CNS intro, Alcohol,Sed/Hyp, GABA (barbituates, benzos) Flashcards

1
Q

CNS Acetylcholine: involved in (8)

A

learning, memory, cognition, attention, wakefulness, arousal, NMJ, nicotinic/muscarinic receptrs

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2
Q

Acetylcholine degenerates in which dz?

A

Alzheimer’s

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3
Q

Norepinepherine/noradrenaline:

a. involved in:
b. acts on:

A

a. mood, attention, arousal, pain regulation, learning, memory
b. acts on G-protein coupled receptors

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4
Q

Dopamine involved in (4 basic processes)

A

reward
reinforcement
motivation
addiction

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5
Q

Dopamine involved in which 2 diseases

A

Parkinson’s

Schizophrenia

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6
Q

Dopamine receptor

A

G-protein coupled receptor

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7
Q

Dopamine receptors: stimulatory, inhibitory

A

D1=stimulatory

D2=inhibitory

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8
Q

D2 receptor is (stim or inhib?)

A

inhibitory

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9
Q

D1 receptor is (stim or inhib?)

A

stimulatory

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10
Q

Serotonin-5HT: involved in (6)

A
mood
promotes sleep
anxiety
OCD
hunger
appetite
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11
Q

Serotonin receptor type

A

G protein coupled receptors

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12
Q

CNS Monoamines (3)

A

Norepinepherine/noradrenaline
dopamine
serotonin

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13
Q

GABA function

A

(Amino Acid)
major INHIBITORY transmitter in the CNS
relieves anxiety & promotes sedation
ACTIVATION OF GABA RECEPTORS ALLOWS CL INTO THE CELL

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14
Q

Glutamate function

A

(Amino Acid)
major EXCITATORY transmitter in the CNS
involved in memory & learning

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15
Q

Glutamate receptor type(s)

A

a. Ionotropic receptors: NMDA, AMPA

b. Metabotropic receptors- post=excitatory, pre=inhibitory

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16
Q

Neuropeptides & their functions (4)

A
  1. Endogenous opioids (endorphins): ↓pain, ↑pleasure-Mu, kappa, delta
  2. Substance P:excitatory-mediates pain transmssn
  3. Neuropeptide Y: regulates food intake & fat storage
  4. Cannabinoids: memory, cognition, pain perception
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17
Q

Alcohol pharmokinetics

A
  1. absorbed in stomach & small intestine
  2. readily crosses BBB & placental barrier
  3. induces CYP450s
    a. ↑acetaminophen toxicity
    b. inhibits breakdown of benzos, barbituates, TCAs, etc
  4. microsomal ethanol oxidizing system induced w/chronic use
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18
Q

Blood alcohol content determinants

A

based on sex, age, body fat

peaks 30-90 mins after last drink

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19
Q

Alcohol metabolism

A
  • ZERO ORDER kinetics
  • broken down by alcohol dehydrogenase to acetaldehyde & then by aldehyde dehydrogenase to acetate
  • oxidation requires NAD+
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20
Q

Disulfiram action

A

inhibits aldehyde dehydrogenase (necessary for metabolism of alcohol)

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21
Q

Alcohol MOA (4)

A
  1. CNS depressant
  2. binds GABA receptor-↑ Cl influx-enhances GABA transmission
  3. long term=downregulation of GABA receptor (tolerance forms)
  4. inhibits glutamate on NMDA receptors=up regulation of NMDA with chronic use
22
Q

Alcohol CNS effects (LOW DOSES) [6]

A
disinhibition
decreased anxiety
mild euphoria
increased confidence
mood swings
decreased concentration
23
Q

Alcohol CNS effects (HIGH DOSES)

A

motor & judgment impairment
slurred speech
ataxia-sedative properties become apparent

24
Q

Alcohol smooth muscle effects

A

vasodilator

hypothermia

25
Q

Alcohol kidney effects

A

decreased ADH=diuresis

26
Q

Alcohol ABUSE definition

A

interference in social life for at least 1 month

27
Q

Alcoholism definition

A

tolerance AND dependence due to prolonged use
CONTINUOUS OR PERIODIC LAC OF CONTROL OVER DRINKING, PREOCCUPATION WITH ALCOHOL, USE DESPITE CONSEQUENCES< DISTORTION OF THINKING (DENIAL)

