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NMBD

Pharm exam 3

QuestionAnswer
what does aminophylline do to NMT stimulates production of cAMP which stimulates NMT
what do calcium channel blockers do to NMT can interfere with NMT
anything that interferes with cAMP does what to calcium and what will it do to your NMBD dose? decreases calcium; will decrease NMT and will make the muscle weaker so you will need LESS NMBD dose
what do low and high doses of lasix do to NMT low doses inhibits cAMP and decreases NMT; high doses inhibits phosphodiasterase which makes more cAMP and speeds NMT (need more NMBD)
which drugs interfere with cAMP (or calcium) and slows NMT (requiring less NMBD)? calcium channel blockers; low dose lasix
which drugs stimulate cAMP (or calcium) and speeds NMT (requiring more NMBD)? aminophylline; high dose lasix
what is the % of receptor blockade when 0 of 4 twitches are seen on the TOF? 100%
what is the % of receptor blockade when 1 of 4 twitches are seen on the TOF? 90-95%
what is the % of receptor blockade when 2 of 4 twitches are seen on the TOF? 80%
what is the % of receptor blockade when 3 of 4 twitches are seen on the TOF? 75%
what is the % of receptor blockade when 4 of 4 twitches are seen on the TOF? 0-75%
when stimulating the ulnar nerve on the PNS, which muscle is being activated? adductor pollicis muscle
nondepolarizers have more rapid onset but less intense block at ________ than on the ______ laryngeal muscles (vocal cords) & diaphragm than on periphery (adductor pollicis)
when stimulating the facial nerve with the PNS, which muscle is being activated? orbicularis oculi
what is the downside of using ulnar nerve during PNS? diaphragm and larynx is not blocked as deep as hand so you may underdose muscle relaxant. PNS may show 0 of 4 twitches but diaphragm may still be moving or patient may still cough when intubating
why is the facial nerve more useful during PNS? more closely resembles timing and depth of blockade at diaphragm and larynx
what is ED95 equal potency between NMBD - is determined by measuring dose needed to produce 95% suppression of single twitch response
describe the history of NMBD; what plant is DTC from and when was it first administered; when was it first used in anesthesia Found in plants in tropical rainforest in South America. Discovered originally from plant sap, and used on blow darts for hunting. D-tubocurarine is an alkaloid from the Chondrodendron Tomentosum vine. 1932; 1942
The muscle fiber is a single skeletal muscle cell. Each muscle fiber contains bundles of cells called myofibrils
what do myofibrils do? carries contractions along muscle fiber
what structures are within myofibrils sarcomeres
what is the plasma membrane of the muscle cell called? sarcolemma
the sections of sarcolemma that separate the sarcomeres are called t-tubules
how large is the synaptic cleft 20-50 nm
what is the synaptic cleft filled with extracellular fluid
what are the folds of the sarcolemma called gyri
where are the nicotinic receptors found on the sarcolemma concentrated on the shoulders of junctional folds so they are close to the active zones
• The bands that boarder the sarcomere are known as z lines
• The band that marks the sarcomeres middle is called the m-line or m-disc
the lightest area of the sarcomere is called the: thin filaments
the contractile protein _______ is found on the thin filaments; inhibitory proteins are also found on thin filaments called ______ & ______ actin; troponin & tropomyosin
thick filaments contain the contractile protein _____ myosin
do thick and thin filaments overlap? yes
the distance between the ends of the thin filaments are known as H zone
the space between the thick filament of one sarcomere and the other is known as I band
which zones/bands shorten during contraction H zone and I band
what does not shorten during muscle contraction (band) A band; the total length of the thick filament
during contraction, the thin filament actin slides toward the: M line of the sarcomere
during resting membrane potential, how is the inside charge maintained? It is maintained by unequal distribution of K+ and Na+ ions across the membrane.
during an action potential, the inside of the cell becomes ______ and the outside becomes ______ positive; negative
what is the role of calcium during NMT Calcium causes the neurotransmitter filled vesicles to undergo exocytosis and release the neurotransmitter into the NMJ.
what is the role of cAMP during NMT cAMP opens calcium ion channels, causing synaptic vesicles to fuse with nerve membrane and release ACh.
