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64 Cards in this Set
- Front
- Back
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what are the 2 major components of the PNS
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Somatic - controls skeletal muscle
ANS - Sympathetic P-Sympathetic |
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Describe the Somatic Nervous System
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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 |
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Describe the ANS
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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 |
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what is a motor unit
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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.
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what is predominant tone
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a tissue is controlled mainly by the sym. or p-sym. system and the other system may override that normal tone
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describe the Parasympathetic Nevous System
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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 |
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what is the neurotransmitter at the pre and post ganglion in parasympathetic system
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acetylcholine
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describe the sympathetic nervous system
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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) |
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what are the neuro transmitters at the pre and post ganglion in sympathetic nervous sys.
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pre - acetylcholine
post - mostly norepinepherine, epinepherine, and dopamine |
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how does the adrenal medulla function in the sympathetic nervous sys.
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1. acts like a giant ganglion, it recieves preganglionic fibers, then outputs transmitter into bloodstream instead of synapse. mechanism for affecting wide range tissue
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what is the ratio that the adrenal medulla secretes epinephrine and norepinephrine
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80 epi (longer lasting): 20 norepi (very brief)
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what are the 2 primary types of nicotinic receptors
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N1 - (autonomic ganglia) blocked by hexamethonium
N2 - (neuromuscular junction) blocked by d-tubocurarine |
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describe the nicotinic recptor
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a pentameric ligand gated ionophoric type receptor made up of 2 alpha, 1 beta, 1gamma, 1 delta subunit.
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what is the neurotransmitter at the at nicotinic recptor
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acetylcholine
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how does activation of the receptor work
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acetylcholine binds to the subunit interfaces of alpha-gamma & alpha-delta
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how is the nicotinic receptor activated
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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
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what are ganglionic blockers
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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.
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what are ganglionic blockers used for and what is the problem with these drugs
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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
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what are the 3 drugs associated with ganglioic blockers
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nicotine
trimethaphan mecamylamine |
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what are the 2 types of drus associated with ganglionic blockers
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depolarizing- nicotine
nondepolarizing - timethaphen,hexamethonium, & mecamylamine |
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how do depolarizing blockers work
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initially stimulate the ganglion like ACh then block due to a persistant depolarization
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how does the non- depolarizers work
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acts by competing for binding sites with ACh
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how does Hexamethonium work
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like a plug; blocking the ion channel after it opens
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explain how nicotine works at the recptor site
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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) |
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what is the only ganglionic blocker on the market today and what does it treat
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severe and malignant HTN
Tourette's Syndrome - Orphan drug Cocaine and Nicotine Addiction |
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what are the symptoms of ganglionic blockade such as seen with Hexamethonium
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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
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the side effects that are seen are due to
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the blockadeof the predominant tone on the tissue, allowing the non-predominate autonomic effects to override
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how does Mecamylamine work in the body specifically in CNS
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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 |
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in what patients should Mecamylamine be avoided
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MI
Glaucoma Stoke Pregnancy - crosses placenta |
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what aqre the adverse reactions seen with Mecamylamine
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N/V, anorexia, mydriasis,syncope,weakness, and fatigue
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how should Mecamylamine be taken
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tablet with meals to lessen risk of hypotension
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describe the history of d-tubocurare
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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 |
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what uses besides skeletal relaxation did d-tubocurare have
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aid in mechanical ventilation
prevent trauma during ECT aid in diagnosis of myasthenia gravis |
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what are the 2 mechanisms of action of neuromuscular blockers
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depolarizing and non-depolarizing
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how does the neuromuscular depolarizer work
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same as the ganglionic, cause an intial depolarization then long term blockade due to receptor stays depolarized and not able to repolarize
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how do the nondepolarizing neuomuscular agents work
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competitive antagonist(affinity, no intrinsic activity) of ACh@ the neuromuscular junction. result in weakness @ low and paralysis @ high doses
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Name the Non-Depolarizing Agents
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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 |
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which drug is the only depolarizing neuromuscular
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succinylcholine
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why is succinylcholine so good for intubating patients
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shortest acting both onset (60 sec.) and duration (1-2 min)
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what can happen with a dose of succinylcholine and an asthmatic pt.
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bronchospasm due to histamine release
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what should a crna be aware that can happen when a pt recieves succinylcholine
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transient bradycardia, arrythmias, tachycardia, arrest by vagal stimulation from P-symp.
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succinylcholine should be avoided in cardia pt taking digoxin why
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succinylcholine can cause hyperkalemia
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what are the 2 short acting non-depolarizing agents
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rocuronium & mivacuronium
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what is a good alternative to succinylcholine for rapid sequence intubation
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rocuronium
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what are the intermiate acting neuromuscular agent
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atrcuium
ciatracurium vecuronium |
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what are the long lasting neuromuscular blockers
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pancuronium
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in pt with decreased plamacholinesterase or reduced pseudocholinesteras activity which NM agent should be avoided
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mivacurium
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what should we keep in mind about the elimination of atracurium and cisatracurium
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metabolized by serum esters by hoffman elimination to produce laudanosine a CNS excitatory metabolite
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pancuronium should have doseage reduction in what type of patient
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renal impaired
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these NM agents are primarily excreted by liver a precaution should be taken if given to pt. w/hepatic disease
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rocuronium &vecuronium
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which NM agents have histamine releasing properties
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succinylcholine - mod.
atracurium - mild to mod mivacurium - mild to mod |
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what NM agents that lack histamine releasing properties & do not block muscarinic receptors are preferred for cardiac & asthma pt.
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rocuronium & vecuronium
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Pt. @ risk for prolonged NM blockade can result from
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pt recieving meds that impair MN function(myasthenia gravis) or that potentiate the pharm actions of NM blockers(electrolyte imbalance)
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what drugs interact with the NM blockers that can potentiate the prolonged NM blockade especially with long acting
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lithium,calcium salts,magnessium salts, inhalational agents, local anesthetics, antibiotics, quinidine, procainamide,lido,
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what is the most common adverse reaction w/ pancuronium due to muscarinic blockade
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tachycardia
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what are the adverse effects seen with the histamine releasing NM agents
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flushing, hypotension, sinus tachycardia, urticaria, wheezing, and bronchospasm
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in asthmatic treated with steriodial NM while on the vent have experienced what
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acute myopathy lasting days to weeks
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what is reported with iv injections of non-depolarizing MN
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phlebitis
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how do NM blocking agent work
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block cholinergic transmission between the motor nerve endings & the nicotinic receptor on NM end plate of skeletal muscle
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what should a crna be aware that can happen when a pt recieves succinylcholine
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transient bradycardia, arrythmias, tachycardia, arrest by vagal stimulation from P-symp.
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succinylcholine should be avoided in cardia pt taking digoxin why
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succinylcholine can cause hyperkalemia
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what are the 2 short acting non-depolarizing agents
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rocuronium & mivacuronium
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what is a good alternative to succinylcholine for rapid sequence intubation
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rocuronium
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what are the intermiate acting neuromuscular agent
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atrcuium
ciatracurium vecuronium |