28
Q

Alcohol kinetics & dynamics

A

Kinetics: ethanol induces CYP2E1-chronic use increases ethanol metabolism
Dynamics: ↓GABA receptors and ↑NMDA receptors – withdrawal due to dynamic tolerance – takes time to reset the receptors

29
Q

Alcohol toxicity symptoms (5)

A

emesis, stupor, coma, respiratory distress, death

30
Q

Tx of alcohol toxicity

A

thiamine, manage symptoms, correct electrolyte disturbances, correct hypothermia

31
Q

What is the cause of alcohol hangovers?

A

buildup of metabolites & dehydration

32
Q

How should you tx a seizure due to alcohol?

A

control w/benzos

33
Q

Effects of chronic alcohol abuse (8 main categories and their manifestions)

A

Malnutrition – folate and thiamine deficiency Gastritis and pancreatitis
Cardiovascular – arrhythmia, cardiac depression, cardiomyopathy, HTN, stroke
Teratogenicity – fetal alcohol syndrome Carcinogenicity – increases carcinogenic effects of tobacco
Sexual dysfunction – testicular atrophy, impotence, gynecomastia
CNS – Korsakoffs & Wernicke’s – peripheral neuropathy
Skeletal muscle atrophy

34
Q

What is the most common dz in alcohol abuse and how does it come about

A

Liver dz due to oxidative stress, tissue damage, lipid peroxidation by acetaldehyde
hepatotoxicity may manifest as: fatty liver, fibrosis, cirrhosis, alcoholic hepatitis, liver cancer

35
Q

TTx of alcohol abuse/dependence should consist of which main elements

A

psychological AND pharmacologic

36
Q

Naltrexone: MOA, used to tx

A

blocks opioid receptor-blocks ability of alcohol to stimulate reward pathyways
[used in tx of alcoholism]

37
Q

Acamprosate: MOA, used to tx

A

analogue of GABA, restores GABA glutamate balance

[used in tx of alcoholism]

38
Q

Disulfiram: MOA, how do SEs com about/what are SEs

A

inhibits acetaldehyde dehydrogenase
ACETALDEHYDE builds up=flushing, HA, nausea, confusion
can have severe effects

39
Q

What other pharm med might you use in the tx of alcohol use disorders?

A

antidepressants

40
Q

Alcohol withdrawal manifestation (mild, severe)

A

CAN BE LIFE THREATENING
mild=anxiety, irritability, insomnia, nausea, tachycardia
severe=hallucinations, DTs, seizures, arrhythmia, hypotension

41
Q

Alcohol withdrawal treatment aims to prevent

A

seizures, DTs & arrhythmia

42
Q

Anxiety disorders: description

A

pervasive feeling of tension or apprehension
ANXIETY THAT BECOME CHRONIC AND INTERFERES WITH NORMAL FUNCTION SHOULD BE TREATED!!
sxs: palpitations, tremor, perspiration, GI effects, dizziness, headache

43
Q

IDEAL ANXIOLYTIC would do what?

A

calm without daytime sedation and drowsiness & would not cause physical or psychological dependence

44
Q

Anxiety: benzos?

A

relieve anxiety without sedation

45
Q

Transient insomnia is due to what & tx how

A

due to situational stress

most effective tx=sedatives/hypnotics

46
Q

Long term insomnia is due to what & tx how

A

psychiatric dz, chronic drug abuse

most effective tx=TLC

47
Q

hypersomnia, narcolepsy tx

A

stimulants

48
Q

enuresis tx

A

TCAs

49
Q

sleep apnea tx

A

CPAP, TLC

50
Q

IDEAL SEDATIVE/HYPNOTIC should

A

allow the person to fall aspeep quickly, stay asleep, without a drug hanglover and has a high margin of safety without effect on the REM sleep