What are the synthetic NON-catecholamines: 1. indirect acting 2. direct acting

1. ephedrine, amphetamines, mephentermine 2. phenylephrine, methoxamine

ANS Flashcards by Arlene D

Describe pre/post ganglia for SNS.

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

How well did you know this?

Not at all

Perfectly

Describe pre/post ganglia for PSNS.

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)

How well did you know this?

Not at all

Perfectly

What is most important function of SNS

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

How well did you know this?

Not at all

Perfectly

Describe a SNS innervated receptor for blood vessel

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

How well did you know this?

Not at all

Perfectly

Describe a SNS innervated receptor for sweat glands

-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)

How well did you know this?

Not at all

Perfectly

Describe a SNS innervated receptor for adrenal medulla

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

How well did you know this?

Not at all

Perfectly

Describe a PSNS innervated receptor for

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

How well did you know this?

Not at all

Perfectly

Most organs have both PSNS and SNS innerv except for?

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)

How well did you know this?

Not at all

Perfectly

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

-drug or hormone = something circulating in the blood

How well did you know this?

Not at all

Perfectly

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

SNS - baseline motor tone via blood vessels

- PSNS - heart rate via Vagus n.

How well did you know this?

Not at all

Perfectly

What are the two main types of cholinergic receptors?

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

2 muscarinic Ach (G protein) = M1-M5

How well did you know this?

Not at all

Perfectly

What are the types of adrenergic receptors?

alpha 1, 2

beta 1,2,3

How well did you know this?

Not at all

Perfectly

What are the endogenous catecholamines?

epi/NE/DOPA

How well did you know this?

Not at all

Perfectly

What are the synthetic/exogenous catecholamines?

dobutamine/isoproteronol

How well did you know this?

Not at all

Perfectly

What are the synthetic NON-catecholamines:

indirect acting
direct acting

ephedrine, amphetamines, mephentermine

2. phenylephrine, methoxamine

How well did you know this?

Not at all

Perfectly

What are the selective alpha-2 agonists?

clonidine, dexmedetomidine (precedex)

sedation/analgesia/

How well did you know this?

Not at all

Perfectly

What are the selective beta-2 agonists?

albuterol, terbutaline, ritodrine

How well did you know this?

Not at all

Perfectly

How do indirect agonists work?

they increase the release of NTs

direct agonists have dif affinities for diff receptors

When do we use sympathomimetics in anesthesia?

inc BP/contractility (anesthetics cause myocardial depression/vasodilation)
bronchodilation (bronchospasm from a/w instrumentation)
anaphylaxis
ACLS
additive to LA’s (epi)
sedation/analgesia (alpha 2)

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

*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

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

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

How do true catecholamines differ from noncatecholamines?

they have diff metabolisms

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

What is the MOA for sympathomimetics?

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

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

type of receptor
receptor density in a tissue
second messenger activation (i.e. PLC or cAMP)

What happens if a patient abruptly stops sympathomimetic therapy?

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

How are catecholamines metabolized?

- reuptake - MAO = metabolize mostly epi - COMT = metabolize all - lungs

How are non-catecholamines metabolized?

- 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

Epinephrine (prototype) 1. receptor affinity 2. lipid solubility 3. onset 4. DOA

* it is the most potent alpha activator* 1. all adrenoreceptors 2. poor lipid solubility 3. SQ = 5-10 min, IV = 1-2 min

Epinephrine - standard bolus dose for resuscitation

10 mcg/kg IV | but can start at 2-8 mcg/kg

Epinephrine - infusion rate based on beta and alpha effects

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

Why might beta blockers affect BP?

-blocking beta1 = dec renin release and dec BP

What effect does epi have on renal vessels?

- a1 = drastic dec in renal blood flow even if BP normal | - b1 = inc renin release

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

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

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

- it is a precursor to NE and inc NE release | - so if no stores = no effect

What pts is DOPA + dobutamine good?

heart failure pts bc it reduces afterload, improves CO | good vasodilation

Why do we not use isoproterenol in asthmatics?

- it has both beta1 and beta2 agonism | - bronchodilation but also affect heart

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

- NO beta blocker, it will dec contraction/HR and kill pt | - give alpha antagonist

What is the dose for epinephrine for resuscitation bolus?

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

What is the infusion rate for epi?

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

What is the infusion rate for NE?

mixed alpha/beta agonist; more alpha/b1 | 4-16 mcg/min

What is the infusion rate for DOPA?

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

What is the infusion rate for isoproterenol?

beta agonist; b1=b2 | 1-5 mcg/min for heart block/bradydysrhythmias

What is the dose for ephedrine?

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

What is the dose for phenylephrine?

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