Psyc 430 Ch 5

Front 1

This and other sedatives reduce excitatory activity or increase inhibitory activity, resulting in lower whole-brain metabolic activity and lower electrical and metabolic activity of brain circuits.

Back 1

Barbiturates

Front 2

the primary excitatory neurotransmitter for barbiturates

Back 2

Glutamate

Front 3

the primary inhibitory neurotransmitter for barbiturates

Back 3

GABA

Front 4

A study that proposed that the amnestic effects of sedatives and anesthetics may be due to glutamate antagonism, since declarative memory formation greatly depends on glutamatergic neurons.

Back 4

Jevtovic-Todorovic and coworkers (1998)

Front 5

An anesthetic that produces amnesia through presynaptic inhibition

Back 5

isoflurane

Front 6

An anesthetic that produces amnesia by reducing cerebral blood flow in right prefrontal and right posterior parietal lobe

Back 6

propofol

Front 7

Barbiturates, benzodiazepines, and ethanol bind to their respective sites on this receptor.

Back 7

GABAa receptor

Front 8

due to facilitation of GABA transmission at GABA-A receptors by opening chloride channels and hyperpolarizing the neuron.

Back 8

sedative-hypnotic and anesthetic actions (of anesthetics, barbiturates, benzodiazepines)

Front 9

increases GABA’s affinity for its receptor and prolongs the opening of chloride channels four- to five-fold (increasing CNS inhibition).

Back 9

Barbiturate binding

Front 10

produce limited CNS depression and greater safety than barbiturates because they cannot open chloride channels when GABA is not present.

Back 10

Benzodiazepines

Front 11

a form of drug-induced, reversible, organic brain syndrome.

Back 11

Ethyl alcohol blackout

Front 12

Which problems did barbiturates treat from 1912 to 1960?

Back 12

Anxiety and insomnia

Front 13

(3-minute redistribution half-life): thiopental; inactivated by redistribution; use = intravenous anesthesia

Back 13

Ultrashort Barbiturates

Front 14

(up to 48-hour elimination half-life): amobarbitol, pentobarbitol, and secobarbitol; Use = Surgical anesthesia and sleep induction

Back 14

Longer Barbiturates

Front 15

(24- to 120-hour elimination half-life): phenobarbitol; use = prolonged sedation and seizure control

Back 15

Very Long Barbiturates

Front 16

Can detect barbiturates from 30 hours to several weeks after ingestion.

Back 16

Urinalysis

Front 17

(anxiety reduction)

Back 17

Anxiolysis

Front 18

Happens with barbiturate withdrawal; dreaming becomes vivid and excessive, producing insomnia and relapse, when drug withdrawal produces

Back 18

REM rebound

Front 19

produce sedation and depress memory.

Back 19

cognitive inhibitors

Front 20

Barbiturates induce enzymes in the liver to metabolize these and other drugs, which results in

Back 20

Cross Tolerance

Front 21

compulsive use to produce a pleasurable effect.

Back 21

Psychological Dependance

Front 22

A barbiturate introduced in 1955 to produce daytime sedation and anxiolysis. Marketed as a “tranquilizer,” like the barbiturates it also produces extended daytime sedation, mild euphoria, and anxiety reduction. A weaker respiratory depressant than other barbiturates

Back 22

Meprobamate (meh pro BA mate)

Front 23

A barbiturate that is converted to meprobamate—its active form—following absorption

Back 23

Carisoprodol (kar eye soe PROE dole)

Front 24

a nonbarbiturate depressant that was widely abused due to the mistaken belief that it was an aphrodisiac (it is actually an anaphrodisiac). Extensive abuse and overdose deaths caused its removal in 1984, although it may be available illicitly.

Back 24

Methaqualone

Front 25

A barbiturate that rapidly metabolizes to the active metabolite, trichlorethanol, which is a nonselective depressant with a plasma half-life of 4-8 hours, reducing the occurrence of next-day hangovers; may be prescribed as a bedtime sedative for elderly patients due to its short half-life. Produces minimal REM rebound, however, sleep disruption and intense nightmares may occur with withdrawal.

Back 25

Chloral hydrate (Noctec)

Front 26

A combination of chloral hydrate and alcohol used to produce increased sedation, stupor, and memory loss (an early date rape drug)

Back 26

"Mickey Finn"

Front 27

(A barbiturate) polymer of acetaldehyde that can be administered rectally or orally to treat delirium tremens (DTs) in patients undergoing alcohol detoxification. Rapidly absorbed by both routes, sleep occurs within 10-15 minutes after a hypnotic dose. Eliminated by the liver and through the lungs (producing a characteristic odor).

