Local Anesthetics Local anesthetics work by rendering a specific portion of the

Local anesthetics local anesthetics work by rendering

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blood brain barrier to concentrate in nerve cell membranes. Local Anesthetics Local anesthetics work by rendering a specific portion of the body insensitive to pain by interfering with nerve transmission. Nerve conduction is blocked only in the area in which the anesthetic is applied, and there is no loss of consciousness. Local anesthetics block both the generation and conduction of impulses through all types of nerve fibers by blocking the movement of certain ions important to this process. They do this by making it more difficult for these ions to move in and out of the nerve fiber. For this reason, some of these drugs are also described as membrane-stabilizing because they alter the cell membrane of the nerve so that the free movement of ions is inhibited. The membrane stabilizing effects occur first, and then pain and other sensory functions are lost. Motor activity is the last to be lost. When the effects of local anesthetic wear off, recovery occurs in reverse order. Classification-CNS Depressant Subclass: Neuromuscular Blocking Dugs Drug Name: Pancuromium(Pavulon) NMBDs are classified into two groups based in mechanism of action: depolarizing and non depolarizing. Depolarizing NMBDs work similarly to the neurotransmitter acetylcholine. They bind in place of Ach to cholinergic receptors at the motor endplates of muscle nerves or neuromuscular junctions. Thus they are competitive agonists. There are two phases of the depolarizing block. During phase I (depolarizing phase), the muscle fasciculate (twitch). Eventually, after continued depolarization has occurred, muscles are no longer responsive to the Ach released; thus muscle tone cannot be maintained and the muscles become paralyzed. This is phase II, or the desensitizing phase. Depolarizing NMBDs include d- tubocurarine and succinylcholine. The duration of action of succinylcholine after a single dose to facilitate intubation is only about 5-9 minutes because of the rapid breakdown of the drug by cholinesterase, the enzyme responsible for metabolizing succinylcholine. Non depolarizing NMBDs also bind to Ach receptors at the neuromuscular junction, but instead of mimicking Ach, they block its actions. Therefore, these drugs are competitive antagonists of Ach. Consequently, the nerve cell membrane is not depolarized, the muscle fibers are not stimulated, and skeletal muscle contraction does not occur. Non- depolarizing NMBD;s include vecuronium and pancuronium and are typically classified into three groups based on their duration of action: short-acting, intermediate acting, and long acting drugs. Antiepileptic Drugs Alter the movement of sodium, potassium, calcium, and magnesium ions. Changes in movement of these ions cause more stabilized and less excitable cell membranes. Major pharmacologic effects of antiepileptic’s are three fold. First, increase the threshold of activity in the area of the brain called the motor cortex. Makes it difficult for a nerve to be excited, or they reduce the nerve’s response to incoming electrical or chemical stimulation. Second, they act to limit the spread of a seizure discharge from its origin. Suppressing the transmission of impulses from one nerve to the next. Third, they
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  • Winter '16
  • Neurotransmitter, dopamine receptor agonists, dopamine replacement drugs

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