Test 2 Flashcards

1
Q

Differentiate BiPolar I, Bipolar II, and Cyclothymic?

A

BP I: cycles b/w manic and hypomanic to depresssion and dysthymia
BI II: like BP I but doesn’t get to mania, only gets up to Hypomania
Cyclothymic: cycles b/w Hypomania and Dysthymia

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2
Q

What’s the correct term for “bipolar” in kids?

A

Kids Bipolar = Disruptive Moods Dysregulation Disorder

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3
Q

Differentiate Mania and Hypomania?

A

Hypomania: >4d but <1w, w/lighter and milder manic type sxs, w/ less impairment and can be IMPROVED, functioning, “genius” can occur
Manic: >1w of sxs

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4
Q

contrast emotional responses and feelings

A

Feelings = conscious experience of emotion
Feelings neurology = pattern of activity across insular cortex, secondary somatosensory cortex, cingulate cortex, hypothalamus, and upper brainstem

Emotions: automatic physiological response experienced

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5
Q

What’s the role of the frontal cortex w/emotional responses and feelings?

A

Frontal Cortex Necessary for emotional responses, esp social emotions and decision making

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6
Q

What are the 3 divisions of the amygdala, and which part is related to feelings/emotions?

A

Amygdala =
1 basolateral: receives input from assoc cortices and sensory structures
2 Central: projects out to emotional response structure
3 Corticomedial: projects to olfaction and appetite centers

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7
Q

What changes in brain structure size correlates w/depression?

A

Depression:
Prefrontal cortex, esp orbitofrontal prefrontal cortex, dorsolateral prefrontal cortex, subgenual prefrontal cortex, amygdala, anterior cingulate cortex, Hippocampus

Prefrontal GABA neuron density reduced
Occipital GABA neuron density reduced

Prefrontal, Anterior Cingulate Cortex neurons and Glial cells in general decreased

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8
Q

What changes in neural activity correlates w/depression?

A

Depression:

Cerebral cortex in general, esp in frontal lobes activity decreases

Anterior cingulate cortex, subgenual prefrontal cortex, hippocampus, striatum have metabolic changes

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9
Q

Which sided lesions generally leads to mania vs depression?

What occurs w/B/L lesions of DorsoLateral prefronal cortex vs Medial OrbitoFrontal cortex?

A

Lt lesion → depression
Rt lesion → mania

B/L DorsoLateral Prefrontal → flat
B/L medial OrbitoFrontal cortex → elevated

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10
Q
Where are these NTs neurons located?
DA
NE
5HT
Histamine
A

DA: Mesostriatal (from SNc = substantia nigra), Mesolimbic (from VTa = ventral tegmental area), and Mesocortical (from VTA and around SN)

NE: Locus ceruleus and Lateral Tegmental area

5HT: Raphe nuclei in midbrain, pons, medulla, Rostral raphe of midbrain and rostral pons, Caudal Raphe nuclei of caudal pons and medulla

Histamine: posterior Hypothalamus

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11
Q

Depression is assoc w/ ___ inflammatory markers and ____ cortisol

A

Depression is assoc w/ INCREASED inflammatory markers and INCREASED cortisol

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12
Q

Differentiate Premsenstrual Dysphoric Disorder vs Post-Partum Depression sxs?
PPD time frame for occurance?

A
• PDD Symptoms include:
○ decreased concentration
○ feelings of sadness
○ tension
○ anxiety
○ fatigue
○ mood swings
○ panic attacks
Seems to be a biochemical deficiency in the neurotransmitter Serotonin

PPD is major depressive or Bipolar w/w/o psychotic features after childbirth >4w but up to 1 yr post
Maybe d/t Progesterone drop?

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13
Q

How to recognize major depression as assoc feature or consequence of medical condition?

A

• Criteria
○ A. A prominent and persistent disturbance in mood predominates in the clinical picture and is characterized by either (or both) of the following:
§ Depressed mood or markedly diminished interest or pleasure in all, or almost all, activities. (-)
§ Elevated, expansive, or irritable mood. (+)
○ B. There is evidence from the history, physical examination, or laboratory findings that the disturbance is the direct physiological consequence of a general medical condition.
○ C. The disturbance is not better accounted for by another mental disorder (as Adjustment Disorder with Depressed Mood in response to the stress of having a general medical condition).
○ D. The disturbance does not occur exclusively during the course of a delirium.
E. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning

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14
Q

Which NTs and neurophysiologic changes are implicated in mood disorders?

A

DA and 5HT implicated in mood disorders

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15
Q

What are types of General Medical Conditions w/mood disorders?

A

○ With Depressive Features: if the predominant mood is depressed but the full criteria are not met for a Major Depressive Episode.
○ With Depressive- Like Episode: if the full criteria are met for a Major Depressive Episode, except disturbance only occurs exclusively during course of a delirium
○ With Manic Features: if the predominant mood is elevated, euphoric, or irritable.
○ With Mixed Features: if the symptoms of both mania and depression are not present but neither predominates.

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16
Q

Define dx criteria of Major Depressive disorder

A

Major depressive disorder: 5+ everyday for 2w+
1. Depressed mood.
2. Loss of interest or pleasure in most or all activities.
□ **
3. Insomnia or hypersomnia.
□ **
4. Change in appetite or weight.
**5. Psychomotor retardation or agitation.
□ **
6. Low energy.
□ ***7. Poor concentration.
□ **8. Thoughts of worthlessness or guilt.
□ **9. Recurrent thoughts about death or suicide.