what is acetylcholine formed from acetate and choline
where does the motor neuron that innervates the muscle arise from? the cell body of the ventral horn of the spinal grey matter
where is acetate supplied by acetyl-coA from mitochondria
where is choline derived from dietary intake and liver production
what is ACh stored in? quanta (vesicles
what types of calcium channels open during NMT fast calcium channels
how many vesicles are released with each depolarization 200-400
Na/K pumps moves... 3 Na+ out and 2 K+ into the cell
what organic functional group is ACh in? ester
describe the structure of ACh has a + charged quaternary ammonium group = 4 carbon atoms attached to 1 nitrogen atom that attaches to a – charged cholinergic receptor.
name the 5 protein subunits of nicotinic receptors beta, delta, epsilon, 2 alpha
besides the NMJ; where else can nicotinic receptors be found? CNS and autonomic ganglia
name the subunits of prejunctional receptors 3 alpha, 2 beta
what happens when you stimulate prejunctional receptors? Stimulation facilitates the release of ACh by stimulating mobilization of ACh in the motor nerve terminal
what class of drugs is fade most observable in? benzylisoquinolines, less with aminosteroids, absent with succs
what two things do prejunctional receptors explain posttetanic facilitation and fade
what is posttetanic facilitation an increase in the strength of muscle contraction after an intense, repetitive electrical stimulus to the nerve (cause presynaptic release of ACh and increase quantal release of the neurotransmitter)
what is fade a decrease in strength of responses to more slowly repetitive stimuli,
some NMBD block prejunctional ______ channels but not ______ channels sodium; calcium.....these drugs may interfere with mobilization of ach from synthesis site to release site
extrajunctional receptors are present when _____; do not give _____ there has been nerve damage; do not give succs; the membrane is unstable and K+ flows freely in and out - succs can cause CV arrest
with succs, the return of function on the TOF is _____ whereas with NDMR it ______ immediate; slowly wears off
why is the volume of distribution small for NMBD Non-depolarizing muscle relaxants (NDMR) because of their quaternary ammonium groups are highly ionized in water soluble compounds at physiologic pH and possess limited lipid solubility.
what are the benefits of the water solubility of NMBD? They do not cross lipid membrane barriers: they do not produce sedation (does not cross BBB), does not affect the fetus, and renal tubular reabsorption is minimal.
the rate of disappearance of NMBD after rapid IV admin is seen as _______ followed by _____ a rapid initial decline (distribution to tissue); slower decline (clearance)
Enhanced NMB by volatile anesthetics reflect ________action as manifested by decreased plasma concentrations of NMBD. pharmacodynamics
are NMBD highly bound to plasma protein? no; it is unlikely that plasma bindind will have a significant effect on renal excretion
which class of drugs do you stay away from with renal disease? aminosteroids?
what is the first sign of clinical effect after defasciculating dose of non-depolarizer is used and why does this happen? the first sign of clinical effect is patient complaint of diplopia bc extraocular muscles exhibit weakness before other areas.
• In cases where strict akinesia must be maintained, it may be necessary to dose NMB at levels deeper than what can be monitored by TOF: in this case, what is a more useful mode of monitoring? posttetanic count
what is the dose of succinylcholine 1-1.5 mg/kg
what is the max dose of succs up to 150 mg total
what is the onset of succs 30-90 seconds
what is the clinical duration of succs 8-15 mins
succs is an ______ to NDMR antagonist
Pretreatment with a nondepolarizer before administration of succs requires a ______dose of succs to be used. larger
leak of K+ by succs will produce an increase in serum K+ by 0.5 mEq/L
do not use succs in patients with SCI, renal patients, CV patients, CVA with paralysis, demyelinating conditions (ALS, MS, muscular dystrophy - duchenne disease - males/peds), children < 12 years old
how is succs broken down (breakdown of the ______) breakdown of the ester linkage in the middle of the molecule by plasma cholinesterase
phase I blocks are potentiated by _______ and antagonized by ______ anticholinesterase drugs (neo); NDMR
what are characteristics of phase I block on PNS decr. contraction to single twitch; decr amplitude but sustained response to continuous stim; TOF > 0.7; absent PTF; augmentation of block by anticholinestase drugs
after giving succs, what must you see before giving NDMR return of function on PNS
how can a phase II/dual block occur? repeated doses of succs, large single dose (>2mg/kg) or with succs infusion --> tachyphylaxis
what happens during phase II block With repeated doses of a depolarizer, the post junction membrane do not respond normally to ACh even when post junctional membranes become repolarized (desensitization). The patients will have a prolonged effect of depolarization.
