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BBDA Spring (Exam 6) > Sedatives and SMR's > Flashcards

Sedatives and SMR's Flashcards

1
Q

Sedative Hypnotics

A

Alcohol

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2
Q

Benzos

A

Xanax, Klonopin, Valium, Ativan, temazepam

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3
Q

Barbiturates

A

phenobarbital, secobarbital

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4
Q

Newer hypnotics

A

zolpidem, zaleplon, eszopiclone

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5
Q

Melatonin receptor agonist

A

Ramelteon (Rozerem)

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6
Q

5-HT agonist

A

buspirone

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7
Q

Centrally acting spasmolytics

A

baclofen, flexeril, soma, metaxalone, methocarbamol, tizanidine

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8
Q

Direct acting muscle relaxant

A

Dantrolene

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9
Q

Sedative hypnotics

A

reduce anxiety and cause drowsiness (sedatives or anxiolytics exert a calming effect) (hypnotics produce drowsiness), may be referred to as CNS depressants, most act via action on GABA receptors in the CNS

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10
Q

GABA

A

major inhibitory transmitters, GABAa and GABAb, responsible for sedation, amnesia, anesthesia, anticonvulsant, antianxiety and muscle relaxation

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11
Q

Drugs that affect GABA

A

Ethanol
Benzos
Barbiturates
Non-BZ sedative hypnotics

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12
Q

Alcohol ADE

A

sedation, euphoria, slowed reaction time, coma, emesis, respiratory depression

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13
Q

Ethanol MOA

A

enhances GABA @ GABAa, inhibits ability of glutamate, depression of contractility of heart, vasodilation in periphery, treatment for essential tremor

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14
Q

Metabolism of Ethanol

A

Ethanol to acetaldehyde via ADH and then to Acetic acid via ALDH

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15
Q

Ethanol ADE

A

hepatitis, cirrhosis, damage to intestines and esophagus, can lead to physical dependence and abuse, increased cardiomyopathy

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16
Q

Treatment of ethanol dependence

A

Disulfiram, Naltrexone, Acamprosate (for acute withdrawal - chlordiazepoxide and clorazepate)

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17
Q

Benzos

A

phase 1 oxidation, phase 2 conjugation,
Short acting- Xanax/Triazolam
Intermediate- clonazepam/ativan
Long acting- Valim/Fluzazepam

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18
Q

Non-BZ hypnotics

A

bind GABAa receptors in different sites than BZ’s, rapidly absorbed, short half-lives,

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19
Q

Flumazenil

A

overdose management of BZ’s, lunesta, ambien, sonata

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20
Q

Anesthesia

A

BZ’s are used IV in combo with other agents

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21
Q

Anticonvulsant

A

Phenobarb, Klonopin, Valium, Ativan

22
Q

Tolerance

A

the need for higher doses to produce response

23
Q

Physical dependence

A

withdrawal symptoms elicited upon d/c

24
Q

Addiction

A

use despite harm, psychological craving and display of addictive behaviors

25
Q

Clinical uses of sedative hypnotics

A

anxiety, insomnia, sedation and amnesia during procedures, tx of epilepsy and seizures, component of anesthesia, for alcohol and sedative hypnotic withdrawal states, muscle relaxation

26
Q

Rozerem

A

ramelteon, no effects on GABA, reduces sleep latency, could decrease testosterone and increase prolactin

27
Q

Buspar

A

buspirone, reduces anxiety w/out sedation, acts via 5-HT and NE, nor for acute anxiety

28
Q

Hydroxyzine

A

Atarax (anthihistamine)

29
Q

Trazodone

A

Desyrel

30
Q

Neuromuscular Blocking Agents

A

Non-depolarizing=pancuronium

Depolarizing=succinylcholine

31
Q

Centrally-acting relaxants

A

BZ’s, baclofen, flexeril, soma, methocarbamol

32
Q

Non-depolarizing blockers

A

antagonize ACh by blocking ACh binding at nicotinic receptors, prevents deplarization and propagation of the action potential, vercuronium etc.

33
Q

Depolarizing Blockers

A

too much depolarizing agonsits also stop the propagation of the action potential, persistent depolarization makes the muscle fiber resistant to ACh, ex succinylcholine

34
Q

Depolarizing Blockers

A

too much depolarizing agonsits also stop the propagation of the action potential, persistent depolarization makes the muscle fiber resistant to ACh, ex succinylcholine

35
Q

Botox

A

blocks ACh at motor endplate, results in paralysis

36
Q

Clinical use of neuromuscular blocking drugs

A

relaxation for surgery, intubation, control of ventilation, tx of convulsions

37
Q

Spasticity

A

exaggerated muscle stretch reflex, occurs when supra spinal control is lost b/c of damage to spinal cord/brain (causes: CVA, CP, MS)

38
Q

Spasticity Triad

A

Painful mass muscle spasms, rigid posturing of limbs, increased reflexes

39
Q

Muscle Spasms

A

increased tension in skeletal muscle following strain, pt is unable to relax, tonic contraction of muscle

40
Q

SMR ADE

A

drowsiness, dizziness, ataxia (w/out control during voluntary mvmt), fatigue and muscle weakness

41
Q

Agents for Spasticity

A

baclofen (Lioresal)
dantrolene (Dantrium)
tizanidine (Zanaflex)

42
Q

Spasticity MOA

A

decrease reflex activity in spinal cord and inhibit motor neuron activity,

43
Q

Baclofen MOA

A

activates pre and post synaptic GABAb receptors, results in hyperpolarization and Ca influx, can be intrathecal

44
Q

Dantrolene

A

directly inhibits skeletal muscle contraction, ONLY one to exert its effects DIRECTLY on the skeletal muscle cell, impairs Ca release from SR, enhances relaxation, used to treat malignant hyperthermia

45
Q

Tizanidine

A

agonist at central alpha-2 receptors, much less blood pressure lowering ability

46
Q

Agents for muscle spasms

A

Soma, chlorzoxazone, Flexeril, Skelaxin, Robaxin, Norflex, Zanaflex

47
Q

Muscle spasms meds MOA

A

blocks inter-neuronal activity of the descending reticular formation

48
Q

Soma Toxicity

A

metabolized via liver into meprobamate which is a sedative hypnotic, causes tremors, hallucinations, and anxiety

49
Q

Flexeril

A

structurally related to TCA

50
Q

Summary:

A

include BZ, barbiturates, non-BZ gabaergic agents, used for sleep, anxiety, convulsions or muscle relaxants, BZ differ in half life and active metabolites, non-BZs used for sleep, SMR include neuromuscular blokcers, centrally acting agents and dantrolene (directly on skeletal muscle), all used for spasticity or muscle spasms

BBDA Spring (Exam 6) (5 decks)

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