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Pharm Spring 2014 > ANS > Flashcards

ANS Flashcards

1
Q

Where is the ANS located?

A

Both the CNS and PNS

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2
Q

Preganglionic neurons of the ANS are (myelinated/unmyelinated)

A

Myelinated

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3
Q

Postganglionic neurons of the ANS are (myelinated/unmyelinated)

A

Unmyelinated

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4
Q

The craniosacral outflow of the PSNS arises from

A

Cranial (Medullary CNS 3, 7, 9, 10)

Sacral (Sinal cord S2-4)

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5
Q

Most important function of the SNS

A

Maintenance of vasomotor tone

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6
Q

Most organs are innervated by both SNS and PSNS, except:

A

Only innervated by the SNS

  • Sweat glands
  • BVs (although muscarinic receptors are here)

Only innervated by the PSNS

  • Ciliary muscles of the eye
  • Bronchial smooth muscle (although B2 receptors here)
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7
Q

Baseline tone of HR and BVs are dominated by

A

HR- Vagal

BVs- SNS

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8
Q

Type of ACh receptor at the NMJ

A

Nicotinic

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9
Q

Type of receptor on sweat glands for SNS innervation

A

Muscarinic (Ach)

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10
Q

Type of receptor at all pre/postsynaptic junctions of the PSNS

A

ACh (nicotinic)

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11
Q

These two medications are anti-muscarinics

A

Atropine and glycopyrrolate

People who receive these will stop sweating and salivating

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12
Q

Types of nAChRs and mAChRs

A

nAChRs: Nn and Nm
mAChRs: M1-5

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13
Q

Types of Adrenergic Receptors

A

Alpha (1&2)

Beta (1, 2, & 3)

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14
Q

Amount of epi and norepi released from the adrenal medulla

A

Epi (80%)

Norepi (20%)

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15
Q

Effect of circulating ACh on BVs

A

Circulating ACh will bind to the muscarinic receptors on BVs, activating NO, resulting in eventual vasodilation

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16
Q

Muscarinics and adrenergics are examples of this type of receptor

A

G-protein coupled receptors

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17
Q

Alpha 1 receptor type and action

A

Alpha 1 is a G-a-q receptor. Stimulated phospholipase C, which increases IP3 and DAG, which raises intracellular calcium. This increase in calcium causes smooth muscle contraction (vasoconstriction).

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18
Q

Alpha 2 receptor type and action

A

Alpha 2 is a G-a-i receptor. This inhibits adenylyl cyclase, reducing cAMP in the cell, causing vasoconstriction and an increase in K+ conductance.

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19
Q

Effect of cAMP in smooth muscle and cardiac cells

A

Smooth muscle- relaxation

Cardiac muscle- increase in force of contraction and rate

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20
Q

Beta 1, 2, & 3 receptor type and action

A

G-a-s. Stimulates adenylyl cyclae, increasing intracellular cAMP. This relaxes smooth muscle and increases cardiac contractility and rate.

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21
Q

Alpha 1 Effects

A

1) Most vascular smooth muscle (BVs, sphincters, & bronchi)- contraction
2) Iris- contraction of radial muscle resulting in pupil dilation
3) Pilomotor smooth muscle- contraction/hair erection
4) Prostate and Uterus- Contraction
5) Heart- Increases the force of contraction (but not as much as B1. Remember this is through Ca, not cAMP)

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22
Q

Alpha 2 Effects

A

1) Platelets- aggregation
2) Presynaptic adrenergic and cholinergic nerve nerminals- inhibits NT release (decrease in BP and HR)
3) Vascular smooth muscle (can cause vasoconstriction due to effect on BV, but more often causes VASODILATION due to the effect of rapidly inhibiting NE release from the presynaptic terminal)
4) GI tract- relaxation (pre-synaptic effect)
5) CNS- sedation and analgesia due to the decrease in SNS outflow

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23
Q

You should think of alpha 2 as being in these three locations

A

1) Brain (works by decreasing SNS outflow, causing sedation and a decrease in BP and HR)
2) BVs (causing vasoconstriction)
3) Pre-synaptic to BV (nerve fiber terminating on BVs)

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24
Q

Negative feedback signal with alpha 2

A

Norepi released from the postsynaptic neuron onto the BV cycles back to that pre-synaptic membrane of the post-synaptic neuron, binds to an alpha 2 receptor, which decreases cAMP and opens K+ channels which hyperpolarize the cell. This reduces the release of norepi. This prevents the system from getting too amped up.

