Autonomics Flashcards
what neurotransmitters are released at presynaptic and postsynaptic sites in the ANS?
presynaptic autonomic motor: acetylcholine
postsynaptic parasympathetic: acetylcholine
postsynaptic sympathetic: acetylcholine
sympathetic ganglionic neurons: norepinephrine
adrenal medulla: epi/NE
what types of cholinergic receptors are found in ANS ganglia?
muscarinic (M1, M2, M3, M4, M5)- postsynaptic parasympathetics, sympathetics to sweat glands
nicotinic (Nn, Nm)- presynaptic parasympathetics
for the sympathetic NS, what types of cholinergic and adrenergic receptors respond to the release of neurotransmitter in the target tissues?
adrenergic receptors: a1- smooth muscle, glands
a2- nerve endings, some smooth muscle
B1- cardiac muscle
B2- smooth muscle, liver, heart
for the parasympathetic NS, what types of cholinergic and adrenergic receptors respond to the release of NTs in the target tissues?
cholinergic: muscarinic, nicotinic
how does sympathetic innervation of eccrine (thermoregulatory) sweat glands differ from the sympathetic innervation of other tissue targets?
acetylcholine is released by sympathetic neurons innervating sweat glands- the receptor is muscarinic. in other sympathetic innervations, primarily norepinephrine is released to adrenergic receptors.
what do specific enzymes in catecholamine synthesis have to do with instances when postsynaptic sympathetics release DA and Epi rather than NE?
absence of dopamine beta hydroxylase determines if dopamine is released
presence of phenethanolamine-N methyltransferase determines if adrenal Epi is released
if DBH is present, NE is released; if PNMT is present, NE is NOT released
definitions/differences between: adrenergic cholinergic cholinoceptor adrenoceptor cholinomimetic sympathomimetic parasympatholytic sympatholytic sympathoplegic
cholinomimetic- mimics action of endogenous NT
sympathomimetic- mimicking adrenaline, etc.
parasympatholytic- blocks action of endogenous NT
sympatholytic/sympathoplegic- blocks action of endogenous NT
the cholinergic, adrenergic are terms to describe the neruons/terminals
list the types of receptors located within each of the target end organs: sweat glands, suprarenal glands, everything involving parasympathetics, everything else in sympathetics
sweat glands- preganglionic sympathetic cholinergic; post ganglionic sympathetic cholinergic
suprarenal glands: preganglionic cholinergic (direct innervation)
parasympathetics: preganglionic cholinergic; post ganglionic cholinergic
sympathetics: preganglionic cholinergic; postganglionic adrenergic
what special role is played by a2 adrenergic receptors in the CNS and PNS?
the 2nd messenger effect is to LOWER the cAMP levels; located in nerve endings
explain how baroreceptor reflex functions as a compensatory mechanism
changes in peripheral resistance changes BP which activates baroreceptors, which through CNS centers regulate both sympathetic and parasympathetic outflow; provides QUICK, HOMEOSTATIC RESPONSES so BP doesn’t shift normally
why might a drug that contracts peripheral vessels result in bradycardia?
contracted peripheral vessels will cause BP to rise, resulting in bradycardia due to the baroreceptor reflex
why might a drug that relaxes peripheral vessels cause tachycardia?
relaxed peripheral vessels will lower BP, causing tachycardia due to the baroreceptor reflex
what are the smooth muscle and epithelial targets for ANS drugs in the eye? what are the autonomic receptors involved?
dilator pupillary muscle (sympathetic), sphinter pupillary muscle (para), ciliary muscle (para), ciliary epithelium
how is pupil diameter and aqueous humour flow altered by specific autonomic related drugs?
pupil diameter: sympathetics contract the dilator pupil muscle (a1 receptor)
aqueous humor: a agonist (phenylephrine) facilitates outflow
b blockers reduce synthesis of aqueous humor
why would a muscarinic agonist be useful in treatment of glaucoma?
a muscarinic agonist would help to increase outflow of aqueous humor; relaxes vessels, so reduces intraocular pressure.
what are the symptoms of muscarinic agonist toxicity? what do the symptoms reflect?
