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Exam 10 > Alcohol Use Disorders > Flashcards

Alcohol Use Disorders Flashcards

1
Q

MOA of benzodiazepines

A

bind to BZ-GABA-A receptor-> positive allosteric-> more Cl ion channel open-> treat withdrawal

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2
Q

Benzodiazepines decrease the duration and severity of symptoms and incidence of ___ and _______

A

seizures and delirium tremens

These can be experienced well past acute withdrawal

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3
Q

Which benzodiazepine is best for treatment of EtOH withdrawal? Which are the most used?

A

all are equal

-chlordiazepoxide, diazepam, lorazepam

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4
Q

Benzos should be dosed _______ for alcohol withdrawal than anxiety or insomnia

A

higher and more frequent

start high, taper slow

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5
Q

The most used barbiturate for alcohol withdrawal is

A

phenobarbital (oral, IM, IV)

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6
Q

Do barbiturates and benzodiazepines bind at the same place

A

no

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7
Q

Where to barbiturates bind and how is that used for alcohol withdrawal

A

subunits on GABA-A receptor complex-> (+) allosteric modulation-> Cl- open longer-> treated

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8
Q

Barbiturates suppresses _______ glutamate receptors and this _______

A

excitatory

decreases glutamate release

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9
Q

Barbiturates are useful as ____ and ____ when compared to benzos for AUD

A

first line and withdrawal refractory

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10
Q

Phenobarbital has a ___ onset of effect and a ____ half life

A

rapid, long

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11
Q

Phenobarbital should be ____ based doing. There is a concern for ____ _____.

A

weight based

respiratory depression

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12
Q

Phenobarbital should be used with caution in ___ and ____ disease. It is an enzyme ______

A

severe liver and renal disease

enzyme inducer

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13
Q

In addition to medications, what other things should be given to someone experiencing alcohol withdrawal

A

multivitamin, thiamine, folic acid, fluids (banana bag)

Likely you need more thiamine than what is in the banana bag

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14
Q

Giving thiamine to someone experiencing EtOH withdrawal can prevent ________. It needs to be given before or with ____.

A

Wenicke’s encephalopathy

D5W

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15
Q

Thiamine is converted to thiamine pyrophosphate which is a cofactor in ____

A

carbohydrate metabolism

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16
Q

Chronic drinking may present with alcoholic _____ and _____

A

ketacidosis and hypoglycemia

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17
Q

Alcohol interferes with hepatic _____ becasue _______

A

glyconeogenesis becasue the energy needed for alcohol metabolism is diverted away

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18
Q

Who is at greatest risk for alcoholic ketoacidosis and hypoglycemia

A

not eaten within 12-14 hours following last drink (N/V and loss of appetite)

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19
Q

Lorazepam is a great drug to use AUD because

A

long half life
few drug interactions (gluconoronidation)
PK are consistent through liver function
many methods of deliver

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20
Q

Alcohol withdrawal may present with___ and ____ which can lead to _______

A

HypoK and HypoMg

QT interval prolongation

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21
Q

Diazepam has a __ half life. What is special about its PK

A

long

active metabolites

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22
Q

Mg is a cofactor needed for converting ___ to ____

A

thiamine to thiamine pyrophosphate

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23
Q

For alcohol withdrawal, you can use ______ and ______ to treat sympathetic symptoms (BP, HR, tremor, sweating, anxiety_

A

clonidine and dexmedetomidine (“clonidine on steroids”, ICU IV only)

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24
Q

In the ED, the treatment is _______

A

symptom-triggered

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25
Q

Should you use anti seizure medications for alcohol withdrawal?

