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29 Cards in this Set

  • Front
  • Back
1. Substance Abuse?
a. Abuse is a pattern of substance use -> impairment or distress for at least 12 months w/one or more of the following manifestation:
1. Failure to fulfil obligations at work, school, or home.
2. Use in dangerous situations (ie, driving a car)
3. Recurrent substance-related legal problems
4. Continued use despite social or interpersonal problems due to the substance use.
2. Dependence?
a. Is substance use ->impairment or distress manifested by at least 3 of the following w/in a 12-month period?
1. Tolerance
2. Withdrawal
3. Using substance more than originally intended
4. Persistent desire or unsuccessful efforts to cut down on use
5. Significant time spent in getting, using, or recovering from substance
6. ↓ social, occupational, or recreational activities because of substance use
7. Continued use despite subsequence physical or psychological problems
3. Note: It is possible to have substance dependence w/out having physiological dependence (i.e w/out having withdrawal or tolerance).
3. Note: It is possible to have substance dependence w/out having physiological dependence (i.e w/out having withdrawal or tolerance).
4. Withdrawal?
a. The development of substance-specific syndrome due to the cessation of substance use that has been heavy and prolonged
5. Tolerance?
a. The need for ↑ amounts of substance to achieve the desired effect or diminished effect if using the same amount of the substance.
6. How do differentiate substance-induced mood sx vs. primary mood sx?
a. Primary mood sx persists during abstinence.
7. What receptors are activated and what receptors are inhibited by alcohol?
a. Alcohol activates GABA and serotonin receptors in the CNS.
b. It inhibits glutamate receptors and voltage-gated calcium channels.
c. Thus, alcohol is a potent CNS depressant.
8. What is alcohol metabolized to and via what 2 key enzymes?
a. Alcohol-> acetaldehyde (via alcohol dehydrogenase)
b. Acetaldehyde -> acetic acid (aldehyde dehydrogenase)
c. There is up-regulation of these enzymes in a heavy drinker.
9. Tx of alcohol intoxication?
a. Monitor: airway, breathing, circulating, glucose, electrolytes, acid-base status.
b. Give Thiamine (to prevent or tx Wernicke’s encephalopathy) and folate
c. Naloxone may be necessary to reverse effects of co-ingested opioids
d. A CT scan of the head may be necessary to rule out subdural hematoma or other brain injury.
e. Severely intoxicated pts may require mechanical ventilatory support w/attention to acid-base balance, temp, and electrolytes while they are recovering.
f. Gastrointestinal evacuation (eg, gastric lavage, induction of emesis, and charcoal) is not indicated in the tx of EtOH overdose unless a significant amount of EtOH was ingested w/in the preceding 30-60 minutes.
10. Leading cause of mental retardation in the US?
a. Fetal alcohol syndrome
11. At what blood alcohol level will most adults show signs of intoxication?
a. BAL > 100
b. Obvious signs w/BAL > 150 mg/dl.
12. Effect of ethanol, as well as w/methanol and ethylene glycol on acid-base balance?
a. They can cause metabolic acidosis w/ ↑ Anion gap.
13. Sx of alcohol withdrawal syndrome?
a. Insomnia, anxiety, hand tremor, irritability, anorexia, nausea, vomiting, autonomic hyperactivity (diaphoresis, tachycardia, HTN), psychomotor agitation, fever, seizures, hallucinations, and delirium.
b. The earliest sx of EtOH withdrawal begin 6-24 hrs after the pt’s last drink and depend on the duration and quantity of EtOH consumption.
c. Generalized tonic-clonic seizures usually occur between 6-48 hrs after last drink, w/a peak around 13-24 hrs.
d. ~1/3 of pts w/seizure develop delirium tremens (DTs).
e. Hypomagnesemia may predispose to seizures; thus, it should be corrected promptly.
14. Tx of seizures due to alcohol withdrawal syndrome?
a. BZDs.
b. Long-term tx w/anticonvulsants is NOT recommended for alcohol withdrawal seizures.
15. Delirium Tremens?
a. Most serious form of EtOH withdrawal.
b. Usually begins 48-72 hrs after the last drink but may occur later (90% of cases w/in 7 days).
c. While only 5% of pts hospitalized for EtOH withdrawal develop DTs, there is a roughly 15-25% mortality rate if left untreated.
d. Physical illness predisposes to this condition.
16. Sx of DT’s in addition to delirium?
a. Hallucinations (most commonly visual)
b. Gross tremor
c. Autonomic instability
d. Fluctuating levels of psychomotor activity
17. Tx of DTs?
a. Chlordiazepoxide (Librium), diazepam (Valium), or lorazepam (Ativan) should be given in sufficient doses to keep the pt calm and slightly sedated, then tapered off slowly.
b. Alternatively, carbamazepine, or valproic acid taper can be used.
c. Antipsychotics and temporary restraints for severe agitation
d. Thiamine, folic acid, and a multivitamin to tx nutritional deficiens (banana bag).
e. Electrolyte and fluid abnormalities must be corrected.
f. Monitor withdrawal signs and sx w/clinical institute withdrawal assessment (CIWA) scale.
g. Careful attention must be given to the level of consciousness, and the possibility of trauma should be investigated.
h. Check for signs of hepatic failure (eg, ascites, jaundice, caput medusae, coagulopathy).
18. Positive screen criteria w/CAGE questionnaire?
a. 2 or more “yes” answers are considered a positive screen.
19. Disulfiram (Antabuse)?
a. Blocks aldehyde dehydrogenase
20. At risk or heavy drinking for men is how many drinks per day?
a. > 4 drinks per day or > 14 drinks per week.
21. At risk or heavy drinking for women is how many drinks per day?
a. > 3 drinks per day or > 7 drinks per week.
22. What lab values suggest excessive alcohol use?
a. AST:ALT ratio ≥2:1 and elevated GGT.
23. Effect of Alcohol on LFT and RBCs?
a. Alcohol can cause ↑ LFTs and macrocytosis (↑ MCV).
24. Action of disulfiram?
a. Blocks the enzyme aldehyde dehydrogenase in the liver and causes aversive reaction to alcohol (flushing, headache, N/V, palpitations, shortness of breath.
b. Contraindicated in severe cardiac disease, pregnancy, and psychosis.
c. Best used in highly motivated pts, as medication adherence is an issue.
25. Naltrexone (Revia, IM-Vivitrol)?
a. Opioid receptor blocker.
b. Works by ↓ desire/craving and “high” associated w/alcohol.
c. Greater benefit is seen in person w/family hx of alcoholism.
d. In pts w/physical opioid dependence, it will precipitate withdrawal.
26. Acamprostate (Campral)?
a. Structurally similar to GABA, thought to inhibit the glutamergic system.
b. Should be started postdetoxification for relapse prevention in pts who have stopped drinking.
27. Contraindication to Acamprostate (Campral)?
a. Severe renal disease
28. Major advantage of Acamprostate (Campral)?
a. Is that it can be used in patients with liver disease!
29. Topiramate (Topamax)?
a. Anticonvulsant that potentiates GABA and inhibits glutamate receptors.
b. Reduces cravings for alcohol