Alcohol Use Disorder > Aud > Flashcards

Aud Flashcards

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1
Q

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2
Q

What is the DSM-5 requirement to diagnose an Alcohol Use Disorder (AUD)?

A

Repeated presence of at least 2 of 11 criteria clustering within a 12-month period (DSM-5). 1

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3
Q

How does ICD-10 diagnose alcohol dependence compared with DSM-5 AUD?

A

ICD-10 requires 3 or more items clustering together; DSM-5 uses ≥2 of 11 criteria (different wording and thresholds). 2

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4
Q

What change to DSM diagnostic items occurred from DSM-IV to DSM-5 for alcohol?

A

One DSM-IV item (legal problems) was dropped and one new item (craving) was added. 3

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5
Q

How does DSM-5 grade AUD severity?

A

Mild = 2–3 criteria; Moderate = 4–5; Severe = ≥6 criteria in the past year. 4

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6
Q

Define ‘early remission’ and ‘sustained remission’ in DSM-5 AUD terms.

A

Early remission: no AUD criteria (except craving) for prior 3 months. Sustained remission: no criteria for ≥12 months. 5

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7
Q

What proportion of middle-class men and women seeking medical care might have alcohol-related problems (as introduced)?

A

About 20–30% of middle-class men and about 15% of women seeking medical care are affected. 6

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8
Q

How many grams of ethanol are in a ‘standard drink’ (US definition) per the PDF?

A

About 10–12 grams of ethanol per standard US drink. 7

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9
Q

Give examples of beverage amounts equivalent to one US standard drink.

A

~12 oz beer (~3.6% ethanol), ~5 oz table wine (~12%), ~1.5 oz 80-proof spirits (~40%). 8

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10
Q

Approximately how much does one standard drink raise blood alcohol concentration (BAC) in an average 70-kg person?

A

About 15–20 mg/dL (0.015–0.020 g/dL) per standard drink. 9

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11
Q

Roughly how long does the body take to metabolize one standard drink?

A

Approximately one hour for the average person. 10

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12
Q

Name the main liver enzyme that metabolizes ethanol and the alternative high-dose pathway.

A

Main: alcohol dehydrogenase (ADH) in cytosol. Alternative at high BAC: microsomal ethanol oxidizing system (MEOS). 11

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13
Q

What toxic intermediate is produced during ethanol metabolism and which enzyme clears it?

A

Acetaldehyde is produced; aldehyde dehydrogenase (ALDH) clears it. 12

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14
Q

How do ALDH2 gene variants affect alcohol reaction and AUD risk (per PDF)?

A

ALDH2*2 homozygotes have an Antabuse-like reaction (nausea, flushing) and near-zero AUD risk; heterozygotes have milder flushing and reduced AUD risk. 13

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15
Q

What neurochemical receptor systems are prominently affected by ethanol?

A

GABA-A (enhanced), NMDA glutamate (inhibited acutely), dopamine (increased), serotonin (increased), opioid systems, adenosine, acetylcholine, CB1. 14

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16
Q

Describe behavioral, pharmacokinetic and pharmacodynamic tolerance to alcohol.

A

Behavioral: learned performance while intoxicated. Pharmacokinetic: increased metabolic clearance. Pharmacodynamic: neuronal adaptation reducing drug effect. 15

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17
Q

What is an alcohol ‘blackout’ and why does it occur?

A

Anterograde amnesia for the drinking period — high doses interfere with encoding/consolidation of memory (depressant effect). 16

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18
Q

How does alcohol affect sleep architecture?

A

Helps sleep onset but fragments sleep, suppresses REM early, reduces stage 4 late, causes awakenings and intense dreams as BAC falls; may take months for sleep normalization in AUD. 17

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19
Q

What neurological syndrome is caused by thiamine deficiency in heavy drinkers?

A

Wernicke encephalopathy (acute signs) and Korsakoff syndrome (persistent amnestic confabulatory disorder) — together Wernicke–Korsakoff. 18

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20
Q

What thiamine dosing protocol is described for Wernicke–Korsakoff in the PDF?

A

IV thiamine 500 mg two to three times daily for 3–5 days, or oral thiamine 100 mg daily for months as needed. 19

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21
Q

List systemic organs/systems commonly damaged by heavy alcohol use (short list).

A

Liver (fatty liver → hepatitis → cirrhosis), pancreas (pancreatitis), heart (cardiomyopathy), nervous system (neuropathy, Wernicke–Korsakoff), immune, cancers. 20

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22
Q

What is alcoholic cardiomyopathy and what are its consequences?

