Week 9

Question 1

Clinical Manifestations of LSD

Answer 1

perceptual distortions: micropsia/macropsia. Derealization, depersonalization. Visual hallucinations. Synesthesia.
Euphoria or lability. Ego fragmentation.
Unmasking psychiatric vulnerabilities

Question 2

Mechanism of LSD

Answer 2

unsure. Serotonergic system (5HT-2 Receptor!), but not exclusively.

Question 3

Clinical Sx PCP (standard/low dose)

Answer 3

Dissociation/Disconnection. Euphoria (peaceful floating). Oblivious to surroundings. Flat affect (schizophrenia-like). Unresponsiveness.

Question 4

Mechanism of PCP

Answer 4

NMDA receptor antagonist. Blocks glutamate. Also monoamines, sigma, other receptors.

Question 5

Clinical Sx MDMA

Answer 5

Euphoria, loving. Loss of boundaries. Disinhibition/decreased defensiveness. Intimacy. Perceptual/cognitive distortions (apathy). Increased anxiety.
BP, heart rate, dry mouth, bruxism, fever/dehydration(?)

Question 6

Mechanism of MDMA

Answer 6

increased vesicular release of dopamine and 5HT (not well characterized)

Question 7

factors increasing drug use

Answer 7

perceived risk; supply

Question 8

route of admin LSD

Answer 8

oral. Powder, solution, blotting paper.

Question 9

Tx LSD trip

Answer 9

Ride the wave. Support. Benzos if extremely anxious.

Question 10

Route of admin PCP

Answer 10

Dipped and smoked.

Question 11

Clinical Sx high-dose PCP

Answer 11

Slurred speech, nystagmus(!), rolling gait, numbness, disturbing depersonlization, distortions of body image/consistency, space/time, perceptual disturbances.

Hyperacusis, amnesia, hostility, excess salivation w/o gag reflex, risk of coma/convulsions/death.

Question 12

Regular PCP use consequences

Answer 12

neuro/cognitive dysfunction for 2-3 wks. (“zombies”)

Question 13

Tx PCP trip

Answer 13

Reassurance NOT EFFECTIVE. Benzo for seizure prophylaxis. Antipsychotic for extreme paranoia. Acidification of urine to increase excretion in extreme cases. Gastric suction for coma.

Question 14

Route of admin MDMA

Answer 14

oral.

Question 15

consequences of chronic MDMA use

Answer 15

permanent destruction of 5HT pathways (?)–>depression

Question 16

Tx of MDMA high

Answer 16

support, prevent dehydration.

Question 17

Anticholinergic administration

Answer 17

rarely taken intentionally. Usually accidental iatrogenic.

Question 18

anticholinergic clinical manifestations

Answer 18

delirium. Waxing and waning of consciousness, impulsivity, impaired judgment, hallucinations, dysphoria. Can be subtle.

Question 19

Treatment of delirium

Answer 19

stop offending agents (e.g. anticholinergics). Physical/chemical restraint (anti-psychotic, not benzo!). Gastric lavage.

Question 20

Huffing

Answer 20

inhalation of volatile hydrocarbons (amyl/butyl nitrates = poppers)

Question 21

Clinical manifestations of huffing

Answer 21

stimulation/disinhibition. Nystagmus. Incoordination. Perceptual distortions. Frank hallucinations?

Question 22

Mechanism of huffing

Answer 22

GABA-A ? not known

Question 23

chronic use of huffing

Answer 23

CNS damage: demyelination/cerebellar atrophy.

Question 24

Sex breakdown of schizophrenia

Answer 24

higher incidence in men, but equal prevalence

Question 25

Cognitive deficits in schizophrenia

Answer 25

1-2 SDs below norm. Verbal/visual learning/memory, attention, speed of processing, executive function

Question 26

Negative symptoms of schizophrenia

Answer 26

alogia, flat affect, anhedonia, avolition, asociality

Question 27

Treatment outcomes of schizophrenia (patterns, prognostic factors)

Answer 27

1/3 Treatment refractory 1/3 episodic relapse 1/3 good response Good prognosticators: later/abrupt onset, shorter duration, better premorbid function, better support, paucity of negative Sx, female, adherence.

