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Psych > 2/16 Rx: Alcohol > Flashcards

2/16 Rx: Alcohol Flashcards

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1
Q

toxicants

A

ethanol, methanol, ethylene glycol

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2
Q

drugs for EtOH w/drawal

A

diazepam (BNZs), VitB1 (thiamine)

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3
Q

drugs for chronic alcoholics

A

naltrexone, acamprosate, disulfiram

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4
Q

MeOH and ethylene glycol are metabolized to toxic products. Prevention of their metabolism is accomplished by admin of what?

A

ethanol or fomepizole

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5
Q

areas of the brain involved in the response to addictive drugs

A

VTA (ventral tegmental area) + NA (nucleus accumbens)

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6
Q

EtOH metabolism + drug inhibiting each step

A

EtOH –> acetaldehyde via alcohol DH
*Fomepizole inhibits this enzyme

acetaldehyde –> acetate via aldehyde DH
*disulfram inhibits this enzyme

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7
Q

Alcohol is _ order process

A

zero: enzymes involved in metabolism are saturates and performing at max capacity
eg. phenytoin, high-dose aspirin

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8
Q

what metabolism pathway becomes more substantiative in chronic alcoholics?

A

CYP metabolism

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9
Q

disulfram

A

used to encourage abstinence from alcohol by preventing acetaldehyde metabolism –> nausea and skin flushing

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10
Q

asian flush

A

diminished aldehyde DH fx due to snp polymorphic changes (ALDH21/22)

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11
Q

dual fx of acetaldehyde build-up

A
  • unpleasant in periphery
  • pleasurable in the VTA, where it promotes dopamine release –> condenses with dopamine to produce salsolinol –> reinforces alcohol-seeking behavior
  • effect seen in asians
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12
Q

Ethanol is an important inducer of which CYP?

A

CYP2E1

*important bc CYP2E1 metabolizes acetaminophen into NAPQI (highly toxic)

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13
Q

what is acetaminophen normally conjugated with?

A

sulfate or glucuronide

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14
Q

normal acetaminophen/Tylenol metabolism

A

acetaminophen –> NAPQI –> rapidly conjugates with cysteine and mercapturic acid (non-toxic) after detoxed by glutathione

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15
Q

acetaminophen metabolism in chronic alcoholics

A

CYP2E1 induction: acetaminophen–> inc NAPQI –> nontoxic conjugates depleted/accumulation of NAPQI in liver –> heptotx

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16
Q

anecdote to NAPQI intoxication (or acetaminophen overdose)

A

N-acetylcysteine –> glutathione: provides fresh conjugate substrate for NAPQI to safely detoxify

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17
Q

what do you use to collect BAL?

A

tiger top, red top; use povidone-iodine, not alcohol wipe

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18
Q

BAL < 50

A

limited muscular incoordination

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19
Q

BAL 50-100

A

pronounced incoordination

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20
Q

BAL 100-150

A

mood and personality ∆; intoxication over the legal limit in most states

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21
Q

BAL 150-400

A

n/v, marked ataxia, amnesia, dysarthria

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22
Q

BAL > 400

A

coma, respiratory insufficiency and death

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23
Q

EtOH receptor?

A

no specific one, instead modulate key pathways: reinforce inhibitory actions of GABA, inhibit stimulatory actions of glutamate

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24
Q

what can inhibition of glutamate pathways cause?

A

blackouts

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25
Q

EtOH –> GABAa effect?

A

GABA release, inc receptor density

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26
Q

EtOH –> NMDA effect?

A

inhibition of postsynaptic NMDA receptors; with chronic use, up-reg

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27
Q

EtOH –> DA effect?

A

inc synaptic DA, inc effects on VTA/NA reward

28
Q

EtOH –> ACTH effect?

A

inc CNS and blood levels of ACTH

29
Q

EtOH –> opioid effect?

A

release of beta endorphins, activation of mu receptors

30
Q

EtOH –> 5-HT effect?

A

inc in 5-HT synaptic space

31
Q

EtOH –> Cannabinoid effect?

A

inc CB1 activity –> changes in DA, GABA, glutamate activity

32
Q

effects of EtOH

A

-CNS depression
-CV depressant
relaxes vascular sm.mm. (vasodilation, possible hypothermia, inc gastric bloodflow)
-relaxes uterine sm.mm. (can prevent premature labor)

33
Q

factors affecting BAL

A
  • VOD
  • BMI
  • female gender
  • metabolism
  • adaptation
34
Q

what does VOD depend on?

A

total body water: more lean –> more body water –> more diluted –> lower BAL

35
Q

which tissue does EtOH not distribute?

