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101 Cards in this Set

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what part of the nervous system does the 'somatic' division control? the 'autonomic'?
somatic: the skeletal muscles, it's voluntary.

autonomic: visceral, vegetative or involuntary (glands & smooth mm).
how does the autonomic nervous system divide?
the efferent (peripheral; motor) divides:

sympathetic (thoracolumbar)

parasympathetic (craniosacral)
where do the divisions of the ANS originate? what do they give off?
both divisions originate in nuclei WITHIN the CNS and give off PREganglionic EFFERENT fibers that exit from the brains stem or spinal cord and terminate in MOTOR ganglia.
what characterizes the sympathetic nerve response?
fight or flight:
1.decreased pulmonary secretions & bronchodilation to increase blood oxygenation.

2.increased heart rate and contractility.

3.arteriolar constriction in skin and digestive tract.

4.glycogen and lipids break down.

5.GI motility decreases, urine retained.
what is the rest and digest response?
PARASYMPATHETIC:
1.slow heart beat.
2.increased digestion.
3.constrict bronchioles
4.constricted pupils.
what is the origin of the sympathetic nervous system? describe it's nerve fibers and ganglia.
thoracolumbar

SHORT pre, long post

ganglia in two paravertebral chains ALONG SPINAL COLUMN
what is the origin of the parasympathetic nervous system? describe it's nerve fibers and ganglia.
craniosacral

LONG pre, short post

ganglia located IN TISSUE INNERVATED
how many neurons are present in a somatic system? what neurotransmitter is used & what receptor? what tissues are innervated?
ONE nueron

acteylcholine, muscarinic.

skeletal muscle
what neurotransmitters are used by the ANS-sympathetic? what tissue type?
Ach at PRE, NE alpha/beta at POST.

smooth muscle
blood vessel
cardiac
gland
with regards to nicotinic Ach receptors, what do the sympathetics and parasympathetics have in common?
both have the same receptor at the ganglia.
what neurotransmitters do the parasympathetics use? what tissues do they innervate?
Ach at pre AND post

smooth muscle
cardiac muscle
gland
what sorts of tissue are known for using dopamine as a neurotransmitter? what are they innervated by?
renal vascular smooth muscle

sympathetic innervation
where are nicotinic receptors found?
somatic skeletal muscle
what types of neurons are considered 'cholinergic'? what does cholinergic mean?
all autonomic PREganglionic and all parasympathetic POSTganglionic are cholinergic.

it means: the parts of the nervous system that use acetylcholine as a neurotransmitter
what can be said about MOST postganglionic neurons?
they are adrenergic (Neurons with norepi as their NT or receptors on which norepi acts)
what gland is considered a modified sympathetic ganglion?
the adrenal medulla.
name some 'effector cells'.
cardiac muscle
smooth muscle
gland cells
some endothelial cells and nerve terminals
how does dopamine get converted to norepinephrine? when does this occur?
via dopamine beta hydroxylase

it occurs when dopamine is being taken up for storage in the vesicle.
what are the two uptake mechanisms involving norepi? what inhibits them?
#1: norepi is taken back to nerve terminal. inhibited by COCAINE or TRICYCLIC ANTIDEPRESSANTS

#2: norepi is taken up by the tissues (no inhibitor)
what stimulates rls of norepi from the nerve terminal? what inhibits it?
influx of calcium stimulates release of norepi.

bretylium (cardiac arrythmia) and guanethidine (antihypertensive) INHIBIT it's release.
what happens to norepi if not stored in a vesicle? what is needed for it's storage? what inhibits it's storage?
MAO will degrade the norepi.
it requires ATP and peptidoglycans for storage in the vesicle.
RESERPINE can inhibit storage (via dopa-norepi transfer)
what amino acid is necessary to synthesize epinephrine? describe the steps.
1.tyrosine
2.dopa
3.dopamine
4.norepinephrine
5.epinephrine
how is Ach rlsd into the synapse?
an action potential is elicited, calcium influx occurs and Ach is released into the synapse with ATP and peptidoglycan.
what are three possible fates of Ach?
1. act on cholin receptors

2.degrades to acetate and choline (via Ach-esterase)

3.binds autoreceptors to initate negative feedback mechanism.
what allows for vesicular storage of Ach? what inhibits it's storage?
ChAT (choline-acetyl transferase?)

