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64 Cards in this Set

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what are the 2 major components of the PNS
Somatic - controls skeletal muscle
ANS - Sympathetic
P-Sympathetic
Describe the Somatic Nervous System
1.Provides CNS contol and reflexive control of skeletal muscle
2.muscle fibers divided into muscle units
3.nerve fibers synsapes at motor end plate
4. transmitter at motor end plate is acetalcholine
Describe the ANS
1. critical in maintance of homeostrasis
2.regulates hormones
3.regulates tone and motility
4. most tissue excpt muscle are innervated by at least one branch of the ANS
what is a motor unit
muscle fiber innervated by a single nerve fiber with axonal branches going to each muscle fiber in the motor unit. the # of muscle fibers in each motor unit varies with the amount of control needed by the body.
what is predominant tone
a tissue is controlled mainly by the sym. or p-sym. system and the other system may override that normal tone
describe the Parasympathetic Nevous System
1. controls sedentary functions
2.exits the spine at the cranial-sacral region
3. synapes at ganglion close to innervated tissue
4. ratio is 1:1 incoming to out going: fine control
5. neurotransmitter is at pre and post ganglionic site is acetylcholine
what is the neurotransmitter at the pre and post ganglion in parasympathetic system
acetylcholine
describe the sympathetic nervous system
1. contols fight or flight
2.exits the spine at the thoraco-lumbar regions
3.synapes at ganglia(paravertebral chain) that lies close to the spinal cord
1:10 to 1:100 incoming to outgoing fibers (gross control)
what are the neuro transmitters at the pre and post ganglion in sympathetic nervous sys.
pre - acetylcholine
post - mostly norepinepherine, epinepherine, and dopamine
how does the adrenal medulla function in the sympathetic nervous sys.
1. acts like a giant ganglion, it recieves preganglionic fibers, then outputs transmitter into bloodstream instead of synapse. mechanism for affecting wide range tissue
what is the ratio that the adrenal medulla secretes epinephrine and norepinephrine
80 epi (longer lasting): 20 norepi (very brief)
what are the 2 primary types of nicotinic receptors
N1 - (autonomic ganglia) blocked by hexamethonium
N2 - (neuromuscular junction) blocked by d-tubocurarine
describe the nicotinic recptor
a pentameric ligand gated ionophoric type receptor made up of 2 alpha, 1 beta, 1gamma, 1 delta subunit.
what is the neurotransmitter at the at nicotinic recptor
acetylcholine
how does activation of the receptor work
acetylcholine binds to the subunit interfaces of alpha-gamma & alpha-delta
how is the nicotinic receptor activated
2 acetylcholine molecules must bind at the subunit interfaces located between alpha-gamma & alpha-delta simultaneously which opens the channel to allow Na+ and Ca++ to enter
what are ganglionic blockers
specifically work on the nicotinic receptors of both the sympathetic and p-sympathetic autonomic ganglia. not selective and block the entire output of the ANS at the nicotinic receptor.
what are ganglionic blockers used for and what is the problem with these drugs
blood pressure contol,even though the nicotinic receptor is blocked other receptor in the cell like muscarinic and adrenergic are believed to amplify or supress the signal. this is where side effect come from
what are the 3 drugs associated with ganglioic blockers
nicotine
trimethaphan
mecamylamine
what are the 2 types of drus associated with ganglionic blockers
depolarizing- nicotine
nondepolarizing - timethaphen,hexamethonium, & mecamylamine
how do depolarizing blockers work
initially stimulate the ganglion like ACh then block due to a persistant depolarization
how does the non- depolarizers work
acts by competing for binding sites with ACh
how does Hexamethonium work
like a plug; blocking the ion channel after it opens
explain how nicotine works at the recptor site
increase HR by symp. ganglia or depressing the P-symp. cardiac ganglia. also works on chemoreceptors and the medullary centers which then sends increased or decreased signals to the heart via compensatory responses.
adrenals - triggers release of epi (increase HR and BP)
what is the only ganglionic blocker on the market today and what does it treat
severe and malignant HTN
Tourette's Syndrome - Orphan drug
Cocaine and Nicotine Addiction
what are the symptoms of ganglionic blockade such as seen with Hexamethonium
Increased blood flow to the skin ( warm and pink), decreased sweating, inhibited lacrimation & salivation, mydriasis and cycloplegia, decreased GI motility, Hypotension, Urinary retention, constipation, and hypoglycemia
the side effects that are seen are due to
the blockadeof the predominant tone on the tissue, allowing the non-predominate autonomic effects to override
how does Mecamylamine work in the body specifically in CNS
Crosses CNS EZ,blocks nicotinic receptors in brain and ganglia. in brain decreasese dopamine and norepi release from specific neuron as well as modulating neuroendocrine responses.
