• Disulfiram - inhibitor of acetaldehyde dehydrogenase, generating severe hangover on alcohol ingestion. Very heterogenous reactions, with cross reaction with alcohol in aftershave and perfume
• Naltrexone - theorized to limit dopamine release upon drinking (modulates nucleus accumbans via opiate receptor); works best with familial alcoholism carried across same sex 
• Acamprosate - opioid receptor antagonist; glutamate antagonist, preventing withdrawal seizures

• Naltrexone - opiate receptor antagonist; causes dysphoria (as opposed to depression seen in alcoholics)
• Methodone - long-acting opiate; tolerance developed at kappa receptor (psychomimetic), leading to heightened alertness; detoxing from methadone takes weeks to month
• Buprenorphine - partial opiate receptor agonist, with ceiling effect. Interacts with benzo's to cause respiratory arrest

• Vaccination, with booster every 90 days
• Despiramine, a TCA

• Buproprion - atypical antidepressant, decreases withdrawal symptoms (taken 2 weeks prior to quitting)
• Nicotine replacement - inhalers, gum (make sure to park gum between cheek and gums)
• Varenicline/chantix - partial nicotine antagonist (increases chance of success from 10% to 50%), severe side effects (psychosis, agitation, suicide attempts)

How are the following psychosocial treatments used with respect to substance abuse?

1. Psychodynamic
2. Cognitive behavioral therapy
3. Family therapy
4. Motivational enhancement

1. Childhood shapes adulthood; patient compensate for deficits in self-worth with self-soothing (note: Brouette dislikes this theory)
2. Challenges false beliefs (e.g. addict is life of the party), perform behavioral intervention (avoid bars and people that use)
3. Address new family dynamic (family has to adjust to new roles)
4. Walk patient through precontemplative (screw you, I like drugs), contemplative (maybe this is bad), action (I'm gonna sober up) and maintenance stages (I'm gonna stay sober)

Both act through GABA_A a receptor-chloride channel complex. However, benzo increases chloride channel frequency, barbiturate directly opens the channel AND decrease dissociation of GABA from receptor

Barbiturate shows a linear progression in dose to cause CNS depressio (benzo doesn't)

Ambien. Non-benzodiazepine benzodiazepine agonist. Decreaes latency of sleep onset and lengthens amount of time patient stays asleep.

Specific to alpha subunit, so does not provide anti-anxiety activity. Causes addiction through dopamine pathway.

• Diazepam and flurazepam
• Triazolam and hydroxytriazolam

• Redistribution to peripheral compartment
• Hypovolemia, increased age, higher BMI, concomitant hypnotics 

• Low dose = hyperalgesic (stimulus experience is more profound)
• Burst suppression (ideal for patient recovering from braun trauma)
• Cardiovascular = venous dilation, decreased cardiac output
• Respiratory = depression
• General = can be necrotizing due to alkaline nature (do not give subQ)

• Generally used in children more than adults due to diminished effects. 
• Induces dissociative state (with protective reflexes intact) and amnesia
  • Stimulates cardiovascular system indirectly, suppresses directly (do not use in people with hx of CAD)
  • Does not depress respiration (good for asthmatics)
• Contraindicated with increased ICP

Imidazole (family of anti-infective drugs) with anesthetic effects. No analgesic activity, great drug for hemodynamically unstable patients.

Can cause hypoadrenalism (suppresses ß-hydroxylase), so watch out for bradycardia and hypotension

• Most popular anesthetic. Metabolites are inactive, leading to zero residual effects.
• Reduces ICP and BP
• Strong respiratory suppressant
• Adverse effects
  • Severe pain on injection (use lidocaine injection prior)
  • Highly contraindicated in hypovolemic patient
  • Vasodilation and hpotension
• No reversal agent, so airway management key

What anesthetic would you use for...

• Routine induction of anesthesia
• Asthmatic patients
• Hypovolemic or exsanguinating patient
• Patient with myocardial dysfunction
• Continuous drip for long surgery

• Propofol or ketamine (bronchodilators)
• Ketamine or etomidate
• Etomidate, midazolam, fentanyl (minimal CV effects)
• Propofol (watch out for hypotension)

• 1 MAC = the percentage of gas required to prevent movement in 50% of people exposed to noxious stimulant (note that 1.3 MAC = 95%)
• MAC-BAR = percentage required to blunt autonomic response (generally higher thean MAC)
• MAC-awake = percentage required to knock patients out (less than MAC)

Oil-gas partition coefficient correlates directly to the potency of the gas; non-immobilizers (halogenated alkanes) are hydrophobic

Theory suggests anesthesia acts on hydrophobic part of cell (membrane)

Amides (two i's) = lidocaine, bupivicaine, ropivicaine, mepivocaine, prilocaine, etidocaine

Esters (short-acting, greater allergenic potential) = chlorprocaine, cocaine, procaine, tetracaine, benzocaine

• Ventricular arrhythmias
• Blunting airway reflexes to intubation/extubation
• Prevent or attenuate the increase in ICP or intraocular pressure (when intubating)

• Increase in temperature, chronic alcohol abuse, hypernatremia, increased CNS transmitters
• Hypoxemia, pregnancy, opposite of the above

Acts on sodium channel, either by modification of lipid membrane or direct interaction with channel.

• The LA is a weak base that needs to be ionized to act (BH⁺), and needs to be in basic pH milieu
• Duration of action is associated with protein binding

Describe the potential clinical implications of the following (with respect to anti-psychotics)

• D₂ antagonism
• 5HT_2A antagonism
• 5HT_1A agonism
• 5HT_2C antagonism
• 5HT_1D antagonism

• Positive symptom efficacy, EPS, endocrine effects
• Negative symptom efficacy, reduced EPS
• Antidepressant/anxiolytic activity, reduced EPS, improved cognition
• Positive symptom efficacy, weight gain
• Antidepressant efficacy

What are the implications of the following:

• Mixed 5HT/NE reuptake inhibition
• M₁ antagonism
• Alpha₁ antagonism
• H₁ antagonism

• Antidepressant and anxiolytic acitiy
• Memory impairment, GI symptoms
• Sedation, hypotension, sexual dysfunction
• Weight gain, sedation

First atypical antipsychotic (D₂ and 5HT_2A antagonism), anatomically selective (blocks mesolimbic but not nigrostriatal dopamine); less EPS/TD.

Last line of defense/used for treatment resistant psychosis because of life threatening agranulocytosis, seizures and bad metabolic profile. Anticholinergic side effects.

Atypical antipsychotic; hyperprolactinemia, EPS and cardiovascular side effects. Moderate weight gain.

Comes in "consta" form (in polymer microspheres, capable of gradually release over the course of 3 weeks)

N-actylecysteine, a glutathione precursor/subsitute

Note: noxious, best given with anti-emetic or via NG tube

Atropine (muscarinic antagonist), oxime (cholinesterase reactivator), diazepam (prevent central mechanism of toxicity)

Nebulized ipratroim to prevent bronchoconstriction