Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm '14 test 2 > Autonomics > Flashcards

Autonomics Flashcards

1
Q

Autonomic preganglionic neurons are

A

myelinated

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

Autonomic postganglionic neurons are

A

unmyelinated

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

Sympathetic preganglionic cell bodies are located where?

A

Intermediolateral horn of T1-L2/3

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

Sympathetic postganglionic cell bodies are located where?

A

Paravertebral chains and prevertebral ganglia (i.e. celiac, superior, inferior mesenteric ganglia)

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

Parasympathetic preganglionic innervation can be described as…

A

Cranio-sacral (CN 3,7,9,10 and spinal segments S2-4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Parasympathetic postganglionic neuron cell bodies are located where?

A

In target organs and discrete ganglia in the head and neck (i.e. ciliary ganglia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Most organs have both SNS and PSNS innervation, name four exceptions

A

Only SNS innervation-
Sweat glands
Blood vessels (muscarinic receptors present, but NO direct innervation)

Only PSNS innervation-
Ciliary eye muscles
Bronchial smooth muscle (B2 receptors present, but NO direct innervation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Blood vessels and bronchial smooth muscle have receptors for PSNS and SNS, respectively, but no direct innervation from these systems. How are the receptors activated?

A

By circulating drug/hormones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Does the heart exhibit baseline SNS or PSNS baseline tone?

A

PSNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Do blood vessels exhibit baseline SNS or PSNS baseline tone?

A

SNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

With respect to the autonomic nervous system, all preganglionic neurons have what type of receptor? Are these ligand gated ion channels or GCPRs?

A

Nicotinic receptors (Nn). Ligand gated ion channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

The somatic efferent system uses what type of receptor for impulse transmission? Is this a ligand gated ion channel or a GCPR?

A

Nicotinic receptors (Nm). These are ligand gated ion channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Within the sympathetic sub-division, what is the primary neurotransmitter?

A

NE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the two exceptions to NE being the primary neurotransmitter of the SNS?

A

Sweat glands- postganglionic receptor is muscarinic and responds to ACh.

Adrenal medulla- Tissue itself is “postganglionic” and release Epi and NE (80/20) directly into the blood stream.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

SNS postganglionic neurons are typically what type of receptors? Are the GCPRs or ligand gated ion channels?

A

Most are adrenergic receptors that respond to NE. These are GCPRs. The exceptions are sweat glands and the adrenal medulla.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

PSNS postganglionic neurons display what type of receptor? What is the bodies neurotransmitter for these receptors? Are the GCPRs or ligand gated ion channels?

A

Muscarinic receptors that respond to ACh. These are GCPRs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cholinergic receptor subtypes in the body-

A

Nicotinic- Nm and Nn

Muscarinic- M1-5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Adrenergic receptor subtypes in the body-

A

Alpha 1, 2
Beta 1,2,3

Grossly simplified, of course!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Sympathetic cholinergic fibers can only be associated with….?

A

Sweat glands.

Remember, anticholinergics don’t touch your SNS, except they will prevent sweating.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Explain the signaling, messengers, and physiologic response of M1 activation.

A

Signal- excitatory, CNS

Messengers- IP3 and DAG –> increased free Ca and decreased K conductance

Response- Increased CNS activity, modulation at ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Explain the signaling, messengers, and physiologic response of the M2 activation.

A

Signal- inhibitory, cardiac

Messengers- inhibit adenylate cyclase –> decrease in cAMP –> increase in K conductance

Physiologic response- decreased HR and decreased contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Explain the signaling, messengers, and physiologic response of the M3 activation.

A

Signal- excitatory, smooth muscle and glands

Messengers- IP3 and DAG –> increased free Ca

Response- Smooth muscle contraction, gland activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Explain the signaling, messengers, and physiologic response of the A1 activation.

A

Signal- excitatory, blood vessels

Messengers- IP3 and DAG –> increased free Ca

Response- Vasoconstriction by smooth muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Explain the signaling, messengers, and physiologic response of the A2 activation.

A

Signal- inhibitory, blood vessels, pre-/post- synaptic CNS

Messengers- inhibit adenylate cyclase –> decrease in cAMP –> increase K conductance

Response- Vasodilation by increased K conductance. Inhibits neurotransmitter release from neurons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Explain the signaling, messengers, and physiologic response of Beta activation.

A

Signal- Excitatory or inhibitory depending on cAMP action (cAMP is INCREASED though).