A

no, seizures usually end before administration of medication/benzodiazepines

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26
Q

Antipsychotics can be used to treat ____ and ____ in alcohol withdrawal. But there is a risk of ___ and ____

A

agitation, hallucinations

QTc prolong, lowering seizure threshold

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27
Q

Do not send a patient out of the hospital while they are still on _____

A

benzodiazepines

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28
Q

Three FDA approved medications for AUD

Two not FDA approved meds for AUD

A

disulfiram (Antabuse), naltrexone (and long acting vivitrol), acamprosate
Topiramate, gabapentin

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29
Q

_____ and _____ are first line for AUD treatment. if they do not respond to these two ______ is used

A

Naltrexone, acamprosate

Disulfiram

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30
Q

Disulfiram works as an alcohol ______ by _______ (MOA). There is ___ effect without alcohol

A

alcohol aversion medication
irreversibly inhibits aldehyde dehydrogenase-> acetaldehyde levels 5-10x normal.
no effect without alcohol, effect seen within 12-14 Horus of taking disulfiram

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31
Q

Alcohol + disulfiram = ?

A

palpitations, facial flushing, sweating, N/V, headache, tachycardia, chest pain, hypotension, dizziness, weakness

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32
Q

For disulfiram, caution when patients are also on/have:

A

metronidazole, cognitive disorder, unstable CVD, cirrhosis

33
Q

Patients can be at risk for disulfiram reaction for ______ after stopping taking it

A

weeks

slow elimination and no aldehyde dehydrogenase needs to be synthsized

34
Q

Disulfiram is pregnancy category __

A

C

35
Q

Naltrexone is an antagonist at ____ which leads to a decrease in _____ in the reward pathway

A

mu-receptors, dopamine activity
this will lesses reinforcing properties of EtOH, decrease cravings, lesses intoxication feeling, lessens euphoria (uncouples drinking and pleasure)

36
Q

What are the short term and long term effect of naltrexone?

A

Short term: reduce relapse, cravings, returning to drinking

long term: unclear if there is a benefit in maintaining abstinence

37
Q

Naltrexone AE? Contraindications?

A

AE: N/V, somnolence
CI: opioids (7-10 days), child Pugh C liver dx, LFTs high (hepatotoxicity)

38
Q

To prescribe naltrexone, need to order _____ and _____

A

urine too screen for opioids and LFTs (synthetic opioids will not show up)

39
Q

Acamprosate modulates glutamate at _____ and is a _______ agonist.

A

NMDA, GABA-A receptor agonist
thought to restore equilibrium of GABA and glutamate systems
(toss up on if it actually works)

40
Q

Acamprosate has a benefit in _______ and dosing is _____

A

maintenance of abstinence

weight based

41
Q

Acamprosate AE? Contraindications?

A

AE: diarrhea
CI: CrCl<30ml/min
Use if worried about liver or pt on opioid or will continue to drink

42
Q

For using acamprosate as a treatment for AUD, opioids, and liver dz: _______ are not a major concern. It is preg category ___.

A

drug drug

C

43
Q

Treatment for AUD should continue for at least __ months

A

6

44
Q

Clonidine and antipsychotics should be combined with ____ for alcohol withdrawal

A

benzodiazepine

45
Q

What is considered heavy drinking

A

5 or more binge days a month (4 for female)

46
Q

___ of EtOH is absorbed in the stomach, with the other amount absorbed in the small intestine

A

20%

47
Q

If there is ______ there will be less EtOH absorbed

A

food in the stomach

48
Q

Metabolism of EtOH

alcohol –alcohol dehydrogenase-> ______ –_______–> Acetic acid -> oxidation ->->-> energy (Krebs)

A

acetaldehyde

acetaldehyde dehydrogenase

48
Q

Metabolism of EtOH

alcohol –alcohol dehydrogenase-> ______ –_______–> Acetic acid -> oxidation ->->-> energy

A

acetaldehyde

acetaldehyde dehydrogenase

49
Q

EtOH elimination is ____ with time because of ___ saturation

A

linear, ADH saturation

you lose about 1 drink an hour

50
Q

What are some reasons for the gender difference in alcohol disposition

A

women weight less, have more fat and less water, less gastric alcohol dehydrogenase (less first pass), eliminate slightly faster

51
Q

What happens if you inhibit alcohol dehydrogenase or aldehyde dehydrogenase

A

You get nausea due to sympathetic NS activation-> bradykinin and His release-> nausea, flushing, hangover

52
Q

Acetaldehyde dehydrogenase is an active ____ in the ____ of cells. There are mutations that cause it to have low affinity for ____ and as a result _______