inhibited by vesamicol
what is the action of Botox?
it inhibts the rls of Ach into the synapse. *cholinergic vesicles = SOA*
what are the effects of vesamicol and reserpine? where do they act?
BOTH prevent storage and deplete transmitters.

v: cholinergic terminals and vesicles.

r: adrenergic terminals and vesicles.
what inhibits tyrosine from being converted to dopa? what enzyme usually acts in this conversion?
metyrosine inhibits

tyrosine hydroxylase usually acts.
what is COMT? what is it's action?
catecho o methyl transferase.

it can break down epi and norepi
where does M1 act? describe it's action.
CNS neurons, autoreceptors

IP3 and DAG are created, intracellular Ca increases.
which cholinoreceptor acts on heart tissue? how does it work?
M2, it opens sodium channels and inhibits adenylyl cyclase.
which two muscarinic receptors have the same activity? do they act on the same tissues?
M1 and M3 BOT form IP3 and DAG, increasing intracellular calcium.

they DON'T work on same tissue:

M1: CNS neurons, autoreceptors
M3: exocrine glands, vessels
how are the two nicotinic receptors similar? how are they different?
BOT open Na/K channels, causing depolarization.

Nn: POSTG neurons, some presynaptic cholinergic terminals

Nm: SKELETAL MUSCLE nt endplates.
how does alpha 1 adrenoreceptor work?
formation of IP3 and DAG, increased intracellular calcium on POSTsynaptic EFFECTOR cells (esp smooth muscle)
what is alpha 2's method of function?
it inhibits adenylyl cyclase, decreasing CAMP. it works on autoreceptors, presynaptic adrenergic nerve terminals, platelets, lipocytes and smooth muscle.
what types of tissue do the three beta adrenoreceptors work on? what is their common method of action? name any additional activities.
beta1: heart
beta2: smooth muscle
beta3: fat

ALL THREE: stimulate adenylyl cyclase and increase cAMP.

beta2 ALSO: activates cardiac G1 under some conditions.
what does D1 do? how does D2 relate to this?
it stimulates adenylyl cyclase and increases cAMP on the brain, effector tissues (esp smooth muscle of renal vascular bed).

D2 INHIBITS adenylyl cyclase on the brain and effector tissues. it also increases K+ conductance and works on presynaptic nerve terminals.
what causes pupil dilation in the eye? what causes constriction of the pupil?
sympathetic innervation to radial smooth muscle.

constricted via parasympathetic innervation to the circular smooth muscle.
where does sympathetic tone predominate? what does this mean?
it predominates in blood vessels meaning it regulates the degree of contraction of vascular smooth muscle, and therefore peripheral resistance and blood pressure.
which division of the ANS largely regulates the heart, eyes, GI tract and bladder?
the parasympathetics.
what does high sympathetic tone cause? high parasympathetic tone?
sympathetic: HYPERtension

para: HYPOtension
which eye muscles are under parasympathetic control? sympathetic?
para:
circular smooth muscle of iris
circular smooth muscle of ciliary muscle

symp:
radial smooth muscle ofiris
what is the function of the ciliary muscle? what innervates it? what happens if the innervation is blocked?
it works in lens accomodation, parasympathetically innervated. if blocked: cycloplegia.
what drains the aqueous humor of the eye? what condition can this cause?
the canal of schlemm. glaucoma.
how is the bladder innervated? what sort of receptor does it use?
autonomic: bladder body and sphincter

somatic: striated mm of external sphincter & maintain tonic contraction of ex.sphincter.
which parts of the bladder are under parasympathetic control?
para contracts the detrusor mm. with relaxtion of the trigone, micturation can occur.
how are the sympathetics involved in bladder control?
they contract the trigone mm. active in urinary retention.
what type of receptor does the detrusor have? the trigone?
detrusor: beta2
trigone: alpha1
which aspects of the GI tract are under parasympathetic stimulation?
it increases GI motility and relaxes sphincters. increases secretions of exocrine glands. inhibition causes constipation. M3 receptors.
how is the GI tract under sympathetic stimulation?
sphincters contract via alpha1 receptors. the GI tract relaxes via beta2 receptors. inhibition causes minimal effects b/c parasympathetic cholinergic system dominates.
what causes a drug to elevate BP? what are some side effects?
increased firing of the carotid sinus and aortic arch baroreceptors increase BP.

causes increased vagal activity.

