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Pharm '14 test 2 > Autonomics > Flashcards

Autonomics Flashcards

1
Q

Autonomic preganglionic neurons are

A

myelinated

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2
Q

Autonomic postganglionic neurons are

A

unmyelinated

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3
Q

Sympathetic preganglionic cell bodies are located where?

A

Intermediolateral horn of T1-L2/3

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4
Q

Sympathetic postganglionic cell bodies are located where?

A

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

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5
Q

Parasympathetic preganglionic innervation can be described as…

A

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

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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)

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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)

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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.

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9
Q

Does the heart exhibit baseline SNS or PSNS baseline tone?

A

PSNS

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10
Q

Do blood vessels exhibit baseline SNS or PSNS baseline tone?

A

SNS

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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.

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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.

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13
Q

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

A

NE

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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.

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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.

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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.

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17
Q

Cholinergic receptor subtypes in the body-

A

Nicotinic- Nm and Nn

Muscarinic- M1-5

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18
Q

Adrenergic receptor subtypes in the body-

A

Alpha 1, 2
Beta 1,2,3

Grossly simplified, of course!

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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.

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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

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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

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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

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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

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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.

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25
Explain the signaling, messengers, and physiologic response of Beta activation.
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)
26
Alpha 1 agonist effects at- ``` Vascular smooth muscle Iris Pilomotor smooth muscle Prostate/Uterus Heart ```
``` Contraction, vasoconstriction Contraction, dilation or mydriasis Erects hair Contraction Increase contractility (B1 more important) ```
27
Alpha 2 agonist effects at- ``` Platelets Presynaptic adrenergic & cholinergic terminals Vascular smooth muscle GI tract CNS ```
Aggregation Inhibits transmitter release (decrease BP and HR) Contraction (post-synaptic) OR dilation (pre-synaptic, CNS) Relaxation (presynaptic) Sedation/analgesia via decrease SNS outflow
28
Beta 1 agonist effects at- Heart Kidneys
Increase force and rate of contraction | Stimulate renin release
29
Beta 2 agonist effects at- Visceral smooth muscle Mast cells Skeletal muscle Liver Pancreas Adrenergic Nerve Terminals
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
30
Beta 3 agonist effects on fat cells
Activate lipolysis, thermogenesis
31
D1 agonist effects on smooth muscle
Post-synaptic location, dilates renal, mesenteric, coronary, and cerebral vascular beds
32
D2 agonist effects on nerve endings
Pre-synaptic location, modulates transmitter release, nausea/vomiting
33
Name the endogenous catecholamines
Epi, Norepi, Dopa
34
Name some synthetic catecholamines
Isoproterenol, Dobutamine
35
Name some synthetic non-catecholamines
Indirect- ephedrine, mephentermine, amphetamine Direct- phenylephrine, methoxamine
36
Name two selective A2 agonists
Clonidine, dexmedetomidine
37
Name some selective B2 agonists
Albuterol, terbutaline, ritodrine
38
All sympathomimetics are derivatives of what?
Beta-phenylethylamine
39
Where are the hydroxyl groups located on a catecholamine?
Positions 3,4 on the benzene ring
40
What is the rate limiting enzyme in catecholamine synthesis in the body?
Tyrosine hydroxylase (Tyrosine --> Dopa)
41
End physiological effects from sympathomimetics usually involve a change in what?
Intracellular calcium, either increased or decreased
42
What terminates the effects of catecholamines?
Reuptake (I- neuronal, II-extraneuronal) MAO A/B COMT Lungs
43
