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Pharm Exam 3 > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

mood disorders - definition:

A

group of diagnoses with disturbances in affect (expressed or observed emotional response)

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2
Q

mood disorder classification is based on…

A

whether patient experienced a manic episode

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3
Q

2 classifications of mood disorders? treatment class for each?

A

1) major depressive disorder (MDD) aka unipolar depression - NO MANIC EPISODES –> treated with antidepressant drugs
2) bipolar disorder - MANIC EPISODES –> treated with mood stabilizing drugs

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4
Q

broad range of symptoms of major depressions

A

1) depressed mood
2) anhedonia (loss of pleasure) and loss of interest in life
3) appetite changes;
sleep abnormalities;
altered cognitive function;
fatigue;
suicidal thoughts/attempts

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5
Q

point prevalence of major depression in USA

A

5-8%

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6
Q

Co-morbidities with major depression?

A 
chronic pain
stroke
CV disease
cancer
and so on...
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7
Q

Etiology of major depression?

What part of brain is most likely causing this disease?

A
  • probably related to stress

- disease of the limbic system

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8
Q

2 main problems with antidepressants?

A

1) delay of therapeutic response: takes weeks or months of regular dosing before most patients derive benefit from antidepressant drugs
2) side effect can limit usage: the elderly are equally responsive to antidepressants but are more likely to experience adverse side effects (SSRIs are preferred in these patients)

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9
Q

What is the monoamine/Biogenic amine hypothesis?

A

-basically that depression is the result of abnormalities in serotonin, norepinephrine and dopamine neurotransmission

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10
Q

What is the neutrophic hypothesis?

A

-basically depression is related to changes in nerve growth factor (ex: BDNF- brain derived neurotrophic factor) signaling = role in cell survival and synaptic plasticity - no nerve growth factor = death

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11
Q

depression is related to a deficiency in which neurotransmitters?

A
  • 5-HT
  • NE
  • DA
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12
Q

First connection between depression and NE depletion?

A

use of reserpine for HTN evoked depression - (reserpine depletes NE)

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13
Q

What do all currently available antidepressants do?

A
  • enhance the synaptic availability of monoamines

- increase BDNF in the brain

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14
Q

neutrophic hypothesis:

-BDNF –> activates? –> results?

A

activates TRK-B receptors = increased neuronal survival and growth

BRAIN FERTILIZER!

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15
Q

Majro antidepressant drug categories:

A

1) Monoamine oxidase inh (MAOI)
2) Tricyclics (TCAs)
3) selective serotonin reuptake inh (SSRI)
4) atypical antidepressants?

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16
Q

What type of drug prescribed for? PTSD?

A

SSRI

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17
Q

What type of drug prescribed for?

Anxiety?

A

SSRI, SNRI, [buspirone ]

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18
Q

What type of drug prescribed for?

Panic disorder?

A

TCAs, MAOI, SSRI, [SNRI(Venlafaxine)]

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19
Q

What type of drug prescribed for?

obsessive compulsive disorder?

A

SSRI, clomipramine

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20
Q

What type of drug prescribed for?

Enurisis?

A

TCAs - imipramine

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21
Q

What type of drug prescribed for?

Chronic pain?

A

TCA and SNRI

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22
Q

What type of drug prescribed for?

Eating disorder - bulimia?

A

SSRI

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23
Q

What type of drug prescribed for?

smoking cessation?

A

bupropion

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24
Q

What type of drug prescribed for?

sedative?

A

trazodone

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25
Q

Potential side effects for 5HT reuptake blockage?

A

GI disturbances
anxiety (dose dependent)
sexual dysfunction

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26
Q

Potential side effects for NE reuptake blockage?

A

tremors

tachycardia

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27
Q

Potential side effects for DA uptake blcokage?

A
  • psychomotor activation,
  • antiparkinsonian effects
  • psychosis
  • increase attention and concentration
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28
Q

Potential side effects for H1 receptor block?

A

sedation
drowsiness
weight gain
hypotension

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29
Q

Potential side effects for muscarinic ACH receptor block?

