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Therapeutics > Exam 5 lecture 1 > Flashcards

Exam 5 lecture 1 Flashcards

1
Q

What is the name of the first antidepressant

A

Imipramine

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2
Q

What are the types of depression?

A

Reactive (60%)
Major depressive disorder (25%)
Bipolar affective (15%)

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3
Q

What are the clinical features of depression (physiologocal, psychological, cognitive)

A

Physiological- Decreased sleep, appetite changes, fatigue, psychomotor fatigue, menstrual irregularities, palpitations, constipation, headaches.

psychological- dysphoric mood, worthlessness, excessive guilt, loss of interest/pleasure

cognitive- decreased concentration, suicidal ideation.

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4
Q

What are the drugs that cause drug induced depression

A

Antihypertensives
(reserpine, methyldopa, propanolol, prazosin)

Sedatives-hypnotics- (Alcohol, BZDs, BBTs, meprobamate)

Anti-inflammatory and analgesics- (Indomethacin, phenylbutazone, opiates)

Steroids- (corticosteroids, OC, estrogen withdrawal)

Misc- anti-parkinsons, anti-neoplastic, neuroleptics

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5
Q

What is the biogenic amine hypothesis of depression

A

Reserpine causes depression by depleting NE and 5HT from vesicles

Agents that increase 5HT and NE are effective for treating depression

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6
Q

Neuroendocrine hypothesis of depression

A

Changes in hypothalamic pituitary adrenal (HPA) axis and and release of CRF caused by stress cause depression.

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7
Q

Neurotrophic hypothesis for depression

A

BDNF is essential

BDNY is brain derived neurotrophic factor

important in neuroplasticity, resilience, neurogenesis

stress and pain- decrease BDNF

Antidepressants- increase BDNF

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8
Q

Integration of hypotheses of depression

A

HPA and steroid abnormalities regulate BDNF levels.

cortisol during stress decreases BDNF by activating hippocampal glucocorticoid receptors

chronic activation of monoamine receptors increase BDNF signalling (>2 wks)

chronic activation of monoamine leads to reduction of HPA axis

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9
Q

main classes of drugs to treat depression

A

MAOIs
TCAs
SSRIs
SNRIs
5-HT2 antagonists

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10
Q

Response time of antidepressants clinically vs biochemically?

Why does this happen?

A

Antidepressants have a delayed therapeutic response.

Biochemically- immediate effect

clinical course- delayed

We are not sure why this happens.

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11
Q

MOA of MAO I drugs

A

MAO is responsible for metabolizing monoamines.

inhibiting MAO leads to increase in amount of NE and 5HT packaged in vesicles

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12
Q

What do MAO-A and MAO-B do?

A

MAO-A breaks down norepinephrine and serotonin

MAO-B breaks down dopamine

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13
Q

What are some non selective MAO inhibitors

A

phenelzine
tranylcyclopromine

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14
Q

What are some MAO-B selective drugs

A

Selegiline
Safinamide

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15
Q

What are some MAO-A selective drugs

A

Moclobemide

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16
Q

identify structural d/c of MAOI, TCA and SSRIs

A
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17
Q

side effects of MAOI drugs

A

severe side effects- headahe, drosiness, dru mouth, weight gain, orthostatic hypotension, sexual dysfunction

Hypertensive crisis (avoid foods and drugs with tyramine)

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18
Q

What are some interactions MAO I drugs have? What to avoid?

A

Interactions with OTC- cole preparations, diet pills.

Interactions with Rx- TCAs, SSRIs, L-DOPA

avoid with TYRAMINE

Interactions with St Johns Wort

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19
Q

What are the targets of reuptake inhibitors?

A

There are two reuptake pumps in the body. VMAT- on vesicles inside synapse
MAO-B transporters (DAT, NAT, SERT)

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20
Q

Where do antidepressants bind reuptake inhibitors?

A

Allosteric site.
This blocks the transport of norepinephrine or serotonin into synapse (More NE or 5HT in extracellular space)

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21
Q

Indication for TCA

A

Depression, panic disorder, chronic pain and enuresis

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22
Q

overdose/toxicity of TCA

A

OD/toxicity- extremely dangerous, depressed patients are more likely to be suicidal.

Patients are more likely to commit self harm or suicide 2 weeks into treatment.

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23
Q

What are the types of TCAs

A

Tertiary amines
secondary amines

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24
Q

What is the difference between tertiary amines and secondary amines

A

Tertiary amines- inhibit both NE and 5HT reuptake and SERT. They also act as receptor antagonists.

Most secondary amines inhibit NET better than SERT.

secondary amines have less sedation, less anticholinergic action, less autonomic, less weight gain, less cardiovascular action.

