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*Pharm > ANS > Flashcards

ANS Flashcards

1
Q

Describe pre/post ganglia for SNS.

A
  • short pre/long post
  • pre cell bodies in thorocolumbar division (T1-L2/L3) in intermediolateral horn of grey matter
  • post cell bodies in paravertebral and prevertebral (celiac/sup/inf mesenteric ganglia) columns
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2
Q

Describe pre/post ganglia for PSNS.

A
  • long pre/short post
  • pre cell bodies in cranio-sacral = CN 3/7/9/10 and s2-s4
  • post cell bodies in target organs or discrete ganglia in head/necl (ciliary)
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3
Q

What is most important function of SNS

A
  • vasomotor tone; regulates BP w/ changes in position, exercise, etc
  • does multiple functions vs PSNS which is discrete, one at a time/selective
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4
Q

Describe a SNS innervated receptor for blood vessel

A

-preganglia causes release of ACH onto NICOTINIC receptor then postganglia causes release of NE into blood stream

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5
Q

Describe a SNS innervated receptor for sweat glands

A

-preganglia causes release of ACH onto NICOTINIC receptor then postganglia causes release of ACH onto a MUSCARINIC receptor
(same as PSNS but sweat glands are only innerv by SNS)

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6
Q

Describe a SNS innervated receptor for adrenal medulla

A

-preganglia causes release of ACH onto NICOTINIC receptor directly on medulla which then acts as ganglia and releases NE (20%) and Epi (80%)

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7
Q

Describe a PSNS innervated receptor for

A

-action potential causes release of ACH onto NICOTINIC receptor which then causes release of ACH onto a MUSCARINIC receptor

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8
Q

Most organs have both PSNS and SNS innerv except for?

A
  • sweat glands = only SNS (but muscarinic receptors present)
  • blood vessels = only SNS
  • ciliary eye muscles = only PSNS
  • bronchial smooth muscle = only PSNS (but B2 receptors present)
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9
Q

If a receptor is present in a tissue but not innervated (nerve releases NT onto it), how is it activated?

A

-drug or hormone = something circulating in the blood

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10
Q

Describe how both SNS and PSNS have baseline tone at rest.

A
  • SNS - baseline motor tone via blood vessels

- PSNS - heart rate via Vagus n.

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11
Q

What are the two main types of cholinergic receptors?

A
  1. nicotinic Ach (ligand gated) = nn (nerve), nm (skeletal)

2 muscarinic Ach (G protein) = M1-M5

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12
Q

What are the types of adrenergic receptors?

A

alpha 1, 2

beta 1,2,3

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13
Q

What are the endogenous catecholamines?

A

epi/NE/DOPA

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14
Q

What are the synthetic/exogenous catecholamines?

A

dobutamine/isoproteronol

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15
Q

What are the synthetic NON-catecholamines:

  1. indirect acting
  2. direct acting
A
  1. ephedrine, amphetamines, mephentermine

2. phenylephrine, methoxamine

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16
Q

What are the selective alpha-2 agonists?

A

clonidine, dexmedetomidine (precedex)

sedation/analgesia/

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17
Q

What are the selective beta-2 agonists?

A

albuterol, terbutaline, ritodrine

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18
Q

How do indirect agonists work?

A

they increase the release of NTs

direct agonists have dif affinities for diff receptors

19
Q

When do we use sympathomimetics in anesthesia?

A
  1. inc BP/contractility (anesthetics cause myocardial depression/vasodilation)
  2. bronchodilation (bronchospasm from a/w instrumentation)
  3. anaphylaxis
  4. ACLS
  5. additive to LA’s (epi)
  6. sedation/analgesia (alpha 2)
20
Q

Describe how phenylephrine/direct vs ephedrine/indirect agonists affect a patient w/ low BP.

A
  • *direct agonists have dif affinities for diff receptors**
  • phenyl - give if pts HR is fast and BP low bc it causes reflex brady
  • ephedrine+ - give if HR is low and BP low
21
Q

What would happen if you give an alpha 2 agonist affecting presynaptic/postsynaptic/brain?