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17
Q

List the associated features of MDD:

catatonic

A

Major depressive disorder: catatonic
• 1. motoric immobility as evidenced by cataplexy or stupor.
□ Catalepsy: immobile position constantly maintained.
□ Cerea flexibilitas (waxy flexibility) can “mold” limb position when moved like wax.
• 2. excessive motor activity (purposeless movement)
• 3. extreme negativism or mutism;
□ Motiveless resistance to instructions or maintenance of a rigid posture against attempts to be moved; mute.
• 4. peculiarities of voluntary movement
□ as evidenced by posturing (voluntary assumption of inappropriate or bizarre postures), stereotyped movement, prominent mannerisms, or prominent grimacing).
• 5. *echolalia- psychopathological repeating of words or phrases (may be in a mocking tone) or *echopraxia- pathological imitation of movements of one person by another.
□ Consider *Mirror neurons: may be involved in feelings of empathy (an understanding “from the inside”) or role in specific human abilities.
• 6. Either of the following, occurring during the most severe period of the current episode:
□ 1. loss of pleasure in all, or almost all, activities.
□ 2. lack of reactivity to usually pleasurable stimuli when something “good happens,”) does not feel much better, even temporarily).

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18
Q

List the associated features of MDD:

Melancholic

A

Major Depressive Disorder-Melancholic
• 1. distinct quality of depressed mood (that is, separate from, say, kind of feeling experienced when your beloved dog died).
• 2. depression regularly worse in the morning.
• 3. early morning awakening (at least 2 hours before usual time of awakening).
• 4. marked psychomotor retardation (-) or agitation (+).
• 5. significant anorexia or weight loss.
• 6. excessive or inappropriate guilt.

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19
Q

List the associated features of MDD:

atypical

A

Major Depressive Disorder-atypical
• A. Mood reactivity (mood actually brightens in response to positive events).
• B. Two or more of the following features:
○ 1. significant weight gain or increase in appetite.
○ 2. hypersomnia
○ 3. leaden paralysis (arms/legs feel “like lead”)
○ 4. long-standing pattern of interpersonal rejection sensitivity resulting in significant social or occupational impairment.
• C. Criteria that are not met for with melancholic features or with catatonic features during the same episode.

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20
Q

Describe dx characteristics of Dysthymia

A

Dysthymia:
• A. Depressed mood for most of the day, for more days than not for 2yrs (adult) or 1yr (kid)
• B. Presence, while depressed, of two or more of the following:
□ 1. poor appetite or overeating.
□ 2. insomnia or hypersomnia.
□ 3. low energy or fatigue.
□ 4. low self-esteem.
□ 5. poor concentration or difficulty making decisions.
□ 6. feelings of hopelessness.

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21
Q

Discuss dx and tx options for Bipolar disorders?
Major depression disorder
dysthymia
Cyclothymia

A

BP: mood stabilizers and antipsychotics w/w/o antidpressants, ECT
Major Depression Disorder: SSRI, SNRI, MAOI, antipsychotic, phototherapy, ECT,
Dysthymia: less pharmacotherapy than MDD if possible
Cyclothymia: Mood stabilizers (Lithium, Valproic Acid > Carbamazepine, Lamotrigine> Gabapentin, Toparamate), Antipsychotics [2st gen Thorazine or 2nd gen Quetiapine], Combo w/w/o antidepressants, and ECT

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22
Q

Diagnostic criteria of Cyclothymia?

A

Cyclothymia:
hypomanic and depressive sxs for 2yrs (adult), 1 yr( kids), but doesn’t meet criteria for Major Depressive or Bipolar… so more chronic but milder

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23
Q

What’s the MonoAmine theory of depression?

A

Depression’s d/t decreased monoamines, and w/initial tx you get an acute decrease d/t presynaptic autoreceptors

Takes weeks to get an increase in Monoamines

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24
Q
For SSRIs, what're the
MOA
TI
PK
*ADEs
A

SSRIs (Fluoxetine, Paroxetine, Citalopram)
MOA: SSRI
TI: Depression, bulimia, all major anxiety disorders (GAD, PTSD, OCD)
ADE: *Reduced libido, *teratogen (cardiac malformation 1st trimester exposure), GI, serotonin syndrome, discontinuation syndrome, dizzy, paresthesias

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25
Q
For SNRIs, what're the
MOA
TI
PK
ADE
A

SNRIs (Venlafaxine, Duloxetine)
MOA: SNRI
TI: Depression, pain, urinary incontinence, all major anxiety disorders (GAD, PTSD, OCD)
ADE: decreased libido, GI, noradrenergic HTN and HR increase, insomnia, anxiety, agitation

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26
Q
For TCAs, what're the
*MOA
TI
PK
*ADE
A

TCAs (Amitryptyline, Nortriptyline, Clomipramine)
MOA: SNRI and inhibition of *mACh, H, Da, NE receptors
TI: depression, OCD, peripheral neuropathy, chronic pain, migraine prophylaxis
PK: needs titration bc potential for OD, serious drug interactions
ADE: *Anticholinergic, *Cardiotoxicity, sedation, orthostatic hypotension, discontinuation syndrome

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27
Q
For MAOIs, what're the
MOA
TI
*PK
ADE
CI/precautions?
A

MAOI-Selegiline
MOA: MAOI
TI: depression, Parkinson’s, anxiety
PK: *transdermal patch avoides hypertensive crisis w/tyramine ingestion (wine/cheese)
ADE: orthostatic hypotension, wt gain, anorgasmia, discontinuation syndrome, Hypertensive Crisis w/tyramine ingestion
CI: SSRI, TCA, St John’s Wort

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28
Q
For Trazodone, what're the
MOA
*TI
*PK
*ADE
A

Trazodone
MOA: selective 5HT Transporter, metabolite=5HT2A antagonist
TI: DEPRESSION AND INSOMNIA
PK: *Major metabolite is the antidepressant
ADE: *Priapism, sedation, nausea, postural hypotension

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29
Q

For atypical antidepressants, what’re the
MOA
TI
ADE

A

atypical antidepressants Bupropion and Vilazodone
MOA: Buproprion=DSNRI, VIlazodone DNRI and enhances 5HT and NE release
TI: Depression
ADE: trouble sleeping, GI, nausea, diarrhea
Bupropion-seizures and psychosis

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30
Q

What are the FDA approved mood stabilizers?