Back 27

Paraldehyde

Front 28

A naturally-occurring four-carbon molecule with a structure similar to GABA. It is synthesized locally from GABA and freely crosses the blood-brain barrier. Has been used to treat sleep disorders, alcohol withdrawal, narcolepsy, and opioid dependence. A sedative-hypnotic drug. Acute withdrawal in dependent patients produces insomnia, anxiety, and tremors that resolve in 3-10 days.

Back 28

Gamma-Hydroxybutyric Acid (GHB).

Front 29

Sudden loss of muscle tone

Back 29

Cataplexy

Front 30

(low-voltage electrical stimulation of the amygdala or hippocampus) appears crucial to antiepileptic drug treatment of both seizures and bipolar disorder.

Back 30

Kindling

Front 31

The first widely effective antiepileptic drug . It replaced the more toxic bromide, which was used during the 19th century

Back 31

Phenobarbital

Front 32

A frequently used anti-epileptic which produces less sedation than barbiturates at an effective plasma level. Daytime sedation can be minimized with bedtime administration due to a half-life of 24 hours.

Back 32

Phenytoin (FEH nih toyn)

Front 33

A GABA agonist that acts postsynaptically by blocking the enzymatic deactivation of GABA by GABA transaminase. An effective and widely prescribed for seizure disorders in children. Rapidly absorbed and due to a 6-12 hour half-life must be administered several times a day. Highly effective in treating bipolar disorder, posttraumatic stress disorder, pathologic aggression, schizophrenia, and alcohol and cocaine dependence.

Back 33

Valproic acid (val PROE ik AH sid)

Front 34

Prescribed for several types of seizures and its sedative effect is weaker than other antiepileptic drugs. Lowers white blood cell count. Increasingly used to treat bipolar disorder in addition to lithium, explosive behavioral disorders, chronic pain syndromes, and alcohol withdrawal.

Back 34

Carbamazepine (kar ba MAH zeh peen)

Front 35

Structurally resembles the anxiolytic drug meprobamate. Concern about serious hematological reactions restricted its use to when it is “absolutely necessary and irreplaceable as an antiepileptic.”

Back 35

Felbamate (fel BAH mate)

Front 36

A structural analogue of GABA and promotes GABA release from presynaptic terminal buttons. Increasingly used as an alternative to lithium and other antiepileptic drugs in treating bipolar disorder. effectiveness in anxiety disorder (phobia) and pain (reflex sympathetic dystrophy). It has been used to treat agitation and aggressiveness in the demented elderly. appears effective in treating alcohol withdrawal and cocaine dependence (although topiramate may be equal or superior).

Back 36

Gabapentin (ga bah PEN tin)

Front 37

Reported to improve mood, alertness, and social interactions in some epilepsy patients. Research has demonstrated antidepressant and antimanic actions. Inhibits sodium ion movement to stabilize neuronal membranes and prevent presynaptic release of excitatory transmitters, principally glutamate. may help protect the brain following hypoxic insult.

Back 37

Lamotrigine (la MOE tri geen)

Front 38

a pathological condition in which the body as a whole or a region of the body is deprived of adequate oxygen supply.

Back 38

Hypoxia

Front 39

A restriction in blood supply, generally due to factors in the blood vessels, with resultant damage or dysfunction of tissue.

Back 39

Ischemia

Front 40

Introduced in the United States to treat epilepsy and has been increasingly used to treat bipolar disorder and other disorders treated by carbamazepine. It does not produce white blood cell toxicity, it is a “safer carbamazepine.”

Back 40

Oxcarbazapine (ox kar BAY zeh peen)

Front 41

Inhibits GABA uptake by terminal buttons and glial cells. It also irreversibly blocks one of the reuptake transporters on presynaptic neurons; Less useful than other antiepileptic neuromodulators in treating bipolar disorder.

Back 41

Tiagabine (tie AY ga been)

Front 42

Has been used to treat bipolar disorder. There have been no reports of comparative efficacy. Risk of decreased sweating and hyperthermia.”

Back 42

Topiramate (toe PEER ah mate)

Front 43

An antiepileptic drug that is also an effective antiobesity drug when combined with a balanced low-calorie diet and has been used to treat binge-eating disorder.

Back 43

Zonisamide (zoe NIH sah mide)

Front 44

Endogenous or synthetic steroid derivatives. Act as neuromodulators, instead of as hormones, and produce anxiolytic, sedative, and anticonvulsant effects.
May work by binding to a steroid-sensitive site on the GABA receptor, facilitating chloride ion entry.

Back 44

Epalons

Front 45

A study that concluded: “With proper management, 90 percent of women with epilepsy can anticipate uneventful pregnancies and normal children.”

Back 45

Cantrell and colleagues (1998)