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IDT > IDT Exam 2 > Flashcards

IDT Exam 2 Flashcards

1
Q

8 subcategories of depression

A

Characterized as mild, moderate, or severe
Reactive
Agitated
Atypical
Dysthymia
PMS
Post-partum
Psychotic
SAD

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2
Q

Treatments for depression

A

Talk
Light
Antidepressants
Exercise
Electroconvulsive

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3
Q

What is the simple biogenic amine hypothesis

A

Antidepressants extend duration of biogenic amines (norepinephrine, serotonin, maybe dopamine) through blocking reuptake or metabolism (SSRIs vs. MAOIs)

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4
Q

Serotonin associated symptoms

A

Agitation
Dysphagia
Dyssomnia
Anxiety
No libido

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5
Q

Norepinephrine associated symptoms

A

Focus/alert
Memory
Energy

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6
Q

Problem with biogenic amine hypothesis

A

Biogenic amines increase in 2-3 hours
Antidepressants take weeks to months to work

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7
Q

Alternative antidepressant and ETC action hypothesis

A

Increase in biogenic amines increases neurotrophic agents (bdnf) and neuronal sprouting leading to structural changes

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8
Q

TCAs block

A

Both NE and 5-HT transporters

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9
Q

Examples of TCAs

A

Imipramine
Amitriptyline
Desipramine
Doxepin
Maprotiline

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10
Q

TCAs SEs

A

Alpha-1 antagonist → vasoconstriction
Muscarinic cholinergic antagonist
NE activation of beta adrenergic receptors
Overall: increased HR
H1 antagonist → sedation
+ alpha1 antagonist → weight gain (worst in amitriptyline and doxepin)
Death if overdosed

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11
Q

MAOIs block

A

NE and 5-HT breakdown

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12
Q

Examples of MAOIs

A

Phenylzine
Tranylcipromine
Isocarboxazid

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13
Q

MAOIs are used for

A

Treatment resistant or atypical depression

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14
Q

MAOI SE

A

Insomnia/daytime sleepiness
Dry mouth
Liver toxicity in phenylzine
Prolongs T1/2 in oxidatively deaminated drugs

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15
Q

What dray combos way cause serotonin syndrome

A

-triptans
SSRI
mepiridine
Dextromethorphan

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16
Q

How to treat serotonin syndrome

A

Oxygen
Sedation
Serotonin antagonist → Cyproheptadine

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17
Q

What foods can be toxic if eaten with MAOI

A

Tyramine rich foods
Fermented, aged, cured, and pickled foods

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18
Q

What is a selective MAOI

A

Selegiline → Parkinson’s

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19
Q

Why are SSRIs better than TCAs

A

They have no affinity for alpha adrenergic, muscarinic, histamine or dopamine receptors

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20
Q

Fluoxetine characteristics

A

Most stimulating ssri
Hyponatremia

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21
Q

How do SSRIs cause hyponatremia

A

They increase vasopressin
Mostly problematic in pts with electrolyte imbalance (bulimia)

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22
Q

What is discontinuation syndrome and do how you treat it

A

When you quit SSRI use
Nightmares
Agitation
Brain zaps
Taper dose instead of cold turkey

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23
Q

SNRI examples

A

Venlafaxine
Deafenlafaxine
Duloxetine
Levomilnacipran

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24
Q

Vilazodone, vortioxetine, and trazadone MOA

A

Serotonin receptor antagonist (5HT:1A, 3, and 7)
and block SERT
Vortioxetine is partial 5HT1A/B agonist
Trazodone is also H1 and Alpha1 antagonist

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25
Q

St Johns Wort characteristics

A

Hyperforin
Similar efficacy and SEs to SSRIs
Induces Cyp3A

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26
Q

Mirtazapine MOA

A

May potentiate NE and 5HT release by blocking autoreceptors
H1 antagonism (sleepy)

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27
Q

Atypical antidepressants

A

Mirtazapine
Bupropion
Esketamine
Dextromethorphan + bupropion
Brexanolone

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28
Q

Mirtazapine MOA

A

Presynsptic autoreceptor antagonist

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29
Q

Bupropion MOA

A

Central nicotinic receptor antagonist

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30
Q

Esketamine MOA

A

NMDA receptor antagonist

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31
Q

Dextromethorphan + bupropion MOA

A

NMDA receptor antagonist

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32
Q

Brexanolone MOA

A

Progesterone metabolite and GABAa receptor positive allosteric modulator

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33
Q

TCA SAR

A

3-4 atoms between N an ring
C3 Monohalogenation
3 amines block 5HT reuptake
2 amines block NE reuptake
3 amines can be converted to 2 amines

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34
Q

3 amines tend to be more

A

Sedating

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35
Q

TCAs are generally metabolized by

A

2D6 and 2C19

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36
Q

Imipramine metabolites and activity

A

Desipramine (desmethylimipramine)
2-hydroxydesipramine
Both active

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37
Q

Common TCA ring systems

A

Dibenzazepine
Dibenzocycloheptenes
Dibenzoxepin

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38
Q

Amitriptyline facts
Gets metabolized to

A

Highest antimuscarinic and sedative fx
Metabolized to nortryptyline which has less above SE

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39
Q

Tetracyclic TCA

A

Maprotiline
500 fold more NET inhibition than SERT

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40
Q

Which MAOI is prodrug

A

Phenelzine

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41
Q

Phenelzine inhibits

A

2B6

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42
Q

Non selective MAOIs

A

Tranylcypromine
Phenelzine
Isocarboxazid

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43
Q

MAOBI

A

Selegiline

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44
Q

Which MAOI are irreversible

A

All

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45
Q

Fluoxetine and norfluoxetine inhibit

A

2D6 and 2C19

46
Q

Sertraline inhibits

A

2D6 weak/moderate

47
Q

Sertraline metabolite

A

N-desmethylsertraline (less active)

48
Q

How is paroxetine metabolized

A

2D6 removes methylene creating an inactive catechol metabolite

49
Q

Fluoxetine SERT fold

A

30-fold SERT over NET

50
Q

Sertraline -fold SERT over NET

A

1400-fold SERT over NET

51
Q

Paroxetine -fold SERT over NET

A

300-fold SERT over NET

52
Q

Fluvoxamine -fold SERT over NET

A

600-fold SERT over NET

53
Q

Citalopram -fold SERT over NET

A

3000-fold SERT over NET

54
Q

How many enantioners does sertraline have?

A

4 but only the 1S, 4S is used

55
Q

Sertraline EWG
Amine

A

Dichloro on benzene
Secondary

56
Q

Fluoxetine EWG
Amine

A

Triflouromethyl
Secondary

57
Q

Paroxetine EWG
Amine

A

Fluorine
Secondary (part of ring)

58
Q

Fluvoxamine EWG
Amine

A

Triflouromethyl
Primary

59
Q

Citalopram EWG
Amine

A

Fluorine and Cyano group
Tertiary

60
Q

Paroxetine inhibits

A

2D6 irreversibly

61
Q

Fluvoxamine inhibits

62
Q

WhichSSRI is UV light sensitive

A

Fluvoxamine can be changed from E to Z isomer (inactive)

63
Q

How does trazodone work

A

N-dealkylation by 3A4 creates mCPP which is a 5HT2a partial agonist

64
Q

How does nefazodone work

A

3A4 metabolizes it to mCPP and alpha-hydroxynefazodone
Both are active

65
Q

Nefanodone inhibits

A

3A4
Nefazodone and alpha-hydroxynefazodone

66
Q

Which antidepressant may cause hepatotoxicicity

A

Nefazodone

67
Q

How is vilazodone different from trazodone and nefazodone

A

No mCPP metabolite
And no active metabolites

68
Q

Vortioxetine metabolism

A

2D6 inactivates it
*reduce dose if used with strong 2D6 inhibitors

69
Q

Venlafaxine metabolism

A

2D6 → O-desmethylvenlafaxine
AKA desvenlafaxine
3A4 → N-desmethylvenlafaxine
Minimal activity
Lastly glucuronidation

70
Q

SNRIs do not have

71
Q

Duloxetine is a moderate

A

2D6 inhibitor

72
Q

Levomilnacipran inhibits

73
Q

Vortioxetine inhibits

74
Q

Bupropion resembles

A

Amphetamine

75
Q

Bupropion metabolism

A

2B6 → hydroxybupropion
Reduction → hydrobupropion
Both active

76
Q

Bupropion inhibits

A

2D6
So does hydroxybupropion

77
Q

Mirtazepine inhibits

78
Q

What causes the decrease in antimuscarinic SEs in Mirtazapine compared to TCAs

A

The basic nitrogen is closer to the ring system

79
Q

How is esketamine metabolized

A

2B6 and 3A4 N-demethylation

80
Q

Esketamine is similar to

A

Phencyclidine/PCP/angel dust
Both are Nmda receptor antagonists

81
Q

What is DSM 5

82
Q

Screening tools for depression

A

PHQ-9 self
GDS geriatric
HAM-D clinician
MADRS both

83
Q

Diagnostic criteria for major depressive disorder

A

Depression
Energy
Sleep
Interest
Guilt
Concentration
Appetite
Psychomotor changes
Suicidality

84
Q

What lowers MDD recovery rates

A

Crisis/trauma
R
Anxiety
Personality disorders
Physical illness
Young

85
Q

What medicines or conditions increase risk of MDD

A

Hypothyroidism
Low T (can be drug induced)
Diabetes
Anemia

86
Q

Sedatives vs. hypnotics

A

Induce sedation and decrease activity
Induce onset and maintain sleep

87
Q

What brain region is Central in the lambic system

88
Q

What does the striatum do in fear response

A

Expression: Fight/flight

89
Q

What does the brainstem do in fear response

A

Regulate autonomic responses

90
Q

What does the hypothalamus do in fear response

A

Hormonal stress response

91
Q

Melatonin comes from

A

Serotonin converted in pineal gland

92
Q

The master clock is located in

A

The suprachiasmatic nucleus in the hypothalamus

93
Q

Why is the ascending arousal system

A

Sleep-wakefulness-excitement-panic

94
Q

Berzodiazopine cons

A

Tolerance
Depressant/sedative
Impaired reasoning and memory
Bad with opioids and alcohol

95
Q

Benzodiazepine pros

A

Quick acting
High therapeutic index
Very effective for anxiety

96
Q

How do gabapentin and pregabalin work

A

Inhibit neurotransmitter release by binding to alpha2delta subunit of presynaptic calcium channel

97
Q

Pregabalin and gabapentin cons

A

Severe/fatal breathing problems esp when used with opioids and in pts with decreased lung function

98
Q

Symptoms of cheese reaction

A

Elevated tyramine (a sympathomimetic) increases NE release which increases blood pressure and can evoke hypertensive crisis

99
Q

Betablockers treat

A

Acute physiological symptoms:
Palpitations
Tremor
GI upset

100
Q

Buspirone acts as a

A

5-HT1A partial agonist

101
Q

What is 1-PP

A

It is the active metabolite of buspirone and alpha2 antagonist which may increase panic attack

102
Q

Barbiturates increase

A
  • GABA efficacy
  • Duration of channel opening
103
Q

Benzodiazepines increase

A
  • GABA affinity
  • Frequency of channel opening
104
Q

Preferred GABAa pentameric combo

A

2 alpha
1 beta
1 gamma
1 beta or gamma

105
Q

Benzodiazepines bind between

A

Alpha and gamma subunits

106
Q

GABA binds between

A

Alpha and beta subunits

107
Q

What is flumazenil

A

Competitive benzodiazepine antagonist

108
Q

Buspirone is metabolized by

109
Q

Buspirone has how many metabolites

A

6 hydroxybuspirone 5HT1A

1PP an alpha2 antagonist

110
Q

Benzodiazepine SAR

A

Must have
7 member ring
C7 EWG
Can have
Groups on 1, 3, and2’

111
Q

Which benzodiazepine has no active metabolites

IDT (5 decks)

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