Messengers- Increase in cAMP

Response- Relaxation of smooth muscle, stimulates cardiac muscle (increase in rate and contractility)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Alpha 1 agonist effects at-

Vascular smooth muscle
Iris
Pilomotor smooth muscle
Prostate/Uterus
Heart
A 
Contraction, vasoconstriction
Contraction, dilation or mydriasis
Erects hair
Contraction
Increase contractility (B1 more important)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Alpha 2 agonist effects at-

Platelets
Presynaptic adrenergic & cholinergic terminals
Vascular smooth muscle
GI tract
CNS
A

Aggregation
Inhibits transmitter release (decrease BP and HR)
Contraction (post-synaptic) OR dilation (pre-synaptic, CNS)
Relaxation (presynaptic)
Sedation/analgesia via decrease SNS outflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Beta 1 agonist effects at-

Heart
Kidneys

A

Increase force and rate of contraction

Stimulate renin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Beta 2 agonist effects at-
Visceral smooth muscle
Mast cells

Skeletal muscle

Liver
Pancreas
Adrenergic Nerve Terminals

A

Smooth muscle relaxation
Decrease histamine release

Dilate vascular beds, tremor, increase speed of contraction, K uptake (decreased serum levels of K)

Glycogenolysis, gluconeogenesis
Increase insulin secretion
Increase NE release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Beta 3 agonist effects on fat cells

A

Activate lipolysis, thermogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

D1 agonist effects on smooth muscle

A

Post-synaptic location, dilates renal, mesenteric, coronary, and cerebral vascular beds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

D2 agonist effects on nerve endings

A

Pre-synaptic location, modulates transmitter release, nausea/vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Name the endogenous catecholamines

A

Epi, Norepi, Dopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Name some synthetic catecholamines

A

Isoproterenol, Dobutamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Name some synthetic non-catecholamines

A

Indirect- ephedrine, mephentermine, amphetamine

Direct- phenylephrine, methoxamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Name two selective A2 agonists

A

Clonidine, dexmedetomidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Name some selective B2 agonists

A

Albuterol, terbutaline, ritodrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

All sympathomimetics are derivatives of what?

A

Beta-phenylethylamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Where are the hydroxyl groups located on a catecholamine?

A

Positions 3,4 on the benzene ring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the rate limiting enzyme in catecholamine synthesis in the body?

A

Tyrosine hydroxylase (Tyrosine –> Dopa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

End physiological effects from sympathomimetics usually involve a change in what?

A

Intracellular calcium, either increased or decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What terminates the effects of catecholamines?

A

Reuptake (I- neuronal, II-extraneuronal)
MAO A/B
COMT
Lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What terminates the effects of non-catecholamines?

A

MAO

Urinary excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Is phenylephrine more selective for A1 or A2?

A

A1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Is clonidine more selective for A1 or A2?

A

A2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Describe norepinephrines receptor selectivity

A

A1=A2, B1 much more than B2 (almost NO activity at B2, no effect at clinical doses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Describe epinephrines receptor selectivity

A

A1=A2, B1=B2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Is dobutamine more selective for B1 or B2?

A

B1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Is isoproterenol more selective for B1 or B2?

A

Equal activity at both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Describe dopamines receptor selectivity

A

D1=D2»B»A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Describe fenoldopam in terms of receptor selectivity

A

D1»D2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Most potent Alpha activator

A

Epi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Routes for Epi

A

SQ or IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Does Epi have CNS effects?

A

No, poor lipid solubility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Epi onset

A

SQ- 5-10min

IV-1-2 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Duration of Epi

A

5-10 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Indications for Epi

A

Bolus- Bronchial asthma, acute allergic reaction, arrest/asystole, PEA, V.fib

Infusion- Increase contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Epi dosing

A

Bolus for resus- 10mcg/kg IV, can start at 2-8mcg/kg

1-2mcg/min- Beta2
4-5mcg/min- Beta1
10-20mcg/min- Alpha and Beta (more of a pure pressor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

CV effects of Epi

A

A1- vasoconstriction- increased BP, CVP, cardiac work
A2- negative feedback- decrease BP
B1- increased HR, CO, contractility, BP
B2- peripheral vasodilation- decrease BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Effect of epi at moderate doses on SBP, DBP, and MAP

A 
SBP increases (B1, A1)
DBP decrease (B2)
MAP tends to be the same, can increase or decrease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What effect does epi have on skeletal muscle vascular beds?