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25
Q

Two examples of Alpha 2 agonists

A

Clonidine and precedex

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26
Q

What is a bad SE of alpha blockers?

A

You lose the negative feedback with NE and the alpha 2 receptor. Thus, NE would keep being released and keep affecting the Beta receptors which would increase HR and BP. Would be better to give a alpha 1 selective blocker.

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27
Q

Why is alpha 2 so important?

A

For negative feedback with NE

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28
Q

Beta 1 Effects

A

1) Heart- increase in force and rate of contraction (high risk of MI)
2) Kidneys- Renin release (this is one way how Beta1 affects BP control)

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29
Q

Beta 2 Effects

A

1) Visceral smooth muscle (GI/GU, resp, uterine, and vascular)- smooth muscle relaxation
2) Mast cells- decrease histamine release
3) Skeletal muscle- dilation of vascular beds, increased speed of contraction, tremor, potassium uptake
4) Liver- glycogenolysis
5) Pancreas- increased insulin secretion
6) Adrenergic nerve terminals- increase in release of NE

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30
Q

This drug (catecholamine) does not work at Beta2

A

Norepinephrine***
This is also why we try to avoid levophed in our patients. It is more potent than epinephrine because it doesn’t have Beta2 effects, but also the lack of balance with Beta2 can result in the loss of fingers and toes.

Beta 2 IS however affected by epinephrine

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31
Q

Beta 3 Effects

A

1) Fat cells- lipolysis and thermogenesis

32
Q

D1 Effects

A

Mostly in smooth muscle.
Located POST-synaptically
DILATES THINGS. Dilates renal, mesenteric, coronary, and cerebral blood vessels.

33
Q

D2 Effects

A

Mostly in nerve endings
PRE-synaptic (provides feedback)
Modulates NT release
Causes nausea and vomiting

34
Q

These are endogenous catecholamines

A

Epi, norepi, and dopamine

35
Q

These are synthetic catecholamines

A

Isoproterenol and dobutamine

36
Q

These are synthetic non-catecholamines

A

Direct Acting
- Phenylephrine and methoxamine

Indirect Acting (increases the release of norepi)
     - Ephedrine, mephentermine, amphetamines
37
Q

Selective Beta 2 agonists

A

ART
Albuterol, ritodrine, and terbutaline
These are mostly used for asthma, but can also be used to treat pre-term labor

38
Q

Is ephedrine direct or indirect?

A

Mostly indirect, but can have some direct effects as well

39
Q

How do indirect agonist work?

A

By increasing the release of NTs (NE)

40
Q

Inhalational agents cause (vasodilation/vasoconstriction)

A

Vasodilation

This wil cause veins to pop out, often making it easier to establish IV access

41
Q

All sympathomimetics are derivatives of

A

Beta-phenylethylamine

42
Q

All catecholamines are derivatives of ______ and have _______ groups on _______

A

Beta-phenylethylamine
Hydroxyl
R3 and R4 of the benzene ring
Remember that catecholamines are the most potent at adrenergic receptors. The OH at R3 and R4 are responsible for this. Non-catecholamines do not have these hydroxyl groups.

43
Q

This enzyme only metabolizes catecholamines

A

COMT

44
Q

How similar are the structures of catecholamines to one another?

A

Very similar. They often only differ by a single side-chain, but produce very different effects.

45
Q

Difference between direct and indirect adrenergic agonists

A

Direct binds to the receptor and activates the receptor itself
Indirect increases endogenous NE release from the post-ganglionic SNS nerve terminals, which then activate the receptor

46
Q

Sympathomimetics work on these types of receptors

A

GPCRs

47
Q

The effect of a sympathomimetic depends on

A

The receptor it stimulates, the receptor density, what second messengers are activated.

48
Q

Where is MAO located?

A

In the mitochondria of cells

49
Q

Effect of the lungs on drug metabolism

A

The lungs can metabolize drugs and also serve as a reservoir for drugs

50
Q

Non-catecholamines rely on this enzyme for metabolism

A

MAO.
Remember that COMT only works on catecholamines, so NON-catecholamines only have MAO for metabolism. This is why giving ephedrine can be disastrous to someone on an MAOI.

