E1/2t is increased markedly in pts with renal disease
Very useful in cardiac patients with CAD

89
Q

Betaxolol dose and effects

A

Cardioselective beta 1 blocker
E1/2t is 11-22hrs
Single dose daily for HTN
Topical useful for glaucoma, with less risk of brochospasm as seen with timolol, so good alternative choice in asthmatics with glaucoma

90
Q

Esmolol dose,action and effects

A

Selective beta 1 antagonist
Rapid onset, short acting
Typical dose of 0.5mg/kg IV (10-180mg IV) DOA= <15mins
Can start infusion 50-300 mcg/kg/min
Effects HR without decreasing BP significantly in small doses
In doses used, it does not occupy sufficient beta receptors to cause negative inotropy

E1/2t is 9 minutes
Rapidly hydrolyzed by plasma esterases
Not the same esterases as cholinesterases responsible for metabolism of sux, therefore no effect on sux metabolism

Only IV. Great for blunting short lived noxious stimuli in OR or for controlled hypotension. Need to be careful of use if patient has profound sympathetic mediated vasoconstriction because can precipitate CV collapse.

91
Q

side effects of betablockers are?

A

CV System-decrease HR, Contractility, BP

Exacerbation of peripheral vascular disease (block of beta -2 vasodilation)

Airway resistance-bronchospasm

Metabolism-alter carbohydrate and fat metabolism, mask hypoglycemic increase in HR

Distribution of extracellular potassium-inhibit uptake of potassium into skeletal muscles

Interaction with anesthetics-may have decrease BP with IAs

Nervous system-fatigue, lethargy
Nausea, vomiting and diarrhea

92
Q

BBlockers contraindication

A

Pre-existing AV heart block or cardiac failure

Reactive Airway Disease

Diabetes Mellitus (without BS monitoring)
Hypovolemia
93
Q

What are the clinical use of BBLockers

A

Treatment of HTN
Management of Angina
Decrease mortality in treatment of post MI pts
Used periop and preop for pts at risk for MI
Suppression of tachyarrythmias
Prevention of excessive sympathetic nervous system activity

94
Q

combined alpha and beta blockers

A

Labetalol
Selective at alpha 1 and beta 1 and 2 receptors

IV Beta to Alpha Blockade 7:1

Metabolism conjugation of glucuronic acid; <5% in the urine

E1/2t of 5-8hrs, prolonged in liver disease
↓ BP, SVR, HR. CO is unaffected

Maximum drop in BP 5-10min after IV administration

Dose 0.1-0.5 mg/kg
Usually 5mg at a time for mild hypertension in the OR

Can cause orthostatic hypotension, bronchospasm, heart block, CHF, bradycardia

95
Q

Name the cholinergic receptor subtypes

A 
Nicotinic receptors 
Pentameric (5 subunit) structures 
Function as ligand-gated ion channels
Muscarinic receptors 
G-protein coupled
M1, M3, M5 inositol phosphate pathway
M2, M4 inhibit adenylyl cyclase reduce cAMP
96
Q

What Location do the Cholinergic receptors innervate

A

M1: CNS, stomach
M2: cardiac muscle, CNS, airway smooth muscle
M3: airway smooth muscle, glandular tissues
M4: CNS
M5: CNS
Nm: skeletal muscle at NMJ
Nn: autonomic ganglia, adrenal medulla, CNS

97
Q

How do the antimuscarinic drugs propagate the process of inhibition

A

Competitively antagonize acetylcholine (Ach) at muscarinic receptors (only)
Cation portion of the drug fits into Ach’s place on the anticholinergic receptor and reversibly inhibits Ach binding

Allow sympathetic responses to predominate

98
Q

Can competitive inhibition of antimuscarinic agents be reversed?

A

yes

This competitive inhibition can be reversed if Ach concentration is ↑

99
Q

Whats the structure of Natural Antimuscarinic drugs

A

Natural (atropine & scopolamine) are tertiary amines – alkaloids of belladonna plants

100
Q

Whats the structure of semisynthetic muscarinic drugs

A

Semi-synthetic (glycopyrrolate/Robinal) - quaternary ammonium derivative

101
Q

Components and characteristics of Atropine

A

IV Atropine onset is 1 minute; duration of action of 30-60 minutes; E1/2t is 2.3 hrs; 18% unchanged via urine the rest is undergoes hydrolysis

102
Q

Components and characteristics of iv Glycopyrolate

A

IV Glycopyrrolate slower onset of 2-3 minutes; duration of action of 30-60 minutes; E1/2t is 1.25 hrs; 80% unchanged via urine