A

Myocardial (striated muscle) toxicity from heavy alcohol leading to heart muscle deterioration, arrhythmias, heart failure — a leading cause of early death in AUD. 21

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23
Q

Which cancers are particularly associated with AUDs?

A

Head and neck, esophagus, stomach, liver, colon, lung, breast — increased risk even after accounting for smoking/nutrition. 22

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24
Q

What fetal outcomes are associated with maternal alcohol use?

A

Fetal alcohol syndrome (low IQ, microcephaly, facial dysmorphology, cardiac defects) and broader fetal alcohol spectrum disorders (FASD) with cognitive/executive deficits. 23

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25
What percent of drinkers report blackout experiences?
About 50% of drinkers have had a blackout at some time; ~15% had ≥3 in a year. 24
26
Give the lifetime risk estimates for AUDs reported in the PDF.
Approximately 15% for men and 10% for women lifetime risk. 25
27
What population groups have especially high rates of AUDs historically per the chapter?
Some Native American and Inuit tribes (very high levels in some tribes); ethnic differences exist (e.g., Irish higher severe problems but also higher abstention). 26
28
What is the typical age at first drink/intoxication/onset of AUD reported?
First drink ~13–15; first intoxication ~15–17; first minor alcohol problem ~16–22; age at onset of AUD ~23–40. 27
29
What percent of patients in psychiatric settings have AUDs per the PDF?
About 30% of psychiatric patients. 28
30
What proportion of people with AUDs report temporary sadness or anxiety?
Up to 80% report temporary sadness or anxiety; ~40% meet full criteria for major syndromes at times. 29
31
How should clinicians distinguish alcohol-induced psychiatric symptoms from independent psychiatric disorders?
Use a timeline: age of AUD onset, periods ≥1 month abstinent, and timing of psychiatric episodes; substance-induced symptoms usually remit within days to weeks of abstinence. 30
32
What is the recommended first step when suspecting an AUD in any patient?
Screen everyone for alcohol-related accidents, interpersonal/work problems, and ask about alcohol history; obtain informant history if possible. 31
33
Name two screening questionnaires mentioned and which is more comprehensive.
AUDIT (10 items) is more comprehensive; CAGE is brief but less sensitive/specific. 32
34
List the 10 core items (themes) covered by AUDIT (not full item wording).
Frequency of drinking; typical quantity; binge frequency (6+ drinks); inability to stop; failure in role obligations; morning drink/eye-opener; guilt/remorse; blackout; injury to self/others; others' concern. 33
35
What are the lab 'state markers' of heavy drinking and one relevant threshold for each?
GGT >35 U/L; CDT >3.0%; MCV >91 μm3; AST (SGOT) >45 IU/L; ALT (SGPT) >45 IU/L; uric acid >6.4 mg/dL (men), >5.0 mg/dL (women). 34
36
What is the sensitivity/specificity of GGT ≥35 U/L and CDT >3% for heavy drinking?
Both have roughly ~60% sensitivity and specificity for ~5+ drinks/day over weeks; combined tests perform better. 35
37
Why is MCV limited as a marker of recent drinking?
Red cell lifespan ~120 days makes MCV insensitive to short-term changes and not useful to detect return to drinking. 36
38
Name three psychiatric disorders that increase the risk for later AUDs (per chapter).
Antisocial personality disorder, bipolar disorder, and schizophrenia. 37
39
What is the risk of AUDs among people with antisocial personality disorder (ASPD)?
About 80% of people with ASPD develop severe alcohol problems and/or other SUDs. 38
40
What is the 'level of response' (LR) to alcohol and its relevance to AUD risk?
Low LR = need for more alcohol to feel effects; genetically influenced; leads to higher consumption and increased AUD risk. 39
41
Name four genetically influenced characteristics affecting AUD risk listed in the PDF.
Alcohol metabolizing enzymes; impulsivity/disinhibition; some psychiatric disorders (e.g., schizophrenia, bipolar); low level of response to alcohol. 40
42
What proportion of AUD risk is attributed to genetic factors according to the chapter?
About 60% of the proportion of risk for AUDs is genetic. 41
43
What historical public health action in the U.S. attempted to prohibit alcohol, and when was it repealed?
The 18th Amendment (Volstead Act) instituted Prohibition in 1920; beverage alcohol became legal again in 1933 (repeal). 42
44
What is the rough annual societal cost of alcohol-related problems in the U.S. mentioned?
About $225 billion per year (lost productivity, healthcare, crime, motor vehicle crashes). 43
45
How common is spontaneous remission among people with AUDs?
Approximately 20% may have spontaneous remission without formal treatment. 44
46
What are the three general steps of AUD treatment outlined?
Intervention, detoxification, and rehabilitation (including relapse prevention). 45
