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52 Cards in this Set
- Front
- Back
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List all the non-depolarizing neuromuscular blockers.
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Cisatracurium
Doxacurium Mivacurium Atracurium Metocurine Tubocurarine Vecuronium Pipercuronium Rocuronium Pancuronium |
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List all the depolarizing neuromuscular blockers.
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Succinylcholine
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How do non-depolarizing neuromuscular blockers work?
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They competitively block Nicotinic Acetylcholine Receptors, thus preventing motor neuron-released Acetylcholine from binding
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How does succinylcholine work?
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It overstimulates the Nicotinic Acetylcholine Receptors, thus fatiguing muscles into relaxation, and desensitizing it to stimulation by Acetylcholine
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Describe how liver metabolism of ND NM-blockers affects duration.
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Hepatic elimination results in medium or short duration, about 20-35 minutes.
Metabolites may accumulate with extended use. |
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Describe how kidney elimination of ND NM-blockers affects duration.
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Renal elimination is slow, >35 minutes duration.
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Describe how spontaneous breakdown applies to ND NM-blockers.
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Spontaneous breakdown follows Hoffmann elimination - duration of effect of drugs is about 20-35 minutes. Breakdown product is Laudanosine and crosses the BBB, causing seizures with prolonged use.
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Describe how plasma cholinesterase affects duration of ND NM-blockers.
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It results in rapid inactivation, duration is only 10-20 minutes.
There is less plasma cholinesterase in patients with renal failure, so duration will be extended in renal failure patients. |
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Which ND NM blockers are eliminated primarily via the Kidney?
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Pancuronium
Tubocurarine Metocurine Doxacurium |
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Which ND NM blockers are eliminated primarily via the Liver?
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Vecuronium
Rocuronium Pipercuronium |
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Which ND NM-blockers are eliminated via Plasma Cholinesterase?
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Mivacurium
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Which ND NM-blockers are eliminated via spontaneous breakdown (Hoffmann elimination)?
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Atracurium (20-35 minutes)
Cisatracurium (25-44 minutes) - takes longer |
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Which ND NM-blocker has the fastest onset?
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Rocuronium
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How can the effects of ND NM-blockers be reversed?
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Cholinesterase inhibitors - results in more Acetylcholine at the NMJ
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Which ND NM-blockers have the least effect on CV? No histamine release?
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Vecuronium
Pipecuronium Doxacurium Cisatracurium Rocuronium |
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Which ND NM-blockers produce bronchospasm and hypotension?
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Tubocurarine
Mivacurium Atracurium |
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How can bronchospasm and hypotension from ND NM-blockers be reduced?
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By administering antihistamines beforehand
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What ND NM-blocker is Vagolytic?
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Pancuronium - vagolytic, resulting in tachycardia, which may be useful in pediatric patients with bradycardia.
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Which ND NM-blockers are derived from steroids?
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Vecuronium
Pipercuronium Rocuronium Pancuronium |
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Which ND NM-blocker has some muscarinic effects on the heart?
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Rocuronium
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Describe the metabolism, duration, etc of Succinylcholine.
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Succinylcholine is structurally similar to Acetylcholine but is less easily degraded.
It is metabolized by Plasma Cholinesterase, has fast onset, and has very short duration. |
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Describe Phase I of the depolarizing effects of Succinylcholine.
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Phase I block (Depolarizing) - Flaccid Paralysis
General disorganized contraction of motor units (muscle fasciculation) Membrane remains depolarized so no "repriming", unresponsive to subsequent stimulus, augmented (NOT reversed) by cholinesterase inhibitors |
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Describe Phase II of the depolarizing effects of Succinylcholine.
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Phase II block - desensitizing - after continued exposure
Endplate depolarization decreases Membrane repolarizes but cannot produce generalized depolarization (channel block?) Late phase II block becomes similar to blockade with nondepolarizing drugs - reversible by acetylcholinesterase inhibitors. |
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Which phase of depolarization can be treated by Acetylcholinesterase Inhibitors?
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Late Phase II - it resembles nondepolarizing drugs.
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What will happen if Cholinesterase Inhibitors are administered during Phase I block?
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The effects will be compounded - since there will be more acetylcholine to add to the overstimulating effects of succinylcholine.
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What side effects are associated with Succinylcholine?
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Arrhythmia (with Halothane)
Bradycardia (better when combined with Atropine) Hyperkalemia (especially in patients with nerve damage) Increased intraocular pressure and intragastric pressure Muscle pain Malignant hyperthermia Caution in Children |
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Which ND NM-blockers may cause seizures with prolonged use?
