L18

Question 1

clonus

Answer 1

reduced ability to lower calcium between stimulations due to increased frequency of stimulation leads to incomplete relaxation

Question 2

tetanic contraction

Answer 2

no appreciable reducing in [Ca2+] between stimuli leads to physiological muscle contraction

Question 3

2 classifications of neuromuscular relaxant drugs

Answer 3

1. non-depolarizing agents (Curare)

2. depolarizing agents (succinylcholine)

Question 4

non-depolarizing drugs mechanism of actions

Answer 4

competitive antagonist at nicotinic Ach receptors. Prevents opening of nicotinic receptor ion channel thus preventing membrane depolarization and end-plate potentials

Question 5

non-depolarizing drugs can be cover come by

Answer 5

excessive Ach through:

1. tetanic stimulation
2. cholinesterase inhibitors

Question 6

T1/2 of non-depolarizing drugs depends on

Answer 6

route of elimination kidney>liver>plasma cholinesterase

Question 7

Pancuronium (mechanism, uses, and excretion and duration)

Answer 7

non-depolarizing neuromuscular relaxant - blocks muscle nicotinic receptors.

used for adjuvant in surgica anesthesia, abdominal wall relaxation and orthopedic procedures

primarily renal excretion

durations 30-60 min

Question 8

Vecuronium

Answer 8

non-depolarizing neuromuscular relaxant

liver and renal excretion

Question 9

mivacurium

Answer 9

non-depolarizing neuromuscular relaxant
good for intubation bc it is fast acting and short lived

excretion: plasma cholinesterases

Question 10

Rocuronium (mechanism, uses, excretion, and duration)

Answer 10

non-depolarizing neuromuscular relaxant

excretion: liver
uses: intubation, muscle relaxation during surgery or ventilation
duration: ~25min

Question 11

receptor reserve and curare compounds

Answer 11

due to the receptor reserve a very high percentage of receptors must be occupied by an antagonist to inhibit contraction (even at 75% occupancy a full strength muscle concentration) therefore even with a long half life the duration of action is short

Question 12

order of effect of non-depolarizing neuromuscular agents

Answer 12

Fine muscles before large limbs before respiratory muscles

extraoccular, hand and feet, head and neck, abdomen and extremities, diaphragm-respiratory muscles

recovery is in the reverse order

Question 13

clinical uses for non-depolarizing neuromuscular agents

Answer 13

Clinical Uses of Non-depolarizing NM relaxants

        Adjuvant to anesthesia during surgery (choice depends on length of surgery and liver/renal function)

Relaxation of larynx for endotracheal intubation (rocuronium and mivacuronium)

Relaxation of chest during mechanical ventilation (choice depends on liver and renal function)

Question 14

Side Effects of non-depolarizing neuromuscular agents

Answer 14

Not analgesic (all)
Apnea (all)

Question 15

inhaled anesthetics affects on non-depolarizing neuromuscular drugs

Answer 15

enhance their effects making the duration unpredictable

Question 16

antidote to non-depolarizing neuromuscular agents

Answer 16

cholinesterase inhibitors- neostigmine

muscarinic blockers - (to minimize the effects of cholinesterase inhibitors) glycopyrrolate

Question 17

depolarizing blocking drugs mechanism of action

Answer 17

agonists ie Succinylcholine

2 phases
phase 1: ion channels are opened depolarizing the membrane. the membrane remains depolarized preventing further APs. Results in a flaccid paralysis. Cholinesterase inhibitors augment block (further prevent repolarization)

phase 2: membrane becomes repolarized
Receptor becomes insensitive to Ach (and other agonists). can be overcome by cholinesterase inhibitors

Question 18

succinyl choline is metabolised by

Answer 18

plasma cholinesterase

Question 19

Depolarizing Agents (Succinylcholine) pharmacokinetics

Answer 19

More rapid onset than non-depolarizing agents

Metabolized by plasma cholinesterase

Action terminated by diffusion away from synapse

Genetic variant of cholinesterase can
prolong T1/2 of Succ

Question 20

Depolarizing Agents (Succinylcholine) clinical uses

Answer 20

Clinical Uses

Endotracheal intubation
Suppression of muscle contraction during ECST
electro-convulsive shock therapy

Question 21

Side effects of Depolarizing Agents (Succinylcholine)

Answer 21

Side Effects

Not analgesic (all)
Apnea (all)
Muscle pain (fasciculations)
Intraocular pressure/intragastric pressure
Stimulation of ganglionic nicotinic receptors (arrhythmia and hypertension)
Stimulation of muscarinic receptors, sinoatrial node
* Hyperkalemia (K+ release from motor endplate)
immediately after burns
several days after widespread tissue injury

Question 22

chemical antidote for Depolarizing Agents (Succinylcholine)

Answer 22

phase I- none

phase II- cholinesterase inhibitors

Question 23

contraindications of Depolarizing Agents (Succinylcholine)

Answer 23

family history of malignant hyperthermia,

burns,

Question 24

Spasmolytic Drugs indications

Answer 24

heightened skeletal muscle tone due to:

1. release from inhibitory supraspinal control
2. increased activity of facilitory pathways
3. increased excitability of α and γ motor systems

Question 25

Goal of spasmolytic therapy is:

Answer 25

reduce 1a afferent-mediated stretch reflex.

enhance activity of inhibitory internuncial neurons

Question 26

Baclofen mechanism of action, uses, side effects

Answer 26

GABA agonists
reduced calcium influx and therefore reduces the release of excitatory transmitters

used for spinal spasticity or spasticity due to multiple sclerosis

side effect: drowsiness

Question 27

Benzodiazepines (Diazepam and clonazepam) (mechanism, uses, and side effects)

Answer 27

facilitate GABA mediated presynaptic inhibition.

used for spinal spasticity and multiple sclerosis

side effects: sedation and drowsiness

Question 28

Tizanidine (mechanism, uses, and side effects)

Answer 28

alpha 2 adrenergic agonist (promotes pre and post synaptic inhibition in the spinal cord.

used for multiple sclerosis and spinal spasticity

side effects: drowsiness, hypotension

Question 29

dantrolene (mechanism, uses, and side effects)

Answer 29

blocks calcium release from sarcoplasmic reticulum in muscle

used for spasticity and malignant hyperthermia

side effects: muscle weakness and sedation