What terminates the effects of non-catecholamines?
MAO | Urinary excretion
44
Is phenylephrine more selective for A1 or A2?
A1
45
Is clonidine more selective for A1 or A2?
A2
46
Describe norepinephrines receptor selectivity
A1=A2, B1 much more than B2 (almost NO activity at B2, no effect at clinical doses)
47
Describe epinephrines receptor selectivity
A1=A2, B1=B2
48
Is dobutamine more selective for B1 or B2?
B1
49
Is isoproterenol more selective for B1 or B2?
Equal activity at both
50
Describe dopamines receptor selectivity
D1=D2>>B>>A
51
Describe fenoldopam in terms of receptor selectivity
D1>>D2
52
Most potent Alpha activator
Epi
53
Routes for Epi
SQ or IV
54
Does Epi have CNS effects?
No, poor lipid solubility
55
Epi onset
SQ- 5-10min | IV-1-2 min
56
Duration of Epi
5-10 min
57
Indications for Epi
Bolus- Bronchial asthma, acute allergic reaction, arrest/asystole, PEA, V.fib Infusion- Increase contractility
58
Epi dosing
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)
59
CV effects of Epi
A1- vasoconstriction- increased BP, CVP, cardiac work A2- negative feedback- decrease BP B1- increased HR, CO, contractility, BP B2- peripheral vasodilation- decrease BP
60
Effect of epi at moderate doses on SBP, DBP, and MAP
``` SBP increases (B1, A1) DBP decrease (B2) MAP tends to be the same, can increase or decrease ```
61
What effect does epi have on skeletal muscle vascular beds?
Vasodilation
62
Epi effects on cerebral vasculature
Minimal vasoconstriction--> increased cerebral blood flow even with normal BP
63
Epi effects on the eye
A1- mydriasis (big wide eyes to see that bear) A1, A2- increase humoral outflow B1- increased aqueous humor production
64
Epi effects on Resp
B2- Dilate smooth muscle, decrease histamine release A1- Reduced mucous secretion
65
Epi effects on GI
A2- Decreased secretions A1, A2, B2- Smooth muscle relaxation A1- Drastically reduced splanchnic blood flow even with normal BP
66
Epi effects on Renal/GU
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
Epi metabolic effects
B2- Liver glycogenolysis B3- lipolysis A2- Inhibition of insulin release
68
Do IDDM patients need more or less insule peri-op?
More!
69
NE dosing
4-16 mcg/min for hypotension
70
Describe NE effects on B2
Minimal, would require "stupid" doses.
71
Why does NE drop HR in an otherwise healthy person?
Vasoconstriction --> increased BP --> baroreceptors activate --> HR decreases
72
What type of drug do you want to use for an infiltrate of NE or Epi?
Alpha blocker given SubQ around the infiltrate (something like phentolamine)
73
Dopamine is a precursor to what in the body?
NE
74
What receptors does dopamine stimulate?
All adrenergic including the dopamine receptors
75
Dopamine dosing
1-3mcg/kg/min- D1 receptors 3-10mcg/kg/min- B1 effects >10mcg/kg/min- Alpha effects (pressor)
76
Dopamine increases/decreases contractility, renal blood flow, urine output, and GFR.
Increases
77
Does dopamine have any indirect effects?
Yes, releases endogenous NE. May be less effective if body stores are depleted
78
Dopamine effects on IO pressure
Increased
79
What nice synergistic effect do dopamine and dobutamine have?
Reduced after load and increased CO
80
Dopamine inhibits what that may alter pt response to hypoxia?
Carotid bodies
81
Isoproterenol is selective for which adrenergic receptors?
B1 and B2
82
Cardio effects of iso
``` Increased HR and contractility Decreased SVR (SPB up, DBP down, MAP down) ```
83
Iso dosing for heart blocks and bradicardia
1-5mcg/min
84
Iso is rapidly metabolised by what enzyme?
COMT
85
You might want to think twice about giving iso to a pt with what disease? Why?
Parkinsons entacapone, tolcapone, and nitecapone are COMT inhibitors used in Parkinsons
86
Dobutamine dosing
2-10mcg/kg/min
87
Dobutamine is selective for which receptors at <5mcg/kg/min
B1
88
Dobutamine is selective for which receptors at >5mcg/kg/min
A1, though somewhat weakly due to stereo antagonism
89
Dobutamine improves CO without doing what?
Without increasing HR or BP, nice for CHF
90
What effect does dobutamine have on the coronary arteries?
Dilation
91
Ephedrine dosing
10-25mg IV, 10-50mg IM
92
Ephedrine acts through what type of mechanism at alpha and beta receptors?
Mostly indirect, also minor direct effects
93
Compared to epi, how long does ephedrine last?
10 times longer
94
Ephedrine. Tachyphylaxis.
Of course.
95
How do we get rid of ephedrine?
40% unchanged in urine. MAO and liver get the rest. E1/2 life of 3 hours.
96
Neo hits what receptors?
Mostly A1, direct acting
97
Does neo work more on the venous or arterial side?
Venous
98
Is neo longer or shorter lasting than NE?
Longer
99
Neo dosing
50-200 mcg IV or infusion of 20-50 mcg/min
100
Will Neo tend to increase or decrease HR?
Decrease. Venous constriction --> increase return --> yada yada --> baroreceptors
101
Should we call neo, neo?
No, sounds like neostigmine
102
Albuterol is selective for
B2
103
Albuterol dosing
MDI- 100mcg per puff, 2 puffs q4-6hrs, max 16-20 puffs Neb for severe asthma 15mg/hr for 2 hours
104
Large doses of albuterol can give you
Tachycardia and hypokalemia
105
Terbualine, Salmeterol, and Ritordine are B2 agonists used for what?
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
Some direct-acting, non-catecholamine, sympathomimetics working at A1