what will you see with phase II block on PNS that you wouldn't see with phase I block fade to repetitive stimulation; PTF; reversibility with ACh inhibitors
when redosing succs, what must you do with the second dose? must give lower second dose and you will have less time; do not give 3rd dose (wake patient up and cancel case)
what is the elimination 1/2 life of plasma cholinesterase? 8-16 hrs (book); 14 days (ppt)
levels < ___ of plasma cholinesterase are necessary for prolongation of SCh 75%
causes of prolonged succs (decreased plasma cholinesterase activity) decr hepatic production (chronic failure); atypical plasma cholinesterase; antichol-ase drugs; insectasides; echothiopate (glaucoma); mestinon (MG); chemo; reglan; parturient (duration of succs not prolonged d/t incr VD)
plasma cholinesterase activity can be measured by ... the ability of the local anesthetic dibucaine to inhibit activity of the enzyme
The dibucaine number reflects _____of the cholinesterase enzyme (ability to hydrolyze), and not the _____of the enzyme in the plasma. quality; quantity
a dibucaine number of 20 reflects what homozygous atypical
what is the expected duration of succs when the dibucaine number is 20 4-6 hours
what is the incidence of homozygous atpical (dibucaine number of 20) 1 in 3000
what does a dibucaine number of 40-60 mean heterozygous atypical
what is the expected duration of succs in heterozygou atypical 30-60 min
what is the incidence of dibucaine number of 40-60 (heterozygous atypical) 1 in 500
what do you do if succs is given to someone with atypical plasma cholinesterase? supportive treatment (vent/sedation) do not give reversal
what is MH triggered by? all VAAs and succs
what is the mechanism of MH problem with calcium reuptake; intracellular calcium increases 500 fold leading to sustained muscle contraction --> severe oxygen debt --> demand of ATP leads to glycolysis and lactic acidosis --> membrane instability, cell rupture and rhabdomyolysis
if person is suspected of MH, what should you do to prep them for their case first case of the day prime circuit to flush residual VAA TIVA
what are clinical features of MH (16) massive uncontrolled metabolic activity; masseter spasm; muscle rigidity; rising ETCO2 & PaCO2; decr sats & PaO2; tacypnea, incr HR, HTN, arrythmias, incr body temp; metabolic acidosis, hyperlactaemia; decr bicarb; hyperkalemia; incr CP; myoglobinuria
what is the treatment for MH (14) dantrolene; resuscitative measures; call for help; VAA stopped; surgery aborted; 100% O2; manually hyperventilate; clean breathing system; sedation; saline iced lavage; IVF for steady UOP; insulin/D50 to reverse hyperkalemia; cardiac arrhythmias tx; ICU
what are some adverse effects of succs (10) cardiac arrythmias; histamine release; anaphylaxis; myalgia; myogloburia; incr intragastric pressure; incr ICP; incr intraocular pressure; sustained muscle spasm; myotonia; pediatrics; hyperkalemia
what cardiac arrythmias happen with succs ventricular and nodal dysrhythmias, junctional rythms, sinus arrest; may cause brady or tachy; reflects actions of SCh at cardiac muscarinic receptors; **tachycardia is more common**
what is myalgia; how can it happen and what can you do to prevent it general muscle pain; from fasciculations of succs; can give defasciculating dose of NDMR, lidocaine, NSAID or self taming dose of succs (10 mg)
what can you pretreat patient with before succs to reduce K+ release pretreatment with Mg or small amount of NDMR; but then succs dose must be increased (1.5 mg/kg); dose does not need to be increased with pancuronium
describe the subunit structure of extrajunctional receptors 1. epsilon subunit is replaced by gamma subunit; or 2. 7 alpha subunits
extrajunctional receptors are more _____ to agonists sensitive
what would a hemiplegic arm demonstrate on PNS false high degree of neuromuscular function compared with rest of body
what is myotonia abnormality in repolarization of muscles;Caused by autoantibodies against or mutation of K+, Na+, or Cl- channels.
