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Antidepressants Flashcards

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1
Q

Why do antidepressants take weeks to show clinical effects?

A

Adaptive changes underlie the response: B-receptors, cAMP and serotonergic neurotransmission, neurogenesis

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2
Q

Antidepressants are not used in pts aged

A

Very high suicide risk

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3
Q

St. John’s Wort. Any good for major depression?

A

No

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4
Q

What is the enzyme that inhibits trafficking of antidepressants across the BBB?

A

MDR1

also P-gp

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5
Q

Which antidepressants are KNOWN substrates of MDR1?

A

citalopram, venlafaxine, paroxetine, amitriptyline

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6
Q

Which antidepressants are NOT substrates of MDR1?

A

mirtazapine and fluoxetine

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7
Q

What determines if a pt will have an increased risk of MDR1 preventing drug passage into the brain?

A

If they have a single polymorphism of T–>C within the MDR1 enzyme gene.

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8
Q

What are the gold standard of tx for depression?

A

SSRIs

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9
Q

What are the indications for TCAs?

A

Major depression. Pain, anxiety disorders (OCD, phobias, panic), ADHD, nocturnal enuresis, depression associated with schizophrenia.

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10
Q

What is the MOA of TCAs?

A

Inhibit reuptake of 5-HT and NE into pre-synaptic terminals.

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11
Q

What other receptors do TCAs effect that can lead to adverse effects?

A

mACh, a-ARs, and Histamine receptors

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12
Q

What are some general behaviors/clinical effects seen by TCA use in the first 2-8wks of use?

A

drowsiness, dysphoria, anxiety, impaired cognition

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13
Q

What are some general behaviors/clinical effects seen by TCA use chronically (>8wks of use)?

A

improved clinical symptoms but NOT euphoria

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14
Q

Describe an adverse effect of TCAs and what causes it.

A

Orthostatic hypotension from blockade of alpha1-ARs

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15
Q

Describe the metabolic/endocrine adverse effects of TCAs.

A

Weight gain, sexual disturbances

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16
Q

What are the overdose effects of TCAs? High or low therapeutic index?

A

CV effects including: arrythmias, direct myocardial depression, worsening of CHF. Acidosis, delirium, seizures.

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17
Q

Describe the pharmacokinetics of TCAs.

A

Incompletely absorbed due to 1st pass metabolism.
High lipid solubility, so good dist. to brain/fat.
Highly bound to plasma proteins, limits excretion, long 1/2 life.

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18
Q

Talk to me about TCA metabolism. Active metabolites?

A

Tertiary amines metabolized to ACTIVE secondary amines by demethylation. Tricyclic ring subject to oxidation and (CYP2D6) and conjugation.

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19
Q

TCAs can block the effects of this a2-adrenergic agonist.

A

Clonidine

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20
Q

What drugs potentiate the effects of TCAs?

A

EtOH and other sedatives

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21
Q

Antiparkinsonian drugs, antipsychotics, and biogenic amines compete with TCAs in what way? What physiological effect does this have?

A

Plasma protein binding –> higher free levels of TCAs–> greater effect.

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22
Q

What is 1st line tx for major depression?

A

SSRIs

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23
Q

What else are SSRIs used for?

A

Panic, OCD, social anxiety disorder, ADHD, and some eating disorders.

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24
Q

Do SSRIs have effects on other receptors?

A

Not like TCAs. No effects on mACh, histamine, a1 receptors like TCAs.

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25
Q

Describe the general behavior/clinical effects of SSRIs in the first 2-6 weeks after starting tx.

A

CNS stimulation (bc more 5-HT available), anxiety, agitation

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26
Q

Describe the general behavior/clinical effects of SSRIs post 6 wks of use.

A

Improvement of most or all clinical symptoms, CNS activation remains.

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27
Q

Describe the ADEs of SSRIs.

A

Nausea, decr. libido, sexual dysfxn. Generally, fewer ADEs compared to other ADs, hence why they are 1st line.
Lower incidence of CV and ACh effects. HIGHER therapeutic index, LOWER INCIDENCE of OD.

28
Q

Use Paroxetine (SSRI) in pregnant women?

A

FUCK NO

29
Q

Which has better bioavailability, TCAs or SSRIs?

A

SSRIs

30
Q

What is Norfluoxetine and why is it relevant?

A

Norfluoxetine is an active metabolite of Fluoxetine (SSRI) that increases the 1/2 life of Fluoxetine to over a week. Hence, weekly dosing of Fluoxetine.

31
Q

Describe the metabolism of SSRIs.

A

CYP2D6, CYP2C19, and 3A4. Inhibition of CYP2D6 and 2C19

32
Q

Give SSRIs to pts on MAOIs?

A

FUCK NO. Must wait 2 weeks.

33
Q

What causes serotonin syndrome?

A

Overstimulation of 5-HT1A receptors in central grey (midbrain) and medulla.

34
Q

What are the symptoms of serotonin syndrome?

A

Hyperpyrexia, hyperreflexa, tremor, shivering, myoclonus, agitation, seizures, confusion, delirium, CV collapse, coma.

35
Q

Can serotonin syndrome be fatal?