47
What does the FRAMES acronym stand for in brief interventions?
Feedback; Responsibility; Advice; Menu of options; Empathy; Self-efficacy. 46
48
Describe the brief intervention structure recommended (visits/workbook example).
Two 15-minute sessions plus workbook (NIAAA), drinking diary between visits, and short follow-up phone contacts. 47
49
What is the first essential step in detoxification?
Thorough physical examination and management of life-threatening medical conditions. 48
50
What is the typical outpatient benzodiazepine approach for mild/moderate alcohol withdrawal described?
Give enough depressant initially to relieve symptoms, then taper over ~4–5 days; examples include lorazepam (short-acting) or chlordiazepoxide/diazepam (long-acting). 49
51
Give the chlordiazepoxide dosing example used in the chapter for initial withdrawal management.
25 mg orally 3–4 times on day 1 (omit if sleepy); up to two extra 25 mg doses if needed; then reduce ~20% per day until off by day 4–5. 50
52
Why might short-acting benzodiazepines like lorazepam require stricter adherence during withdrawal?
Missed doses of short-acting agents can cause rapid concentration changes that may precipitate seizures. 51
53
What adjuncts may be used but do NOT reduce seizure or delirium risk during withdrawal?
β-blockers (propranolol) and α2-agonists (clonidine) — they reduce autonomic signs but don't reduce seizure/delirium risk and may mask severity. 52
54
What percentage of AUD patients experience severe withdrawal (DTs) per the chapter?
Less than 3% experience severe withdrawal with delirium tremens (DTs). 53
55
What is the role of high-dose benzodiazepines and antipsychotics in DTs?
High-dose benzodiazepines are primary; antipsychotics (e.g., haloperidol) can control severe agitation/hallucinations but benzodiazepines remain first-line. 54
56
If benzodiazepines fail to control DTs, what ICU options are mentioned?
Induce arousable deep sleep with propofol or use dexmedetomidine (α2-agonist) under ICU care and then wean by ~day 5. 55
57
What is the approximate peak timing of alcohol withdrawal symptoms?
Begin ~8 hours after last drink, peak on days 2–3, diminish by days 4–5. 56
58
What percentage of patients may have a single grand mal seizure during withdrawal?
About 1% may have a single grand mal convulsion (peak ~day 2). 57
59
What is 'protracted withdrawal' and how long may symptoms persist?
Mild anxiety, insomnia, autonomic overactivity may persist for 2–6 months after acute withdrawal. 58
60
Which medication is mentioned as possibly helpful for protracted withdrawal symptoms?
Acamprosate may diminish some protracted withdrawal symptoms. 59
61
What are the three core goals of rehabilitation after detox?
Maximize motivation for abstinence; restructure a sober lifestyle; and relapse prevention. 60
62
What psychotherapeutic approach is emphasized for rehabilitation and relapse prevention?
Cognitive-behavioral therapy (CBT) and CBT-based relapse prevention (skills, coping, identifying high-risk situations). 61
63
How should clinicians treat independent psychiatric disorders comorbid with AUD?
Treat the independent disorder appropriately (e.g., lithium/valproate for bipolar I, antipsychotics for schizophrenia) while addressing withdrawal and then rehabilitation. 62
64
What two medications have double-blind evidence of modest benefit for AUD when combined with CBT?
Acamprosate and naltrexone (~15–20% better than placebo in trials). 63
65
Describe acamprosate: mechanism, usual dosing, and effect size per chapter.
Mechanism: NMDA/glutamate antagonism (modulates excitability); dosing ~2,000 mg/day (often 666 mg TID); studies show ~15–20% better outcome vs placebo; usually prescribed ~6 months. 64
66
Describe oral naltrexone: mechanism and dosing described in the chapter.
Opioid receptor antagonist reducing reward/craving; usual dose 50 mg/day; evidence ~15–20% better outcome vs placebo; injectable 380 mg monthly (Vivitrol) available. 65
67
What genetic variant may predict better response to naltrexone?
A variant at Asn40Asp in the OPRM1 (mu opioid receptor) gene has been associated with better outcomes on naltrexone in some studies. 66
68
What is the rationale and usual dose for disulfiram (Antabuse) and what are its limitations?
Dose ~250 mg/day; causes aversive reaction to alcohol (nausea, vomiting, BP changes). Limited evidence vs placebo; rare severe adverse effects (psychosis, hepatitis); contraindicated in certain medical conditions. 67
69
Name three other pharmacological agents mentioned as being studied or used off-label for AUDs.
Topiramate (300 mg/day), ondansetron (4 mcg/kg in some studies), baclofen; SSRIs (e.g., sertraline) have mixed data. 68
70
What is the approximate efficacy improvement of acamprosate or naltrexone vs placebo reported?
About a 15–20% better outcome than placebo in many trials. 69
71