Midodrine- postural hypotension Oxymetazoline, xylometazoline- nasal/ocular decongestants
107
A2 selective agonists your pt might be taking
Clonidine- partial agonist | Methyldopa
108
Drugs your patient might be taking: Indirect-acting Sympathomimetics
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
Drugs Your Patient Might Be Taking: Inhibitors of Catecholamine Storage and Reuptake
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
A-antagonists, A1 selective
Prazosin, terazosin, doxazosin- super A1 selective
111
A-antagonists, non-selective
Phentolamine
112
A-antagonists, A2 selective
Yohimbine, tolazoline - modestly A2 selective
113
Mixed A,B antagonists
Labetalol, carvedilol B1=B2>A1>A2
114
B-antagonists, B1 selective
Metoprolol, atenolol, esmolol
115
B-antagonists, non-selective
Propranolol, nadolol, timolol
116
B-antagonists- B2 selective
Butoxamine
117
A1-antagonist effects on BP
Decreased PVR--> lower BP Postural hypotension common side effect. Venoconstriction responsible for compensation when standing.
118
A2-antagonist effects
Increased NE release from nerve terminals, removes normal negative feedback mechanism
119
A-antagonist effects at GU, eyes, nose
GU muscle relaxation, eases micturition Causes miosis Increased nasal congestion
120
Most A-antagonists bind competitively. Name one that binds covalently. In what case might we want to use such a drug?
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
Phentolamine dosing
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
Phentolamine CV effects
Decrease BP, increase HR and CO.
123
Phenoxybenzamine effects, onset, E1/2 time
A1>A2 Decrease SVR, vasodilation 1 hour onset time, pro-drug needs to be metabolized. E1/2 time of 24 hours.
124
Uses for Prazosin
Control BP in pheochromocytoma Mostly A1, minimal reflex tachycardia
125
Uses for Terazosin and Tamulosin
Long acting A1a used for prostatic smooth muscle relaxation (BPH)
126
``` Beta-antagonist effects at- Heart Airway Blood vessels Juxtaglomerular cells Pancreas ```
``` Improved O2 supply/demand Can provoke bronchospasm Vasoconstriction in skeletal muscles, increase PVD Decrease renin release--> decrease BP Decrease insulin release ```
127
Chronic B-antagonist administration can cause what? What do we need to be careful about regarding this?
Up-regulation of B-receptors, need to be careful about suddenly stopping B-antagonists (like, don't)
128
Can beta blockade be overcome with agonist?
Yes, large doses will compete with antagonists for binding sites
129
B-antagonists are derivatives of what drug class?
Sympathomimetics (specifically isoproterenol). They can maintain some of these effects. Substitution occurs on the benzene ring.
130
B-antagonists, non-selective
Propranolol, nadalol, timolol, pindolol
131
Cardioselective (B1) antagonists
Metoprolol, atenolol, acebutolol, betaxolol, esmolol Large doses lead to selectivity loss
132
Propranolol basics
Pure antagonist B1=B2 Dose increased until HR of 55-60 is achieved
133
Propranolol CV effects
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
``` Propranolol pharmacokinetics Dose Protein binding Metabolism E1/2 time Interactions ```
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
Timolol uses, effects
Nonselective, used in glaucoma. Reduces production of aqueous humor--> decrease IOP Decrease in BP, HR, increase in airway resistance
136
Nadolol highlights
Nonselective No significant metabolism (renal/bile excretion) E1\2 time of 20-40hrs, taken 1x daily
137
Metoprolol dosing
60% first pass PO 50-400mg IV 1-15 mg
138
Metoprolol basics
B1 selective Decrease inotropy and chronotropy Nonselective at higher doses
139
E1/2 time of metoprolol
3-4hrs
140
Which beta blocker is MOST selective at B1?
Atenolol. Also has the lowest CNS effects.
141
E1/2 time of atenolol
6-7hrs
142
How is atenolol eliminated?
Renally
143
Atenolol is great for
Cardiac pts with CAD
144
When is betaxolol usful?
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
Esmolol dosing
0.5mg/kg IV (10-180mg IV) DOA= less than 15 minutes Infusion can be started at 50-300mcg/kg/min
146
Esmolol CV effects
Decrease in HR without significant BP effects at small doses Does not cause negative inotropy at clinical doses
147
E1/2 time of esmolol. How is it metabolized?
9 minutes. Broken down by plasma esterases.
148
In pts known to have difficulty breaking down sux, what type of precautions are needed when giving esmolol?
None, different set of plasma esterases for each drug. Esmolol away.
149
B-blocker side effects
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
Relative B-blocker contraindications
AV block, heart failure (short term) Reactive airway DM (needs vigilant BS monitoring) Hypovolemia
151
Indications for B-blockers
HTN Angina Post-MI mortality reduction Peri-op for pts at high MI risk Tachyarrythmias Excessive SNS disorders, NAP student
152
Labetalol basics
Combined A/B blocker- selective at A1, B1, B2 7:1 Beta to Alpha blockade
153
Labetalol dosing, effects, E1/2 time
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
Labetalol side effcts
Orthostatic hypotension, bronchospasm, heart block, CHF, bradycardia

Pharm '14 test 2 (5 decks)

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