Antidepressants Flashcards

1
Q

What form of drugs best crosses the BBB?

A
  • lipophilic/hydrophobic
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2
Q

Name 4 classes of Monoamine Reuptake Inhibitors?

A
  • tricyclics
  • SSRIs
  • NA reuptake inhibitors
  • other non-selective reuptake inhibitors
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3
Q

What do Monoamine Transmitters contain structurally?

A

-a single AMINE (NH2) group

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4
Q

What is the relation between Monoamine NT and Depression?

A
  • one of the many reasons depression occurs is d/t the DEFICIT of M-NT; esp. 5-HT and NA
  • why CSF of depressed patients contain REDUCED Monoamine levels
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5
Q

What are Raphe Nuclei?

A
  • nuclei found running down from the brain stem to the spinal cord
  • 2 groups- caudal and rostral
  • said location for SEROTONIN prodn
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6
Q

What is the Caudal- Raphe nuclei responsible for?

A
  • Analgesia
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7
Q

What is the Rostral Raphe nuclei said to regulate?

A
  • sleep
  • mood
  • feeding
  • sensory perception
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8
Q

What enzyme converts 5-OH-Tryptophan to 5-HT?

A

L-AA Decarboxylase

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9
Q

What metabolized 5-HT?

A

-Monoamine Oxidase

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10
Q

Where is the Main site of noradrenaline neurones in the brain?

A
  • Locus Caeruleus
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11
Q

What is the major REGULATORY role of Locus CAERULEUS?

A
  • regulation of arousal, attention and stress response
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12
Q

Name 2 monoamine oxidase inhibitors.

A
  • Phenelzine

- Moclobemide

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13
Q

How do MOA-Is help increase NT levels?

A
  • less NT is metabolized in the post-synaptic neurone
  • less NT will be re-uptaken
  • More NT remains in the synaptic cleft==>more activity
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14
Q

What is the risk of using Irreversible MAO-Is? (1)

A
  • “CHEESE REACTION” may occur (a hypertensive crisis)
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15
Q

How does the cheese reaction come about?

A
  • irreversible MAO-Is permanently deactivates MAO; it would then take a couple of weeks for the enzyme levels to be restored
  • therefore essential to control tyramine intake
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16
Q

How does Tyramine levels cause malignant hypertension?

A
  • tyramine is a potent releaser of NE.

- with the use of MAO-Is and intake of tyramine; NE levels will surge ==> ^BP

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17
Q

What other S/Es do MOA-Is bring about?

A
  • insomnia
  • postural HYPOTENSION
  • peripheral edema
  • potentiates other drugs (benzos) by decreasing their metabolism
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18
Q

Where is tyramine found?

A
  • in cheese
  • yeast containing products (beer, wine, sauces)
  • old food
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19
Q

Which irreversible Monoamine Oxidase Inhibitor must one carefully monitor their diet for?

A
  • Phenelzine
20
Q

Name 3 tricyclic Antidepressants.

A
  • imi- and Lofe-pramine
  • amitriptyline
  • dosulepin
21
Q

How do Tricyclic antidepressants act?

A
  • blocks the reuptake of MONOAMINES (NE and 5-HT) into the presynaptic terminals
22
Q

What are the COMMON s/es of TCAs?

A
- Anticholinergic S/Es: 
blurry vision, dry mouth, constipation, urinary retention
-SEDATION, WGT GAIN
- tachycardia, Arrhythmia
- HYpotension
23
Q

Why should TCAs not be considered for cardiac patients?

A
  • cardiotoxic
  • postural hypotension
  • tachycardia
  • arrhythmias
24
Q

Name a SSRI and its mode of axn.

A
  • FLUOXETINE

- block the serotonin reuptake transporter

25
Q

Name 3 other SSRIs.

A
  • citalopram
  • sertraline
  • Paroxetine
26
Q

What are the s/es of SSRIs?

A
  • Nausea
  • Headache
  • Sweating
  • Anxiety worsened
  • WGT gain, sedation
  • sexual DYSFXN
  • hyponatremia (in the old)
27
Q

Which age group of individuals should you be wary about with SSRIs?

A
  • pts < 25Y.O

- risk of SELF-HARM and suicidal ideation

28
Q

Why are there a no. of GI s/es with use of SSRIs?

A
  • d/t stimulation of serotonin receptors in the GIT
29
Q

Name 2 DUAL reuptake inhibitors.

A
  • Venlafaxine
  • Duloxetine
  • both blocks NE and 5-HT
30
Q

Why are dual reuptake inhibitors preferred?

A
  • d/t their LACK of major receptor blocking axns
31
Q

Name an atypical antidepressant and what receptors it blocks.

A

Mirtazapine

blocks alpha2, 5-HT2 and 5-HT3

32
Q

What are the s/es of Mirtazapine?

A

incr. appetite>WGT gain and confusion

33
Q

which other anti-depressants may be given adjunct to SSRIs to reduce its s/es?

A

mirtazapine - because it blocks post-synaptic serotonin receptors; highly serotonergic

34
Q

Name a dopamine uptake inhibitor.

A

Bupropion

35
Q

How efficient are anti-depressants, in general?

A
  • all of them: 40-70% efficacy
  • most: delayed ONSET of action
  • BEST used for only SEVERE depression
36
Q

What is the MOA of Lithium?

A
  • said to block the second messnger sys. / inhibit GLYCOGEN SYNTHASE KINASE 3BETA
37
Q

What is a sign that blood level of Lithium is very high?

A
  • ATAXIA
  • vomitting
  • diarrhea
  • convulsions
  • coma
38
Q

Other s/es of Lithium?

A
  • dry mouth
  • polydipsia/polyuria
  • hypothyroidism
  • tremor
  • long term reduced renal function
  • wgt gain
  • NEPHROGENIC diabetes insipidus
39
Q

What is given as long term treatment as Mood Stabilizers?

A
  • Valproic Acid, Lamotigrine, Carbamazepine (ANTICONVULSANTS)
40
Q

What MAJOR risk does Valproic Acid hold?

A

teratogenecity

—others: ataxia, drowsiness, liver enzyme induction (shared with CARBAMAZEPINE)

41
Q

What risk does lamotigrine hold?

A

small risk of STEVEN-JOHNSON $

42
Q

What is lithium used for?

A
  • as a mood stabilizer in Bipolar d/o
43
Q

What anti-psychotics can be given as a mood stabilizer?

A
  • olanzapine
  • quetiapine
  • lurasidone
  • Aripiprazole
44
Q

What is the MOA of anti-psychotic?

A

-dopamine antagonist and serotonin antagonist

45
Q

What are the S/Es of antipsychotics?

A

sedation, wgt gain, METABOLIC SYNDROME

- extrapyramidal effects (aripiprazole)

46
Q

What to give an obese pt who has come in with depression?

A
  • avoid: Mirtazapine, TCA, Lithium, Atypical Anti-psychotic

GIVE VENLAFAXINE, BUPROPION