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Atracurium, Cisatracurium - due to the elimination product Laudanosine
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What are the indications for ND NM-blockers?
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Used during surgical procedures and in the ICU to cause paralysis
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What effect do ND NM-blockers have on Succinylcholine?
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Antagonism - they prevent the overstimulation form occurring by preventing Succinylcholine from binding to the Nicotininc receptors, just as they prevent Acetylcholine from binding.
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What are the drug interactions associated with NM-blockers?
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Inhaled anesthetics augment activity
Antibiotics increase activity Local anesthetics and antiarrhythmics augment activity Antagonism from Cholinesterase Inhibitors |
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Can NM blockers also be used to control ventilation and convulsions?
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Yes
Control of ventilation - eliminates chest wall resistance Treatment of convulsions, seizures - no central effect |
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Define spasticity, as a clinical problem.
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Diseases with abnormally high reflex activity in neuronal pathways that control skeletal muscle.
Examples: Cerebral Palsy, MS, Stroke |
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What are some symptoms of Spasticity?
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Increase in tonic stretch reflexes and flexor muscle spasms
Together with muscle weakness (painful spasms) Abnormal bowel, bladder, and skeletal muscle function Stretch reflex arc is intact, but UMN lesion, damage to descending motor tract. |
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Name the Spasmolytic drugs.
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Dantrolene
Baclofen Diazepam Barbiturates Tizanidine Gabapentin Glycine, Progabide Riluzole Cyclobenzaprine, Carisoprodol, Chlorphenesin, Chlorozoxone, Metaxalone, Methocarbamol, Orphenadriene |
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How does Baclofen work as a spasmolytic?
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It is a GABA-B agonist - metabotropic receptor activation increases K+ channel activity, resulting in hyperpolarization, and a decrease in excitatory NT release in stretch reflex arc.
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How does Baclofen compare to Diazepam and Dantrolene?
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Baclofen is as efficacious as Diazepam but without sedation
Baclofen does not work by reducing muscle strength, as does Dantrolene |
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When is intrathecal administration of Baclofen by pump indicated?
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For severe spasticity and pain - greatly increases quality of life
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What are the toxicities of Baclofen?
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Transient drowsiness, Seizures in Epileptics
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What is Tizanidine?
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Congener of Clonidine (alpha-2 adrenoceptor agonist)
Reinforces postsynaptic and presynaptic inhibition of the motor neuron in the spinal cord |
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What other Spasmolytics are of comparable efficacy to Tizanidine?
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Baclofen, Dantrolene, Diazepam
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What are the toxicities of Tizanidine?
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Drowsiness, Hypotension
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How does Gabapentin act as a spasmolytic?
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May be useful in spasms of patients with MS - increases GABAergic transmission
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What are the side effects of Gabapentin?
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Somnolence, Dizziness, Ataxia, Headache, Tremor
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What do Glycine and Progabide do?
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They activate GABA B and A receptors, help spasticity in some patients
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What is Riluzole?
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A primary treatment for ALS, but also treats ALS-induced spasms - inhibits glutaminergic transmission in the CNS
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How does Dantrolene treat Spasticity?
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It reduces skeletal muscle strength - binds to Ryanodine calcium channels in the sarcoplasmic reticulum and inhibits release of calcium from the SR, preventing contraction.
Cardiac and Smooth Muscle are hardly affected due to difference in Ca2+ release mechanisms. |
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What toxicities are associated with Dantrolene?
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Muscle weakness, Sedation
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What are some special applications of Dantrolene?
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Treatment for Malignant Hyperthermia for patients with hereditary defect in Ca2+ sequestration - prompt IV dantrolene is treatment
Also for neuroleptic malignant syndrome associated with neuroleptic drugs |
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How is Botulinum Toxin used for Spasticity?
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It prevents release of ACh from vesicles, used ophthalmologically, also a single ingestion can work for weeks-months in patients with generalized spastic disorders following a stroke.
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What are some drugs for acute local muscle spasm?
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Cyclobenzaprine
Carisoprodol Chlorphenesin Chlorozoxone Metaxalone Methocarbamol Orphenadriene |
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What are the toxicities associated with Cyclobenzaprine and related drugs used for acute local muscle spasm?
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Sedation, antimuscarinic effects, Fatigue, Asthenia, Nausea, Constipation, Dyspepsia, Taste Changes, Blurred Vision, Headache, Nervousness, Confusion, Transient Visual Hallucinations
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How does Cyclobenzaprine treat acute local muscle spasms?
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It is related to TCAs...
Interferes with polysynaptic reflexes in the brainstem that maintain skeletal muscle tone. Ineffective in cerebral palsy, spinal cord injury. |