what conditions may be subject to prolonged sustained muscle contraction (5 min after succs) - under myotonia  Neuromyotonia (Isaac’s syndrome or continuous muscle fiber activity syndrome)  Myotonic dystrophy (Steinert’s disease)  Myotonia congenital (Thomsen’s disease)  Paramyotonia congenital  Periodic hyperkalemic paralysis
what is dose, onset and duration of doxacurium 0.07 mg/kg 4-6 min 100-120 min
what is the brand name of doxacurium nuromax
what is dose, onset and duration of pancuronium 0.1 mg/kg 3-6 min 60-90 min
what is the brand name of pancuronium pavulon
what is dose, onset and duration of pipercuronium 0.1 mg/kg 2-4 min 90 min
what is dose, onset and duration of atracurium 0.5 mg/kg 2-3 min 40 min
what is the brand name of atracurium tracrium
what is dose, onset and duration of vecuronium 0.08-0.15 mg/kg 3 min 40 min
what is the brand name of vecuronium norcuron
what is the brand name of rocuronium zemuron
what is the brand name of mivacurium mivacron
what is dose, onset and duration of rocuronium 0.4-1.12 mg/kg 1-2 min 20-45 min
what is dose, onset and duration of cisatracurium 0.15 - 0.25 mg/kg 2-3 min 45-60 min
what is dose, onset and duration of mivacurium 0.15 - 0.25 mg/kg 2-3 min 12-20 min
what 4 NDMR can you run drips on pancuronium, atra, vec, cisatra
what is the infusion rate for pancuronium 1-1.7 mcg/kg/min
what is the infusion rate for atracurium 9-10 mcg/kg/min
what is the infusion rate for vecuronium 1 mg/kg/min
what is the infusion rate for cisatracurium 1-3 mcg/kg/min
what are the long acting NDMR dox, pan, piper
what are the intermediate acting NDMR cisatra, atra, vec, roc
what is the short acting NDMR mivacurium
what are the characteristics of NDMR seen on PNS decr response to single twitch; unsustained reponse (fade) during continuous stim; TOF ratio < 0.7; PTF; potentiation of other NDMR; antagonized by anticholinesterase drugs
selection of NDMR is based on... SE profile, desired timing, rate of recovery, metabolism and clearance
describe priming for NDMR; speeds onset of induction dose; give 10% of dose before starting, wait 3-6 min; give full dose
succs followed by NDMR does what to NDMR block enhances d/t desensitization of succs at post junctional membranes
how does calcium channel blockers affect NMT blocks L-subtype (slow) calcium channels on the motor nerve terminal (synergistic with nondepolarizing relaxants); these drugs do not influence fast calcium channels.
drugs that induce microsomal enzymes can increase degradation of what class of NMBD steroidal NDMR bc partially metabolismed bye CYP450 system
increased synergistic effect is demonstrated when intubating dose of roc is followed by maintenance dose of _______ cisatracurium
Drugs that influence activity of plasma cholinesterase may impair metabolism of succs: The following impair plasma cholinesterase reglan, pancuronium, oral contraceptives, neostigmine, echothiopate
Muscle relaxants + _________are associated with myopathy. corticosteroids
what are some effects of histamine release flushing, hypotension, rebound tachycardia
why is atracurium not good for asthmatics histamine release
unlike atracurium, cisatracurium does not cause what side effect histamine release
how does pancuronium produce tachycardia? blocking cardiac muscarinic receptors
what cases is pancuronium good for and why CV surgery - Pancuronicum is a good drug to use with high dose opioid induction (fentanyl) to counterbalance effects of bradycardia from opioid.
