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Pharm main > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

Where is the monoamine system located

A

Upper brainstem and limbic system

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2
Q

What are the NT involved in the monoamine system

A

NE,5HT, DA

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3
Q

What is the purpose of NE

A

Study and get things done

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4
Q

What is the purpose of 5HT

A

Everyday life NT- appetite, mood, emotion, sleep

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5
Q

What is the purpose of DA

A

Joy of life, feel good and party, attention

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6
Q

What other receptors are involved in the monoamine system

A

5HT3,2
H1
Alpha 1adrenergic
M- cholinergic

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7
Q

5HT3

A

Agonist- N/V/D

Antagonist- anti emetic

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8
Q

5 HT2

A

Agonist- insomnia, anxiety, akathesia, sexual dysfunction

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9
Q

H1

A

Weight gain and sedation

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10
Q

M cholinergic

A

Antagonist- constipation, dry mouth, drowsiness and confusion

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11
Q

Alpha 1 adrenergic

A

Orthostatic hypotension

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12
Q

Rules for diagnosing depression

A

Must have 5 of the SIGECAPS symptoms (1 of them must be from the interest category), change from normal functioning, and must rule out physical problems- tsh, hgb, b12

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13
Q

SIGECAPS

A

S- sleep- insomnia or hypersomnia
I- interest- depressed mood or adhedonia
G- guilt- feelings of worthlessness
E- energy- decreased energy
C-concentration- inability to make decisions or focus
A-appetite- wit changes or loss of enjoyment of food
S-suicidie- recurring thoughts of suicide

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14
Q

Who is most successful at suicide

A

Older men

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15
Q

What questions should you ask about suicide and when should you’ve concerned?

A

Always be concerned

Be especially concerned and make sure to ask if they have a plan

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16
Q

Etiologic hypothesis of depression

A

Stress diathesis- threshold for depression, environment determines if we exceed it
Biological hypothesis- aided by fact that drugs help
Catecholamine hypothesis- body runs out of NE AND 5HT
Dsregulation hypothesis- imbalance between NE and 5HT

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17
Q

Role of psychotherapy and CBT

A

Used in mild to moderate depression- works synergistically with antidepressants.
Takes longer to help but has a lower rate of remission

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18
Q

When do you use pharmacotherapy for depression

A

In severe depression

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19
Q

ECT

A

Safe for pregnant and elderly
Very quickly down regulates beta receptors in the brain which correspond to a decrease in depression.
Use if patient has depression that is refractory to 2-3 drugs that have been used for at least 12 weeks

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20
Q

Pharmacotherapy

A

Takes 4 -6 weeks to see mood changes

Changes in mood correspond to decrease in beta receptor density not changes in hormone or NT levels

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21
Q

Pharmacotherapy AE

A

Transient insomnia, anxiety, and jitteriness

Sexual dysfunction occurs but this is not transient

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22
Q

Types of drugs used to tx depression

A 
SSRI
TCA
MOA
venlafaxine
Duloxetine
Nefazodone
Trazodone
Bupropion
Mirtazapine
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23
Q

SSRI- drug names

A 
Fluoxetine
Citalopram
Paroxetine
Sertaline
Fluvoxamine
Escitalopram
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24
Q

SSRI MOA

A

Blocks serotonin reuptake
5HT2 agonist
Down regulation of beta receptors

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25
Q

SSRI AE

A

Insomnia, anxiety, diarrhea
Sexual dysfunction
Serotonin syndrome

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26
Q

How is sexual dysfunction Dealt with

A

PDE5 inhibitor

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27
Q

What is serotonin syndrome

A

Occurs when have excess serotonin, have taken to many drugs that stimulate serotonin
Fishing, wheezing, hyperthermia, N/V/D
Hypertension, myoclonus, headache, seizure, ataxia
Treat by stopping the serotonin drugs, cooling blankets, nifedipine for HTN, clonazepam for the myoclonus, and anti convulsants for the seizures

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28
Q

SSRI withdrawal

A

Shooting electric pains, anxiety, flu like symptoms
Headache, insomnia, dizziness
Must titration down the dosage especially if using SSRIs with a short half life ie paroxetine or venlafaxine
Fluoxetine doesn’t have to be titrated down BC it has a long half life and active metabolite

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29
Q

Fluoxetine

A

SSRI with very long half life and most psychomotor activating of the SSRI so good for pts with motor depression

30
Q

Citalopram

A

Least psychomotor activating of the SSRI so good for pts with psychomotor activation

31
Q

Paroxetine

A

Short half life,must be tapered down

Do not give to pregnant woma

32
Q

What SSRI do you not give in pregnancy

A

Paroxetine

Sertaline

33
Q

SSRI USE

A

DOC for depression with comorbid anxiety

Can change between them if one doesn’t work another might

34
Q

TCA drug names

A

Imipramine –> desipramine
Amotryptaline–> nortriptaline
Dsipramine and nortriptaline are metabolites

35
Q

TCA- MOA

A

Inhibit NE AND 5HT reuptake

Muscarinic, alpha 1, and H1 antagonists

36
Q

TCA AE

A

Orthostatic hypotension, Weight gain, and anti cholinergic
Sexual dysfunction
Serotonin syndrome if given with other antidepressants
Lowers the seizure threshold
Cardiac events
OD- can kill

37
Q

Mechanism of cardiac toxicity for TCA

A

Block the NA Channels causing prolonged QT interval leading to torsades des pointes –> vfib–> death
Tx OD with NAHCO3 BC it act on NA channels

38
Q

TCA’s and teratogenicity

A

The non metabolite TCA (Imipramine and amitriptalline) can cause heart failure, tachycardia, seizures, and urinary retention in newborns.

