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ARCHIVED: Pharmacology for Nurse Anesthesia > Exam 2: ANS Pharmacology > Flashcards

Exam 2: ANS Pharmacology Flashcards

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1
Q

Organs that are only innervated by SNS:

A 
Sweat glands 
Blood vessels (though they have M receptors)
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2
Q

Organs only innervated by PSNS:

A

Ciliary muscle of eye

Bronchial smooth muscle (though they have B2 receptors)

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3
Q

Receptors on skeletal muscle:

A

Nicotinic (Nm)

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4
Q

Receptors on blood vessels and other smooth muscle:

A

Adrenergic (alpha/beta)

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5
Q

Receptors on sweat glands:

A

Muscarinic (M1-5)

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6
Q

Receptors on adrenal medulla:

A

Nicotinic - preganglionic

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7
Q

Receptors on salivary glands etc:

A

Muscarinic

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8
Q

How is the adrenal medulla an anomaly?

A

Acts like a ganglia but releases NE/Epi as hormones

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9
Q

Norepi/epi % release:

A

Norepi 20%

Epi 80%

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10
Q

How are the sweat glands an anomaly?

A

Innervated by the SNS, but postganglionic neuron releases ACh onto a muscarinic ACh receptor

Sympathetic cholinergic!

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11
Q

How are the blood vessels an anomaly?

A

No PSNS innervation, although muscarinic ACh receptors present (require circulating ACh)

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12
Q

Name the endogenous catecholamines:

A

Epi
Norepi
Dopa

ENDogenous

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13
Q

Name the synthetic catecholamines:

A

Isoproterenol

Dobutamine

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14
Q

Name the indirect acting synthetic non-catecholamines:

A

Mephentermine
Ephedrine
Amphetamines

MEA culpa is an INDIRECT way of saying “my bad!”

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15
Q

Name the direct acting synthetic non-catecholamines:

A

Phenylephrine
Methoxamine

Don’t comment publicly, just PM me directly…

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16
Q

Name the selective α2 agonists:

A

Clonidine

Dexmedetomidine

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17
Q

Name the selective β2 agonists:

A

Abuterol
Terbutaline
Ritodrine

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18
Q

How do direct agonists work?

A

Either mimic the endogenous substance or directly activate the receptor

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19
Q

How do indirect agonists work?

A

Stimulate release of NTs

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20
Q

Structure of all sympathomimetics:

A

Beta-phenylethylamine derivatives

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21
Q

Chain of catecholamine formation:

A 
Tyrosine
DOPA
Dopamine
Norepinephrine
Epinephrine
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22
Q

Termination of effect of catecholamines:

A

Reuptake (I/II)
MAO
COMT
Lungs

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23
Q

Termination of effect of non-catecholamines:

A

MAO

Urinary excretion

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24
Q

Reuptake I vs II:

A

I: Neuronal (80%)
II: Extraneuronal

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25
Q

How do MAO inhibitors cause problems with sympathomimetics?

A

Non-catecholamines are unable to be broken down and have an increased effect

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26
Q

Relative receptor activation of α-agonists:

A

Phenylephrine: α1 > α2
Clonidine: α2 > α1

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27
Q

Relative receptor activation of mixed α/β agonists:

A

Norepi: α1=α2; β1&raquo_space;> β2
Epi: α1=α2; β1=β2

Equal Epi
Nonequal Norepi

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28
Q

Relative receptor activation of β-agonists:

A

Dobutamine: β1 > β2
Isoproterenol: β1 = β2
Terbutaline/albuterol: β2 > β1

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29
Q

Relative receptor activation of dopamine agonists:

A

Dopamine: D1 = D2
Fenoldopam: D1&raquo_space; D2

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30
Q

MoA of epinephrine:

A

α and β receptor activation

Most potent α receptor activator!

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31
Q

PK of epinephrine:

A

Very poorly lipid soluble (no CNS effect)
IV onset: 1-2 min
Duration: 5-10 min

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32
Q

Indications for epinephrine:

A

Bronchial asthma
Acute allergic rxn
Cardiac arrest/asystole
Vfib unresponsive to defib

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33
Q

Resuscitation dose of epinephrine:

A

10mcg/kg IV

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34
Q

Infusion dose of epinephrine:

A

1-2mcg/min: β2 for bronchospasm
4-5mcg/min: β1 for ↑ contractility
10-20 mcg/min: α (more prominent as dose ↑) and β

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35
Q

CV effects of epinephrine:

A 
BP regulation is major role
α1: Vasoconstriction, ↑BP / CVP / work 
α2: Negative feedback ↓ BP 
β1: ↑ contractility, HR, CO, BP
β2: Peripheral vasodilation ↓ BP

At moderate doses:
SBP increases
DBP decreases
MAP stays the same

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36
Q

Cerebral effects of epinephrine:

A

Minimal vasoconstriction

↑ CBF

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37
Q

Ocular effects of epinephrine:

A

Dilation of pupils/mydriasis (α1)

Increased humoral outflow (α1/α2), production of aquaous humor (β1)

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38
Q

Respiratory effects of epinephrine:

A

Bronchodilation (β2)
Decreased histamine release (β2)
Reduced mucosal secretions (α1)

Good for treating bronchospasm, anaphylaxis

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39
Q

GI effects of epinephrine:

A

Decreased digestive secretions (α2)
Decreased peristalsis (α, β2)
Decreased blood flow (α1)

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40
Q

GU effects of epinephrine:

A

Renal blood flow dramatically reduced! (α1)
Increased renin release (β1)

Contraction of urethral sphincter (α1) and bladder relaxation (β2)

Inhibition of labor (β2)

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41
Q

Metabolic effects of epinephrine:

A

↑ glycogenesis, insulin release (β2) - inhibition of release by α2, but minor

Peri-op pts need more insulin than usual

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42
Q

Hypotension dosing for norepi:

A

4-16mcg/min

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43
Q

Indications for norepi perioperatively:

A

Hemorrhage (redistribute remaining blood)

Septic shock last line

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44
Q

Effects of norepi:

A 
Intense vasoconstriction (α1 with no β2 to balance!!)
↑ BP activates baroreceptors so ↓ HR
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45
Q

Dosing of dopamine:

A

1-3 mcg/kg/min: D1 receptor dominates
3-10 mcg/kg/min: β1 receptor dominates
> 10 mcg/kg/min: α receptor dominates

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46
Q

Effects of dopamine:

A

↑ contractility, renal BF, UOP, GFR
↑ endogenous norepi release
Inhibition of carotid bodies / altered response to hypoxia
↑ ocular pressure

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47
Q

Dopamine and dobutamine:

A

Synergistic; reduces afterload, improves CO

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48
Q

MoA of isoproterenol:

A

β1 and β2 agonist

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49
Q

Effects of isoproterenol:

A

↑ HR, contractility

↓ SVR means ↑ SBP, ↓ DBP, ↓ MAP

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50
Q

Dosing of isoproterenol for block/dysrhythmias:

A

1-5 mcg/min

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51
Q

PK of isoproterenol:

A

Rapidly metabolized by COMT (need to infuse)

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52
Q

Why increased MI risk with isoproterenol?

A

↑ HR means ↓ O2 delivery to the myocardium

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53
Q

Dosing for dobutamine:

A

2-10 mcg/kg/min

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54
Q

Receptors targeted by dobutamine:

A

β1 selective at < 5 mcg/kg/min

Weak a1 stimulation > 5 mcg/kg/min

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55
Q

Effects of dobutamine:

A

↑ CO without increasing HR/BP

Coronary artery vasodilator

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56
Q

MoA of ephedrine:

A

Indirect agonist at α and β receptors

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57
Q

Indications for ephedrine:

A

Hypotension with bradycardia

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58
Q

Dosing for ephedrine:

A

10-25 mg IV

10-50 mg IM

59
Q

Negative effect of ephedrine:

A

Tachyphylaxis d/t norepi depletion

60
Q

PK of ephedrine:

A

Excreted unchanged in urine
Metabolized by MAO and conjugated in liver
Et1/2: 3 hrs

61
Q

MoA of phenylephrine:

A

Direct α1 agonist

62
Q

Effects of phenylephrine:

A

Venoconstriction ( > arterial)
↑ BP, SVR
↓ HR, CO

63
Q

Indications for phenylephrine:

A

Hypotension (not d/t hypovolemia)

64
Q

Dosing for phenylephrine:

A

50-200 mcg IV

Infusion: 20-50 mcg/min

65
Q

Overdose of phenylephrine or epinephrine:

A 
Give phentolamine (α1 antagonist) or NTG/NTP
NOT a β-blocker, which will ↓ contractility and rate and leave massive vasoconstriction
66
Q

Indications for β2 agonists:

A

Premature labor, asthma, COPD

67
Q

Side effects of β2 agonists:

A

Tremor

Reflex tachycardia

68
Q

Indications for albuterol:

A

Asthmatic bronchospasm

69
Q

Dosing of albuterol:

A

100mcg/puff
2 puffs q4-6hr

Nebulization: 15mg/hr for 2 hours

70
Q

Side effects of albuterol:

A

Tachycardia, hypokalemia

71
Q

Indications for terbutaline:

A

Asthma

Premature labor

72
Q

Difference between salmeterol and albuterol:

A

Salmeterol duration > 12 hrs

73
Q

Indication for ritordine:

A

Premature labor

74
Q

Side effects of ritordine:

A

↑ HR/CO d/t β1 activity

Can cause pulmonary edema

75
Q

MoA and indication for midodrine:

A

α1 agonist

Postural hypotension

76
Q

Effects of amphetamine:

A

↑ release of norepi, dopamine, 5HT
Blocks reuptake
Blocks vesicular transport
Inhibits MAO

77
Q

Difference between amphetamine and methamphetamine:

A

Methamphetamine has higher CNS effects

78
Q

MoA of cocaine:

A

Prevents reuptake of catecholamines (norepi, dopamine, 5HT)

79
Q

MoA of reserpine:

A

Vesicles lose ability to store norepi/dopamine/5HT

80
Q

CV effects of α1 antagonism:

A

Vasodilation ↓ PVR, BP

Postural hypotension

81
Q

CV effects of α2 antagonism:

A

↑ norepi release by blocking negative feedback

82
Q

GI effects of α-antagonism:

A

Muscle relaxation and easier urination

83
Q

ENT effects of α-antagonism:

A

Miosis

Nasal congestion

84
Q

Competitive α-antagonists:

A

Phentolamine
Prazosin
Yohimbine

85
Q

Covalently binding α-antagonist:

A

Phenoxybenzamine

86
Q

MoA of phentolamine:

A

Nonselective α-blocker

87
Q

Effects of phentolamine:

A

Vasodilation
↓BP
↑HR, CO

88
Q

Indications for phentolamine:

A 
Hypertensive emergencies (pheochromocytoma, ANS dysreflexia)
Extravascular infiltration of sympathomimetics
89
Q

Dosing/timing of phentolamine for HTN crisis:

A

30-70 mcg/kg IV
Onset: 2 min
Duration: 10-15 min

90
Q

Dosing of phentolamine for extravasation:

A

2.5 - 5mg in 10ml NS

91
Q

MoA of phenoxybenzamine:

A

Binds covalently to α1 receptors

92
Q

Effects of phenoxybenzamine:

A

↓ SVR, vasodilation

93
Q

PK of phenoxybenzamine:

A

Pro-drug
Onset: 1hr
Et1/2: 24 hrs

94
Q

Indications for phenoxybenzamine:

A

Pheochromocytoma

Raynaud’s disease

95
Q

MoA of prazosin:

A

Selective α1 antagonist

96
Q

MoA of yohimbine:

A

Selective α2 antagonist

97
Q

Indications for yohimbine:

A

Orthostatic hypotension

Impotence

98
Q

MoA and indications for terazosin and tamulosin:

A

α1 antagonists for BPH

99
Q

Effects of β antagonists:

A 
Improve O2 supply/demand
Can provoke bronchospasm
Vasoconstriction in skeletal muscles
↓ renin release
↓ insulin release
100
Q

MoA of β antagonists:

A

Competitive and reversible inhibition of β receptors

101
Q

Chronic use of β antagonists:

A

Upregulation in receptors

MUST take β-blocker on DOS or ↑ risk of intra-op MI

102
Q

Non-selective β antagonists:

A

Propranolol
Nadalol
Timolol
Pindolol

Not Too Particularly Picky

103
Q

Cardioselective/β1 antagonists:

A 
Metoprolol
Atenolol
Acebutolol
Betaxolol 
Esmolol

MAABE they’re block your receptor, but they’re selective

104
Q

Receptor activity of propranolol:

A

β1 = β2

105
Q

MoA of propranolol:

A

Lacks sympathomimetic activity; pure antagonist

106
Q

CV effects of propranolol:

A

↓ HR, contractility, CO
Especially during exercise

↑ PVR, coronary VR

O2 demand lowered

Sodium retention d/t ↓ renin

107
Q

PK of propranolol:

A 
Significant first pass effect
Highly protein bound (90-95%)
Metabolized in liver
Et1/2: 2-3 hrs
↓ clearance of amide LAs
↓ pulmonary first pass effect of Fentanyl
108
Q

Indications for timolol:

A

Glaucoma

109
Q

Indications for nadolol:

A

Long-term tx; preferred d/t daily dosing

Et1/2: 20-40 hrs!