A 
blurred vision,
dry mouth
sinus tachycardia
constipation
urinary retention
memory dysfunction
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30
Q

Potential side effects for alpha1 receptor block (adrenergic)?

A

postural hypotension
reflex tachycardia
dizziness

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31
Q

MOAI

1) used for? clinical use?
2) drug names?
3) MOA
4) problem with MAOIs?

A

1) -not first line but used for depression - we have better drugs now.
- in tx resistant MDD patients
- atypical depressions
- anxiety states (social and panic)
2) -phenelzine**
- tranylcypromine**
- selegiline**
- moclobemide (not available in US)
3) increase sympathetic availability of NE and 5HT by blocking their catabolism via inh of MAO enzymes (A and B)
4) toxicity and potentially lethal food and drug interactions

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32
Q

Phenelzine

  • selective for which MOA?
  • reversible or not?
  • non-specific side effects?
  • review MAO common side effects and interactions
A
  • non-selective for MAO-A and B
  • irreversible
  • side effects are worse than other MAOI - like tranylcypromine
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33
Q

MAO-A targets what chemicals?

A

targets tyramine, NE, 5HT and DA

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34
Q

MAO-B targets what chemicals?

A

targets DA

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35
Q

Tranylcypromine

  • selective for which MOA?
  • reversible or not?
  • non-specific side effects?
  • review MAO common side effects and interactions
A
  • non-selective MAO-A and MAO-B
  • irreversible
  • side effects are worse than other MAOI - like phenelzine
36
Q

Selegiline

  • selective for which MOA?
  • reversible or not?
  • treatment of what at low dose vs high dose?
  • non-specific side effects?
  • review MAO common side effects and interactions
A
  • MAO-B but NON-selective at high doses
  • irreversible
  • low dose = parkinsons (inh DA breakdown
  • high dose = antidepressant
  • prone to sudden discontinuation syndrome
37
Q

**MAO most common side effects:

Less common side effects?

A
  • *common:
  • orthostatic HTN
  • weight gain

less common:
-dry mouth, constipation, blurry vision, urinary retention,…

38
Q

**MAO important food/chemical interaction?
What happens?
what foods?

A

1) tyramine –> results in HTN crisis!
2) interaction triggers release of catecholamines in the synapse =
- increase NE circulation
- overwhelming vasoconstriction–> HTN crisis
- headaches, intracranial bleed, stroke, MI, organ damage
3) -cheese (except cottage and cream cheese)
- chianti wines and beers that contain yeast
- coffee
- chocolate
- fava beans

39
Q
  • *Tricyclic antidepressants

- clinical uses?

A
  • major depression if SSRI are not effective
  • phobic and panic anxiety states
  • **chronic pain conditions - neuropathic pain
  • OCD

-selection base on relative incidence of side-effects

40
Q

neuropathic pain - use what antidepressant drug class?

A

Tricyclic antidrepressant - desipramine

41
Q

**TCAs: MOA?

A
  • *1) block re-uptake of both 5-HT and NE by inhibiton of SERT and NET
    2) desensitize presynaptic autoreceptors
    3) reduce central beta receptor responsiveness and density
  • 4) potent antagonist at cholinergic histinergic and alpha-adrenergic receptors
42
Q

Prototype TCA?

A

imipramine

43
Q

TCA drugs to remember:

A
  • *1) imipramine
  • *2) desipramine for neuropathic pain
  • *3) amitriptyline
44
Q

Imipramine

-MOA and treatment?

A
  • anticholinergic –> ***treats enurisis (bed wetting)

- strong 5HT and NE reuptake inh

45
Q

Desipramine

-MOA and treatment?

A

(-metabolite of imiprmine)

  • weak anticholinergic
  • strong NE and 5HT reuptake inh

-effective in treating neuropathic pain

46
Q

Amitriptyline

-MOA and treatment?

A
  • highly anticholinergic
  • highly alpha antagonist

-uses: sedative effect

47
Q

**Most serious side effect of TCAs?

A

**-cardiac tox: Na/Ca channel antagonism = lethal cardiac arrhythmias

48
Q

TCAs

-Side effects:

A

1) antagonists:
a) H1 = sedation and WG
b) alpha1=orthostatic intolerance/hypotension (HIP BREAKERS IN OLD PPLE)
c) muscarinic=anti-cholinergic (dry-mouth, constipation, blurred vison, urinary retention, confusion)
2) CNS tox:
a) delirium (WORSE IN ELEDERLY)
b) seizure, tremor
3) sexual dysf: anorgasmia,no libido
* **4) cardiac tox: lethal cardiac arrhyth (NA/Ca channel blocK)
* *5) overdose: (3 C’s)
a) convulsions
b) coma;
c) cardiac arrhyth

49
Q

TCA drug interactions?

A

with MAOI and SSRIs

50
Q

SSRI antipressant drugs:

A
  • fluoxetine
  • sertaline
  • paroxetine
  • citalopram
  • escitalopram
  • fluvoxamine
51
Q

What are the dirty drugs?
What drugs are used instead?
Used for what?

A

-MAOIs (selegiline, phnelzine, tranylcyproamide)

  • SSRIs instead (fluoxetine-sertaline-paroxetine-citalopram
  • escitalopram-fluvoxamine)

-for major dpression and a bunch of other stuff

52
Q

SSRI - clinical uses:

A

1) Major depression:
a) ease of use
b) safety in OD
c) relative tolerable cost (ALL GENERICS)
d) broad spectrum of use
2) other stuff:
a) generalized anxiety diso (GAD)
b) PTSD
c) OCD
d) panic diso
e) Premenstrual dysphoric disor (PMDD)
f) bulimia

53
Q

most commonly prescribed antidepressant drug?

A

SSRI - fluoxetine

54
Q

Primary long term Tx for PTSD?

A

SSRI

55
Q

SSRI MOA?

A
  • selectively inh SERT and block reuptake of 5HT into the pre-synaptic terminal
  • down-reg or desenitize autoreceptors
56
Q

SSRIs side effects:

  • short term?
  • long term?
  • OD?
  • interactions?
A
  • “safest” of antidepress
  • short term: nausea, GI upset, diarrhea
  • long term: sexual dysf, nervousness, agitation, sweating, fatigue, headache, WL, WG, insomnia
  • OD - low risk
  • interact with other ** antidepressants = serotonin syndrome
57
Q
  • *serotonin syndrome:
  • why does it happen?
  • what is messed with specifically?
  • which drug most often?
  • which drug is safer?
A
  • rare side effect of SSRIs due to long halflife - esp if in combo with other SSRI, TCA, or MAOI
  • most inhibit p450 enzymes (esp fluoxetine, fluvoxamine)
  • fluoxetine has longest half life - has to be discontinued for 4-5 weeks prior to using other antidepressants;
  • other SSRIs only discontinued for 2 weeks

-citalopram is safer!

58
Q
  • *serotinin syndrome
  • early symptoms?
  • late symptoms?
A

early: -lethary-restlessness-mental confusion-flushing-diaphoresis-tremor
late: -HTN-hyperthermia-hypertonicity-rhabdomyolysis-renal failure-death

59
Q
  • Discontinuation syndrome
  • which drug type?
  • what ahppens?
  • Why?
A
  • SSRIs
  • sudden discontinuation of short halflife SSRIs may cause AE in some patients 1-7 days after stopping
  • ex) paroxetine and sertaline –> dizziness, parethesias, anxiety
  • Why? clearance is occuring faster that re-adaptation to receptor regulation and therefore sensitization can occur
  • may want to switch to longer halflife SSRI
60
Q

SNRIs - serotonin-NE reuptake inh

  • what class?
  • MOA?
  • why better?
A
  • atypical antidepressants
  • inh both serotonin SERT and NE NET transporters
  • unlike TCAs these do not have affinity for other receptors = fewer side effects
61
Q

SNRI drugs?

A
  • venlafaxine

- duloxetine

62
Q

Venlafaxine

  • MOA?
  • used for?
  • side effects?
A

SNRI

  • weak NET inh
  • Strong SERT inh

-used for severe depression

  • —similar to TCA but not as severe:
  • Serotonergic: GI nausea, sex dysf, WG –> DISCONTINUATION SYNDROME,
  • noradrenergic: inc BP and HR, CNS activation (insomnia and anxiety)
63
Q

Duloxetine

  • MOA?
  • usef for?
  • side effects/
A

SNRI
-balanced SERT and NET blockde

-use for chronic back pain over TCAs/

  • —similar to TCA but not as severe:
  • Serotonergic: GI nausea, sex dysf, WG –> DISCONTINUATION SYNDROME,
  • noradrenergic: inc BP and HR, CNS activation (insomnia and anxiety)
64
Q

What drug to use for chronic back pain?

A

SNRI - duloxetine

65
Q

5-HT antagonists:

  • drug class?
  • MOA?
A
  • atypical anti-depressants

- block 5-HT2, weak SERT and NET inh

66
Q

5_HT antagoinst drugs?

A

**Trazodone

67
Q

Trazodone

  • MOA?
  • type of drug?
  • uses?
  • problems?
  • side effects?
A

-blocks H1 receptor = sedative effect
-5-HT antagonist - atypical anti-depressant
-used as unlabeled hypnotic (for insomnia)
-causes priapism (peripheral alpha1 block
-side effects: GI disturbances
; sedation and priapism

68
Q

Brupropion

  • MOA?
  • uses?
  • side effects?
A
  • blocks NE and DA re-uptake
  • inc presynaptic release of catecholamines
  • uses: MDD, smoking cessation
  • lower seziure threshold; agitation; insomnia
69
Q

Mirtazapine

  • MOA?
  • uses?
  • side effect?
A
  • blocks presynaptic alpha2 receptors
  • increase synaptic release of 5HT and NE
  • blocks 5-HT2 and 5HT3 = anti-emetic
  • blocks H1 = sedation, WG, few sexual side effects

SEDATION!

70
Q

How long until therapeutic effects seen with antidepressants?

A

2-4 weeks

71
Q

problematic sort of issue with antidepressants?

A

suicidal patients

72
Q

WHich antidepressants are safer in larger doses?

A

SSRIs

73
Q

Which antidepressant has serious cardiac issues?

A

Cardiac tox ith TCAs - blocknig Na/Ca channels = arrhythmias

74
Q

Which antidepressant drugs should not be combined?

A

SSRI
MAOI
TCA

75
Q

Bipolar disorder drugs?

A
  • lithium

- valproic acid and carbamazepine

76
Q

Most all antidepressants inh what CYPs?

A

2D6 and 3A4

77
Q

potent inh of CYP2D6?

A

paroxetine, fluoxetine and fluvoxamine

78
Q

never combine which two drugs and allow time to clear before switching?

A
  • TCA and SSRI - long half lives!

- serotonin syndrome and TCA toxicity

79
Q

Lithium

  • drug of choice for?
  • what type of drug?
A
  • manic and depressive phases of bipolar disorder

- mood -stabilizing drug

80
Q

Valproic acid and carbamazepine:

-used for?

A

-anticonvulsants but when combined with antipychotics (olanzapine, quetiapine, risperidone) used for severe bipolar disorders or patients who dont respond to lithium

81
Q

lithium treatment administration?

A

maintentance treatment, slow onset of action

82
Q

valproic acid and carbamazepine used to treat?

A

acute mania

83
Q

Lithium MOA?

A

-mostly unknown

  • prevents recycling of inositol phos(IP–> PIP2) = mood dampening effect
  • inhibits release of NE (prevents mania)
  • may also inh 5HT1a/1b autoreceptors
  • reduces synaptic glutamate by enhacing reuptake
84
Q

Lithium side effect?

A

***-tremor - most common- flu like symptoms, seziures, edema WG (not water)
GI upset

  • hypothyroidism -reversible -interferes with diodination of T4 –>T3
  • neprogenic diabetes insipidus - reversible - blocks ADH response –> polydipsia and polyuria
  • skin reactions: acne vulgaris and psoriasis
85
Q

***Lithium drug interactions:

A

-Thiazides and loop diuretics == diminish Li clearance = toxicity

these diuretics deplete Na (lose Na) = reabsorb Li and Na from proximal tubules = less excretion of Li –> high Li plasma concentration

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