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NMBD
Pharm exam 3
| Question | Answer |
|---|---|
| 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
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