110
Q

MoA of metoprolol:

A

Selective β1 antagonist

111
Q

Effects of metoprolol:

A

Prevents inotropy, chronotropy

112
Q

PK of metoprolol:

A

60% first pass effect

Et1/2: 3-4 hrs

113
Q

Dosing of metoprolol:

A

1-15 mg (1mg at a time)

114
Q

MoA of atenolol:

A

Most selective β1 antagonist with the least CNS effects

115
Q

PK of atenolol:

A

Not metabolized in liver; excreted via renal system (VERY polar)
Et1/2: 6-7 hrs

116
Q

Indications for atenolol:

A

Cardiac patients with CAD

117
Q

MoA of betaxolol:

A

Selective β1 antagonist

118
Q

Et1/2 and indications for betaxolol:

A

Et1/2: 11-22 hrs
Daily dose for HTN
Topical for glaucoma with less bronchospastic risk

119
Q

MoA of esmolol:

A

Selective β1 antagonist

120
Q

PK of esmolol:

A

Rapid onset
Et1/2: 9 min
Short duration (< 15 min)
Hydrolyzed by plasma esterases

121
Q

Indications for esmolol:

A

Controlled hypotension
Tourniquet pain
Short noxious stimuli
Wakeups

122
Q

Dosing for esmolol:

A

0.5 mg/kg IV

Infusion: 50-300 mcg/min

123
Q

Side effects of β blockers:

A 
↓ HR, contractility, BP
Exacerbation of PVD 
Bronchospasm
Inhibit uptake of K+ into muscles
↓ BP with inhaled agents
Fatigue, lethargy
N/V/D
124
Q

Relative contraindications for β blockers:

A

Heart block or cardiac failure
Asthma
DM w/o BG monitoring
Hypovolemia

125
Q

Indications for β blockers:

A 
HTN
Angina
Post-MI
Tachyarrythmias
↓ SNS tone
126
Q

MoA of labetalol:

A

α1, β1, β2 antagonist

β blockade 7x higher

127
Q

PK of labetalol:

A

Conjugation metabolism
Very little in the urine
Et1/2: 5-8 hrs

128
Q

Effects of labetalol:

A

↓ BP, SVR, HR - maximum drop 5-10 mins after administration

129
Q

Dose of labetalol:

A

0.1 - 0.5 mg/kg

Usually 5mg/time for HTN in OR

130
Q

Side effects of labetalol:

A 
Orthostatic hypotension
Bronchospasm
Heart block
CHF
Bradycardia
131
Q

Which muscarinic receptor most affects the heart?

A

M2

132
Q

MoA of antimuscarinics:

A

Competitively, reversibly antagonize ACh at muscarinic receptors

133
Q

Tertiary amines vs. quaternary ammonium antimuscarinics:

A

Tertiaries: atropine, scopolamine
Quaternary: glycopyrrolate

Tertiary will cross BBB, quarternary will not

134
Q

PK of IV atropine:

A

Onset 1 minute
Duration 30-60 min
Et1/2: 2.3 hours
18% unchanged, rest hydrolysed

135
Q

PK of IV glycopyrrolate:

A

Onset 2-3 min
Duration 30-60 min
Et1/2: 1.25 hrs
80% unchanged via urine

136
Q

PK of scopolamine:

A

Extensively metabolized

137
Q

Indications for antimuscarinics:

A 
Antisialogogue
Sedation
PONV prevention
Bradycardia
Reversal of NMB (with anticholinesterase)
Amnesia promotion in unstable pts
Bronchodilation
Mydriasis
Reduce biliary/ureteral spasm
138
Q

Dosing for ipratropium:

A

40-80 mcg/puff
2 puffs

0.25 - 0.5 mg via nebulizer

Not fast onset - 30-90 min

139
Q

Scopolamine dosing:

A

Pre-op: 0.3 - 0.5 mg

1.5 mg transdermal for 72 hours’ N/V prevent

140
Q

Atropine dosing:

A

0.2 - 0.4 mg IV pre-op
0.4 - 1.0 mg IV for bradycardia
2 mg in 5ml NS nebulized for bronchodilation

141
Q

Glycopyrrolate dosing:

A

0.1 - 0.2 mg IV pre-op or bradycardia

142
Q

S/s of central anticholinergic syndrome:

A 
Restlessness
Hallucinations
Somnolence
Unconsciousness
Delayed emergence
143
Q

Tx for central anticholinergic syndrome:

A

Physostigmine (anticholinesterase) 15-60 mg/kg IV PRN q1-2hrs

ARCHIVED: Pharmacology for Nurse Anesthesia (20 decks)

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