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PSYCH > Pharm of Alch > Flashcards

Pharm of Alch Flashcards

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1
Q

how does alcohol work as an NT?

A

GABA A agonist–>increases effect

NMDA/glutamate antagonist–>inhibits release of glutamate

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2
Q

HABA major action

A

inhibitory

–relaxation, loss of coordination, motor slowing

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3
Q

net effects of glutamate antagonism

A

sedation
impaired memory
impaired cognition

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4
Q

how do opioids work?

A

indirect stimulation of b endorphins

–>pleasurable, euphoric effects via mu receptors

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5
Q

two ways that alcohol inhibits glutamate system

A

Presyn action on meGluR and presyn voltage-sens Ca channels–>inhibit glutamate release

inhibit post-synp ionotrpic glutamate receptors (NMDA)

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6
Q

chronic exposure to alcohol

A

compensatory increase in NMDA activity and R density leads to tolerance

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7
Q

rate limiting step of alcohol metabolism

A

oxidation of each ethanol molecule requires 2 NAD+

–limited supply of NAD+ in the liver

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8
Q

where does alcohol go?

A

2-10% excreted in urine

~90% removed by oxidation

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9
Q

what causes a hang over?

A

acetaldehyde

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10
Q

cystolic increase in NADH/NAD+ drives 4 biochemical pathways:

A
  • inc. production of lactic acid–>hyperuricemia & gout
  • inc ketone bodies–>ketosis
  • inc triglyceride synthesis–>fatty liver
  • inc gluconeogenesis and liver glycogen–>hypoglycemia
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11
Q

microsomal liver enzyme

A

as the concentration of ethanol increases above 100 mg/dl, there is an increased contribution of MEOS, therefore increased NADPH (via cytochrome p450)

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12
Q

acetyladehyde metabolism

A

acetyladehyde–aldehyde dehydrogenase–> acetate–>CO2 and H20–>acetyl-CoA

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13
Q

Disulfiram/Antabuse

A

inhibitor of ALDH–> acetaldehyde accumulates

-causes extreme discomfort in patients who drink alcoholic beverages

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14
Q

metabolism in GI tract

A

ADH in stomach and small intestine

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15
Q

proof

A

% alcohol by volume x 2

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16
Q

BAC

A

weight of alcohol per volume of blood, measured in mg of alcohol per 100cc of blood

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17
Q

worsening, decrease in temp, decrease in bp, excessive sleepiness, amnesia

A

0.30-0.40 300-400%

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18
Q

mood, behavioral changes
reduced coordination
impaired driving, machinery operation

A

20-100mg% (0.02-0.1)

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19
Q

unresponsiveness
serious decrease in pulse, temp, bp, resp
urinary and bowel incontinence

A

400-800%

0.40-0.80

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20
Q

markedly impaired thinking, memory, coordination
marked reduction in level of alertness
memory black outs
nausea and vomiting

A

200-300 mg%

0.20-0.30

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21
Q

nervous system adverse alcohol effect

A

generalized symmetric peripheral nerve injury

22
Q

Wernicke-Korasakoff encephalopathy is because of

A

a thiamine deficiency

23
Q

Werncke’s enceph

A

Opthalmoplegia
nystagmus
ataxia
confusion

24
Q

Korsakoff’s psychosis

A

anterograde and retrograde amnesia
confabulation
lack of insight
apathy

25
Q

liver disease track

A

alcoholic fatty liver–>alcoholic hepatitis–>cirrhosis–>liver failure

26
Q

how does tolerance develop

A
  • induction of hepatic enzymes with increased metabolism

- neuroadaptation–>induction dec GABA inc glutamate, inc dopamine

27
Q

alcohol withdrawal is problematic because

A

increased glut
decreased GABA
decreased DA

28
Q

primary goals of treatment of alcohol withdrawl syndrome

A

prevent serizures
delirium
werickes

29
Q

days of withdrawal for seizures

A

1-2

30
Q

days of withdarwal for remors

A

peak at 3-4

31
Q

purpose of thiamine

A

helps correct nerve problems due to ack of thiamine in WKS

32
Q

how is thiamine absorbed and metablolized

A

abosrbed- GI

metab- liver

33
Q

lorazapam class-

A

benzo

GABA modulator

34
Q

lorazapa/librium mechanism

A

binds to central benzo receptors–>interact allosterically to potetiate effect of inhibitory GABA

35
Q

librium/chloradiazepoxide issues

A

build up of active metabolites makes it less appropriate for eldely, hepatic metabolism bad for liver disease, cog effects persist for days-weeks

36
Q

chloradiazepoxide benefit

A

logner acting

37
Q

Gabapentin class

A

GABA analogue, anticonvulsant

38
Q

gabapentin action

A

interacts with voltage gated Ca channels

39
Q

Gabapentin benifits vs. disadvantages

A

benefits- non addictive

disadvantages- not FDA approved for this- not or high risk pts

40
Q

Naltrexone class

A

opiod antgonist

41
Q

most common adverse effect of naltrexone

A

nausea

42
Q

disadvantage of naltrexone

A

cant use with patients on opiates

non-compliance

43
Q

topiramate class

A

anti epileptic

44
Q

topiramate mechanism

A

blocking of voltage-gated Na+ channels,
augmentation of GABA at GABAR
antag of AMPA

45
Q

topiramax avantages

A

more robust than naltrexone

46
Q

topiramax disadvantages

A

not fda approved

47
Q

acamprosate class

A

analogue of GABA

48
Q

acamprosate action

A

NMDA antaonist + GABA R activator

may restore neuronal excitation and inhibit balance

49
Q

acamprosate adverse effects

A

caution in depressed patients or renal impairment patients

50
Q

gabapentin alcohol mech

A

not active at gabaR

modulates synthesis of GABA and glutamate release resulting in net + GABA effect

PSYCH (25 decks)

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