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50 Cards in this Set

  • Front
  • Back
Sedative or anxiolytic agents do what?
reduce anxiety, exert calming and relaxing effects
Hypnotics do what?
produce drowsiness, and onset and maintainance of sleep
Treatment of anxiety states: To treat or not to treat
Meds, substance related: don't give more drugs.

Dz related: Trt the Dz, may use short term sedative-hypnotic.

Situational anxiety: i.e. acute stress disorder, death, divorce etc. Use short term seds-hyps.

Chronic anxiety: treat underlying condition, though responds well to seds-hyps.
Treatmen of sleep disorders: treat or not to treat?
Sleep apnea: no, don't treat... might decrease arousal to hypoxia.

circadian rhythm: hypnotics helpful in reseting internal clock

Dz related insomnia: trt underlying medical condition

Meds, substancee related: alter current med dosing or med choices.

Transient Insomnia: due to stree, lifestyle changes etc. Limit hypnotic use to 1-3 days. , no more than 3 wks b/c of withdrawal effects, should be tapered off hypnotics.

Chronic Insomnia: investigate underlying cause. Change in behavior, excercise diet plus hypnotics for trt.
allosterically enhance affinity of GABA for GABAa-R, resulting in inhibition due to GABA induced prolong duration Cl- channel opening.
Barbiturates at high doses
Also directly activate GABAa receptor, inhibit AMPA receptor function, and inhibit nAChR at autonomic gn and muscle.
So what's the consequence of direct activity of barbiturates on GABAa-Rs?
it has a dose-proportional effect causing sedation, then sleep, anesthesia, coma and death. Benzodiazapenes don't do this.
Problems with barbiturates
Low TI, do not induce physiological sleep, rx interactions,m abuse and addiction, residual CNS effects afterwards, tolerance, withdrawal.
Long acting barbiturates:
daytime seedative, antiseizure agent

Phenobarbital*: 80-120 hrs, also used for hypnosedative withdrawal.

mephoobarbital: 10-70 hr
Intermediate acting barbiturates:
Pentobarbital*: 15-50 hr

hypnotic, preoperative sedative, emergency mgmt of seizure

Pentobarbital*: 15-50 hr
amobarbital (amytal): 10-40 hr

secobarbital: 15-40 hr
Short-acting barbiturates:
induction or maitainance of anesthesia:

Thiopental*: 8-10 hr

methohexital: 3-5 hr
barbiturate metabolism
short acting barbiturate affect limited by their redistribution from CNS to lipids and muscle (they are very lipophylic).

Metabolism/conjugation occurs in liver. Still 30% excreted unchanged in urine.
Barbiturate poisoning
Sx: Moderate resemble alcohol intox,

Severe: coma, hypothermia, hypotension, bradyapnea, bradycardia, hypoxia, shock, cold sweaty skin.

Treatment: supportive, respiration, cardiovascular. Most deaths due to cardiovascular collapse, respir and renal failure.
Treatment for barbiturate poisoning
supportive, remove drug, NEVER give CNS stimulants b/c it can result in massive withdrawal reactions.
Increase GABAa-R affinity for GABA by allosteric effects similar to barbiturates HOWEVER, no DIRECT effects on GABAa-R in absence of GABA. Do not inhibit nAchR and AMPA.
What makes Benzodiazepines better than barbiturates?
No coma or death with overdose. But depressant action are additive with CNS depressants, so NO ALCOHOL.
Benzodiazepines: alprazolam
for anxiety, 10-14hrs
Benzodiazepines: chlordiazepoxide
anxiety, alcohol withdrawal, preanestheic med, 7-13 hrs
Benzodiazepines: clonazepam
seizures, mania, movement disorders, 20-27 hrs
Benzodiazepines: diazepam
anxiety, status eplilepticus, muscle relaxation, preanesthetics, 43 pm 13 hrs
Benzodiazepines: flurazepam
insomnia, 74 pm 24 hrs
Benzodiazepines: Lorazepam
anxiety, status epilepticus,, preanesthetics, 14 pm 5 hrs
Benzodiazepines: midazolam
preanesthetic and intraoperative med, 1.9 pm .6 hrs
insomnia, 11 pm 6 hrs
Benzodiazepines adverse effects
alter normal sleep pattern, impaired mental/motor fxn, ataxia, daytime sedation, anterograde amnesia, additve with other CNS depressants ie. Eth.

