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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
Describe the general behavior/clinical effects of SSRIs in the first 2-6 weeks after starting tx.
CNS stimulation (bc more 5-HT available), anxiety, agitation
26
Describe the general behavior/clinical effects of SSRIs post 6 wks of use.
Improvement of most or all clinical symptoms, CNS activation remains.
27
Describe the ADEs of SSRIs.
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
Use Paroxetine (SSRI) in pregnant women?
FUCK NO
29
Which has better bioavailability, TCAs or SSRIs?
SSRIs
30
What is Norfluoxetine and why is it relevant?
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
Describe the metabolism of SSRIs.
CYP2D6, CYP2C19, and 3A4. Inhibition of CYP2D6 and 2C19
32
Give SSRIs to pts on MAOIs?
FUCK NO. Must wait 2 weeks.
33
What causes serotonin syndrome?
Overstimulation of 5-HT1A receptors in central grey (midbrain) and medulla.
34
What are the symptoms of serotonin syndrome?
Hyperpyrexia, hyperreflexa, tremor, shivering, myoclonus, agitation, seizures, confusion, delirium, CV collapse, coma.
35
Can serotonin syndrome be fatal? | How do you treat it?
Yes, can be fatal. | Discontinue treatment immediately. Good progn. if discontinued before 24 hrs.
36
What is venlafaxine and why is it wonderful. | What ADEs does it cause?
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
What is the most potent SNRI? | Fun facts?
Duloxetine. Highly protein bound. Metabolized by CYP2D6 and 1A2 1/2 life 12 hrs
38
What is amoxamine? Fun facts? | How does it work?
Atypical antidepressant. Retains DA receptor antagonism---> extrapyramidal effects Mixed inhibition of NET>SERT~DAT
39
``` How does bupropion work? What class of ADs is it in? ADEs? ```
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
Maprotiline. How does it work? What kind of AD is it? ADEs?
NRI Atypical R/O SEIZURES
41
Mirtazepine. What's going on. | ADEs?
Atypical Enhances the release of serotonin and NE by antagonizing presynaptic a-2ARs. Antagonizes 5-HT receptors. ADEs: Potent antihistaminergic ---> sedation! WEIGHT GAIN
42
Name the two SARIs (serotonin antagonists and reuptake inhibitors.
Atypicals | Trazodone and Nefazodone
43
What is trazodone used for, primarily?
Atypical | Depression characterized by anxiety and sleep disturbances.
44
Why have we discontinued nefazodone?
Atypical | Hepatotoxicity.
45
What is vilazodone? How does it work?
Atypical | Potent 5-HTa1 partial agonist and SSRI
46
What is Vortioxetine?
Atypical | Potent blocker of SERT and high efficacy partial agonist at 5-HT1a/1b receptors. Weak block of NET and B1-AR.
47
List the MAOIs.
Tranylcypromine Isocarboxazid Phenelzine
48
Why use MOAIs?
Last option, pt does not respond to other drugs or ECT.
49
What is the MOAI MOA?
Blocks oxidative metabolism of monoamines by IRREVERSIBLE inhibition of MAO-A/B in nerve terminals (presynaptic).
50
What MAO primarily metabolizes NE, 5-HT, and tyramine?
MAO-A
51
What MAO primarily metabolizes Dopamine?
MAO-B
52
Describe the acute (2-6 wks) effects of MAOIs. | Chronic?
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
ADEs of MAOIs?
insomnia, orthostatic hypotension, weight gain, sexual dysfxn
54
How do we dose MAOIs?
Daily, despite irreversible action. Drug effects persist 1-3 weeks.
55
Avoid these foods when on MAOIs:
Tyramine rich foods like cheese
56
Your pt takes MAOIs with sympathomimetics. What might happen?
Acute hypertensive reaction
57
Meperidine or Dextromethorphan + MAOIs. What happens?
Hyperpyrexia, delirium, convulsions, coma, death.
58
What are the mood stabilizers?
Lithium, VPA, carbamazepine
59
Mood stabilizers are needed for?
Manic depression (bipolar affective disorder)
60
Acute mania tx w/?
antipsychotics and/or benzos
61
1st line tx for bipolar disorder? | How does it work?
Lithium- inhibition of inositol phosphate signaling and inhibits NT stimulated adenylyl cyclase activity.
62
Tell me about lithium distribution. Metabolism?
Dist. to total body water. Same concentration in bone. | No metabolism, cleared in urine ~20hr 1/2 life
63
Adverse effects of Lithium?
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
This AD inhibits its own metabolism and the metabolism of other drugs:
VPA
65
ADEs of VPA:
Nausea, abdominal pain, heartburn. Hepatotoxicity. Monitor liver fxn.
66
This AD INDUCES its own metabolism and has 100% abs. from intestines
Carbamazepine- strong inducer of CYP2C/3A
67
ADEs of carbamazepine:
diplopia, ataxia. GI upset, Aplastic anemia, Agranulocytosis.

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