Alcohol Abuse- Pharm Flashcards

1
Q

What is alcohol abuse

A

Compulsive use of alcohol

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2
Q

What is alcohol dependence

A

Alcohol abuse, physical dependence, tolerance, and s/s upon withdrawal

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3
Q

Alcohol withdrawal syndrome

A

Insomnia, tremor, agitation, seizure, autonomic instability

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4
Q

Delirium tremens

A

Severe alcohol withdrawal w/ sweating, tremor, confusion, and hallucinations

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5
Q

Fetal Alcohol Syndrome

A

Craniofacial dsymorphia, heart defects, mental retardation

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6
Q

Wernicke-Korsakoff syndrome

A

Ataxia, confusion, extraocular paralysis due to chronic alcoholism and thiamine deficiency

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7
Q

Explain ADH metabolism

-what inhibits ADH? What is a use of one of the inhibitors

A

Ethanol is converted to acetaldehyde via ADH which also converts NAD to NADH (accumulation of NADH contributes to metabolic disorders, lactic acidosis, and hypoglycemia)

ADH is inhibited by aspirin and FOMEPIZOLE which is used to treat acute methanol/ethylene poisoning

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8
Q

Explain ALDH metabolism

-what inhibits ALDH and what is its use

A

ALDH converts acetaldehyde to acetic acid which is then metabolized to CO2 and water; NAD is converted to NADH

Disulfiram inhibits ALDH and is used to treat alcohol abuse and dependence

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9
Q

Explain polymorphisms in ALDH

  • who does it commonly affect
  • what is the result
  • what does it protect against and what does it inc risk of
A

ALDH polymorphisms are common in Asians resulting in flushing, light headedness, palpitations, and hangover symptoms

Helps protect against alcohol dependence and abuse; alcoholics w/ this polymorphisms are at inc risk of liver disease

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10
Q

Explain the MEOS system of metabolism; what does it lead to

A

If NAD is depleted MEOS (cyp450) use NADPH as cofactor in metabolism of ethanol; MEOS system activity inc toxins, free radicals, and hydrogen peroxide

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11
Q

Explain effects of acute ethanol consumption w/ regards to:

  • CNS
  • NMDA and GAGA
  • Heart
  • Smooth M
A

CNS- alcohol causes sedation and relieves anxiety but inc [ ] leads to slurred speech, ataxia, impaired judgement/behavior

NMDA- alcohol inhibits ability of glutamate to open NMDA-R; depress CNS and memory loss

GABA- alcohol inc effects of GABA at R which depresses CNS

Heart- depress myocardial contractility

Smooth m- vasodilate and hypothermia

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12
Q

Explain effects of chronic alcohol consumption w/ regards to:

  • esophagus
  • stomach
  • intestines
  • pancreas
  • liver
A

Esophagus- esophageal dysfunction, reflux, barretts, esophageal cancer

Stomach- acute/chronic gastritis and epigastric pain

Intestines- chronic diarrhea, nutritional malabsorption, and vit deficiency

Pancreas- #1 cause pancreatitis; Ca stones

Liver- #1 cause cirrhosis and need for transplant; fatty liver, hepatitis, cirrhosis, LF

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13
Q

Explain chronic alcohol abuse w/ regards to:

  • peripheral n
  • Wernicke-Korsakoff
  • Korsakoff psychosis
  • vision
A

Peripheral n- symmetric peripheral n injury causing distal parathesias, gait abnml, and ataxia

WK- extraocular paralysis, ataxia, confusion due to thiamine deficiency

KP- chronic disabling memory disorder post-WK syndrome

Vision- optic n degen and blurred vision

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14
Q

Explain effects of chronic alcohol abuse w/ regards to CV system and relationship between alcohol and CAD

A

Inc risk of dilated cardiomyopathy, ventricular hypertrophy, cardiac fibrosis, arrhythmias, HTN, folate deficient anemia, and stroke

Mod alcohol- dec risk of CAD by inc HDL and inhibiting inflammatory processes of atheroslcerosis

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15
Q

Explain effects of chronic alcohol abuse on endocrine system

A

Gynecomastia, testicular atrophy, hypoglycemia, ketosis, and abnml K levels

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16
Q

Relationship between alcohol and diuresis

A

Alcohol inhibits vasopressin leading to diuresis; during withdrawal vasopressin inc leading to water retention and hyponatremia

17
Q

Explain goals and mgmt of acute alcohol intoxication

A

Goals- prevent resp depression and aspiration

Glucose for metabolic disturbances
Thiamine to prevent wernicke-korsakoff
K if pt is vomiting severely

18
Q

Explain goals and mgmt of alcohol withdrawal syndrome; class of drug used (compare interdrug classes pros and cons)

A

Goals- prevent seizure, delirium, and arrhythmias and correct electrolytes and thiamine levels

Substitute LA sedative for alcohol and taper
LA benzodiazepine (clor and diazepam-have built in tappering but CI w/ liver dysfunction)
Short acting benzodiazepine (l/o-zepam- can use in pt w/ liver dysfunction)
19
Q

Explain mgmt of alcohol dependence

  • primary treatment
  • list the 3 drugs
A

Alcohol dependence

  • psychosocial therapy #1
  • drugs- naltrexone, acamprosate, disulfiram
20
Q

Naltrexone

  • use
  • MOA
  • effects
  • metabolism
  • what must pt be free of; why?
  • AE and CI
A

Naltrexone

  • used for alcohol dependence
  • MOA- LA mu-antagonist
  • effects- reduce cravings and relapse
  • extensive 1st pass effect
  • pt must be opioid free or will lead to acute withdrawal syndrome
  • AE-hepatocellular injury
  • CI- acute hepatitis or liver failure
21
Q

Acamprosate

  • MOA
  • effects
  • caution in what pt
A

Acamprosate

  • MOA- NMDA antagonist and GABAa agonist
  • effects- reduce relapse
  • caution in pt w/ kidney disease
22
Q

Disulfiram

  • MOA
  • who is it used in
  • who is it never used in
A

Disulfiram
MOA- irreversibly inhibitors ALDH and causes extreme discomfort in pt who drink alcohol
Used in pt who are highly motivated and have supportive therapy
Never use in pt who are drunk

23
Q

What are earliest signs of alcohol withdrawal syndrome? When do they first appear and how long can they last? When does delirium tremens develop?

A

Earliest signs- anxiety, tremor, insomnia, palpitations, anorexia, seizure, hallucinations w/ in 24 hr

Delirium tremens develops between 48-72 hrs since alcohol discontinuation

24
Q

Methanol

  • who does methanol poisoning effect
  • what does it lead to
  • how do you treat
A

Methanol

  • poisoning due to accidental ingestion or in alcoholics using it as substitute
  • causes very blurry vision
  • treat- resp support, hemodialysis, alkalinization w/ bicarb, and inhibit its metabolism by ADH w/ ethanol (higher affinity) and fomepizole (inhibits ADH)
25
Q

Ethylene Glycol

  • who gets poisoned by it
  • how do you treat
A

Ethylene Glycol

  • accidental OD by pets or kids due to drinking antifreeze
  • treat- hemodialysis, ethanol, fomepizol