abrupt withdrawal can cause anxiety, nausea, seizures

Tolerance and abuse
Benzodiazepines Metabolism
Daizepam has active metabolites, Lorazepam does not have active metabolites. These active metabolize under estimate the duration of drug effect.

metabolized in liver by CYP4503A4, so drug interraction with 3A4 inhibitors.
Non-Benzodiazepines (z-drugs)
most widely used hypnotics.
Advantages: an anxiolytic, muscle relaxant or antiseizure properties ,maintain normal sleep pattern, less rebound insomnia and withdrawal sx, low potential for tolerance, dependance or abuse.
Why are non-bz drugs free of anti-seizure or muscle relaxing properties?
b/c it affects alpha 1 receptors subunit only, which is sedation only.

alpha 2 subunit is anxiolytic, muscle relaxant.
more on the receptors
GABAa-R: alpha 1-6) beta (1-3) plus other variable subunits.

BZ site: alpha 1-3, 5 and gamma 2. (no beta)
adverse effects of z drugs
headache, additive with other cNS depressants, bitter aftertaste, memory impairment during first week with eszopiclone, pyscholigical habbit forming? , sleepwalking, sleep eating with zolpidem. BZ and non-BZ can cause amnesia and not remember night time actions.
Z drugs: Zolpidem
aka ambien. Incrase sleep duration, for short term use upto 10 days.
decrease latency to sleep, no sleep maintainance, short term use only upto 10 days.
aka lunesta. increase sleep duration, approved for long term use (upto 6 months), potential for tolerance, dependance or abuse.
Z-drug antagonist
Flumazenil: competitive antagonist. Decrease recovery time, rapid metabolism so might require multiple doses.

adverse: agistation, confusion, dizziness, nausea, risk of seizures
About Melatonin
derived from Serotonin, snyth and secreted by pineal gland, synth controlled by light. Meltanonin lightens skin pigment, supress ovarian function, role in biological rhythm.
What's Melatonin commonly have been used for?
promote sleep (through MT1-R), reduce jetlag (MT2-R).
MT1: regulate sleepiness.//

MT2: reg. circadian rhythm.//

both found in suprachiasmatic nucleaus (SCN)
MT1/MT2-R Agonist
Ramelteon (Rozeram)

use: hypnotic (no sleep maintainance though).

CYP1A2, 3A4, 2C9 inhibitors increase the drug.
Advantages of MT-R agonist
Ramelteon: no gen. CNS depression, no moter/cognitive impairment, little change in sleepiness, approved for long term use.
Disadvantages of MT-R agonist
Ramelteon: increase Prolactin >> hypogonadism, infertility, decreased libido, osteoporosis, decrease Testosterone.
Serotonergic Agents
Buspirone: partial agonist at 5-HT1a-R.

Uses: anxiety, depression, psych disorders.

advantages: safter, less abuse potential, less psychomotor

disadvantages; weak anxiolytic, dizziness, headache, nausea
Antihistamines as sleeping aid
Doxylamine, diphenhydramine://

issue due to rapid dev'p of tolerance, residual day time sedation, dry mouth, urinary retention.
ancient root from stems of valerian plant, used to treat sleep disorders but data in clinic inconclusive.
gamma-hydroxybutyrate (GHB) aka sodium oxybate
a metabolite and precursor for GABA. Injested GHB will activate both GHB-R and GABAb-Rs.

GHB is sched. 1 controlled drug, highly addictive, euphoric, hallucinogenic. Replacing Flunitrazepam as 'date rape' drug.
What are spasmolytic drugs?
subclass of muscle relaxants, used in symptomatic treatment of MS, ALS, cerebral palsy, stroke or local muscle trauma.
Which spasmolytic drug is approved for musculoskeletal problems?
benzodiazepines... that's it!
spasmolytics: Baclofen
spasmolytic drug, GABAb-R agonist, increase K permeability >> decrease Glu release.

adverse effects: drowsiness, seizures, less sedation than benzodiazepines
spasmolytics: Tizanidine
central alpha 2 adrenergic receptor agonists. inhibit pre and post synap motor neurons.

adverse: drowsiness, hypotension, dry mouth, weakness
spasmolytics: Dantrolene
decrease Ca relase from sarcoplasmic reticulum << DIRECT ACTION ON MUSCLE. //

also used in malignant hypethermia.

adverse: general muscl weakness. CONTRAINDICATED IN ALS., sedation, rare but serious hepatotoxicity.
spasmolytics: benzodiazepines
diazepam and clonazepam

adverse: sedation, respir. depression in advance ALS.