A

Vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Epi effects on cerebral vasculature

A

Minimal vasoconstriction–> increased cerebral blood flow even with normal BP

63
Q

Epi effects on the eye

A

A1- mydriasis (big wide eyes to see that bear)

A1, A2- increase humoral outflow
B1- increased aqueous humor production

64
Q

Epi effects on Resp

A

B2- Dilate smooth muscle, decrease histamine release

A1- Reduced mucous secretion

65
Q

Epi effects on GI

A

A2- Decreased secretions

A1, A2, B2- Smooth muscle relaxation

A1- Drastically reduced splanchnic blood flow even with normal BP

66
Q

Epi effects on Renal/GU

A

A1- Drastic reduction in renal blood flow even with normal BP
B1- Increased renin release

A1- Increased urethral sphincter tone
B2- Bladder relaxation–> reduced urine output

A1- Facilitates ejaculation

B2- Relaxes uterus

67
Q

Epi metabolic effects

A

B2- Liver glycogenolysis

B3- lipolysis

A2- Inhibition of insulin release

68
Q

Do IDDM patients need more or less insule peri-op?

A

More!

69
Q

NE dosing

A

4-16 mcg/min for hypotension

70
Q

Describe NE effects on B2

A

Minimal, would require “stupid” doses.

71
Q

Why does NE drop HR in an otherwise healthy person?

A

Vasoconstriction –> increased BP –> baroreceptors activate –> HR decreases

72
Q

What type of drug do you want to use for an infiltrate of NE or Epi?

A

Alpha blocker given SubQ around the infiltrate (something like phentolamine)

73
Q

Dopamine is a precursor to what in the body?

A

NE

74
Q

What receptors does dopamine stimulate?

A

All adrenergic including the dopamine receptors

75
Q

Dopamine dosing

A

1-3mcg/kg/min- D1 receptors
3-10mcg/kg/min- B1 effects
>10mcg/kg/min- Alpha effects (pressor)

76
Q

Dopamine increases/decreases contractility, renal blood flow, urine output, and GFR.

A

Increases

77
Q

Does dopamine have any indirect effects?

A

Yes, releases endogenous NE. May be less effective if body stores are depleted

78
Q

Dopamine effects on IO pressure

A

Increased

79
Q

What nice synergistic effect do dopamine and dobutamine have?

A

Reduced after load and increased CO

80
Q

Dopamine inhibits what that may alter pt response to hypoxia?

A

Carotid bodies

81
Q

Isoproterenol is selective for which adrenergic receptors?

A

B1 and B2

82
Q

Cardio effects of iso

A 
Increased HR and contractility 
Decreased SVR (SPB up, DBP down, MAP down)
83
Q

Iso dosing for heart blocks and bradicardia

A

1-5mcg/min

84
Q

Iso is rapidly metabolised by what enzyme?

A

COMT

85
Q

You might want to think twice about giving iso to a pt with what disease? Why?

A

Parkinsons

entacapone, tolcapone, and nitecapone are COMT inhibitors used in Parkinsons

86
Q

Dobutamine dosing

A

2-10mcg/kg/min

87
Q

Dobutamine is selective for which receptors at <5mcg/kg/min

A

B1

88
Q

Dobutamine is selective for which receptors at >5mcg/kg/min

A

A1, though somewhat weakly due to stereo antagonism

89
Q

Dobutamine improves CO without doing what?

A

Without increasing HR or BP, nice for CHF

90
Q

What effect does dobutamine have on the coronary arteries?

A

Dilation

91
Q

Ephedrine dosing

A

10-25mg IV, 10-50mg IM

92
Q

Ephedrine acts through what type of mechanism at alpha and beta receptors?

A

Mostly indirect, also minor direct effects

93
Q

Compared to epi, how long does ephedrine last?

A

10 times longer

94
Q

Ephedrine. Tachyphylaxis.

A

Of course.

95
Q

How do we get rid of ephedrine?

A

40% unchanged in urine. MAO and liver get the rest. E1/2 life of 3 hours.

96
Q

Neo hits what receptors?

A

Mostly A1, direct acting

97
Q

Does neo work more on the venous or arterial side?

A

Venous

98
Q

Is neo longer or shorter lasting than NE?

A

Longer

99
Q

Neo dosing

A

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

100
Q

Will Neo tend to increase or decrease HR?

A

Decrease. Venous constriction –> increase return –> yada yada –> baroreceptors

101
Q

Should we call neo, neo?