51
Q

Methods of termination of effect/metabolism of catecholamines

A

1) Re-uptake (main mode of termination of effect)
2) MAO
3) COMT
4) Lungs

52
Q

Methods of termination of effect/metabolism of NON-catecholamines

A

1) MAO

2) Excreted unchanged through the kidneys

53
Q

Methods of the reuptake of catecholamines

A

Uptake I- Neuronal (main means for endogenous NE)
Uptake II- Extraneuronal uptake (neighboring cells and tissues take up NE or other drugs. This is not as rapid as Uptake I)

54
Q

Beta 2 receptors are located in many tissues, but are not directly innervated because

A

NE is the main NT of the adrenergic system, so so innervating B2 receptors would have no effect

55
Q

Ocular effects of SNS

A

A1- mydriasis
A1 & A2- increase in humoral outflow
B1- increase in production of aqueous humor
(many people with glaucoma may be on a B1 blocker)

56
Q

Prototype of endogenous catecholamines

A

Epinephrine

57
Q

Effect of epinephrine on cerebral circulation

A

With epinephrine, unimportant vascular beds are constricted, shunting blood flow to the important organs. With epinephrine, cerebral perfusion is usually increased.

Only at EXTREMELY high doses will cerebral blood flow be restricted. Think about fight or flight! We need brain function. Epinephrine preferentially vasoconstricts vessels that are less important (skin, mucosal, mesenteric, renal).

58
Q

Three vascular beds usually spared from the vasoconstrictive effects of epinephrine

A

Cerebral, Pulmonary, and Coronary

The three most important sites we need when running from a bear!

59
Q

Pulmonary effects of epinephrine

A

B2- Bronchial smooth muscle dilation. Decreased histamine release in bronchial vasculature.
A1- Decongestion (vasoconstriction of mucosal beds)

60
Q

GI effects of epinephrine

A

Think about what you would want to happen in fight or flight!

Decreased digestive secretions (hyperpolarizing effect of A2
Direct smooth muscle relaxation (A2 and B2)
Decreased splanchnic blood flow (A1)- splanchnic blood flow is DRASTICALLY reduced, even if BP is normal

61
Q

GU effects of epinephrine

A

1) Renal vasculature (very important!!!!!!)
- A1 causes reduction
- B1 increases renin release, which turns into angiotensin II, which constricts renal casculature even more!
2) Bladder
- A1 causes constriction of urethral sphincter- urinary incontinence
- B2 relaxation- decreases urinary output
3) Erectile tissue
- A1- facilitates ejaculation (phosphodiesterase inhibitors target this)
4) Uterus
- B2 relaxation- inhibits labor

62
Q

Metabolic effects of epinephrine

A

Glycogenolysis and insulin release (B2)
Lipolysis (B3)
Inhibition of insulin release (A2)
Overall, there is an increase in insulin production.

63
Q

Why is norepi so powerful for hypotension?

A

Because it doesn’t have B2 effects. SBP, DBP, and MAP will all go up!

64
Q

Effect of epinephrine on BP

A

SBP goes up (A1 and B!)
DBP goes down (B2)
MAP stays about the same (or may decrease slightly)

65
Q

Do we typically give NE in anesthesia?

A

No. Usually only in septic shock, or we can’t increase pressure with fluids fast enough and we’re getting desperate.

66
Q

Effect of dopamine on catecholamine levels

A

Causes levels to be all over the place. Because of this, it’s really difficult to determine what rate will cause what effect. We have set standards, but only because we don’t have anything better.

67
Q

Vascular beds dilated by dobutamine

A

Skin and skeletal muscle

68
Q

How is isoproterenol metabolized?

A

COMT

69
Q

Why does it take longer to metabolize beta-2 agonists?

A

Their hydroxl groups are in different locations, meaning that it cannot be metabolized by COMT

70
Q

When are beta-2 agonists useful?

A

1) Bronchiole smooth muscle relaxation (for asthma and COPD)

2) Relaxation of uterine smooth muscle (for preterm labor)

71
Q

Side-effects of B2 agonists

A

Muscle tremor (B2 effect on skeletal muscle) and reflex tachycardia (from B2 vasodilation)

72
Q

Most common route for B2 agonists

A

Inhalation

73
Q

When would we give B2 agonists IV?

A

If the person is so bronchoconstricted that we can’t get our inhalational agent in

74
Q

This B2 agonist carries a risk for sudden death when taken with a steroid

A

Salmeterol

75
Q

When should we stop ADHD meds?

A

A week prior to surgery

76
Q

What is a sympathomimetic?

A

A drug that mimics the effects of epi, norepi, and dopamine

Pharm Spring 2014 (13 decks)

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