SLUDGE: salivation, lacrimation, urination, defecation, GI upset, emesis
they reflect the role of muscarinic receptors in various target tissues.
what is the difference in the way that acetylcholine and catecholamines are cleared from the synaptic cleft?
acetylcoline is degraded by AChE enzyme; catecholamines are diffused away, reuptake or metabolized
what is the difference between a direct-acting and indirect-acting cholinomimetic? what about sympathomimetics?
direct-acting: act like acetylcholine
indirect-acting: cholinesterase inhibitors- compete with ACh for the enzyme
sympathomimetics: direct-acting: a or B agonists
indirect-acting: increase the conc of endogenous catecholamines in the synaptic cleft by increasing release of NT or inhibiting reuptake
list the 5 classes of ANS drugs and specific examples of what drugs fall into each class (blue)
direct-acting cholinomimetics- bethanecol
cholinoceptor blockers- atropine, scopolamine (anti-muscarinic)
indirect-acting cholinesterase inhibitors- neostigmine, organophosphates
sympathomimetics (direct/indirect)- direct: epi, NE, phenylephrine, albuterol; indirect: tyramine, amphetamine, cocaine, tricyclic antidepressants
adrenoceptor blockers- prazosin, propanolol
how do cholinergic agonists effect changes in peripheral vascular vessel diameter when these vessels lack direct autonomic fiber inputs?
vasodilation from cholinomimetics even when parasympathetic fibers don’t innervate the blood vessels, because muscarinic receptors are located in endothelial cells, receptor activation leads to release of NO, which diffuses to adjacent vascular smooth muscle, relaxes the vessels
what specific types of receptors do ganglionic blockers work on?
nicotinic receptors
why were drugs that fall into ganglionic blocker class once used but are now NOT used to treat hypertension?
too many side effects: they block sympathetic and parasymp. outflow; not tolerated well.
what type of autonomic drugs would result in bronchodilation versus bronchoconstriction in the lungs?
bronchodilation: anti-muscarinic
what type of autonomic drugs would exacerbate or relieve the urinary retention seen in patients with benign prostatic hyperplasia? what receptors are involved?
alpha blockers (adrenoceptor blocker)
some drugs like the tricyclic antidepressants have side effects that reflect the action of….
anti-muscarinic action
how do indirect-acting cholinomimetics differ from direct acting cholinomimetics?
indirect-acting cholinomimetics inhibit the enzymes that breakdown ACh
explain in a general sense how neostigmine works to augment the conc of acetylcholine in the synaptic cleft?
neostigmine inhibits AChE activity by binding to it and undergoing hydrolysis (competes with ACh for the active site)
how do sympathetic fibers constrict cutaneous blood vessels while dilating skeletal blood vessels?
different receptors: cutaneous blood vessels have alpha receptors, skeletal blood vessels have B2 receptors
compare and contrast the mechanism underlying the sympathomimetic effects of tyramine, amphetamine, cocaine, and tricyclic antidepressants
tyramine and amphetamine: induce release of stored catecholamines from terminal
cocaine- blocks reuptake at the NE or DA transporter
tricyclic antidepressants- blocks reuptake at the NE transporter
why are sympathomimetic drugs sometimes added to local anesthetics?
they cause local vasoconstriction, which controls spread of anesthesia from the site and causes hemostasis
what is the functional difference in the activation of a and B adrenergic receptors with respect to smooth muscle in the walls and sphincters of the GI tract?
the B2 receptor relaxes smooth muscle (walls)
the a2 receptor causes contraction (sphincters)
what specific drugs have the potential to alter the level of thermoregulatory sweating?
anti-muscarinic drugs
The ANS is under the control of….