decreased sympathetic activity causes decreased heart rate, CO and total peripheral resistance (TPR). vasodilation is INCREASED.
what is the formula for BP?
CO x TPR
what is the effect of a drug which LOWERS BP?
decreased firing of baroreceptors.
decreased vagal activity
increased:
sympathetics
HR, CO, vasoconstriction and TPR

*with tendency for BP to increase again, ie postural reflex.
what largely determines TPR (degree of vasoconstrict/dilate)?
determined by sympathetic tone:

increased s.t.: vasoCONSTRICT

decreased s.t.: passive vasodilate (decreased TPR)
what type of innervation do most vessels have?
most have muscarinic cholinergic receptors present, but they do NOT have parasympathetic innervation.
name three choline esters. what type of drugs are they?
Ach
carbachol
bethanechol

choline esters, cholinergic AGONISTS
name three cholinomimetic alkaloids. what type of drugs are they?
muscarine
pilocarpine
nicotine

all cholinergic AGONISTS
name three carbamates. what type of drug are they?
physostigmine
neostigmine
pyridostigmine

all cholinesterase INHIBITORS
what is edrophonium?
a cholinesterase inhibitor
name two organophosphates. what types of drugs are these?
echothiophate
malathion

both are cholinesterase INHIBITORS
what is the MOA of cholinergic agonists? include receptor types.
binds Ach RECEPTORS, ie effector cells innervated by:
postg para fibers
presyn autoreceptors (M1, M2)
symp and para ganglia
motor end-plates on skeletal muscle (nicotinic)
CNS (M1)
what effects do cholinergic agonists have on the cardiovascular system?
M2 receptors: decreased HR, AV conduction.
M3: increased vasodilation and EDRF + NO synthesized.

indirectly: baroreceptor reflexes & adrenergic effects due to rls of catecholemines.
can Ach produce vasodilation alone?
NO. it needs endothelium stimulated NO synthetase. the NO diffuses thru into smooth muscle, stimulates guanylate cyclase and causes relaxation.
what are the effects of cholinergic agonists on nonvascular smooth mm?
eye: miosis

bronchioles: constrict. M3

UT (esp bethanechol): micturation. M3

GI: increased peristalsis.
what happens to the exocrine glands as a side effect of certain cholinergic agonists? what receptor is involved?
SLUD symptoms. M3 receptor.
name three choline esters. what type of drugs are they?
Ach
carbachol
bethanechol

choline esters, cholinergic AGONISTS
name three cholinomimetic alkaloids. what type of drugs are they?
muscarine
pilocarpine
nicotine

all cholinergic AGONISTS
name three carbamates. what type of drug are they?
physostigmine
neostigmine
pyridostigmine

all cholinesterase INHIBITORS
what is edrophonium?
a cholinesterase inhibitor
name two organophosphates. what types of drugs are these?
echothiophate
malathion

both are cholinesterase INHIBITORS
what is the MOA of cholinergic agonists? include receptor types.
binds Ach RECEPTORS, ie effector cells innervated by:
postg para fibers
presyn autoreceptors (M1, M2)
symp and para ganglia
motor end-plates on skeletal muscle (nicotinic)
CNS (M1)
what effects do cholinergic agonists have on the cardiovascular system?
M2 receptors: decreased HR, AV conduction.
M3: increased vasodilation and EDRF + NO synthesized.

indirectly: baroreceptor reflexes & adrenergic effects due to rls of catecholemines.
can Ach produce vasodilation alone?
NO. it needs endothelium stimulated NO synthetase. the NO diffuses thru into smooth muscle, stimulates guanylate cyclase and causes relaxation.
what are the effects of cholinergic agonists on nonvascular smooth mm?
eye: miosis

bronchioles: constrict. M3

UT (esp bethanechol): micturation. M3

GI: increased peristalsis.
what happens to the exocrine glands as a side effect of certain cholinergic agonists? what receptor is involved?
SLUD symptoms. M3 receptor.
what can higher doses of cholinergic agonists stimulate?
autonomic ganglia and neuromuscular junction, esp carbachol and nicotine.

this results in para and symp effects.

skeletal mm contraction may result.
how is Ach absorbed? why are the other agonists better?
Ach is poorly absorbed orally. Ach is rapidly hydrolyzed by AchE.