what NMBD can alter heart rate pancuronium, rocuronium, succs
which class of drug is more likely to cause histamine release benzylisoquinolines d/t presence of tertiary amine (vss. aminosteroids)
how are aminosteroids generally metabolized and cleared? 10-30% through hepatic microsomal enzymes; remained is excreted unchanged in urine
increased age causes variability in duration of action by how long 15-20 min except in cisatra
what class of drugs are most desirable in elderly and why benzylisoquinolines (atra and cisatra) bc organ INdependent metabolism
why do infacts have a shorter onset but prolonged recovery vs. adults? larger volume of distribution, immature NMJ, immature hepatic metabolism
who requires highest dose of NMB based on age children
gender differences in NMBD requirements may be d/t what body composition (muscle mass), VD, plasma protein concentration
vec requirements for men vs. women women require 22% less vec
roc requirements for men vs. women 30% less roc (ouellette) 30% more roc (ppt)
what drug classes may enhance response of NDMR and less NDMR will be needed antibiotics, VAAs, local anesthetics, CV dysrhythmic drugs, diuretics, mag, lithium, ganglionic blocking drugs, anticonvulsants, corticosteroids
what other factors (non-drug factors) may potentiate effects of NDMR acetylcholine in excessive amounts; acidosis, guillain-barre disease, hypothermia, muscular dystrophy, MG, myasthenic syndrome, hypokalemia
what factors cause resistance to NDMR burn injury/thermal injury; denervation; myasthenia gravis (succs); azathipine (imuran); hyperkalemia; paresis/hemiplegia after CVA; allergic reactions
what do antibiotics do to NDMR enhances drug; less drug will be needed; causes direct blockade of ion channels
what class of antibiotics and drugs within class enhance NDMR aminoglcosides: gentamycin, bleomycin, streptomycin
how do VAAs affect NDMR enhance block; depression of CNS causes decr tone of skeletal muscles; decreased sensitivity of NMJ to depolarization
how do local anesthetics affect NMBD small doses enhance block; large doses may block NMT; interfere with prejunctional release of ACh, stabilize postjunctional membrane, depress skeletal muscle fibers; compete for plasma cholinesterase and prolong succs
what CV dysrhythmic drugs prolong NDMR calcium channel blockers; lidocaine; quinidine
azathioprine does what to succs augments succs; works similar to lasix
how does mag affect NMBD decreases ACh release from nerve terminals; reduces senstivity of post junctional membrane to ACh (stabilization); enhances NMBD; phase II block may occur more readily
how does lithium affect NMBD enhances NMBD; interferes with Na transport
how does hypothermia affect NMBD prolongs duration of drugs d/t slowing of hepatic enzyme activity and biliary and renal clearance. decr degradation by hoffman elimination and ester hydrolysis; decr clerance and slowed equilibrium
how does hypokalemia affect NMBD decreased extracellular K+ increases transmembrane potential causing hyperpolarization of cell membranes. Efflux of K+ or influx of Cl- causes the membrane potential to be more negative (-70 to -90). resistant to succs , but incr sensitivity to NDMR
how does thermal injury affect NMBD and when would you see effect resistance to NDMR; seen 10 days after injury, peaks at 40 days, decr after 60 days; >30% of body must be burned to produce resistance
how does hyperkalemia affect NMBD increased K+ decreases the resting membrane potential and partially depolarizing cell membranes. This change increases the effects of depolarizers and opposes the action of non-depolarizers.
does pancuronium cause histamine release? hell no
pan decreases MAC of halothane
enhanced block of pan is seen with respiratory/metabolic acidosis/alkalosis respiratory acidosis
pan is antagonized by what drugs neostigmine or any anticholinesterase drugs
describe the metabolism and clearance of pan 10-40% - hepatic deacetylation 80% eliminated unchanged in urine
how much decr in plasma clearance is seen with pan 33-50%
what does pan do to plasma cholinesterase inhibits p.c.
which NDMR most closely related structurally to ACh pan
doxacurium pharmacokinetically resembles what NDMR pan
what are some positives and negatives of doxacurium + no histamine , no CV changes - longer duration with elderly
pipecuronium resembles what drug and why pan; dependence on renal clearance
how does hepatic cirrhosis affect pipecuronium does not alter pharmacokinetics or dynamics
what is a positive aspect of pipecuronium no histamine or CV changes
how are intermediate acting drugs different from long acting drugs they possess efficient clearance mechanisms that minimize likelihood of significant accumulation effects with repeated doses or infusions; however more costly