A

No, sounds like neostigmine

102
Q

Albuterol is selective for

A

B2

103
Q

Albuterol dosing

A

MDI- 100mcg per puff, 2 puffs q4-6hrs, max 16-20 puffs

Neb for severe asthma 15mg/hr for 2 hours

104
Q

Large doses of albuterol can give you

A

Tachycardia and hypokalemia

105
Q

Terbualine, Salmeterol, and Ritordine are B2 agonists used for what?

A

Terbutaline- Asthma or premature labor SC dose 0.25mg

Salmeterol- Asthma, MDI lasts >12 hours, otherwise similar to albuterol

Ritordine- premature labor. Some B1, so HR and CO increase. Can cause pulm. edema r/t decreased Na, K, and H2O excretion

106
Q

Some direct-acting, non-catecholamine, sympathomimetics working at A1

A

Midodrine- postural hypotension

Oxymetazoline, xylometazoline- nasal/ocular decongestants

107
Q

A2 selective agonists your pt might be taking

A

Clonidine- partial agonist

Methyldopa

108
Q

Drugs your patient might be taking: Indirect-acting Sympathomimetics

A

Amphetamine (Adderall, Dexedrine)- increases NE, 5HT, and dopamine release. Blocks reuptake. Blocks vesicular transport. MOA inhibitor.

Methamphetamine- similar to amphetamine, but stronger CNS effects

Methylphenidate (Ritalin), Pemoline (Cylert)- amphetamine like variants for ADHD

109
Q

Drugs Your Patient Might Be Taking: Inhibitors of Catecholamine Storage and Reuptake

A

Reserpine- Vesicles lose ability to store NE, 5HT, and dopamine. MAO breaks down excess except in high doses. Hypotension, depression common.

Cocaine- Blocks NE, DA, 5HT reuptake. Interferes with their transport as well.

110
Q

A-antagonists, A1 selective

A

Prazosin, terazosin, doxazosin- super A1 selective

111
Q

A-antagonists, non-selective

A

Phentolamine

112
Q

A-antagonists, A2 selective

A

Yohimbine, tolazoline - modestly A2 selective

113
Q

Mixed A,B antagonists

A

Labetalol, carvedilol B1=B2>A1>A2

114
Q

B-antagonists, B1 selective

A

Metoprolol, atenolol, esmolol

115
Q

B-antagonists, non-selective

A

Propranolol, nadolol, timolol

116
Q

B-antagonists- B2 selective

A

Butoxamine

117
Q

A1-antagonist effects on BP

A

Decreased PVR–> lower BP

Postural hypotension common side effect. Venoconstriction responsible for compensation when standing.

118
Q

A2-antagonist effects

A

Increased NE release from nerve terminals, removes normal negative feedback mechanism

119
Q

A-antagonist effects at GU, eyes, nose

A

GU muscle relaxation, eases micturition

Causes miosis

Increased nasal congestion

120
Q

Most A-antagonists bind competitively. Name one that binds covalently. In what case might we want to use such a drug?

A

Phenoxybenzamine binds covalently to A receptors. Useful where risk of overwhelming catecholamine release is high, such as in pheochromocytoma resection or highly resistant hypertension

121
Q

Phentolamine dosing

A

Hypertensive emergency- 30-70mcg/kg IV, onset 2 minutes.

Extravascular sympathomimetic administration- 2.5-5.0 mg in 10ml given SubQ around the site.

122
Q

Phentolamine CV effects

A

Decrease BP, increase HR and CO.

123
Q

Phenoxybenzamine effects, onset, E1/2 time

A

A1>A2

Decrease SVR, vasodilation

1 hour onset time, pro-drug needs to be metabolized. E1/2 time of 24 hours.

124
Q

Uses for Prazosin

A

Control BP in pheochromocytoma

Mostly A1, minimal reflex tachycardia

125
Q

Uses for Terazosin and Tamulosin

A

Long acting A1a used for prostatic smooth muscle relaxation (BPH)

126
Q 
Beta-antagonist effects at- 
Heart
Airway
Blood vessels
Juxtaglomerular cells
Pancreas
A 
Improved O2 supply/demand
Can provoke bronchospasm
Vasoconstriction in skeletal muscles, increase PVD
Decrease renin release--> decrease BP
Decrease insulin release
127
Q

Chronic B-antagonist administration can cause what? What do we need to be careful about regarding this?