supraspinal centers
what is the role of the hypothalamus with respect to regulation of the ANS? what part of the hypothalamus is the regulating center for parasympathetics? for sympathetics?
principal CNS integration center for ANS; separate parasympathetic and sympathetic regulating areas; except the area for cholinergic sweating is located in anterior hypothalamus with parasympathetics; the rest of sympathetics are located in the posterior hypothalamus
what receptors are used by the parasympathetic and sympathetic innervation of the bladder?
sympathetics inhibit bladder wall: activate B receptors, decreasing the presynaptic a2 receptors from parasympathetics
sympathetics excite internal urethral sphincter via a1 receptors (constrict)
parasympathetics excite bladder wall through activation of muscarinic receptors
what are two ways in which the sympathetic input to the bladder inhibits the tone of the detrussor muscle?
relaxes the detrussor muscle via B2 receptors
distinguish the type of neurogenic bladder seen after different CNS lesions. what type of lesion would be seen after a bilateral lesion of the sacral spinal cord?
LMN type; areflexic, flaccid bladder, incontinence, severe urinary retention could result in renal damage
what type of lesion would be seen between the lumbar cord and the pons? above the pons?
between lumbar spinal cord and pons: UMN; loss of voluntary control; hyperreflexia; spastic bladder, doesn’t empty fully; incontinence
above the pons: no desire to control micturition or urgency to urinate but can’t delay; uninhibited reflex bladder (infantile)
parasympathetics release ___ at the postsyn site
acetylcholine
presynaptic receptor of parasympathetics is what type of receptor? the post synaptics of parasympathetics?
nicotinic
muscarinic
sympathetics that go to sweat glands are this type of receptor
muscarinic
presynaptic adrenergic autoreceptors are what type of receptor?
a2 - for negative feedback control of NT release
muscarinic receptor blocker (used clinically to block postgang parasympathetics)
atropine
blocks release of acetylcholine
botulinum toxin
blocks monoamine reuptake at synapse to prolong action of neurotransmitters
cocaine
blocks binding of ACh to its nicotinic receptor on skeletal muscle
curare
inhibits AChE activity, prolonging, ACH activity
neostigmine
irreversibly inactivates AChE
organophosphates
blocks monoamine reuptake
tricyclic antidepressants
varenicline is what type of drug?
direct-acting cholinoceptor agonist
donepezil, neostigmine, physostigmine, pyridostigmine: what type of drugs?
indirect-acting cholinoceptor agonists
atropine, scopolamine, solifenacin: what type of drugs?
muscarinic cholinoceptor antagonists
albuterol, amphetamine, ephedrine, epi, methamphetamine, methylphenidate, norepi, phenylephrine, pseudoephedrine: what class of drugs?
sympathomimetic drugs
tamsulosin: what class of drugs?
adrenergic receptor antagonists
direct-acting cholinomimetic
bethanecol
mushroom poisoning is synonymous with..
cholinomimetic toxicity (SLUDGE)
how does vasodilation from cholinomimetics occur when parasympathetics do not innervate blood vessels?
there are muscarinic receptors on endothelial blood vessel cells; when activated, they release NO, diffuses to adjacent smooth muscle, increases cAMP, relaxation of vessels– causes sweating, tachycardia, vasodilation
prototypical cholinesterase inhibitor
neostigmine
what’s unique about neostigmine?
doesn’t work if injected into plasma; more stable, longer half life; doesn’t enter CNS
direct acting sympathomimetics (prototype?)
epi (prototype), norepi, phenylephrine, albuterol
two modes of action of indirect acting sympathomimetics
- increase release of NT
2. inhibit reuptake, thereby increasing action
-zosin indicates
a1 blocker
prototypical non-selective B blocker
propranolol
beta blockers: what affect do they have on secretion of aqueous humor?
decrease secretion of aqueous humor
location of lesion for spastic bladder. for flaccid bladder?
spastic bladder-between lumbar spinal cord and pons
flaccid bladder: sacral spinal cord/cauda equina