What practical role do self-help groups (AA) play in rehabilitation?
AA encourages lifestyle change, sober peer group, models of recovery, 24-hour availability; participation is associated with improved outcomes and clinicians should help patients find suitable meetings. 70
72
What family interventions are important in AUD rehab?
Education/support for family, help to rebuild relationships, and avoid enabling/protecting behaviors that reduce patient motivation for abstinence. 71
73
What is the chapter's advice regarding routine use of antidepressants for alcohol-induced mood symptoms after withdrawal?
Routine antidepressant use is not supported for alcohol-induced mood disorder; these symptoms often improve within days–weeks of abstinence and meds may pose interaction risks. 72
74
Which sleep/pharmacologic approach is recommended for lingering insomnia/anxiety in recovery?
CBT, education, reassurance; avoid routine benzodiazepines because of tolerance and misuse risk. Acamprosate may help protracted symptoms. 73
75
What is the role of genetic testing in tailoring AUD pharmacotherapy according to the chapter?
Some genotypes (OPRM1 Asn40Asp, serotonin transporter, etc.) show associations with response to medications (naltrexone, ondansetron, SSRIs) but further research is needed before routine clinical use. 74
76
What monitoring strategy is useful after initiating detox/treatment to detect return to drinking using labs?
Monitor GGT and CDT (combine both) — GGT returns to normal in 2–4 weeks; CDT half-life ~16 days so useful for monitoring abstinence. 75
77
What are the core elements to assess when taking an alcohol timeline to distinguish induced vs independent disorders?
Age of AUD onset; periods ≥1 month of abstinence; ages when full major psychiatric syndromes occurred — to see if psychiatric disorder predates or persists independent of AUD. 76
78
What advice does the chapter give about diagnosing personality disorders in AUD patients?
Defer diagnosing personality disorders other than ASPD and borderline until ≥1 month abstinent unless personality symptoms clearly predated the AUD. 77
79
How common is alcohol-induced psychosis and what is its usual course?
~3% experience hallucinations/paranoid delusions in clear sensorium; often clear within days–weeks of abstinence but may recur with resumed heavy drinking. 78
80
List three physical exam or history clues that should alert clinicians to possible heavy drinking.
Frequent bruising, enlarged liver or signs of cirrhosis, history of pancreatitis or head/neck cancers; mornings irritability and sleep disruption reported by family. 79
81
What are the key components of relapse prevention counseling?
Identify high-risk situations; develop coping strategies for craving and stress; reframe slips as learning opportunities; build sober social network. 80
82
What percentage of treated AUD patients do well after completing a program according to the chapter?
A majority do well and develop long-term abstinence; good outcomes most likely without ASPD and with job/family support (approx figures given: ~60% chance for >1 year abstinence with good predictors). 81
83
What is the mortality impact of long-term AUDs on life expectancy per the chapter?
On average, heavy ongoing AUD decreases lifespan by about a decade (≈10 years). 82
84
What suicide risk figure is associated with AUDs in the chapter?
Approximately 10% risk for suicide, often during depressive episodes. 83
85
Which comorbid substance use disorder is especially elevated among people with AUDs?
Nicotine use disorders are markedly elevated among individuals with AUDs. 84
86
What practical points about benzodiazepine choice for withdrawal are noted?
Long-acting agents (chlordiazepoxide, diazepam) permit smoother taper but risk oversedation; short-acting (lorazepam) safer in hepatic impairment but require strict adherence to avoid seizures. 85
87
How should clinicians respond to brief relapses during early treatment?
Use relapse as a learning opportunity: reinforce relapse prevention training, re-engage in aftercare/AA, review triggers, and continue treatment rather than treat slip as failure. 86
88
What combined pharmacotherapy pairing is discussed as possibly more effective than monotherapy?
Combination of acamprosate (666 mg TID) plus naltrexone (50 mg/day or other schedules) may be more effective, though results are mixed. 87
89
What safety warnings are emphasized for disulfiram use?
Risk of severe reactions with alcohol; rare psychosis and potentially fatal hepatitis; contraindicated in heart disease, stroke, diabetes and other medical conditions. 88
90
Summarize the chapter's practical discharge/aftercare plan used for the case JP.
Inpatient detox + group counseling; start acamprosate (666 mg TID) + naltrexone (50 mg/day); couples counseling; twice-weekly aftercare groups; selection of suitable AA and Al-Anon groups. 89
Alcohol Use Disorder
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