Question 28

Schizophrenia etiology

Answer 28

neurodevelopmental disorder: vulnerability x environment. heritable, but no high-contribution genes. 3rd trimester development (flu, nasal cavity)

Question 29

Dopamine hypothesis of schizophrenia

Answer 29

too much DA leads to inappropriate salience attributed to random stimuli. (antipsychotics block D2)

Question 30

glutamate hypothesis of schizophrenia

Answer 30

``` NMDA antagonists (PCP, ketamine) mimic both positive and negative Sx. NMDA blockade of interneuron leads to loss of inhibitory tone-->loss of synchrony of cortical areas NMDA hypomorphs are reasonable model for schizophrenia. ```

Question 31

Anorexia Nervosa criteria

Answer 31

A: 85% body weight B: intense fear of gaining weight, even though underweight C: Disturbance in body weight/shape experience or lack of recognition D: Absence of 3 consecutive menstrual cycles

Question 32

Anorexia nervosa onset

Answer 32

following crisis, loss of self-esteem. Dieting to "take control" Serotonin might play a role.

Question 33

Anorexia nervosa Tx

Answer 33

impatient if indicated. SSRIs not useful. atypical antipsychotics might be. Very hard to treat. Boot camp rehab and psychotherapy. Bring parents in before returning to independent eating (controversial)

Question 34

Bulimia Nervosa criteria

Answer 34

``` A: recurrent episodes of binging B: recurrent compensatory behavior C. Binge/compensation 1/wk for 3 months D. self evaluation unduly influenced by weight and shape E. Does not occur during AN ```

Question 35

Bulimia Nervosa neurobio

Answer 35

less activation of fronotstriatal areas---> less impulse control

Question 36

Bulimia Nervosa course

Answer 36

May occur in all weights. First occurrence usually in response to caloric deprivation while dieting

Question 37

Bulimia Nervosa complications

Answer 37

erosion of enamel, hypokalemia--> weakness, lethargy, arryhthmias, parotid gland enlargement.

Question 38

Bulimia Tx

Answer 38

fluoxetine (SSRI), CBT (alone not sufficient for many patients). Only eating disorder where pharm Tx indicated

Question 39

Binge Eating Disorder criteria

Answer 39

``` A. Binging + lack of control B. Associated binging practices C. Marked distress D Frequency E. not associated with compensatory behavior, not AN or BN ```

Question 40

Neuro of Binge Eating

Answer 40

similar to cocaine. Food addiction?

Question 41

Tx of BED

Answer 41

CBT and behavioral weight control equivalent for reducing binging. BWC superior for reducing weight

Question 42

Night eating syndrome

Answer 42

25% of food intake. 2/wk. distress

Question 43

Leading preventable cause of death in US

Answer 43

smoking

Question 44

Pharm of nicotine

Answer 44

NAchR modulated Da release presynaptically and response of post-synaptic neuron

Question 45

Interventional therapy for nicotine addiction

Answer 45

Brief advice is pretty good relative to behavior therapy

Question 46

Pharm therapy for nicotine

Answer 46

replacement therapy, bupropion SR, varenicline (partial agonist)

Question 47

Only antipsychotic that works on negative Sx of schizophrenia

Answer 47

clozapine (but has AE of agranulocytosis)

Question 48

Dexamethasone suppression test

Answer 48

Exogenous steroid: should be able to suppress (feedback) Dysregulation of HPA --> failure to suppress (anxiety, depression). Only works for severe melancholic depression (2/3 depression overall)

Question 49

Benzos vs SSRIs for GAD

Answer 49

Benzos treat symptoms!! (GABA). To treat underlying disorder, need SSRIs! First-line is SSRI, sometimes with "benzo-bridge." Prescribe benzo for situational anxiety only (e.g. flight phobia), where treating underlying disorder would be exposure therapy