PNS Flashcards
preganglionic NT for all systems is….
acetylcholine (ACh)
dominant NT for the parasympathetic nervous system
acetylcholine
receptors of the PNS; what is the overall term they’re referred to as?
nicotinic + muscarinic* ; cholinergic
dominant NT for the sympathetic nervous system
epinephrine + norepinephrine
receptors of the SNS; what is the overall term they’re referred to as?
alpha + beta; adrenergic
epinephrine is released by what?
adrenal medulla
SNS division S+S
dilated pupils (MYDRIASIS), increased HR + BP, bronchodilation (increased RR), decreased salivation, decreased peristalsis + digestion, decreased voiding (relaxation of detrusor muscle), increased blood glucose, inhibit sex organs
PNS division S+S
constricted pupils (MYOSIS), decreased HR + BP, bronchoconstriction (decreased RR), increased salivation, increased peristalsis + digestion, gallbladder stimulation, voiding (contraction of detrusor muscle), stimulates sex organs
SNS stimulation drugs nomenclature:
stimulating?
blocking?
stimulating: sympathomimetics, adrenergic agonists
blocking: adrenergic antagonists
what do sympathomimetics / adrenergic agonists do? which receptors do they act on? what is the effect on the receptors?
- stimulate/mimic SNS*
- act on alpha + beta receptors
- alpha: vasoconstriction
- beta1: increase HR / beta2: bronchodilation
which of the PNS drugs are LIFE SAVING/EMERGENCY based?
sympathomimetics/adrenergic agonists
what are alpha receptors responsible for?
blood vessels
- constriction, increase HR, increase BP
- pushing blood back to heart!*
what are beta 1 receptors responsible for?
heart + kidneys
-increase HR, contraction, strength of impulse
what are beta 2 receptors responsible for?
lungs
-bronchodilation
+glycogenolysis –> glucose!!
what do adrenergic antagonists do? what effect do they have on the receptors?
BLOCK the SNS
- block alpha + beta receptors
- -> vasodilation - decrease HR + BP
- -> decrease HR, contraction, impulse
- -> bronchoconstriction
parasympathetic nervous system drug nomenclature:
stimulating?
blocking?
stimulating: parasympathetomimetics, muscarinics
blocking: anticholinergics
what are parasympathetomimetics/muscarinics doing? what receptors are they acting on?
stimulating the PNS
-acting on cholinergic receptors (nicotinic + muscarinic)
what are anticholinergics/muscarinic antagonists doing?
- BLOCKING the PNS
- block acetylcholine
SE mneumonics for anticholinergics
can’t see, can’t pee, can’t spit, can’t shit :)
(pupil dilation, urinary retention, dried up, decreased peristalsis)
BLOCKING PNS
what is the ONLY NT that activates beta 2 receptors?
epinephrine
beta 2=lungs
what is the muscarinic receptor responsible for? (think, what are the S+S of parasympathetic nervous system…)
increased secretions, contraction of smooth muscle (peristalsis, bronchi, detrusor muscle), slow HR, miosis
activation of beta 2 receptors causes which process to happen in the liver? and what can happen in patients with existing DM?
glycogenolysis –> glucose
can cause hyperglycemia in patients with DM
prototype for parasympathtomimetics
bethanechol (Urecholine)
use for bethanechol
urinary retention (postpartum/post op)
when should we give bethanechol?
1 hour BEFORE meals - this med causes smooth muscle contraction –> increased peristalsis / GI effects and food can make this worse
when should we NOT use bethanechol? (4 scenarios/diagnoses)
asthma (can cause bronchoconstriction), obstruction, BPH, post op bowel surgery
main SE of bethanechol
GI issues (discomfort, NVD)
prototype for anticholinergics/muscarinic antagonist
atropine
atropine is contraindicated in patients with which condition?
glaucoma (can increase IOP)
SE of atropine
think S+S of SNS stimulation
blurred vision, photophobia (b/c of dilated pupils), increased HR, anhidrosis (can’t sweat)
can’t see, can’t pee, can’t spit, can’t shit
tx for atropine overdose + what is the MOA for the tx drug?
physostigmine (cholinisterase inhibitor –> more ACh)
what does atropine overdose present as? what other S+S do we need to check for to confirm OD?
psychosis
need to look for “can’t see, can’t pee, can’t spit, can’t shit” symptoms
sympathomimetics and adrenergic agonists can be divided into which 2 categories? what are the main differences?
catecholamines + noncatecholamines
catecholamines: (Epi, NE)
- can’t take orally (1st pass effect)
- short half life
- can’t cross BBB
* EMERGENCY*
noncatecholamines: (ephedrine, phenylephedrine)
- can take orally
- longer half life
- crosses BBB
* OTC drugs*
prototype for sympathomimetics/adrenergic agonists
epinephrine
which receptors does epinephrine act on? what effects would you see?
alpha 1+2, beta 1+2
alpha: vasoconstriction (Get blood to heart)
beta1: increase HR, BP, CO
beta2: bronchodilation
epinephrine is which type of adrenergic agent?
catecholamine
what is drug of choice for anyphylaxis?
epinephrine
noteworthy AEs of epinephrine (4)
hyperglycemia, HTN crisis, dysrhythmias, necrosis
prototype for adrenergic antagonist (alpha)
prazosin (Minipress)
what does prazosin work on? what effects would you see?
blood vessels –> smooth muscle relaxation –> vasodilation
which drug do we see first dose orthostatic hypotension with? how do we combat this?
prazosin - give @ bedtime or have them lay down/educate them on how to get up
which drug do we see reflex tachycardia with?
prazosin
which drug do we see nasal congestion with? why?
prazosin - b/c the smooth muscles are relaxed, including in nasal passages, and this allows secretions to flow –> congestion
prototype for adrenergic antagonist (beta)
propranolol (Inderal LA)
what receptor is propranolol working on? based on the receptor(s) it works on, what is that type of drug called? what effects would you see?
beta1 +2 = “nonselective beta”
beta1: decreased HR, BP, contraction, rate of impulse
beta2: bronchoconstriction, inhibits glycogenolysis
because propranolol blocks beta 1 AND 2, what process is blocked in the liver and what could this lead to?
it blocks glycogenolysis –> hypoglycemia
r/t SNS, which drug should you not stop taking immediately and why
propranolol - because the SNS has been blocked for so long, an abrupt cessation of the med could cause MI