which NDMR is bound to plasma protein and by how much atracurium; 82% bound
how is atracurium metabolized 10-40% hoffman elim 2/3 by ester hydrolysis
what kind of patients is atracurium good for and why renal patients; no renal involvement
what is a major metabolite of hoffman elim and ester hydrolysis laudanosine; released at slightly alkaline states and further degradation occurs
how is laudanosine metabolized liver - 70% excreted in bile; remainder in urine
vec is structurally similar to and more potent than what drug pan
what is a positive aspect of vec wide margin of safety; very predictable time frame
how is vec metabolized hepatic deacetylation 50% in liver 30 min after admin 40% unchanged in bile up to 24 hrs after 30% unchanged in urine up to 24 hrs after
why does redistribution occur rapidly with vec more lipophilic; monoquaternary compound; increase doses
what SE could you see with vec modest vagotonic effect (brady); SA node exit block and cardiac arrect (rare)
compare roc to vec structurally similar to vec but smaller number of molecules; less potent than vec but more rapid onset
how should roc be dosed in obese patients should be dosed by ideal body weight and not actual body weight
how can onset of roc be altered by changes in cardiac output incr CO speeds onset (ephedra); decr CO slows onset (beta blocker)
what are some positives and negatives to roc + no histamine release - slight vagolytic effect (tachy) lower potency compared to other aminosteroids prolonged effects in renal failure decreased hepatic clearance in elderly
how is roc metabolized and cleared NO deacetylation; 50% unchanged in bile 2 hrs after; >30% renal excretion in 24 hours
compare cisatra to atra similar to atra except onset is slower; hoffman elim but unlike atra, nonspecific plasma esterases are not involved in cisatra
describe the metabolism and clearance of cisatra 77% hoffman clearance; 16% renal clearance
what is a downside to cisatra onset slower in elderly d/t slower equilibrium
describe the metabolism of mivacurium hydrolysis by plasma cholinesterase; 7% appears in urine
what common anesthetics can prolong mivacurium VAAs (sevo) and pancuronium bc they inhibit plasma cholinesterase
what are some downsides to mivacurium histamine release (decr. MAP), bronchospasm
which anticholinesterases work presynaptically edrophonium and physostigmine initiate release of ACh
which anticholinesterases work postsynaptically pyridostigmine, neostigmine, physostigmine by inhibiting ACh-E action
patients with renal and liver disease have less effects of _____ but have greater effects on the _____ recurarization; muscarinic receptors
if there is no response on the PNS, why would you not give a reversal will have a synergistic effect on block
which drug reversals are faster than others edrophonium is faster than neostigmine
describe the physical structure of neostigmine and how it works as an anticholinesterase consist of a carbamate moiety and quaternary ammonium group; carbamate moiety forms a covalent bond to ACh-E; renders the molecule lipid insoluble so it doesn't cross the BBB
what is the brand name of neostigmine prostigmine
what is the dose of neo 0.04 - 0.08 mg/kg (max 5 mg for adults)
how is neo packaged 10 cc...1 mg/cc
what is the onset and duration of neo 5-10 min; 54 min - > 1 hr
how is neo metabolized 50% hepatic clearance 50% renal clerance
what muscarinic effects can be caused by neo increased gastric motility, bradycardia, PONV
how can you treat muscarinic effects of neo glyco 0.2 mg : 1 mg neo atropine 0.4 mg : 1 mg neo ratio usually 1 cc: 1 cc
what is neo contraindicated in cardiac transplant; mechanica, intestinal and urinary obstruction.
does pyridostigmine cross biologic barriers? does not cross BBB or placenta; does cross GI tract (more effective when absorbed through GI tract)
how does mestinon work as an anticholinesterase forms a carbamyl ester with reversible inhibition of ACh-E
describe the metabolism of mestinon hepatic metabolism accounts for 25% of drug in pts without renal function; 75% is eliminated renally unchanged
what is the principle metabolite of mestinon 3-hydroxy-N-Methylpyridium
what is the dose of mestinon (pyridostigmine) 0.1-0.4 mg/kg
how is mestinon available 5 mg/cc solution
what is the onset and duration of mestinon 10-16 min 76 min
what is the recommended dose of atropine and glyco to give after mestinon 0.2-0.6 of glyco (preferred d/t slower onset) 0.6 - 1.2 mg of atropine for 10-20 mg of mestinon
what is the brand name for edrophonium tensilon
describe the physical properties of edrophonium/tensilon quaternary ammonium; lacks carbamate group; produces reversible inhibition (prevents ACh from approximating correctly with enzyme)
