Week 9 Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Clinical Manifestations of LSD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mechanism of LSD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Clinical Sx PCP (standard/low dose)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Mechanism of PCP

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Clinical Sx MDMA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Mechanism of MDMA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

factors increasing drug use

A

perceived risk; supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

route of admin LSD

A

oral. Powder, solution, blotting paper.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Tx LSD trip

A

Ride the wave. Support. Benzos if extremely anxious.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Route of admin PCP

A

Dipped and smoked.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical Sx high-dose PCP

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Regular PCP use consequences

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Tx PCP trip

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Route of admin MDMA

A

oral.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

consequences of chronic MDMA use

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Tx of MDMA high

A

support, prevent dehydration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Anticholinergic administration

A

rarely taken intentionally. Usually accidental iatrogenic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

anticholinergic clinical manifestations

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Treatment of delirium

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Huffing

A

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

21
Q

Clinical manifestations of huffing

A

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

22
Q

Mechanism of huffing

A

GABA-A ? not known

23
Q

chronic use of huffing

A

CNS damage: demyelination/cerebellar atrophy.

24
Q

Sex breakdown of schizophrenia

A

higher incidence in men, but equal prevalence

25
Q

Cognitive deficits in schizophrenia

A

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

26
Q

Negative symptoms of schizophrenia

A

alogia, flat affect, anhedonia, avolition, asociality

27
Q

Treatment outcomes of schizophrenia (patterns, prognostic factors)

A

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.

28
Q

Schizophrenia etiology

A

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

29
Q

Dopamine hypothesis of schizophrenia

A

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

30
Q

glutamate hypothesis of schizophrenia

A
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.
31
Q

Anorexia Nervosa criteria

A

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

32
Q

Anorexia nervosa onset

A

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

33
Q

Anorexia nervosa Tx

A

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)

34
Q

Bulimia Nervosa criteria

A
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
35
Q

Bulimia Nervosa neurobio

A

less activation of fronotstriatal areas—> less impulse control

36
Q

Bulimia Nervosa course

A

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

37
Q

Bulimia Nervosa complications

A

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

38
Q

Bulimia Tx

A

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

39
Q

Binge Eating Disorder criteria

A
A. Binging + lack of control
B. Associated binging practices
C. Marked distress
D Frequency
E. not associated with compensatory behavior, not AN or BN
40
Q

Neuro of Binge Eating

A

similar to cocaine. Food addiction?

41
Q

Tx of BED

A

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

42
Q

Night eating syndrome

A

25% of food intake. 2/wk. distress

43
Q

Leading preventable cause of death in US

A

smoking

44
Q

Pharm of nicotine

A

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

45
Q

Interventional therapy for nicotine addiction

A

Brief advice is pretty good relative to behavior therapy

46
Q

Pharm therapy for nicotine

A

replacement therapy, bupropion SR, varenicline (partial agonist)

47
Q

Only antipsychotic that works on negative Sx of schizophrenia

A

clozapine (but has AE of agranulocytosis)

48
Q

Dexamethasone suppression test

A

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)

49
Q

Benzos vs SSRIs for GAD

A

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