Kruse CIS Flashcards
alpha 1 do what?
beta 2 do what?
muscarinic receptors do what?
stimulate contraction of all smooth muscle. vasoconstriction / secretion
relax smooth muscle - vasodilation
contract smooth muscle
adult diapers and bladder training. symptoms are consistent with what division of the nervous system?
parasympathetic
knowing someone is having trouble with urination, what is going to be administered to alleviate symptoms?
beta 2 receptor agonist direct-acting cholinergic agonist indirect-acting cholinergic agonist muscarinic AchR antagonist Nicotinic AChR
it has to be something sympathetic, so it’ll probably be inhibiting muscarinic AChR.
Muscarinic AChR antagonist.. they are causing contraction of smooth muscle. if we block that surrounding the bladder, it’ll increase volume of the bladder and decrease the frequency
Beta 2 relaxes smooth muscle.. IT’LL INCREASE BLADDER CAPACITY but it won’t work because it doesn’t inhibit bladder contraction
direct/indirect acting cholinergic agonists –> used for paralysis of the bladder during surgery.
nicotinic AChR antagonist –> no effect because not part of the parasympathetics.
what works on the sphincters usually?
alpha 1
How does activation of mAChRs cause trigone and sphincter relaxation?
what do they do though??
if we have acetylcholine and give it to the endothelial cells there is going to be vasodilation due to NO!
activating muscarinic in endothelial cells results in production of NO.
relaxation of the sphincter through muscarinic is due to NO.
contract smooth muscle!
Oxybutinin – nonselective muscarinic antagonist..
what adverse effect could you have?
constipation lacrimation miosis salivation vomiting
blocking muscarinic which is responsible for parasympathetic.
parasympathetics are moving stuff through the GI so constipation is the answer.
Lacrimation = tears is PNS Miosis = constriction of the pupil... PNS salivation = PNS vomiting = PNS??
other than constipation, what else would you see happen from a muscarinic antagonist (nonselective)
dry mouth/eyes, dizziness, blurred vision
feelings of impending doom and tremors.. this often happens after exercise or drinking coffee..
super high blood pressure
positive free metanephrine test!
what is it?
pheochromocytoma
what is a pheochromocytoma?
what are the common symptoms
adrenaline secreting tumor.
Epi/NE secreting tumor sitting on the adrenal medulla.
spills out catecholamines from exercise or coffee..
common symptoms are headache, perspiration, palpitations!
what is a metanephrine test?
they’re searching for catecholamine breakdown and this is what they find
someone has a pheochromatoma.. which of the following is going to immediately reduce a pheochromocytoma?
alpha 1 antagonist alpha 2 antagonist beta 1 antagonist mAChR M2 agonist Thiazide diuretic
alpha 1 deals with blood pressure vasoconstriction.. so blocking those would lead to vasodilation.
Alpha 2 doesn’t really make sense because they’re most often found presynaptically in the CNS so that won’t be super fast.
beta 1 antagonist = reduces blood pressure (it’s a beta blocker), but the most immediate effect will be ones that are directly targeting the vasculature.
mAChR M2 agonist also slows it down but it’s not the fastest acting.
thiazide diuretic is a slow acting blood pressure regulatar
an antagonist of what receptor is going to reduce heart rate (remember, not blood pressure)
Alpha 1 Beta 1 Beta 2 mAChR M2 mAChR M3
Beta 1! Remember Beta 1 are primarily found on the heart, when they are active they increase strength and force. so blocking that will best lower it.
the only other ones found on the heart are muscurinic but those will have to be agonists, not antagonists
person with pheochromocytoma…
if we give a beta-receptor selective agonist (propranolol) is administered, which of the following is most expected?
bronchial smooth muscle relaxation Diarrhea increase heart rate uncontrollable urination worsening of hypertension
Beta receptor antagonist… if you’re antagonizing that you’re going to lower blood pressure.. but we have spilling of tons of catecholamines and blocking Beta is going to have more available for alpha, which vasoconstriction, worsening hypertension.
we know that Beta are going to increase heart rate.. so blocking that won’t do anything
Beta 2 normally cause smooth muscle relaxation.. so antagonist would block smooth muscle relaxation.. so not that.
in a pheochromocytoma, what results if you use a beta blocker?
you’re going to have unopposed alpha stimulation (i.e. vasoconstriction).. worsening hypertension
if you use an alpha 2 receptor agonist (clonidine) on a patient with a pheochromoscytoma.. what’s going to happen?