A
FDA approved mood stabilizers:
Lithium
Lamotrigine
Valproic Acid (rapid cyclers)
Carbamazepine
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31
Q

what meds can be used off label for Bipolar Disorder?

A
non-FDA-approved mood stabilizers
Oxcarbazepine
atypical antipsychotics
some typical antipsychotics
Olanzapine
Benzodiazepine
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32
Q
For Lithium? 
theorized MOA 
ADEs
drug-drug interaction
drug-disease interaction
A

Lithium
theorized MOA: alters Na and NT transport, and 2nd messenger systems like IP3 and DAG in alpha and muscarinic adrenergic systems
ADEs: prone to high serum levels
Most common nausea, diarrhea, polyuria, polydipsia, weight gain, tremor, fatigue, confusion, somnolence… Hypothyroidism, skin reactions, leukocytosis, cardiac abnormalities, diabetes insipidus
drug-drug interaction: renal elimination, so NSAIDs, diuretics esp thiazides, ACEI or ARB
drug-disease interaction: pregnancy category D

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33
Q
For Valproic Acid
theorized MOA 
ADEs
drug-drug interaction
drug-disease interaction
A

Valproic Acid
theorized MOA: enhance GABA and block Na
ADEs:
drug-drug interaction:
Transient: GI effects, sedation, dizziness, tremor, thrombocytopenia
Weight gain, polycystic ovary syndrome (PCOS), menstrual changes, mild alopecia
Rare: agranulocytosis, hepatotoxicity, pancreatitis, SJS
drug-disease interaction: pregnancy category D

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34
Q

How do you prescribe mood stabilizers?

A

Acute mania/manic
§ Lithium and/or valproic acid
§ +/- Antipsychotic (if psychotic symptoms, severe, or mixed symptoms)
§ Antipsychotic monotherapy (hypomania or milder mania)
§ +/- Adjunctive short term benzodiazepine (select symptoms)
§ Alternatives are carbamazepine, oxcarbazepine

Acute depression/depressive
§ Lithium and/or lamotrigine
§ Consider valproic acid
§ Fluoxetine + olanzapine (co-formulated)
§ Antipsychotics as monotherapy (e.g., quetiapine, lurasidone, olanzapine, select others)
§ Adjunctive antidepressant
□ Often done, but avoid monotherapy with an antidepressant
□ Ideal duration unknown; typically discontinued (tapered) a few months following episode remission
§ Adjunctive antipsychotic (if psychotic symptoms)

• Lithium
○ Best in both states (mania and depression)
○ Limited by monitoring, pregnancy, adverse effects
• Valproate
○ Good for mania/hypomania state
○ Also good for rapid cyclers and mixed features
• Carbamazepine, Oxcarbazepine
○ Good for mania/ hypomania state
○ Limited by drug interactions
• Lamotrigine
Good for bipolar depression

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35
Q
For Lamotrigine
theorized MOA 
ADEs
drug-drug interaction
drug-disease interaction
A

Lamotrigine
theorized MOA: Glutamate inhibition
ADEs: Rash; SJS (rare)—titrate slowly! Avoid new medications, foods, products in first few months, Nausea and headache
Somnolence and fatigue
drug-drug interaction: anticonvulsants, so decrease dose for Valporate, increase dose w/Carbamazepine, Phenytoin, Primidone, Phenobarbital, Rifampin
drug-disease interaction: Pregnancy Category C (fine)

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36
Q
For Carbamazepine
theorized MOA 
ADEs
drug-drug interaction
drug-disease interaction
A

Carbamazepine
theorized MOA: Na channels, Aspartate and Glutamate
ADEs: Somnolence, confusion, dizziness, blurred vision, GI effects, diplopia, SIADH
Rare: SJS/TENS, blood dyscrasias, hepatic failure
Test those with Asian ancestry for HLA-B*1502 gene since SJS linked to this gene
drug-drug interaction: Inducer of 1A2, 2C9, 2C19, and 3A4; Autoinduction (3A4) Complete after 3-4 weeks; Need 2nd form of birth control; Avoid with MAOIs
drug-disease interaction: can cause SJS

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37
Q
For Oxcarbazepine?
theorized MOA 
ADEs
drug-drug interaction
drug-disease interaction
A

Oxcarbazepine
theorized MOA: Na channels, Aspartate and Glutamate; prodrug of 10, 11-epoxycarbamazepine
ADEs: like Carbamazepine but less blood cell effects and more SIADH
drug-drug interaction: maybe d/t 3A4 induction, but NOT autoinducer
drug-disease interaction: pregnancy category C (fine)

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38
Q

Which Benzodiazepine, antidepressant, and atypical antipsychotic can be used for BiPolar?

A

Benzodiazepine: Lorazepam
Antidepressant
Atypical Antipsychotic: Olanzapine

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39
Q

For Atypical antipsychotics, which is used for BP and what’s the theorized ADE relevant to BP?

A

Olanzapine for Bipolar interacts w/other drugs

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40
Q

When do you use TCAs for Bipolar?

whatre the possible ADEs relevant to BP?

A

TCA for BP can theoretically induce mania or rapid cycling

Use as adjunct when getting some response from optimal dose of mood stabilizer

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41
Q

For Benzodiazepines, which is used for BP, when, and what’re the precautions?

A

Lorazepam for BP can be used for
agitation, insomnia, or anxiety as adjunct, or IM in emergency
avoid chronic use

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42
Q

What’s the tx for Clyclothymia?