describe the metabolism of edrophonium/tensilon 30% hepatic metabolism (undergoing glucuronidation and forming edrophonium glucuronide which is an inactive metabolite) 75% renal elimination
what is the dose of tensilon 0.5 - 1 mg/kg max
how is tensilon available 10 mg/cc
what is the onset and duration of edrophonium 1-2 min 1 hour
what is edrophonium primarily used for to determine anticholinesterase overdose vs. myasthenic crisis
what anticholinergic is used with tensilong/edrophonium atropine 0.014 mg
what is physostigmine used for a parasympathomimetic (a reversible choinesterase inhibitor) used to treat glaucoma, and delayed gastric emptying; used to treat CNS effects of atropine and scopolamine (central anticholinergic syndrome)
does physostigmine cross BBB? why or why not yes bc of tertiary amine
what is the dose of physostigmine for anticholinergic syndrome? 15-60 mcg/kg 2 mg/kg for reversal of somnolence associated with opioids and VAAs 0.01-0.03 mg/kg for reversal dose (although no longer used as reversal agent in anesthesia)
what are the SE of physostigmine N
how does cholinergic crisis occur in patients with MG when there is too much cholinesterase inhibition
what are clinical features of cholinergic crisis muscle fasciculations; sweating; excessive salivation; constricted pupils; bronchospasm; CNS effects
what is the treatment of cholinergic crisis withdrawal cholinesterase drug administer atropine 35-75 mcg/kg supportive measures
what are examples of synthetic cholinergic agonists derivatives of ACh; methacholine, carbachol, bethanacol
what is the significance of synthetic cholinergic agonists actions of these drugs are blocked by atropine;
what is bethanachol used for urinary retention
what is carbachol used for used to treat narrow angle glaucoma and produce miosis for intraocular surgery
what are examples of cholinomimetic alkoloids pilicarpine, muscarine and arecholine
pilicarpine, muscarine and arecholine are examples of what cholinomimetic alkoloids; used for topical miosis and decrease IOP
how are anticholinergic agents derived scopalamine and atropine are naturally occurring tertiary amine and are alkoloids of belladonna plant; glyco is synthetic conoger of same plant but are quaternary ammonium
how do anticholinergic drugs work competitively antagonize effects (parasympatholytic) of ACh at the muscarinic receptors (antimuscarinic); competitive antagonist
what drug has the greatest cholinergic effect and fast onset effects atropine
what is the location of M1 receptors CNS; stomach - H+ ion secretion
M2 location heart, lungs, CNS - bradycardia
M3 location CNS, airway smooth muscle - salivation and bronchospasm
M4 location CNS, heart - ?
M5 location CNS - ?
what is the antisialogogue doses for atropine, glyco, and scopalamine 10-20 mcq/kg (0.4-0.6 mg) - atropine 5 - 8 mcg/kg glyco - most used 5 mcg/kg (0.3 mg) scopalamine
does atropine produce sedation? hell yes
what is the onset and duration of atropine 1 min 30-60 min
what is the onset and duration of glyco 2-3 min 30-60 min
how is glyco clearance more rapid than atropine; 80% unchanged in urine
how is scopalamine broken down in body almost entirely in body; 1% excreted unchanged in urine
what are the clinical uses of anticholinergics (test) premedicant antisialogogue tx of bradycardia reversal of effects of anticholinesterase drugs opthalmic uses bronchodilator
rank antisialogogue effects from greatest to least scop > glyco > atropine
doses for treatment of bradycardi 0.5-1 mg atropine 10-20 mcg/kg in children glyco 0.1-0.4 mg (slowr onset than atropine) scop not used
does scopalamine cross BBB yes (tertiary amine)
what are CNS effects of anticholinergics amnesia drowsiness sedation
rank in order from greatest to least sedative effects of anticholinergics scop> atropine > glyco
how can anticholinergics be administered for NV or sedation (premedicant transdermal patch : 1.5 mg premedicant for adults: 0.3-0.6 mg
for bronchodilating effects; how can atropine be administered neb 1-2 mg in 3-5 cc
highlights of ipratropium anticholinergic used for aerosol admin; quaternary ammonium 40-80 mcg 2-4 puffs or neb 0.25 - 0.5 mg slower onset 30-90 min
when is central anticholinergic syndrome seen mostly with admin of scopalamine bc it crosses the BBB
what are S&S of central anticholinergic syndrome restlessness - hallucinations somnolence - unconsciousness
what is a treatment of central anticholinergic syndrome physostigmine 15-60 mg
what are S&S of overdose symptoms of anticholinergics dry mouth, difficulty swallowing and talking, blurred vision, photophobia, tachycardia,dry-flushed skin, incr body temp
what is the tx for anticholinergic OD physostigmine 15-60 mg
Created by: rwilson