Alpha 2 are present in the CNS.. and they suppress further sympathetic outflow in the CNS so suppresses sympathetics.. but pheochromocytoma is going to keep secreting a bunch of stuff so it’s not going to do anything
clonidine function?
activate central pre-synaptic alpha 2 receptors to suppress release of catecholamines form neurons.
they block the further release of catecholamines from the nerve terminal in the adrenergic nerve!!
smoker has wheezing but no chest pain.. what would you give them to help him?
Remember that alpha receptors are for blood pressure
we need something that will relax smooth muscle. the only thing that does is B2 agonists or mAChR antagonist
beta 2 = relaxation
alpha 1 = vasculature
alpha 2 = CNS only really
you give someone a mAChR antagonist.. what adverse symptoms are you going to see of the following?
excess perspiration excess salivation Delierium Diarrhea Decreased Mucus Production
blocking parasympathetic
it would be decreased mucus production in the bronchial glands because the muscarinic stimulates secretions… but inhibiting that would decrease because mucus production in the bronachial glands.
so not salivation
not diarrhea
excess perspiration –> activation of muscarinic receptors causes this, so block will be less perspiration.
excess perspiration is coming from what?
what happens if you inhibit them?
muscarinic receptors.. so if you inhibit muscarinic you will have less perspiration!
Inhibiting mucus production may lead to what?
increased infection
someone has super dry eyes or mouth, what are you going to do to increase this?
AChE inhibitor AChE regenerator Charged mAChR antagonist mAChR agonist Uncharged mAChR antagonist
mAChR agonist
you want to increase tear production and secretions and that’s done by mAChR
AChE inhibitor = inhibits AChE and that will lead to more in the presynaptic cleft, but not necessarily work faster
Cevimeline (mAChR Agonist) is prescribed to someone with dry eyes and mouth. what is the adverse effect that could happen?
nausea increased BP dry eyes diaphoresis decreased urinary frequency
you would have increased frequency of urine, so not that
no sweating would probably be the answer
increasing BP (maybe)
dry eyes. no that’s not it
nausea (not necessarily)
diaphoresis is directly acted upon by muscarinic receptors
diaphoresis is acted on by what?
directly by Ach and muscarinic.. so having an agonist will have a ton more sweat than normal
which concomitant condition would be exacerbated by cevimeline if prescribed?
remember, it’s an mAChR agonist
smooth muscle contraction is what mAChR is doing… so agonists to that will increase asthma.
muscarinic agonist and…
heart failure
myasthenia gravis?
xerostomia?
xerostomia is dry mouth, so no.
myasthenia graves is caused by antibodies attacking nicotinic receptors on skeletal muscle… so muscarinic has nothing to do with it.
heart failure –> muscarinic line M2 receptors on the heart and could slow down the heart… but there is baroreceptor reflex that overtakes that to fix it
someone found that peed themself, muscle fasciculations, oral foaming.
receptor is most likely involved?
Cholinergic (muscle fasciculations leads to nicotinic… the rest is muscarinic)
someone found that peed themself, muscle fasciculations, oral foaming.
an agent from which drug class was most likely ingested?
AChE inhibitor…
this is because if they’re doing both muscle fasciculations and peeing themselves, there has got to be more ACh in the system
symptoms of acetylcholineesterase inhibitors?
SLUDGE
salivation, lacrimation, urination, defecation, gastrointestinal pain, gas, emesis
DUMBELS - defecation, urination, mitosis, bronchorrhea/bronchospasm/bradycardai, emesis, lacrimation, salivation
when you take an AChE inhibitor, which symptoms occur first?
if you drink it
GI symptoms occur first if you drink it
if it’s a crop duster, you’d have sweating and muscle fasciculations because of the percutaneous absorption
Antidote for AChE inhibitor toxicity? what does it do?
atropine
muscarinic antagonist. so it’s not going to inhibit the muscle fasciculations