A

Cyclothymia tx

same as BP, mood stabilizers +/- antidepressants

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43
Q

Define personality disorder

A

enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual’s culture
is pervasive and inflexible
has an onset in adolescence or early adulthood
is stable over time
leads to distress or impairment
representative of long-term functioning and are not limited to episodes of illness

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44
Q

Differentiate Paranoid PD, Schizoid, Schizotypal, and Paranoid Schizphrenia
Who seeks tx?

A

Paranoid PD: paranoia grounded in REALITY

Schizoid: solitary, little interest in sex, emotionless, indifferent, no close friends, FUNCTIONAL

Shizotypal: odd beliefs, magical thinking, excessive social anxiety d/t paranoid fears that they can tell are delusional/apart from reality

Schizophrenia paranoia: paranoia not grounded in reality, that they CAN’T differentiate from reality

Schizotypal seeks tx for stress and anxiety, (+) results w/Haloperidol

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45
Q

Differentiate Antisocial and Borderline personality disorder?
Tx?
Problems when experiencing illness?

A

Antisocial: fails to conform to social norms of lawful behavior, indifferent and w/o remorse
-complies w/psychotherapy but usually substance abusers so maybe use meds

Borderline: frantically avoiding ‘abandonment’ but alternates b/w extrerme idealizing and devaluing people, HIGH IMPULSIVITY
-psychotherapy + meds

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46
Q

Differentiate Histrionic, and Narcissistic personality disorder?
Tx?
problems while treating?

A

Histrionic: inappropriately demanding center of attention, shallow, melodramatic, BUT FUNCTIONAL
-psychotherapy +antidepressants if symptomatic

Narcissistic: grandiosity, no empathy, arrogant, requires admiration, less manipulative/impulsive than borderline PD
-long term psychotherapy goals of tolerating disappointments and appreciating others needs, but they usually don’t seek help

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47
Q

Differentiate Avoidant and Dependent personality disorder?
tx?
problems while treating?

A

Avoidant: avoids interpersonal contact, hypersensitive to rejection and embarrassment, socially awkward and timid,
tx: psychoanalytic therapies, SSRI, MAOIs, beta-blockers for social phobias
tends to abandon tx abruptly

Dependent: starting in early adulthood, dependent on others for everything, difficulty disagreeing w/others or initiating projects
Tx: meds given during crisis, psychotherapy

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48
Q

Differentiate OCD and OCPD?
tx?
problems while treating?

A

OCD: true obsessions and compulsions, makes them NON-FUNCTIONAL bc deep seated fear/anxiety, and they understand they are abnormal!
-Clomipramine

OCPD: FUNCTIONAL, perfectionism that can interfere w/task completion, over-conscientious/scrupulous/inflexible on morals/ethics/values/rules, excessive hoarding of worthless items, but they think they’re normal!
-SSRIs

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49
Q

What’s found in REM and non-REM stages of sleep? (behavior, EEG)

A

nonREM
Stage 1: some muscle activity, low V, mixed f
Stage 2: episodic bursts of Sinusoidal waves that’re high V
slow-wave
Stage 3: high a, slow Delta waves
Stage 4: increased slow waves
REM: low V, mixed F, paradoxical sleep, no muscle activity, rapid eye movements

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50
Q

Compare peds to YA to elderly sleep patterns

A

newborns 50% REM
YA 25% REM, mostly Stage 2 sleep
elderly <25% REM, less nonREM stage 4 sleep

as you age, sleep cycles increase in duration

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51
Q

What’s the neural correlate of Circadian Rhythm

A

Circadian Rhythm:
Suprachiasmatic nucleus = endogenous clock, releases hormones on 24hr cycle
proteins PER and TIM regulate hormone release
TIM’s degraded by light, so build up occurs at night, allowing PER and TIM to form complex and limit hormone transcription

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52
Q

What are the patterns of sleep cycles?

A

Cycle: nonREM 1-2-3-4-3-2 to REM (skips 1 on the way back)

REM occurs every 60-90m, increasing in duration and intensity throughout the night

2nd half of night is mostly REM and Stage 2 (very little Stages 3-4 slow wave sleep)

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53
Q

What are the role of the brainstem and thalamic neurons w/regards to sleep?

A

Midbrain Reticular Formation (part of ascending reticular activating system) above Pons = wakefulness
Medulla = sleep center, inhibits wakefulness

Posterior Hypothalamus = arousal via Histamine
Anterior Hypothalamus = sleep via GABA, inhibiting Post Hypothalamus

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54
Q

What are the monoamine mechanisms for REM and nonREM sleep?

A

REM (and switching between nonREM and REM) = ACh
non-REM = histamine, NE, 5HT… get shut off between waking to stage 1 through stage 4; GABA cells in Nucleus Reticularis oscillate d/t VgCaCh, inhibiting Thalamocortical relay cells

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55
Q

What are the theories of benefits for sleep in terms of memory consolidation?