39
Q

TCA uses

A

Alternative to SSRI.
Used in depression with comorbid pain- fibromyalgia, Migraine, chronic pain, and atypical depression.
B/c NE IS THE NT OF PAIN

40
Q

TCA contraindications

A

History of CAD, seizure history, BPH, dementia, or constipation

41
Q

MOA- drugs

A

Isocarboxacid
Phenelzine
Tranycypromine

42
Q

TCA MOA

A

Blocks MAOA (5Ht, NE, and Tyrammine) and MAOB (DA)

43
Q

MAO AE

A

Orthostatic hypotension, weight gain, anti cholinergic
Sexual dysfunction
Serotonin syndrome if given with other antidepressants or meperidine, tramadol, or dextrometorphan
Wine and cheese syndrome
TERATOGENIC

44
Q

Wine and cheese syndrome

A

Hypertensive crisis that leads to fatal hemmorhages
Wine and cheese have a lot of tyrammine, normally it’s cleared nfirst pass metabolism, if there is an mao inhibitor then it might not be cleared this causes excess release of NE from peripheral neurons.

45
Q

Mao drug interactions

A

Meperidine, phenylephrine, and sympathmimetics

Lead to hypertension, fever, and delirium

46
Q

MAO uses

A

Atypical depression for tx refractory depression
Other drugs have better safety profiles.
When switching to Mao from another antidepressant make sure to taper off it the previous drug for at least two weeks and 5-6 weeks if it is fluoxetine.

47
Q

Venlafaxine MOA

A

At low doses acts as a 5HT reuptake inhibitor, at high doses acts as a NE reuptake inhibitor

48
Q

Venlafaxine AE

A

At low doses has the same AE as SSRI, including withdrawal BC of the short half life
Be careful inpatients with uncontrolled HTN

49
Q

Duloxetine MOA

A

Blocks NE AND 5HT reuptake at low doses

50
Q

Duloxetine uses

A

Depression with pain , it is FDA approved for diabetic pain

51
Q

Duloxetine AE

A

Drug interactions

Hepatotoxicity

52
Q

Nefazodone MOA

A

Blocks 5HT and NE reuptake

5HT2A, H1, M antagonist

53
Q

Nefazodone uses

A

Good for depression with anxiety and insomnia and sexual dysfunction

54
Q

Nefazodone AE

A

Sedation, GI complaints, drumouth, constipation

55
Q

Nefazodone- AE

A

Drug interactions

Hepatotoxicity

56
Q

Trazodone- MOA

A

5ht reuptake inhibitor and 5HT2 antagonist

Blocks H1 and alpha 1

57
Q

Trazode AE

A

Orthostatic hypotension
Very sedating
Priapism

58
Q

Trazondone uses

A

Used for sedation to counter insomnia with other antidepressants and hypotonic

59
Q

Bupropion MOA

A

Blocked NE AND DA reuptake

This is the same MOA AS COCAINE

60
Q

Buproprion AE

A

CAN INCREASE SEIZURES AND SEXUAL FUNCTION
Psychomotor activation, headache, insomnia, psychosis,and anorexia
Can cause weight loss

61
Q

Bupropion use

A

Help patients quit skiing and to counter sedation

62
Q

Bupropion CI

A

Seizure history
Anxiety
Bulimia

63
Q

Mirtazapine MOA

A

Antagonizes the presynaptic alpha 2 receptors increasing NE RELEASE
Block 5HT3 and 2,and H1

64
Q

Mirtazapine uses

A

Good for DEPRESSION with comorbid anxiety, reduced sexual function and has a low risk of OD
This is the sleep, sex, and food antidepressant

65
Q

Mirtapazine AE

A

Sedative effect, weight gain, neutropenia, and agranulocytosis

66
Q

What to think about when prescribing antidepressants

A

Comorbid conditions
Which drugs has pt had success with, or their first degree relatives
Adverse events

67
Q

Treating depression phases

A

Acute, continuation, maintenance

68
Q

Acute phase

A

Week 1- Improvement in sleep and appetite
1-3 weeks- everyday life improvements- activity, sex drive, self care, sleeping and appetite normalization
2-6 weeks- suicide and depression subside

69
Q

Continuation phase

A

4-9 months of maintaining the same dose as during the acute phase to keep it in remission

70
Q

Maintenance phase

A

Long term therapy depends on the person and their circumstances

71
Q

Treatment outcomes

A

Response- dec symptoms by 50%, this occurs in 60% of patients
Remission- attitude returns to normal, this occurs in 30% of patients, has a decreased chance of relapse

72
Q

Treatment regimen in depression

A

Start with SSRI they are the safest, least AE, and most studied
If that doesn’t work can change meds, add bupropion or another agent, or augment to with- lithium, anticonvulsant, th, or buspirone.

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