How do you treat it?

A

Yes, can be fatal.

Discontinue treatment immediately. Good progn. if discontinued before 24 hrs.

36
Q

What is venlafaxine and why is it wonderful.

What ADEs does it cause?

A

It is an atypical AD. It works similarly to TCAs but does not have the ADEs caused by blockage of histamine, ACh, and a1 receptors.

ADEs: short, sustained HTN, sweating, N/D, anxiety

37
Q

What is the most potent SNRI?

Fun facts?

A

Duloxetine.
Highly protein bound.
Metabolized by CYP2D6 and 1A2
1/2 life 12 hrs

38
Q

What is amoxamine? Fun facts?

How does it work?

A

Atypical antidepressant.
Retains DA receptor antagonism—> extrapyramidal effects
Mixed inhibition of NET>SERT~DAT

39
Q 
How does bupropion work? 
What class of ADs is it in?
ADEs?
A

It is a weak DAT, NET, SERT inhibitor.
Atypical AD.
Active metabolite is an NET blocker as well.
ADEs: agitation, anxiety, restlessness. R/O SEIZURE!

40
Q

Maprotiline. How does it work? What kind of AD is it? ADEs?

A

NRI
Atypical
R/O SEIZURES

41
Q

Mirtazepine. What’s going on.

ADEs?

A

Atypical
Enhances the release of serotonin and NE by antagonizing presynaptic a-2ARs. Antagonizes 5-HT receptors.
ADEs: Potent antihistaminergic —> sedation!
WEIGHT GAIN

42
Q

Name the two SARIs (serotonin antagonists and reuptake inhibitors.

A

Atypicals

Trazodone and Nefazodone

43
Q

What is trazodone used for, primarily?

A

Atypical

Depression characterized by anxiety and sleep disturbances.

44
Q

Why have we discontinued nefazodone?

A

Atypical

Hepatotoxicity.

45
Q

What is vilazodone? How does it work?

A

Atypical

Potent 5-HTa1 partial agonist and SSRI

46
Q

What is Vortioxetine?

A

Atypical

Potent blocker of SERT and high efficacy partial agonist at 5-HT1a/1b receptors. Weak block of NET and B1-AR.

47
Q

List the MAOIs.

A

Tranylcypromine
Isocarboxazid
Phenelzine

48
Q

Why use MOAIs?

A

Last option, pt does not respond to other drugs or ECT.

49
Q

What is the MOAI MOA?

A

Blocks oxidative metabolism of monoamines by IRREVERSIBLE inhibition of MAO-A/B in nerve terminals (presynaptic).

50
Q

What MAO primarily metabolizes NE, 5-HT, and tyramine?

A

MAO-A

51
Q

What MAO primarily metabolizes Dopamine?

A

MAO-B

52
Q

Describe the acute (2-6 wks) effects of MAOIs.

Chronic?

A

Acute: CNS stimulation, agitation. Possibly euphoria

Chronic: Improvement of most or all symptoms, CNS activation remains. (common to all ADs we have seen so far)

53
Q

ADEs of MAOIs?

A

insomnia, orthostatic hypotension, weight gain, sexual dysfxn

54
Q

How do we dose MAOIs?

A

Daily, despite irreversible action. Drug effects persist 1-3 weeks.

55
Q

Avoid these foods when on MAOIs:

A

Tyramine rich foods like cheese

56
Q

Your pt takes MAOIs with sympathomimetics. What might happen?

A

Acute hypertensive reaction

57
Q

Meperidine or Dextromethorphan + MAOIs. What happens?

A

Hyperpyrexia, delirium, convulsions, coma, death.

58
Q

What are the mood stabilizers?

A

Lithium, VPA, carbamazepine

59
Q

Mood stabilizers are needed for?

A

Manic depression (bipolar affective disorder)

60
Q

Acute mania tx w/?

A

antipsychotics and/or benzos

61
Q

1st line tx for bipolar disorder?

How does it work?

A

Lithium- inhibition of inositol phosphate signaling and inhibits NT stimulated adenylyl cyclase activity.

62
Q

Tell me about lithium distribution. Metabolism?

A

Dist. to total body water. Same concentration in bone.

No metabolism, cleared in urine ~20hr 1/2 life

63
Q

Adverse effects of Lithium?

A

VERY NARROW therapeutic window!
Neuro/psych: tremor, axatia, hyperactivity, aphasia, sedation, fatigue.
Glandular: edema, mild hypothyroidism
Renal: polydipsia, polyuria (nephrogenic diabetes inspidus)
Cardiac: bradycardia-tachycardia
other: acne, folliculitis, and exacerbates psoriasis

64
Q

This AD inhibits its own metabolism and the metabolism of other drugs:

A

VPA

65
Q

ADEs of VPA:

A

Nausea, abdominal pain, heartburn. Hepatotoxicity. Monitor liver fxn.

66
Q

This AD INDUCES its own metabolism and has 100% abs. from intestines

A

Carbamazepine- strong inducer of CYP2C/3A

67
Q

ADEs of carbamazepine:

A

diplopia, ataxia. GI upset, Aplastic anemia, Agranulocytosis.

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