A

why sleep for Memory consolidation?
slow wave sleep reactivates hippocampus
REM sleep consolidates memories in cortical areas for long-term storage

56
Q
Benzodiazepines used for insomnia?
MOA
TI
*PK
*ADEs
CI
A

Temazepam, Triazolam
MOA: increases frequency of Cl- channel opening
TI: short term insomnia (7-10d)
PK: *short to intermediate 1/2 life
ADEs: *rebounding insomnia, sedation, anterograde amnesia, cog impairment
CI: pregnancy

57
Q
Z-drugs used for insomnia?
MOA
TI
PK
*ADEs
CI
A

Zolpidem
MOA: Binds to alpha1 subunit of Benzodiazepine site (BZ1), facilitating GABAA action
TI: short term insomnia (7-10d)
PK: short 1/2 life
ADEs: *sleep driving and other complex behaviors, HA, dizzy, drowsy, diarrhea
CI: known hypersensitivity

58
Q
Ramelteon
MOA
TI
PK
ADEs
CI
A
Ramelteon:
MOA: Melatonin1 and 2 receptor agonist
TI: insomnia, esp sleep onset
PK: active metabolist = M-II
ADEs: sleepy, fatigue, dizzy
CI: angioedema w/previous Ramelteon use, or use w/Fluvoxamine
59
Q
Suvorexant
MOA
TI
PK
ADEs
CI
A
Suvorexant
MOA: Orexin receptor antagonist
TI: insomnia
PK: CYP3A4
ADEs: somnolence
CI: narcolepsy, or taking strong CYP3A4 inhibitor like Clarithromycin or Ritonavir
60
Q
Modafinil
MOA
TI
ADEs
CI
A

Modenafil
MOA: UNK, stimulates wakefullness like amphetamines
TI: narcolepsy, obstructive sleep apnea, shift work disorder
ADEs: HA, back pain, nausea, nervousness
CI: known hypersensitivity

61
Q

How do Orexin neurons regulate sleep?

How do Orexin mutations cause Narcolepsy?

A
Orexin neurons (aka Hypocretin) stimulate MonoAminergic neurons, stimulates thalamus
MOA inhibit VLPO indirectly regulates Ventral Lateral Preoptic area aka Sleep Center

Narcolepsy when Orexin neurons shut off, and VLPO and MOA try to inhibit each other simultaneously

62
Q

What’s the only non-substance disorder that can be grouped under substance addiction/dependency?
why?

A

Gambling and Gaming disorder had enough data to justify including with drug/alcohol categories
See similar low 5HT and decreased Ventral Medial Prefrontal Cortex activity (assoc w/impulsive decision making in risk-reward assessments)

63
Q

Define alcohol use intoxication, withdrawal, and chronic CNS effects

A

Acute: EtOH binds GABA receptor sites thus increasing GABA activity;
blocks Glutamate and Glycine (NMDA) activity;
increases endogenous opioids

Chronic: chronic upregulation of Glutamate and GABA suppression

Withdrawal: CNS hyperexcitability bc Glu/Glycine won’t be suppressed and GABA won’t be secreted… can have Delirium Tremens in 3-5d

64
Q

What can occur when treating PD pts w/DA?

A

PD pts treated with DA agonists or replacement tx, have increased risk for behavioral additions

65
Q

what’s tx for Behavioral addictions, including gambling?

A

No Med tx for behavioral addictions!

try CBT, 12 step programs

66
Q

Smokers have a low incidence of which neurological disease?

A

Smokers have lower incidence of Parkinsonism!

67
Q

Withdrawal of Benzos or Barbituates is more severe?

A

Barbiturate withdrawal more severe than bnezodiazepine

68
Q

What’s the most common cause of Wernicke’s Encephalopathy?
2nd most common?

What’s the triad of sxs?

A
#1 gastric bypas
#2 alcoholism

confusion/delirium/encephalopathy + Ataxia + Nystagmus

69
Q

What can Wernicke’s Encephalopathy lead to?

A

Wernicke’s can lead to Korsakoff syndrome, a chronic deficit in ability to establish new memory stores, will confabulate to fill in gaps in memory, a non-progressive dementia

70
Q

What is Wernicke’s Encephalopathy?

A

Wernickes = Vit B1 Thiamine deficiency that causes neurological sxs

71
Q

Differentiate Naltrexone and Naloxone?

A

Naltrexone: reversible opioid receptor antagonist, prevents alcohol-opioid effects but must be opioid free at least 1w prior

Naloxone: Opioid antagonist, blocks or reverses effects of opioids, treats OD, acute use (not used for alcohol withdrawal)

72
Q

Do Hallucinogen’s have withdrawal sxs?

What’s the exception?

A

Hallucinogen’s do NOT have withdrawal

except MDMA/ecstasy, have stimulant-like withdrawal effects

73
Q

What is Captogon? Kratom?

A

Captogon = amphetamine/theophylline, used for ADHD tx but now used by ISIS for fighting

Kratom = herbal ‘speedball’ banned in US

74
Q
Differentiate between street names of
MDMA
MDA
MDEA
Methamphetamine
crystal meth
A

MDMA: Ecstasy, similar to 5HT, stimulant = MDA: Love Drug, intense euphoria
MDEA: Eve, rave drug for sexual stimulant
Methamphetamine: Rx
crystal meth: rock form of Ephedrine/pseudoephedrine

75
Q

Differentiate between Fentanyl and Meperidine?

A

Both strong synthetic opioid analogs,
Fentanyl: used as preop anesthesia or post op pain
Meperidine: pain medicine, can cause Parkinsonism

76
Q

Differentiate PCP and Ketamine

A

Both NMDA receptor antagonist in cerebral cortex and limbic structures, directly effecting DA and 5HT receptors, causes violent behaviors, seizures, psychosis, and hyperthermia w/rhabdomyolosis
PCP = Angel Dust
Ketamine = general anesthesia, esp kids

77
Q

Differentiate Synthetic Cathinones and Cannabinoids

A

Bath Salts = synthetic cathinones, from Khat plant, sympathomimetic syndrome w/adrenergic stimulation and hallucinogenic effects, causes Parkinsonian sxs
SPICE = synthetic cannabinoids, causes stroke, MI, and kidney failure

78
Q

Walk through reward pathway

A

VTa (mesolimbinc domapimnergic path) to
NAc (nucleus accumbens) to
Prefrontal cortex to
Amygdala

79
Q

What are the 3 classes of addictive drugs?