@ low doses few peripheral side effects
in what patients should Mecamylamine be avoided
MI
Glaucoma
Stoke
Pregnancy - crosses placenta
what aqre the adverse reactions seen with Mecamylamine
N/V, anorexia, mydriasis,syncope,weakness, and fatigue
how should Mecamylamine be taken
tablet with meals to lessen risk of hypotension
describe the history of d-tubocurare
plant alkloid from chondodendron Tomentosum, used by S. american indians to kill animalsby skeletal paralysis.
1st used to tx tetanus and spasticity (1932)
1940's used with anesthesia for muscle relaxation
what uses besides skeletal relaxation did d-tubocurare have
aid in mechanical ventilation
prevent trauma during ECT
aid in diagnosis of myasthenia gravis
what are the 2 mechanisms of action of neuromuscular blockers
depolarizing and non-depolarizing
how does the neuromuscular depolarizer work
same as the ganglionic, cause an intial depolarization then long term blockade due to receptor stays depolarized and not able to repolarize
how do the nondepolarizing neuomuscular agents work
competitive antagonist(affinity, no intrinsic activity) of ACh@ the neuromuscular junction. result in weakness @ low and paralysis @ high doses
Name the Non-Depolarizing Agents
Tubocurarine - D/C
Pancuronium - long - 1-2hr
Atacurium - med. - 30-60 min
cisatracurium - med - 30-60
vencuronium - med - 30-60
mivacurium - short - few min
rocuronium - short - few min
which drug is the only depolarizing neuromuscular
succinylcholine
why is succinylcholine so good for intubating patients
shortest acting both onset (60 sec.) and duration (1-2 min)
what can happen with a dose of succinylcholine and an asthmatic pt.
bronchospasm due to histamine release
what should a crna be aware that can happen when a pt recieves succinylcholine
transient bradycardia, arrythmias, tachycardia, arrest by vagal stimulation from P-symp.
succinylcholine should be avoided in cardia pt taking digoxin why
succinylcholine can cause hyperkalemia
what are the 2 short acting non-depolarizing agents
rocuronium & mivacuronium
what is a good alternative to succinylcholine for rapid sequence intubation
rocuronium
what are the intermiate acting neuromuscular agent
atrcuium
ciatracurium
vecuronium
what are the long lasting neuromuscular blockers
pancuronium
in pt with decreased plamacholinesterase or reduced pseudocholinesteras activity which NM agent should be avoided
mivacurium
what should we keep in mind about the elimination of atracurium and cisatracurium
metabolized by serum esters by hoffman elimination to produce laudanosine a CNS excitatory metabolite
pancuronium should have doseage reduction in what type of patient
renal impaired
these NM agents are primarily excreted by liver a precaution should be taken if given to pt. w/hepatic disease
rocuronium &vecuronium
which NM agents have histamine releasing properties
succinylcholine - mod.
atracurium - mild to mod
mivacurium - mild to mod
what NM agents that lack histamine releasing properties & do not block muscarinic receptors are preferred for cardiac & asthma pt.
rocuronium & vecuronium
Pt. @ risk for prolonged NM blockade can result from
pt recieving meds that impair MN function(myasthenia gravis) or that potentiate the pharm actions of NM blockers(electrolyte imbalance)
what drugs interact with the NM blockers that can potentiate the prolonged NM blockade especially with long acting
lithium,calcium salts,magnessium salts, inhalational agents, local anesthetics, antibiotics, quinidine, procainamide,lido,
what is the most common adverse reaction w/ pancuronium due to muscarinic blockade
tachycardia
what are the adverse effects seen with the histamine releasing NM agents
flushing, hypotension, sinus tachycardia, urticaria, wheezing, and bronchospasm
in asthmatic treated with steriodial NM while on the vent have experienced what
acute myopathy lasting days to weeks
what is reported with iv injections of non-depolarizing MN
phlebitis
how do NM blocking agent work
block cholinergic transmission between the motor nerve endings & the nicotinic receptor on NM end plate of skeletal muscle
what should a crna be aware that can happen when a pt recieves succinylcholine
transient bradycardia, arrythmias, tachycardia, arrest by vagal stimulation from P-symp.
succinylcholine should be avoided in cardia pt taking digoxin why
succinylcholine can cause hyperkalemia
what are the 2 short acting non-depolarizing agents
rocuronium & mivacuronium
what is a good alternative to succinylcholine for rapid sequence intubation
rocuronium
what are the intermiate acting neuromuscular agent
atrcuium
ciatracurium
vecuronium