103
Q

Components and characteristics of Scopalamine

A

Scopolamine extensively metabolized with only 1% excreted unchanged in the urine

104
Q

Uses of anticholinergic drugs

A

Pre-operative – antisialagogue or sedation, nausea prevention
Treatment of bradycardia (especially vagal stimulation related)
Magnitude of effect depends on baseline vagal tone
Young patients high tone = more tachycardia
Elderly patients less tone= less pronounced tachycardia
With anticholinesterase drugs (always given when antagonizing NMB)
Promoting amnesia in unstable patients

105
Q

In Treatment of bradycardia,what does the magnitude of effect depend on

A

Magnitude of effect depends on baseline vagal tone
Young patients high tone = more tachycardia
Elderly patients less tone= less pronounced tachycardia

106
Q

When might a CRNA use these drugs

A

Bronchodilation (Ipratropium)
MDI 40-80mcg 2 puffs
0.25-0.5 mg via nebulizer
Onset 30-90 minutes
Consider in asthmatics, COPD, and smokers prior to airway instrumentation
Mydriasis and cycloplegia (ophtho cases)
Note: anticholinergics may be dangerous in patients with narrow angle glaucoma (increases IOP)
To reduce biliary and ureteral spasm r/t opioids

107
Q

Scopolamine

dose

A
  1. 3-0.5 mg or 5mcg/kg IM (pre-op)

1. 5mg transdermal (5mcg/hr X 72 hrs - nausea)

108
Q

ATropine dose

A

0.2-0.4 mg IV (pre-op)
0.4-1.0 mg IV (bradycardia)
2mg in 5ml NS via nebulizer (bronchodilate)

109
Q

Glycopyrolate dose

A

0.1-0.2 mg IV (pre-op and bradycardia)

110
Q

What is Physostigmine used for

A

Central ACH syndrome

111
Q

Dose of Physostigmine

A

15-60mcg/kg iv prn q1-2 hrs

112
Q

What are the symptoms of Central ACH syndrome and what drug causes it.

A

Scopolamine and atropine (unlikely with glycopyrrolate)
Restlessness, hallucination
Somnolence and unconsciousness
Delayed emergence/recovery in PACU

113
Q

Other ANti muscarinic agents and their use are?

A

Ipratropium (Atrovent), tiotropium (Spiriva) - COPD
Bronchodilator
Oxybutynin (Ditropan), tolterodine (Detrol) - overactive bladder
Nonspecific M-rec
Darifenacin (Enablex), solifenacin (Vesicare) - overactive bladder
M3 specific

114
Q

What is the mechanism of action of AchE inhibitors

A

Elevates concentration of endogenously released ACh in synapse by decreasing its metabolism
Increases transmission at Nm junction (reverses competitive NMB)
Increases parasympathetic tone
Increases central cholinergic activity

115
Q

What do we use AchE for?

A

Useful in diseases of the Nm junction
Myasthenia gravis - pyridostigmine, neostigmine
Glaucoma
Increases outflow of aqueous humor - physostigmine (Isopto)
Abdominal distension
Increases smooth muscle motility - neostigmine
AD and other forms of cognitive dysfunction
Tacrine (Cognex), donepezil (Aricept), rivastigmine (Exelon), galantamine (Razadyne)

116
Q

ADverse effects of AChE

A

Peripheral ACh effects of GI tract
N/v/d, anorexia, flatulence, abdominal cramping
Dose-dependent

117
Q

Contraindications of ACHE

A

Unstable or severe cardiac disease
Uncontrolled epilepsy
Active PUD

118
Q

NAme the Muscarinic agents your patient may be taking at home

A

Diagnosis of asthma
Methacholine

Miosis and decreased intraocular pressure
Carbachol

GI and urinary tract motility - post-op and post-partum urinary retention, neurogenic bladder
Bethanechol

119
Q

Give an example of Nicotinic Agonists

Depolarizing Muscle Relaxant and how it functions

A

Succinylcholine

Continuous activation of nicotinic receptor channels results in depolarization blockade

120
Q

Phenelephrine cahracteristic and effects emergency drug

A 
Synthetic non-catecholamine
Primarily alpha1-adrenergic receptor stimulant
Mostly direct acting
Venoconstriction>arterial constriction
Less potent than norepinephrine
Longer lasting
Treat hypotension in OR due to various reasons
inc MAP, SBP, DBP, SVR decreaseHR, CO
121
Q

Phenylephrine dose and mix

A

Dose: 50-200g IV, can be used as continuous infusion (20-50 mcg/min)
Standard concentration in vial= 10mg/ml
Standard concentration for administration= 100mcg/ml
Needs double dilution/or in1ml of 10mg/ml in 100mL bag of saline

Double dilution: mix 9ml saline + 1ml of 10mg/ml phenylephrine then discard 9ml and replace with 9ml sale

122
Q

ephedrine Characteristics and action emergency drugs

A

Synthetic non-catecholamine
Indirect acting-stimulates B and A adrenergic receptors (with some direct action at receptors as well)
Treat hypotension in OR due to various reasons
CV effects similar to epinephrine, longer lasting (~10X)
SVR effected minimally
CV effects mostly due to inc contractility– inc MAP, SBP, DBP, HR, Coronary BF, dec renal, splanchnic BF.