A

tetramer in the mitochondria

low affinity for NAD, short half life with virtually no activity

53
Q

EtOH inhibits toxic _____ ______ acutely due to inhibition of CYP2E1. However in chronic alcohol, there is CYP2E1 induction and if _____ is taken there will be:

A

acetominophen metabolism

acetaminophen, depletion of antioxidants and inactive conjugates leading to liver damage

54
Q

What is the major MOA of EtOH in the brain

A

It is a GABA-A agonist and a glutamate (NMDA) antagonist

55
Q

Typical sedating effects of EtOH

A

disinhibition, muscle relaxant, reinforcement, vasodilation, diuresis, sexual behavior

56
Q

EtOH causes diuresis by _______

A

inhibition of ADH secretion

57
Q

At what level of BAC will there be loss of motor coordination? What level is major impairment of mental and physical control? What level conscious but stupor? What level is lethal for 50%

A

0.08-0.10
0.14-0.16
0.3
.45

58
Q

Consequences of regular binge drinking on major body organs

A

Brain-> memory, attention, exec function
Liver-> fatty liver, fibrosis, cirrosis
CV-> HTN, MI, stroke, atherosclerotic
Kidney-> glomerulonephritis
Cancer-> oral, pharynx, larynx, colorectal
Other-> pancreas, FAS, depression, impaired fertility

59
Q

Main mechanism for alcohol tolerance

A

Decrease in GABA receptor function (internalization)
Increased NMDA function
(minor is metabolism change in liver)

60
Q

Which things of alcohol withdrawal can be life threatening and should be treated with benzos

A

CNS hyper excitability, ANS hyper excitability, tremor and motor abnormalities

61
Q

When alcohol releases β endorphins, inhibits GABA what gets released

A

dopamine

62
Q

With tolerance to alcohol, there is enhanced ___ release which promotes GABA inhibition of DA release

A

glutamate

63
Q

What causes Wenicke Korsakoff

A

thiamine deficiency

64
Q

What causes encephalopathy

A

liver failure-> accumulation of ammonia

65
Q

Mild deficits with alcohol will be seen with more than ___, moderate at ____ drinks/episode, substantial with 10 drinks/episode

A

5 drinks/episode
7-9
10 (6-7 days/week)

66
Q

Brain damage from alcohol will cause increased _____ and loss of ______

A

increased ventricular space

loss of grey matter (dendrites and cell bodies

67
Q

What is the process of hepatocytes turning into CT due to EtOH

A

Fatty liver with abnormal fat metabolism-> ROS + hepatic inflammation (alcoholic steahepatitis)-> alcoholic fibrosis from stellate cells making collagen-> liver failure
also 1-2% get hepatocellular carcinoma

68
Q

What liver functions are lost with cirrhosis (there are 4)

A

blood clotting, albumin, growth and immune factors, drug and toxin metabolism

69
Q

Sx of cirrhosis? (4)

A

hemorrhage, edema+ascites, immune dysfunction, decreased toxin removal

70
Q

Acetaldehyde will cause ____ in blood vessels

A

fibrosis

71
Q

EtOH can cause _____ due to disruption of potassium homeostasis

A

Arrhythmias

72
Q

With modest alcohol consumption, what are some protective effects from EtOH

A

less atherosclerosis, stroke, PAD, decreased clotting, inflammation, increased plasminogen

73
Q

Adolescents will have ____ sedation and motor impairment from alcohol. They suffer ____ memory loss

A

decreased
greater
(easier to continue drinking to high BAC)

74
Q

What are some CNS dysfunction things caused by fetal alcohol spectrum disorder (behavioral + neuropsychological)

A

B: poor impulse, judgement, concentration and attention, fail to consider consequences
Neuro: trouble with math and reading, low IQ, poor exec fxn, short term memory problems, lack of social skills, visual spatial deficits

75
Q

What is worse in FASD, binging or continual drinking?

A

binging

76
Q

FASD: aspect of development at _______ determine outcomes

A

time of drinking

77
Q

____ is an antibiotic that can also inhibit acetaldehyde dehydrogenase

A

Metronidazole

Exam 10 (4 decks)

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