A

addictive drugs

1) Gio protein coupled receptors = Opiates
2) Transporters of biogenic amines = Psychostimulants
3) Ionotropic receptors/channels = Nicotine, Ethanol

80
Q

What changes in neurocircuitry that leads to addiction?

A

addiction:
Prefrontal cortex gets compromised and undermined d/t
-Nucleus accumbens, responsible for learning/motivation, hijacks control of reward pathway
-Amygdala, maldapation leads to increased reactivity to stress and (-) emotions

81
Q

What’s the MOA of opiods?

A

Opioid MOA:
mu-opioid GPCR receptors INHIBIT Ca+ influx that would normally lead to GABA release
mu-opioid receptors ACTIVATE K+ channels, hyperpolarizing cell
K+ hyperpolarization and no GABA release, no inhibition of DA neurons

82
Q

What’s the MOA of Cocaine? Amphetamine?

A

Cocaine MOA: blocks Dopamine Transporter (DAT) causing addiction… and blocks Na channels
Amphetamine: increases catecholamine (CA) release, blocks CA storage and MOA

83
Q

What’s the Dopamine Hypothesis?

A

Addictive drugs always cause Dopamine Release, usurps reward pathway

84
Q

What causes opioid withdrawal sxs?

A

Opioid withdrawal:
using opiates causes increased production of AC, PKA, cAMP bc opiates decrease them
Withdrawing opiates causes massive increases in cAMP
cAMP causes diarrhea and withdrawal sxs

85
Q

Differentiate Opioids and Cocaine addiction (reference reward pathway)

A

Opioids: Dopamine-independent mechanism to block DA’s inhibitors, so blocking DA receptors won’t change much. Plus there’s opiate receptors on NAc that also reinforce reward seeking pathway

Cocaine: blocks Dopamine Transporters, so blocking the DA receptors will change behavior

86
Q

Differentiate Nicotine and Ethanol abuse addiction neurocirtuity pathways

A

Nicotine: binding nAChR in VTa AND stimulating Glu input from amygdala’s PPT/LDT, stimulates DA release in NAc

EtOH: somehow affects GABA, Cannabinoid, and Glu receptors

87
Q

How do you treat alcohol toxication?

Alcohol Withdrawal?

A

EtOH toxication: Banana bag w/B1, B9, multivitamins, fluid, +/- Mg

EtOH Withdrawal: Benzos first
can try antiadrenergic, or antipsychotics

88
Q

What are drug-drug and drug-disease interactions for meds used to treat alcohol withdrawal

A

Diazepam can cause hepatic accumulation impairment

Antipsychotics can increase seizure risks

89
Q

What are the short acting Benzos?
What are the fact acting Benzos?
any drawbacks?

A

Short acting: Lorazepam, Oxazepam

Fast acting: Diazepam (can cross BBB, but accumulates hepatic impairment)

90
Q

What are the FDA approved drugs used for Alcohol Dependence/Abstinence?

A

Alcohol addiction drugs:
1 Naltrexone
2 Disulfram
3 Acamprostate

91
Q

What’s the MOA, *ADE, drug-drug and drug-disease interactions for Naltrexone?

A

Naltrexone
MOA: reversible opioid receptor antagonist
ADE: *hepatic impairment, GI intolerance, injection rxns
drug-drug: blocks opioid effects
drug-disease: must be opioid free for at least 1w

92
Q

What’s the MOA, *ADE, drug-drug and drug-disease interactions for Disulfiram?

A

Disulfiram
MOA: Aldehyde dehydrogeanse antagonist, causes acetaldehyde buildup as ‘aversion therapy’
ADE: *hepatic impairment, metallic taste, drowsy, visual changes… avoid in pts w/psych or heart disease
drug-drug: EtOH, Metronidaze (additive CNS effects)
drug-disease: wait till patient is currently abstinent

93
Q

What’s the MOA, *ADE, drug-drug and drug-disease interactions for Acamprosate?

A

Acamprosate
MOA: UNK, maybe blocks NMDA receptor to decrease Glu hyperexcitability during abstinence
ADE: *renal impairment, GI, insomnia, anxiety, sleep changes

94
Q

What’s the MOA, sxs of use, sxs of abuse, sxs of withdrawal, and tx for Cocaine and Ampethamine

A

Cocaine and Amphetamine
MOA: NE/DA Reuptake Inhibitors
sxs use: stimulation
sxs abuse: Euphoria, hypervigilance, irritability, insomnia, confusion, decreased appetite, ↑HR, ↑/↓BP, arrhythmias, respiratory depression, N/V, diaphoresis
sxs withdrawal: Fatigue, sleep changes, nightmares, depression, appetite changes, bradyarrhythmias, tremor, altered mental status
Tx: Supportive, Lorazepam if agitated, Haloperidol if psychotic agitation,

95
Q

What’s the MOA, sxs of use, sxs of abuse, sxs of withdrawal, and tx for Ecstasy?

A

MDMA = MDA = stops reuptake of CatecholAmines (5HT, DA, DE)
sxs use/abuse: Euphoria, empathy, muscle tension, sweating, increased HR/BP, tremors, memory loss, can cause serotonin syndrome
sxs withdrawal: insomnia, depression
Tx: supportive ONLY

96
Q

What’s the MOA, sxs of use, sxs of abuse, sxs of withdrawal, and tx for Marijuana?

A

MOA Marijuana: activates cannabinoid receptors and increases DA
sxs use/abuse: Euphoria, increased senses, increased appetite, apathy, amotivation, hallucinations, dry mouth
sxs Withdrawal: In general, not physically threatening but can occur with routine use (e.g., sleep disturbances, anxiety, restlessness, sweating), Usually resolves within a few weeks, most symptoms within first week, Preliminary data suggests long-term CNS effects, particularly if used during adolescence; limited data on long-term physical effects
Tx: Supportive (acute)

97
Q

What’s the MOA, sxs of use, sxs of abuse, sxs of withdrawal, and tx for Benzodiazepines?

A

Benzo
MOA: GABA agonist, increases frequency of opening
sxs use/abuse: memory impairment, drowsy, confused, slurred speech, nystagmus
sxs withdrawal: similar to alcohol withdrawal, and seizures
tx: Supportive, and Flumazenil in acute OD but don’t use for chronic users bc it’ll cause seizures

98
Q

What’s the MOA, sxs of use, sxs of abuse, sxs of withdrawal, and tx for GammaHydroxyButyrate?

A

GHB
MOA: alters DA transmission, GABA analog
sxs use/abuse: slurred speech, respiratory depression, vomiting, seizures, amnesia, anesthesia
sxs withdrawal: Similar to alcohol withdrawal, but more severe psychiatric symptoms and less severe physical symptoms
tx: supportive, consider benzos

99
Q

What’s the MOA, sxs of use, sxs of abuse, sxs of withdrawal, and tx for Inhalants?

A

Inhalants
MOA: CNS depression via inhibitory NTs
sxs use/abuse: Distorted time/space, headache, nausea, slurred speech, fear, anxiety, depression, motor impairment, glassy eyes, red nose or mouth, respiratory depression
sxs withdrawal: hallucinations, tremor, diaphoresis, chills, HA, seizures
tx: supportive

100
Q

What are the 2 drugs that maintain alcohol abstinence? which is Aversion therapy?

A

Disulfiram=aversion therapy

Acamprosate

101
Q

What’s the triad of opioid poisoning?

A

opioid poisoning:
pinpoint pupils
unconsciousness
respiratory depression

102
Q

What’s the MOA and ADE of Methadone

A

Methadone:
MOA: FULL opioid agonist
ADE: respiratory depression, sedation

103
Q

What’s the MOA and ADE of Buprenorphine

A

Buprenorphine:
MOA: PARTIAL opioid agonist
ADE: Hepatoxicity, respiratory depression, sedation

104
Q

What’s the MOA and ADE of Suboxone?

A

Suboxone:
MOA: Buprenorphine + Naloxone
ADE: Hepatotoxicity, respiratory depression, sedation

105
Q

What’s the MOA and ADE of Naltrexone?

A

Naltrexone:
MOA: Opioid antagonist
ADEs: GI, fatigue, insomnia

106
Q

What are the types of Nicotine Replacement Therapy drugs?

A

Nicotine replacement rx:
Varenicline
Bupropion

107
Q

What’re the MOA of Varenicline and Bupropion?

When do you start them?

A

Varenicline: α4β2 nAChR partial agonist

Buproprion: DNSRI

*initiate both prior to quit date

108
Q

What’re the drug-drug and drug-disease interactions of
Buproprion
Varenicline
general Nicotine Replacement Therapies

A

Buproprion: can induce seizures
Varenicline: don’t combine w/Nicotine Replacement Therapy drugs
general Nicotine Replacement Therapy can affect HR, BP (avoid in hx MI), dizzy, HA, patch: skin irritation, insomnia
lozenge/gum: mouth sore, taste change, GI upset
inhaler: concern w/asthma or COPD

Drug-drug: smoking cigarettes induces CYP1A2 and nicotine affects BP, HR, etc.

109
Q

What are off-label rx for smoking cessation?

A

smoking cessation off label rx:
Clonidine (alpha2 agonist)
Nortriptyline (TCA aka SNRI)

110
Q

What are 3 drugs given in pts who look like they’ve been poisoned and experiencing CNS dysfunction?

A

poisoned pt w/CNS dysfunction?
1 Dextose
2 Naloxone
3 Thiamine

111
Q

How is Activated Charcoal administered, and how does it help poisoning?

A

Activated Charcoal
MOA: binds to diverse substances, making them less available for systemic absorption; except for hydrocarbons, alcohols, and most metals except THallium
Give within 1hr of poison ingestion, be careful of aspiration, Multiple Doses of Activated Charcoal (MDAC) enhances elimination by inerrupting enterohepatic recirculation and DI dialysis, pulling toxins from bloodstream back into intraluminal space

112
Q

When can you use Whole Bowel Irrigation?

what is it?

A

Use WBI when poisoning by Enteric-coated Aspirin, sustained-release Lithium tablets, Verapamil, metals, and asymptomatic drug packers
Polyethylene glycol

113
Q

How does Ion Trapping work, esp for Salicylate OD?

A

Ion trapping alkalinizes urine, so weak acid drugs like Aspirin get trapped in renal tubules
how? give IV sodium bicarb

114
Q

Describe Serotonin Syndrome?
moa?
sxs:
tx?

A

Etiology: SSRIs, MAOIs

Sxs: Agitation (restlessness), diaphoresis, diarrhea, DIC, fever, hyperreflexia, incoordination/ataxia, mental status changes (confusion, hypomania), multi-organ failure, myoclonus, ocular clonus, rhabdomyolysis, shivering, tonic-clonic seizures, tremor

Tx: remove drug, supportive, use Benzos, 5HT2A antagonist (Cyproheptadine) and neurmuscular block (Rocuronium) if necessary

115
Q

Describe Neuroleptic malignant syndrome
moa?
sxs:
tx?

A

Etiology: no DA activity, can come from Haloperidol and other antipsychotics
Sxs: Diaphoresis, dysphagia, tremor, incontinence, confusion-coma, mutism, tachy, elevated/labile BP, leukocytosis, elevated CrKinase
Tx: remove drug, supportive, use Benzos, neuromuscular blocks if necesary

116
Q

Describe Cholinergic toxidrome
moa?
sxs:
tx?

A

Etiology: nerve gases or organophosphate poisoning (insecticides) causing increased ACh by blocking AChE
Sxs: diarrhea, urination, miosis, brady, bronchoconstriction, emesis, lacrimation, salivation, diaphoresis
Tx: Atropine (blocks mAChR, crosses BBB) and Pralidoxime (regenerations AChE, doesn’t cross BBB)

117
Q

Describe Anticholinergic toxidrome
moa?
sxs:
tx?

A

Etiology: TCAs, Typical antipsychotics, and other anticholinergics
Sxs: tachy, tachypnea, hyperthermia, Dry mouth, blurred vision, mydriasis, flushed skin, agitation/delirium, decreased bowel sounds
Tx: Physostigmine salicylate (AChE inhibitor)

118
Q

Describe Opioid toxidrome
moa?
sxs:
tx?

A

Etiology: Opiates
Sxs:
Tx: Naloxone aka Narcan, low dose reverses respiratory depression but maintains analgesia

119
Q

How do Atropine and Pralidoxime treat organophosphate (malathion/parathoin) poisoning?

A

Atropine: crosses BBB to block mAChR

Pralidoxime: regenerates AChE

120
Q

How to dose Naloxone?

A

High dose if you want to reverse completely

Low dose if you want to maintain analgesia but reverse respiratory depression

121
Q

Why is acetylcysteine used to treat acetaminophen OD?

A

Aceytlcysteine restores Glutathione stores

Glutathione removes the toxic intermediates that can form from Acetaminophen breakdown

122
Q

Why is ethylene glycol toxic?

Tx?

A

Ethylene glycol at first looks like alcohol poisoning, but causes metabolic acidosis, *renal tubular damage, and blindness
Tx: Fomepizole, competitive inhibitor of alcohol dehyrogenase

123
Q

Why is Methanol toxic?

Tx?

A

Methanol causes metabolic acidosis, renal tubular damage, and *blindness
Tx: Fomepizole, competitive inhibitor of alcohol dehyrogenase

124
Q

What are Cyanide poisoning, etiology?
presentation?
tx?

A

Etiology: uncouples mitochondrial oxidative phosphorylation, preventing cellular respiration
Found in seeds, smoke, and chemicals
Pt smells like bitter almonds
Sxs: CNS, respiratory, and CV sxs
Tx:
1 Triad:Amyl nitrate, sodium nitrate, and sodium thiosulfate
2 Cyanokit = hydroxycolbalamine aka B12

125
Q

What is the Minimum Alveolar Concentration for inhaled anesthetics?

A

MAC = [drug] where 50% of pts are immobile… so low MAC is high potency and vice versa

126
Q

What’s the MOA of inhaled anesthetics?

PK?

A

MOA: strengthens GABAA (inhibitory), with decreased 5HT/Glu/NMDA/AMPA (excitatory
PK: decreased solubility = faster induction/recovery time, bc if it doesn’t dissolve there’s more available to get into brain

127
Q

Differentiate Nitrous oxide and Sevoflurance as inhaled anesthetics
Effect on organ systems?
*ADEs?

A

NO: gaseous at room temp
Sevoflurane: liquid at room temp
Decrease cerebral metabolic rate, decrease myocardial fx, decrease MAP (mean arterial pressure), bronchodilate and cause respiratory depression
ADEs: *decrease MAP, Sevoflurane nephrotoxocity, NO megaloblastic anemia, Halothane hepatitis

128
Q

What’s the cause and tx for Malignant Hyperthermia?

A

Malignant hyperthermia d/t general anesthetics or neuromuscular blocking drugs (esp Sevoflurane and Succinylcholine)
Tx: Dantrolene, inhibits CA release from SR by blocking Ryanodine1 receptors

129
Q

For Thiopental
MOA
*PK
organ system effects

A

Thiopental: Barbiturate
MOA: increase duration of Cl- opening at GABAA
PK: 1/2 life skyrockets w/>30m infusion, so not really used anymore
organ system effects: post-op N/V

130
Q

For Propofol
MOA
*PK
*organ system effects

A

GABAA Potentiator Propofol
PK: *most frequently used for induction, AND it’s 1/2 life doesn’t increase much w/increased infusion duration
organ system effects: antiemetic activity

131
Q

For Etomidate
who?
PK
organ system effects

A

GABAA Potentiator Etomidate
who: compromised myocardial contractility
organ system effects: , endocrine effects, adrenocortical suppression
ADEs: post op N/V

132
Q

For Midazolam
MOA
PK
organ system effects

A

Midazolam: Benzo
MOA: increase Cl- channel open frequency at GABAA receptor, anxiolytic, anterograde amensia
PK: terminate w/Flumazenil
organ system effects: pain during injection

133
Q

For Ketamine
MOA
PK
organ system effects

A

Ketamine
MOA: inhibit NMDA receptor
PK: * only IV anesthetic that doesn’t cause respiratory depression, bc “dissociative anesthesia” where pt’s conscious but in catatonic state, good for kids, most profound analgesia
organ system effects: Psychotropic

134
Q

When do you use ElectroConvulsive Therapy (ECT)? and why?

ADE?

A

For Major Depressive Disorder, Schiphrenia, mania, cataonia… if unresponsive to therapy w/90% efficacy! but 50% relapse in 6mo
superior to placebo, antidepressants, and MAOIs!
ADEs: memory loss, cognitive dysfunction, amnesia

135
Q

What’s theorized to cause Seasonal Affective Disorder?

Tx?

A

SAD: temporal change causing depression, maybe d/t Melatonin, NT5s 5HT, NE, and DA, and low 5HT in thalamus and hypothalamus

Tx: Tryptophan, d-fenfluramine, Sertraline, Fluoxetine (all enhance 5HT levels)