A
  • alpha 2 = g alpha i
  • cAMP normally causes smooth muscle relaxation
  • w/ g alpha i cAMP is inhibited;
  • you will have dilation presynaptically w/ smooth muscle contraction POST synaptically
  • presynaptically at adrenergic/cholinergic terminals you will have dec HR/BP d/t inhibited NT release
  • at the brain you will have sedation
22
Q

How do true catecholamines differ from noncatecholamines?

A
  • they have diff metabolisms

- non tend to last longer d/t lack of hydroxyl

23
Q

What is the MOA for sympathomimetics?

A
  • activation of G proteins (PLC or cAMP)
  • direct agonist = drug binds to receptor and activates g protein
  • indirect agonist = drug inc NE release from SNS post ganglionic nerves that then activate receptor
24
Q

What does the specific effect of a G protein receptor depend on?

A
  1. type of receptor
  2. receptor density in a tissue
  3. second messenger activation (i.e. PLC or cAMP)
25
Q

What happens if a patient abruptly stops sympathomimetic therapy?

A
  • receptors upregulate/downregulate in response to plasma concentration
  • w/ therapy = upregulation - if stopped may cause rebound effect
26
Q

How are catecholamines metabolized?

A
  • reuptake
  • MAO = metabolize mostly epi
  • COMT = metabolize all
  • lungs
27
Q

How are non-catecholamines metabolized?

A
  • MAO (generally found everywhere)
  • urine excretion (unchanged, liver doesn’t alter it)
  • *lack of MAO will cause an issue bc this is their main mechanism of reuptake
28
Q

Epinephrine (prototype)

  1. receptor affinity
  2. lipid solubility
  3. onset
  4. DOA
A
  • it is the most potent alpha activator*
    1. all adrenoreceptors
    2. poor lipid solubility
    3. SQ = 5-10 min, IV = 1-2 min
29
Q

Epinephrine - standard bolus dose for resuscitation

A

10 mcg/kg IV

but can start at 2-8 mcg/kg

30
Q

Epinephrine - infusion rate based on beta and alpha effects

A

1-2 mcg/min IV for Beta2 effects
4-5 mcg/min IV for Beta1 effects
10-20 mcg/min IV for alpha/beta effects

31
Q

Why might beta blockers affect BP?

A

-blocking beta1 = dec renin release and dec BP

32
Q

What effect does epi have on renal vessels?

A
  • a1 = drastic dec in renal blood flow even if BP normal

- b1 = inc renin release

33
Q

In perioperative period do you think IDDM patients need more or less insulin?

A

-less? if given epi or other beta2 agonists = inc insulin release

34
Q

Why is DOPA not as useful when catecholamine stores are depleted?

A
  • it is a precursor to NE and inc NE release

- so if no stores = no effect

35
Q

What pts is DOPA + dobutamine good?

A

heart failure pts bc it reduces afterload, improves CO

good vasodilation

36
Q

Why do we not use isoproterenol in asthmatics?

A
  • it has both beta1 and beta2 agonism

- bronchodilation but also affect heart

37
Q

if pt gets overdose of phenylephrine or epinephrine how would you treat it?

A
  • NO beta blocker, it will dec contraction/HR and kill pt

- give alpha antagonist

38
Q

What is the dose for epinephrine for resuscitation bolus?

A

10 mcg/kg IV (can start 2-8 mcg/kg)

39
Q

What is the infusion rate for epi?

A

mixed alpha/beta agonist; all equal
1-2 mcg/min for beta 2
4-5 mcg/min for beta 1
10-20 mcg/min for alpha

40
Q

What is the infusion rate for NE?

A

mixed alpha/beta agonist; more alpha/b1

4-16 mcg/min

41
Q

What is the infusion rate for DOPA?

A

dopa agonist; D1=D2>b»a
1-3 mcg/kg/min = d1 dominant
3-10 mcg/kg/min = beta dominant
>10 mcg/kg/min = alpha dominant

42
Q

What is the infusion rate for isoproterenol?

A

beta agonist; b1=b2

1-5 mcg/min for heart block/bradydysrhythmias

43
Q

What is the dose for ephedrine?

A

indirect non catecholamine
IV = 10-25 mg
IM = 10-50 mg

44
Q

What is the dose for phenylephrine?

A

direct non catecholamine
IV = 50-200 mcg
infusion = 20-50 mcg/min

*Pharm (6 decks)

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