A

Up-regulation of B-receptors, need to be careful about suddenly stopping B-antagonists (like, don’t)

128
Q

Can beta blockade be overcome with agonist?

A

Yes, large doses will compete with antagonists for binding sites

129
Q

B-antagonists are derivatives of what drug class?

A

Sympathomimetics (specifically isoproterenol). They can maintain some of these effects.

Substitution occurs on the benzene ring.

130
Q

B-antagonists, non-selective

A

Propranolol, nadalol, timolol, pindolol

131
Q

Cardioselective (B1) antagonists

A

Metoprolol, atenolol, acebutolol, betaxolol, esmolol

Large doses lead to selectivity loss

132
Q

Propranolol basics

A

Pure antagonist
B1=B2
Dose increased until HR of 55-60 is achieved

133
Q

Propranolol CV effects

A

Decreased HR, contractility, CO particularly during exercise/SNS outflow

B2 blockade increases PVR, increased coronary vascular resistance

Overall, CV work/O2 requirement is lowered

Na retention related to drop in CO effects at the kidneys

134
Q 
Propranolol pharmacokinetics 
Dose
Protein binding
Metabolism E1/2 time
Interactions
A

Large first-pass effect (90-95%), oral dose much larger than IV. 0.05mg/kg IV or 1-10mg. Max 1mg/min.

Highly protein bound (90-95%)

Metabolized in the liver, E1/2 time 2-3hrs

Reduces clearance of amide LAs due to drop in hepatic blood flow

Decreases the pulmonary first pass effect on fentanyl

135
Q

Timolol uses, effects

A

Nonselective, used in glaucoma.

Reduces production of aqueous humor–> decrease IOP

Decrease in BP, HR, increase in airway resistance

136
Q

Nadolol highlights

A

Nonselective

No significant metabolism (renal/bile excretion)

E1\2 time of 20-40hrs, taken 1x daily

137
Q

Metoprolol dosing

A

60% first pass

PO 50-400mg

IV 1-15 mg

138
Q

Metoprolol basics

A

B1 selective

Decrease inotropy and chronotropy

Nonselective at higher doses

139
Q

E1/2 time of metoprolol

A

3-4hrs

140
Q

Which beta blocker is MOST selective at B1?

A

Atenolol. Also has the lowest CNS effects.

141
Q

E1/2 time of atenolol

A

6-7hrs

142
Q

How is atenolol eliminated?

A

Renally

143
Q

Atenolol is great for

A

Cardiac pts with CAD

144
Q

When is betaxolol usful?

A

Medication regimen complexity reduction (taken once a day) E1/2 time of 11-2hrs

Also used in glaucoma when pt is susceptible to bronchospasm (more selective than timolol)

145
Q

Esmolol dosing

A

0.5mg/kg IV (10-180mg IV) DOA= less than 15 minutes

Infusion can be started at 50-300mcg/kg/min

146
Q

Esmolol CV effects

A

Decrease in HR without significant BP effects at small doses

Does not cause negative inotropy at clinical doses

147
Q

E1/2 time of esmolol. How is it metabolized?

A

9 minutes. Broken down by plasma esterases.

148
Q

In pts known to have difficulty breaking down sux, what type of precautions are needed when giving esmolol?

A

None, different set of plasma esterases for each drug. Esmolol away.

149
Q

B-blocker side effects

A

Decreased HR, contractility, BP

PVD exacerbation

Increased airway resistance

Altered fat/carb metabolism. Masks HR increase in hypoglycemia

Increased serum K

Decreased BP with inhaled anesthetics

Fatigue, lethargy, n/v, diarrhea

150
Q

Relative B-blocker contraindications

A

AV block, heart failure (short term)

Reactive airway

DM (needs vigilant BS monitoring)

Hypovolemia

151
Q

Indications for B-blockers

A

HTN

Angina

Post-MI mortality reduction

Peri-op for pts at high MI risk

Tachyarrythmias

Excessive SNS disorders, NAP student

152
Q

Labetalol basics

A

Combined A/B blocker- selective at A1, B1, B2

7:1 Beta to Alpha blockade

153
Q

Labetalol dosing, effects, E1/2 time

A

0.1-0.5mg/kg IV (5mg at a time IV for mild hypertension)

Decreased BP, SVR, HR. CO about the same.

E1/2 time 5-8hrs, longer in liver disease

154
Q

Labetalol side effcts

A

Orthostatic hypotension, bronchospasm, heart block, CHF, bradycardia

Pharm '14 test 2 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions