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Anes. Pharm I Test 1
pathophysiologic issues with depolarizing and non depolarizing NMB agents
| Question | Answer |
|---|---|
| What are the 5 drugs associated with resistance to non depolarizing NMB agents | Phenytoin (Dilantin), Corticosteroids, Aminophylline, Theophylline, Fursosemide (1 - 4 mg/kg dosages) |
| Why does Phenytoin (Dilantin) cause shorter duration of non depolarizing NMB agents? | increased metabolism due to induction of cytochrome P-450 or decreased activity of acetylcholinesterase |
| How long is the duration of Rocuronium (Zemuron) in patients taking Phenytoin (Dilantin)? | 4 - 7 minutes (20% of normal duration) |
| How long is the duration of Vecuronium (Norcuron) in patients taking Phenytoin (Dilantin)? | 16 - 22 minutes (37% of normal duration) |
| How long is the duration of Pancuronium (Pavulon) in patients taking Phenytoin (Dilantin)? | 24 - 36 minutes (40% of normal duration) |
| Chronic use of Corticosteroids has been reported to cause resistance to the ___________ class of non depolarizing NMBs. | steroidal |
| Why are Aminophylline and Theophylline associated with resistance to non depolarizing NMB? | they inhibit phosphodiesterase, increasing the cAMP needed to make and release ACh. more ACh = greater dose of NMB needed to compete |
| Why do large doses (1 - 4 mg/kg) of Furosemide (Lasix) cause resistance to non depolarizing NMB? | inhibits phosphodiesterase and increases cAMP needed to make and release ACh, so more ACh = greater dose of NMB needed to compete |
| Why are burn patients resistant to non depolarizing NMB? | caused by decreased sensitivity (affinity) of post junctional receptors to either ACh or non depolarizing NMB |
| When does the resistance to non depolarizing NMB in burn patients begin and how long does it last? | begins 10 days after injury, peaks at 40 days and declines after 60 days; requires > 30% or more BSA burned |
| How does hyperkalemia affect non depolarizing and depolarizing NMB agents? | non depolarizing = resistance; depolarizing = sensitivity |
| How does hypokalemia affect non depolarizing and depolarizing NMB agents? | non depolarizing = sensitivity; depolarizing = resistance |
| How does hypermagnesemia affect blockade by non depolarizing NMB agents? | decreases release of ACh from pre junctional receptors causing an enhanced block |
| How does hypernatremia affect blockade by NMB agents? | dehydration causes decreased volume of distribution, so prolonged blockade r/t more drug reaching receptors |
| How does significant hypothermia affect blockade by NMB agents? | prolongs duration by slowing metabolism via kidneys, liver, and Hofmann elimination and plasma esterases |
| How do volatile anesthetics enhance the effect of non depolarizing NMBs? | volatiles decrease skeletal muscle tone, so requires less dose of NMB to produce same effect; weaker twitches and stronger blockade; can be used to our advantage. |
| How do local anesthetics enhance the effect of non depolarizing NMBs? | they interfere with release of ACh from pre junctional receptors, block ion channels and directly suppress skeletal muscle tone |
| How do certain antibiotics enhance the effect of non depolarizing NMBs? | magnesium type effect (anti calcium = decreased release of ACh) |
| What antibiotics increase sensitivity to non depolarizing NMBs? | aminoglycosides: genatmycin, neomycin, streptomycin, kanamycin, amikacin, tobramycin, and vancomycin too |
| What antibiotics have no effect on blockade by NMBs? | penicillins and cephalosporins |
| Why does lidocaine enhance the effect of non depolarizing NMBs? | blocks pre junctional release of ACh |
| True or False: Quinidine (an anti arrhythmic drug) prolongs blockade by both non depolarizing and depolarizing NMBs. | true |
| Although Lithium has a variable effect on blockade by non depolarizing NMB, why does it cause a prolonged onset and duration of depolarizing NMB? | acts similarly to sodium ion. influx hypopolarizes membrane and potentiates depolarizing NMBs (SCh) |
| Why does Lasix (in doses < 1 mg/kg) enhance blockade by non depolarizing NMBs? | decreased cAMP production, so less ACh released |
| Does cyclosporine (anti rejection drug) cause sensitivity or resistance to non depolarizing NMBs? | sensitivity (prolonged blockade) |
| How does the administration of SCh affect the blockade by a non depolarizing NMB? | it enhances the block (deepens it) but does not prolong it. so it reduces the dose of the non depolarizing NMB needed. |
| What must you always check for after administration of Succinylcholine but before administration of any non depolarizing NMB? | return of twitches |
| Combination of non depolarizing NMB causes a __________ effect, allowing for a smaller doses of each. | synergistic |
| Do Verapamil and other calcium channel blocking drugs cause sensitivity or resistance to non depolarizing NMBs? | sensitivity |
| Doe acute administration of Hydrocortisone potentiate or lessen a blockade by a non depolarizing NMB? | potentiate |
| The antihypertensive drugs Trimethaphan and Hexamethonium cause prolongation of blockade by depolarizing and non depolarizing NMB agents, Why? | inhibit plasma cholinesterase activity and cause relaxation on their own |
| What groups of patients will typically receive aminoglycoside antibiotics during anesthetic? | GU cases = gentamycin suspected endocarditis = clindamycin allergic to PCNs or cephalosporins = vancomycin |
| Succinylcholine administration for intubation ________ dose required of non depolarizing NMB | reduces |
| Untreated myasthenia gravis patients are ________ to non depolarizing NMBs because they have _______ receptors for which to compete | sensitive decreased |
| Treated myasthenia gravis patients are ________ to non depolarizing NMBs | resistant |
| Treated myasthenia gravis patients are sensitive to Succinylcholine. Why? | because part of treatment is anticholinesterase drugs which inhibit plasma cholinesterase needed to metabolize SCh |
| Myasthenic Syndrome or Eaton Lambert is seen in what kind of cancer? | oat cell carcinoma of the lungs |
| What is an autoimmune disease where presynaptic calcium channels are destroyed by antibodies | Myasthenic syndrome (Eaton Lambert) |
| Why are anticholinesterase drugs ineffective in Myasthenic Syndrome (Eaton Lambert) patients? | because there is no ACh released into the NMJ |
| Myasthenic Syndrome (Eaton Lambert) patients are _____ sensitive to NMB agents (both SCh and non depolarizers) than myasthenia gravis patients. | more |
| What would be the goal when giving non depolarizing NMB agent to myotonia dystrophica patient? | dose them in order to avoid giving reversal. reversal drug = increase of ACh = possible prolonged contraction in these patients |
| Succinylcholine causes prolonged muscle contraction in patients with _______ ________ | myotonia dystrophica |
| Why is pediatric dosing for non depolarizing NMB essentially unchanged from adult dosing despite increased sensitivity in pediatric patients? | pediatric patients have a larger volume of distribution |
| With regard to non depolarizing NMB, elderly patients typically have _______ duration and ________ onset time. | prolonged duration prolonged onset time |
| Obese patients typically have _______ blockade with non depolarizing NMBs | prolonged (especially with Vecuronium) |
| Rocuronium (Zemuron) dose is based on ______ body weight | ideal |
| Succinylcholine dose is based on _______ body weight | total |
Created by:
Mary Beth
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