structural modifications resist hydrolysis & prolong DOA.
which cholinergic agonists are resistant to cholinesterases?
carbamacol and bethanechol
what are possible toxic effects of cholinergic agonists?
how can they be treated?
syncopy with heart block (M3 at SA node)
cardiac arrest
hypotension
asthma, dyspnea

tx: atropine (1-2mg IV, IM) pharm antagonist

or - epi (IV,SC - for asthma)
physiological antagonist.
what is muscarine?
natural alkaloid found in mushrooms. interacts with muscarinic cholinergic receptors at effector cells and not at ganglia.
what is pilocarpine?
alkaloid with predominantly muscaranic effects, it's orally active. use is mainly limited to local application to eye for glaucoma (drops, film)
what is nicotine?
a potent ganglionic ('nicotinic') and CNS stimulant.
stimulation of autonomic ganglia leads to mixture of parasympathomimetic and sympathomimetic effects.

chronic use: cancer, CHD, peptic ulcer, flaccid paralysis, convulsion, coma, hypertension.
how are the cholinesterase inhibitors classified?
short act: edrophonium

interm: pyridostigmine, physostigmine, neostigmine

long act: echothiophate
what is the MOA of cholinesterase inhibitors?
there are reversible and irreversible inhibitors, but BOTH result in accumulation of Ach at cholinergic synapses througout the body. some may have direct effects (neostigmine)
how does a reversible cholinesterase inhibitor work?
either reversibly bound (edrophonium) or gradually hydrolyze (physostigmine and neostigmine); or compete with ach for binding sites.
*these are SHORT lived*
how do 'irreversible' cholinesterase inhibitors work?
they phosphorylate the enzyme at esteratic site via a stable bond; return of activity requires synthesis of NEW enzyme (aging)
what are the net effects of cholinesterase inhibitors?
parasympathetic domination:
decreased HR, AV conduction, CO.
blood vv and BP minimal.
what effect do cholinesterase inhibitors have on NON vascular smooth muscle?
eye: miosis, low IOP. M3

GI: increased peristalsis

Bronchioles: wheezing

urinary tract: micturation

exocrine glands: SLUD
what effect do cholinesterase inhibitors have on skeletal m neuromuscular junctions?
initial stimulation and subsequent depolarization blockade and paralysis of voluntary mm (flaccid paralysis).

*neostigmine may have some direct Ach-like actions as wel.
what are some CNS effects of cholinesterase inhibitors?
stimulation followed by inhibition.

high dose can result in convulsions, coma and respiratory arrest.
describe the moa of tacrine and donepezil.
high affinity for AchE; lipophilic, cross BBB; long DOA
how does physostigmine work?
it's a NON-quaternary ammonium agent. readily absorbed, widely distributed, including CNS; hydrolyzed by AchE.
what do neostigmine and other quaternary ammoniums have in common?
they don't readily enter the CNS; destroyed by plasma enterases.
what are some characteristics of organophosphorous anticholinesterases?
lipid soluble
readily absorbed from all sites
widely distributed (include CNS)

EXCEPT: echothiophosphate, highly polar and more stable

malathion - safe
parathion - dangerous
what are some adverse effects of organophosphorous anticholinesterases.
increased mm weakness or paralysis.
who is most likely to suffer an acute overdose toxicity of organophosphorous anticholinesterases?
farmers during spraying. also oral route.
what are some symptoms of organopho anticholinesterases?
autonomic: muscarinic predominance (SLUD, decreased HR, BP; wheezing)
CNS: anxiety, confusion, etc.

tx: symptomatic and supportive tx. monitor AChE levels.
ATROPINE in large doses to antagonize the muscarinic actions, including some CNS effects (2-4 mg IV, IM every 5-10 minutes)
what is a cholinesterase reactivator?
pralidoxime (protopam, 2-PAM) for organophosphate poisoning. it chemically interacts with the phosphorylated AchE to split off the phosphorous compound. *regenerates enzyme*
1gm IV (can be repeated)
what are some clinical uses of cholinomimetics?
eye: for glaucoma. reduce IOP by facilitating outflow of aqueous humor.

effective in open-angle, secondary glaucoma and brief tx of angle closure glaucoma prior to surgery.
what are some examples of cholinergic drugs used for glaucoma?
pilocarpine
pysostigmine
echothiophate
what drugs can cause GI and urinary tract problems?
bethanechol and neostigmine can cause postop ileus and congenital megacolon.