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29 Cards in this Set
- Front
- Back
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What is common to all neuromuscular blockers? What does this mean?
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All 4º amines. ∴ highly polar they must be given IV only & and do not cross the BBB.
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What is significant about the metabolism of pancuronium?
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• Renal elimination
• Slow elimination, LONG duration • Steroid PANcuronium action sPANs a long time. |
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What is significant about the metabolism of vecuronium & rocuronium?
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• Hepatic elimination
• Fast elimination. • Metabolic accumulation w/ extended use. • Steroids. |
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What is significant about the metabolism of atracurium?
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• Spontaneous breakdown - Hoffman elimination
• Metabolite = laudanosine which crosses BBB and can cause seizures w/ prolonged use. • Isoquinolone. |
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What muscle relaxant can cause seizures w/ prolonged use? Why?
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• Atracurium.
• Laudanosine (metabolite) crosses BBB. |
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What is significant about the metabolism of mivacurium?
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• Rapid inactivation by plasma cholinesterase
• Isoquinolone. mne: MIvacurium gone in MInutes. |
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What is of concern in certain patients when administering succinylcholine?
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• Certain patients have abnormal cholinesterase
• Measured "dibucaine number" • Abnormal cholinesterase causes prolonged duration (normal is very rapid hydrolysis) |
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What is phase I of succinylcholine? What is phase II? Which phase is reversible by acetylcholinesterase inhibitors? Why?
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• Phase I: depolarizing or "flaccid paralysis phase." Maxes out muscle.
• Phase II: block or desensitizing phase. • Phase II is similar to blocking by antagonists. *Reversible by Ach inhibitors* |
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What non-depolarizing muscle relaxant drug has the fastest onset?
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• Rocuronium (1-2 mins)
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What non-depolarizing muscle relaxant drug has duration of 15 mins? Or 60 mins?
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• Mivacurium: duration 15 mins
• Tubocurarine: duration 60 mins |
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What it the mechanism for the reversal of non-depolarizing muscle relaxants?
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• Non-depolarizing muscle relaxants are antagonists at the ACh receptor. Using Acetylcholinesterase inhibitors (Neostigmine, etc) allows ACh to remain at the NMJ and surmount the antagonists.
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Which muscles are most sensitive to non-depolarizing muscle relaxants?
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Face > Foot & Hand >>>> Abdomen & trunk
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Which muscles are most sensitive to succinylcholine?
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after IV admin:
• transient muscle fasciuclations • paralysis of arm, neck, leg muscles • paralysis of facial & pharngeal muscles • paralysis of respirtaory muscles |
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What patients have ↑ sensitivity to NM blockers? Who has ↓ sensitivity?
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• ↑ Myasthenica gravis, older age
• ↓ burn patients |
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What non-depolarizing muscle relaxant drug is notable for moderate block at cardiac muscarinic ACh receptors? What can this cause?
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Pancuronium
• Can cause vagolytic tachycardia *think* long duration, stays in blood longer, better chance of affecting heart |
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What non-depolarizing muscle relaxant drug is notable for weak block at autonomic ganglia nicotinic ACh receptors and for moderate histamine release?
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Tubocurarine
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What muscle relaxant can cause stimulation of both autonomic ganglia ACh receptors, cardiac muscarinic receptors, and slight histamine release? What does this cause?
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Succinylcholine
• Bradycardia (which can be alleviated w/ co-admin of atropine) *think* structure is 2 Ach molecules, thus non-discriminate also means there are a lot of side effx. |
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What drugs can cause bronchospasm and hypotension? Why? How can these effects be attenuated?
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• Tubocurarine, Micacurium, atracurium
• All have slight effects on Histamine release Can be attenuated w/ antihistamine premedication. |
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What drug can cause arrythmias when administerd w/ Halothane? What else can it cause? Why?
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• Succinylcholine
• Bradycardia (which can be alleviated w/ co-admin of atropine) • Stimulates all autonomic cholinorecepotrs and muscarinic receptors on the heart. |
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What are the side effects of succinylcholine?
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• Bradycardia
• Arrythmias (when administered w/ Halothane) • Hyperkalemia • ↑ IOC • ↑ intragastric pressure/emesis • muscle pain • Malignant hyperthermia |
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What drug interatctions are important to keep in mind when considering the use of muscle relaxants?
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• Succinylcholine + Halothane = cardiac arrythmias
• Tubocurarine + Isoflurane = ↑ NM block • Tubocurarine + Halothane = ↑ NM block • NM block is enhanced by general anesthetics, local anesthetics, antiarrythmic drugs, aminoglycoside antibiotics |
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How does Baclofen act as a spasmolytic drug?
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• Baclofen ↓ Ia fber activity (which excites motor neurons).
• Baclofen binds to the GABA-B metabotropic receptor on both the excitatory neuron in the LCST & the Ia motor neuron. • Baclofen causes hyperpolarization (by ↑ gK+) of the excitatory neuron (which synapses on the motor neuron) and the motor neuron itself. • Overall this ↓ activity of the stretch reflex arc |
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What are the toxicities of Baclofen?
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• Baclofen is a GABA-B agonist
• Toxicities = drowsiness & seizures in epileptics |
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How does Tizanidien act as a spasmolytic drug? What are the toxicities?
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• Tizanidine acts on α2 adrenoreceptor.
• ↑ pre-synaptic & post-synaptic inhibition of motor neuron in the cord. Toxicities: drowsiness & hypotension |
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In addition to pain (neuropathies, centrally mediated pain) what is Gabapentin used for?
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• Spasms in MS pts.
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What is Riluzole used for?
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• ALS induced spasm.
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What drug reduces muscle strength by binding to the ryanodine calcium channel in the SR therby ⊣ Ca++ release?? What is the final effect?
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• Dantrolene
• ↓ Skeletal muscle strenght, used as a spasmolytic. (also indicated for Malignant Hypertension) |
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What is the MOA of botulinum toxin? In addition to cosmetic applications, what is it used for?
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• Prevents release of ACh from vesicles by inhibiting docking proteins
• Generalized spastic disorders dues to neurologic injury. |
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What is the MOA of cyclobenzaprine? What are the toxicities?
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• Interfers w/ polysynaptic reflexes in the brainstem that maintain skeletal muscle tone
• Toxicities: sedation, antimuscarinic effects, fatigue, taste changes, blurred vision, headache, nervousness, visual hallucinations (can't drive) |