A

adipose

-thus, high BMI tend to have higher BAL

36
Q

female gender on BAL

A

high BAL

  • inc absorption (5-10%) compared to men
  • weight is lower
  • higher % body fat
37
Q

metabolism of EtOH

A

zero order process (same AMOUNT per time), 1 standard drink per hour

38
Q

types of adaptation? which is more significant?

A

behav and neural adaptation > enzyme induction

39
Q

chronic effect of EtOH on LIVER

A

dec GNG –> hypoglycemia

fatty liver: hepatitis, cirrhosis, failure

40
Q

chronic effect of EtOH on GI

A

bleeding, scarring –> absorptive and nutritional def

41
Q

chronic effect of EtOH on CNS

A

peripheral neuropathy (MC neuro presentation), W-K syndrome

42
Q

sx of W-K syndrome

A

Confusion,
Ataxia
Nystagmus (ocular muscle paralysis)

tx: thiamine (vit b1)

43
Q

chronic effect of EtOH on ENDOCRINE

A

steroid insufficiency –> gynecomastia, testicular atrophy

44
Q

4 effects of alcohol consumption on thiamine

A

1) dec thiamine in diet due to poot nutrx
2) dec thiamine absorption from GI
3) dec thiamine storage in liver
4) dec thiamine phosphorylation in brain

these lead to dec thiamine pyrophosphate (“active thiamine”) in the brain

45
Q

conseq of thiamine def

A

dec biosynth of a.a. and proteins (esp those in CNS), dec energy (ATP)

46
Q

chronic effect of EtOH on CV

A
  • HTN, anemia, dilated cardiomyoopathy
  • modest alcohol consumption inc HDL and may protect against CDH

(arrhythmia with BINGE DRINKING-acute)

47
Q

chronic effect of EtOH on NEOPLASIA

A

inc risk for GI cancer

48
Q

chronic effect of EtOH on IMMUNE SYSTEM

A
  • enhanced inflammation in liver and pancreas
  • reduced immune response in other tissues
  • chronic alcoholics susceptible to infectious pneumonia (2˚ to immune suppression)
49
Q

does alcohol cross the placenta?

A

YES!

levels in fetal blood reflect mom’s (bc fetus can’t metabolize it)

50
Q

effect on EtOH on developing CNS

A
  • triggers apoptosis

- incorrect neuronal and glial migration in developing nervous system

51
Q

FAS

A
  • typically early prego
  • IUGR, microcephaly, poor coordination, mid facial underdev (flat), minor joint anomalies, congenital heart defects, neuro deficits
52
Q

tx of intoxicated pt

A

1) ABCS
2) thiamine
3) THEN dextrose (earlier admin can exacerbate W-K if present)
4) correct electrolytes

53
Q

tx of w/drawal pt

A

BNZ sedative, thiamine, correct electrolytes

54
Q

BNZ sedative of choice in w/drawal pt

A

1) long-acting DIAZEPAM
2) if hepatic fx impaired, give LORAZEPAM (bc processed only by glucuronidation (phase II) and therefore less susceptible to a prolongation in half-life)

55
Q

signs of a w/drawing pt

A

insomnia, tremor, anxiety, rarely seizures and “DTs”, N/V, diarrhea, arrhythmias

56
Q

disulfiram-like effect

A

drug + EtOH –> inc acetaldehyde

drug is a non-alcoholism, medical condition

57
Q

drugs with disulfiram-like effect

A

SURs, cefotetan, ketoconazole, procarbazine

58
Q

PK effects of alcohol

A

inc teratogenicity through metabolism changes,

inc absorption of either component

59
Q

PD effects of alcohol

A
  • additive CNS depressive actions with drugs
  • inc toxx of acetominophen
  • inc risk of bleeding with NSAIDs and anticoags
  • inc risk of hypoglycemia in diabetics on meds
60
Q

naltrexone

A

mu opioid antagonist: felt to dec drinking through dec feelings of reward w/alcohol or dec craving

61
Q

acamprosate

A

weak NMDA antagonist, activator of GABAaR (major); may dec mild protracted abstinence syndromes with dec feelings of “need” for alcohol

62
Q

Alcohol, and its effects on several NTxs, target what system?

A

corticomesolimbic dopaminergic pathway (extends from VTA to NA)

63
Q

ethylene glycol metabolism

A

(alcohol DH) –> oxalic acid –> acidosis, nephrotx

64
Q

methanol metabolism

A

(alcohol DH) –> formaldehyde, formic acid –> severe acidosis, retinal damage

65
Q

tx for ethylene glycol and methanol intoxication

A

fomepizole, ethanol (enough to maintain BAL >100, to ensure enzyme saturation)

Psych (17 decks)

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