Term
|
Definition
|
|
Term
| Postsynaptic relaxants (3) |
|
Definition
Cisatracurium
Vecuronium
Succinylcholine |
|
|
Term
| Spinal interneuron relaxants (2) |
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Definition
|
|
Term
| Skeletal muscle contractile relaxant |
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Definition
|
|
Term
| Reasons to block NMJ transmission (4) |
|
Definition
Facilitate intubation
Adjunct to surgical anesthesia: decrease reflex mvmt and relax muscles to gain access to operative sites
Facilitate mechanical ventilation
Reduce muscle contractions and decrease local pain reflexes (botulinum) |
|
|
Term
| Reasons to inhibit spinal interneuron trasmission = centrally acting (2) |
|
Definition
Decrease spasticity = excessive motor reflex activity due to sprains, arthritis, myositis, fibrositis
Decrease hypertonia |
|
|
Term
| Reasons to disrupt skeletal muscle contractile process = peripherally acting(2) |
|
Definition
Prophylaxis of malignant hyperthermia
Spasticity due to UMN lesions: strokes, MS, postencephalitic athetosis and dystonia |
|
|
Term
|
Definition
| Cleaves SNARE proteins = presynaptic ACh vesicles aren't attached to the exocytic membrane = can't release ACh |
|
|
Term
| Botulinum toxin: pharmacodynamics |
|
Definition
|
|
Term
| Vecuronium, cisatracurium: MOA |
|
Definition
Non-depolarizing competitive blockade
-Has an NH4+ group that attracts the postsynaptic negatively-charged ACH-R a-subunit
-Binds, but has no intrinsic activity
-Muscle relaxes due to lack of input (but will contract if directly electrically stimulated)
Can be overcome with increased ACh, which can be accomplished by inhibiting its breakdown = AChE inhibitors reverse the block |
|
|
Term
|
Definition
Depolarizing non-competitive blockade
-Has 2 NH4+ groups that attract the postsynaptic negatively-charged ACH-R a-subunit
-Binds and actually depolarizes the postsynaptic membrane
-It keeps the gate open = initial stimulation but no cycling of depol/pol, appears as fasciculation
-Remains on the ACh-R until it diffuses away and is broken down
Phase I: initially ACh/AChE intensify the blockade, because it's like there's more ACh available to the NMJ, but the NMJ feels like there's too much ACh in the first place
Phase II: eventually, the receptor is desensitized to succinylcholine and repolarizes, it's now equivalent to competitive blockade and can be reversed by ACh/AChE |
|
|
Term
| Most of cisatracurium undergoes ___ at normal body temp/pH by a ___ with the rest cleared by ___ |
|
Definition
Spontaneous metabolism
Base-catalyzed hydrolysis (Hoffman elimination)
Hepatic metabolism |
|
|
Term
| Hypothermia can intensify both ___ and also prolong ___ |
|
Definition
Non-depol and depol blockade
Duration of muscle relaxation |
|
|
Term
| Succinylcholine has a ___ duration while cisatracurium has an ___ |
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Definition
|
|
Term
| Patients with MG are more sensitive to ___ because ___ and so they need ___ |
|
Definition
Competitive blockers
Have fewer ACh-R
Smaller dose |
|
|
Term
| Succinylcholine has a short duration of action because ___ and ___ (also means that only a small amount reaches the NMJ) |
|
Definition
Diffusion
Rapid hydrolisis |
|
|
Term
| Patients with atypical/low AChE exhibit ___ with succinylcholine |
|
Definition
|
|
Term
|
Definition
Bradycardia, cardiac dysrhythmias
Increased IOP, ICP, intragastric pressure
Myalgia
Myoglobinuria |
|
|
Term
| Patients with MG are less sensitive to ___ because ___ |
|
Definition
Succinylcholine
Fewer ACh-R to depolarize |
|
|
Term
| Post burn/trauma there's a proliferation of ___, which ___ and ___ when given succinylcholine |
|
Definition
AChR on muscle
Causes contraction of the muscle and release of K |
|
|
Term
| Factors that augment vecuronium, cisatracurium blockade |
|
Definition
Inhaled anesthetics (dose-dependent)
Ab, especially aminoglycosides |
|
|
Term
| If using succinylcholine + drugs that decrease serum K, you'll have to ___ |
|
Definition
| Probably increase the dose of the serum K drug since succinylcholine can cause hyperkalemia |
|
|
Term
|
Definition
| Enhances GABA to decrease spinal interneuron signaling |
|
|
Term
| Centrally acting muscle relaxants: MOA |
|
Definition
| Depress excess activity in spinal/supraspinal interneurons and motor reflex pathways responsible for hypertonia |
|
|
Term
|
Definition
| Decreases glutamate release from spinal neurons = decreased interneuronal excitation |
|
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Term
|
Definition
| Binds to and inhibits SR ryanodine-R = inhibits release of Ca during excitation/contraction |
|
|
Term
| Malignant hyperthermia is ___ when triggered (anesthetic, muscle relaxant, etc.), causing ___, which leads to ___ and ___ |
|
Definition
Severe muscle spasms
Sustained SR-release of Ca
Hypermetabolism, spasms, rigidity
Rapid increase in body temperature |
|
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Term
|
Definition
| Generalized muscle weakness, fatigue |
|
|
Term
| Patients are usually treated with Dantrolene Na ___ |
|
Definition
| Prior to the potential trigger |
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