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2/16 Rx: Alcohol Flashcards

(65 cards)

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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
EtOH --> GABAa effect?
GABA release, inc receptor density
26
EtOH --> NMDA effect?
inhibition of postsynaptic NMDA receptors; with chronic use, up-reg
27
EtOH --> DA effect?
inc synaptic DA, inc effects on VTA/NA reward
28
EtOH --> ACTH effect?
inc CNS and blood levels of ACTH
29
EtOH --> opioid effect?
release of beta endorphins, activation of mu receptors
30
EtOH --> 5-HT effect?
inc in 5-HT synaptic space
31
EtOH --> Cannabinoid effect?
inc CB1 activity --> changes in DA, GABA, glutamate activity
32
effects of EtOH
-CNS depression -CV depressant relaxes vascular sm.mm. (vasodilation, possible hypothermia, inc gastric bloodflow) -relaxes uterine sm.mm. (can prevent premature labor)
33
factors affecting BAL
- VOD - BMI - female gender - metabolism - adaptation
34
what does VOD depend on?
total body water: more lean --> more body water --> more diluted --> lower BAL
35
which tissue does EtOH not distribute?
adipose | -thus, high BMI tend to have higher BAL
36
female gender on BAL
high BAL - inc absorption (5-10%) compared to men - weight is lower - higher % body fat
37
metabolism of EtOH
zero order process (same AMOUNT per time), 1 standard drink per hour
38
types of adaptation? which is more significant?
behav and neural adaptation > enzyme induction
39
chronic effect of EtOH on LIVER
dec GNG --> hypoglycemia | fatty liver: hepatitis, cirrhosis, failure
40
chronic effect of EtOH on GI
bleeding, scarring --> absorptive and nutritional def
41
chronic effect of EtOH on CNS
peripheral neuropathy (MC neuro presentation), W-K syndrome
42
sx of W-K syndrome
Confusion, Ataxia Nystagmus (ocular muscle paralysis) tx: thiamine (vit b1)
43
chronic effect of EtOH on ENDOCRINE
steroid insufficiency --> gynecomastia, testicular atrophy
44
4 effects of alcohol consumption on thiamine
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
conseq of thiamine def
dec biosynth of a.a. and proteins (esp those in CNS), dec energy (ATP)
46
chronic effect of EtOH on CV
- HTN, anemia, dilated cardiomyoopathy - modest alcohol consumption inc HDL and may protect against CDH (arrhythmia with BINGE DRINKING-acute)
47
chronic effect of EtOH on NEOPLASIA
inc risk for GI cancer
48
chronic effect of EtOH on IMMUNE SYSTEM
- enhanced inflammation in liver and pancreas - reduced immune response in other tissues - chronic alcoholics susceptible to infectious pneumonia (2˚ to immune suppression)
49
does alcohol cross the placenta?
YES! | levels in fetal blood reflect mom's (bc fetus can't metabolize it)
50
effect on EtOH on developing CNS
- triggers apoptosis | - incorrect neuronal and glial migration in developing nervous system
51
FAS
- typically early prego - IUGR, microcephaly, poor coordination, mid facial underdev (flat), minor joint anomalies, congenital heart defects, neuro deficits
52
tx of intoxicated pt
1) ABCS 2) thiamine 3) THEN dextrose (earlier admin can exacerbate W-K if present) 4) correct electrolytes
53
tx of w/drawal pt
BNZ sedative, thiamine, correct electrolytes
54
BNZ sedative of choice in w/drawal pt
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
signs of a w/drawing pt
insomnia, tremor, anxiety, rarely seizures and "DTs", N/V, diarrhea, arrhythmias
56
disulfiram-like effect
drug + EtOH --> inc acetaldehyde | drug is a non-alcoholism, medical condition
57
drugs with disulfiram-like effect
SURs, cefotetan, ketoconazole, procarbazine
58
PK effects of alcohol
inc teratogenicity through metabolism changes, | inc absorption of either component
59
PD effects of alcohol
- 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
naltrexone
mu opioid antagonist: felt to dec drinking through dec feelings of reward w/alcohol or dec craving
61
acamprosate
weak NMDA antagonist, activator of GABAaR (major); may dec mild protracted abstinence syndromes with dec feelings of "need" for alcohol
62
Alcohol, and its effects on several NTxs, target what system?
corticomesolimbic dopaminergic pathway (extends from VTA to NA)
63
ethylene glycol metabolism
(alcohol DH) --> oxalic acid --> acidosis, nephrotx
64
methanol metabolism
(alcohol DH) --> formaldehyde, formic acid --> severe acidosis, retinal damage
65
tx for ethylene glycol and methanol intoxication
fomepizole, ethanol (enough to maintain BAL >100, to ensure enzyme saturation)

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