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5 Cards in this Set
- Front
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MECHANISM
Nondepolarizing Neuromuscular Blocking Drugs |
Nondepolarizing drugs prevent the action of ACh at the skeletal muscle end plate (Figure 27–1). They act as surmountable blockers. (That is, the blockade can be overcome by increasing the amount of agonist [ACh] in the synaptic cleft.) They behave as though they compete with ACh at the receptor, and their effect is reversed by cholinesterase inhibitors
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MECHANISM
Depolarizing Neuromuscular Blocking Drugs |
Succinylcholine acts like a nicotinic agonist and depolarizes the neuromuscular end plate (Figure 27–1).
The initial depolarization is often accompanied by twitching and fasciculations (prevented by pretreatment with small doses of a nondepolarizing blocker). Because tension cannot be maintained in skeletal muscle without periodic repolarization and depolarization of the end plate, continuous depolarization results in muscle relaxation and paralysis |
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MECHANISM
Drugs for Chronic Spasm |
Three of the drugs (baclofen, diazepam, and tizanidine) act in the spinal cord
Baclofen acts as a GABA B agonist at both presynaptic and postsynaptic receptors, causing membrane hyperpolarization. Presynaptically, baclofen, by reducing calcium influx, decreases the release of the excitatory transmitter glutamic acid; at postsynaptic receptors, baclofen facilitates the inhibitory action of GABA. Diazepam facilitates GABA-mediated inhibition via its interaction with GABAA receptors (see Chapter 22). Tizanidine, an imidazoline related to clonidine with significant 2 agonist activity, reinforces presynaptic inhibition in the spinal cord. All 3 drugs reduce the tonic output of the primary spinal motoneurons. Dantrolene acts in the skeletal muscle cell to reduce the release of activator calcium from the sarcoplasmic reticulum via interaction with the ryanodine receptor (RyR1) channel. Cardiac muscle and smooth muscle are minimally depressed. |
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MECHANISM
Drugs for Acute Muscle Spasm |
Most of these drugs are sedatives or act in the brain stem. Cyclobenzaprine, a typical member of this group, is believed to act in the brain stem, possibly by interfering with polysynaptic reflexes that maintain skeletal muscle tone
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