123
Q

Ephedrine dose,dilution and adverse effects

A

Dosage: 5-25mg IV
Tachyphylaxis is common with this agent-due to indirect effect and occupying of receptors
Dilute once
1ml of 50mg/ml + 4ml saline = 10mg/ml OR
1 ml of 50mg/ml in 9 ml saline = 5 mg/ml

124
Q

ATropine characteristic

Emergengy drugs

A

Anticholinergic-antagonizes effect of Ach at cholinergic post ganglionic muscarinic receptors.
Muscarinic receptors are present in: heart, salivary glands, smooth muscles of GU and GI tract.
No/minimal effect at nicotinic receptors.
Tertiary amine-naturally occurring, is an alkaloid of belladonna plant.
Resembles cocaine in structure, and has mild analgesic activity.
Combines reversibly with muscarinic receptors and prevents Ach from binding to these sites, competitive inhibitors.

125
Q

Atropine dose and action

A

Drug of choice for treating intra-op bradycardia
Available in 2 “standard concentrations”

Dose: 15-75MCg/kg IV OR 0.4-1mg (max dose 3 mg)
Other effects: antisialagogue, bronchodilation, mydriasis, dec GI motility and acid production, bronchodilation, sedation

126
Q

Glycopyrolate characteristics and dose

A

Similar to atropine.
Quaternary ammonium-does not easily cross BBB so no sedative effects.
Uses similar to atropine, similar effects, more potent antisialagogue, less potent at HR.
Dosage: 0.2-0.4mg IV
Combine with anticholinestrase drugs (i.e. neostigmine) for reversal, 0.05-0.07mg/kg (or 1cc of robinul for each cc of reversal drawn)

127
Q

Lidocaine Emergency drugs characteristics

A

Amide local anesthetic
Prevents transmission of nerve impulses by inhibiting passage of sodium ions through voltage gated sodium channels in nerve membranes.
Slows the rate of depolarization such that the threshold potential is not reached and an action potential is not propagated.
In the cardiac conduction system and myocardial muscle it reduces intracellular sodium activity and intracellular calcium activity (by the sodium-calcium exchange mechanism).
Reduction of the “arrhythmogenic transient depolarization” and a reduction of contractility by decreasing the inward sodium current.
Overdose causes CNS toxicity/seizures.

128
Q

Lidocaine dose and use

A

Used for local anesthetic activity, numbness of veins for propofol (about 30mg), and ablating response to laryngoscopy (1mg/kg).
Used as an anti-dysrhythmic-suppresses ventricular dysrhythmias, especially PVCs, and ventricular tachycardia-2mg/kg IV followed by infusion of 1-4mg/min

129
Q

Succ characteristics and effects

A

Depolarizing muscle relaxant
SCh attaches to each of alpha subunits of the nicotinic cholinergic receptor and mimics the action of ACh, depolarizing the post-junctional membrane.
Hydrolysis of SCh is slower than ACh resulting in sustained depolarization of the receptor ion channels.

130
Q

Succs dose and effects

A

Dose: 0.5-1.5mg/kg
Duration of action: 3-5minutes
Used for emergency a/w situations (0.5mg to break laryngospasm), rapid sequence induction (1-1.5mg/kg).
Can cause: dysrhythmias (bradycardia, arrest-acts at cardiac muscarinic receptors mimics ACh), hyperkalemia, myalgias, inc GI pressure, ICP and IOP.

131
Q

Labetalol characteristics and dose

A

Non selective beta blocker as well as alpha blockade.
B:A in a ratio of 7:1.
Bolus of 10mg-typical
Can repeat q 10 mins.
Hypertensive emergency IV dose is 40-80 mg (usually titrate up to this with smaller boluses).
Duration of action of 2-18hrs
Make sure patient has adequate HR, do not give to asthmatics.

132
Q

Esmolol characteristics and dose

A

Beta-1 selective agent at small doses.
Onset of 2 minutes.
E1/2 life of 9 minutes-metabolized by non-specific plasma esterases found in the cytosol of RBCs.
Bolus dose of 500ug/kg (IV loading dose)
In OR we typically use 10-15mg, and then dose according to response.

Pharmacology (9 decks)

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