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25
side effects of tertiary amines
These agents cause the most sedation, autonomic side effects and weight gain.
26
What are some tertiary amine drugs
Imipramine- Metabolized to desipramine. Enuresis and ADHD Amitriptyline- metabolized to norttriptamine Trimipramine Clomipramine Doxepin
27
Secondary amine drugs
Desipramine Nortriptyline Protriptyline Mapotiline
28
ALL TCAs have which side effects
Anticholinergic, CV (elderly), neurological, weight gain Patients may be suicidal
29
mechanisms of SSRIs
SSRIs block serotonin pumps and increase amount of 5 HT in synapse, which activate the 14 serotonin receptors
30
SSRI drugs
Fluoxetine Fluvoxamine Paroxetine Sertraline Citalopram Escitalopram
31
Uses of SSRIs? Side effects?
Uses- depression, alcoholism, OCD, Enuresis, PTSD, Eating disorder, social phobias, panic anxiety, GAD Side effects- N/V, headaches, sexual dysfunction, anxiety, insomnia
32
symptoms of SSRI dyscontinuation syndorme
brain zaps, dizziness, sweating, N/V, confusion, vertigo
33
What is serotonin syndrome? Symptoms? Treatment?
Happens when SSRIs given with MAOIs, TCAs, metoclopramide, tramadol, triptans, St johns work symptoms include- hyperthermia, muscle ridgiddity, restlessness, sweating, shivering, seizures treatment- dx of medication and management of symptoms. administration of serotonin antagonists, BZDs to control seizures
34
name a partial serotonin 1A agonist used in anxiety
Busperinone
35
What are some SSRI + 5HT1A partial agonists
Vilazodone- reduced sexual side effects vs SSRI Vortioxetine-
36
Name tetracyclic and unicyclic drugs and what receptor they inhibit
Maprotiline- NET inhibitor Amoxapine- NET inhibitor, D2 antagonist Mirtazapine- a2 antagonist, 5HT2 and 5HT3 antagonist H1 antagonist Bupropion- DAT inhibitor NET & SERT inhibitor also treats GAD
37
Name 5HT2 antagonists/SERT inhibitors
Trazodone- Weak SERT inhibitor, 5HT 2a antagonist Nefazodone- Weak SERT, 5HT2 antagonist
38
Name SNRI drugs
Duloxetine Milnacipran Levomilnacipran
39
What receptors do the 4 SNRI drugs act on? What do they treat?
Duloxetine- NET and SERT inhibitor Treats GAD and peripheral neuropathy Milnacipran- NET and SERT inhibitor approved for fibromyalgia Levomilnacipran- Active enantiomer of milnacipran NET and SERT inhibitor
40
What are the NSRI drugs? What are they used for?
Reboxetine- FDA declined in US Atomoxetine- uses for ADHD
41
What are the selectivity profiles of amitriptyline vs nortriptyline? Clomipramine? Maprotiline, SSRIs? NSRIs?
amitriptyline- 1:7 ratio (binds to serotonin better) Nortriptyline- 8:1 more NET selective clomipramine- 1:136 (serotonin selective) Maprotiline- 523:1 NET selective
42
What are some NMDA antagonists
Ketamine- subanesthetic doses Scopolamin (muscarinic and NMDA antagonist)
43
MOA of ketamine
blocks NMDA and keeps it in a partially inactive state
44
What percent of pregnant mothers have post partum depression (PPD)> How to treat
PPD occurs in 10-15% (within 4 weeks and can last >1 yr) SSRIs- fluoxetine and paroxetine and venlafaxine BREXANOLONE- MOA involves GABA receptors
45
MOA of brexanolone
Allopregnanolone levels increase during pregnancy. GABA receptors get desensitized Allopregnanolone levels return to normal post partum Brexanolone resensitizes GABA A receptor
46
What are some new agents in development to treat depression
psychadelics (MDMA, psilocybin, LSD) 5HT2C antagonists metabotropic glutamate receptor agonists reversible inhibitors of monoamine oxidase A
47
Non-pcol
Electroconvulsive therapy psychotherapy hospitalization
48
What does filbanserin treat? MOA?
hypoactive sexual desire disorder Agonist as 5HT1A, antagonist at 5HT2A/C
49
Bipolar disorder onset, etiology and how widespread is it?
Approximate 1.5-3% onset<30 Biological, environmrntal and genetic
50
Types of bipolar disorder? symptoms?
Bipolar I Bipolar II Cyclothymia disorder Unspecified bipolar and related disorder Substance-induced mood disorder Symptoms- mania, hypomania, depression, mixed mania, depression
51
Features of mania
Euphoria, irritability/anger, impulsive high risk behavior, aggressive, grandiose ideas, decreased sleep and appetite, difficult concentrating, delusions, hallucinations Hypomania is just less severe mania Depression
52
Treatment of bipolar
Hospitalization Psychotherapy Pharmacotherapy
53
What is the pharmacotherapy used in bipolar treatment
Li, Anticonvulsants, atypical antipsychotics CCB (verapamil, nimodipine) combo tx + BZDs
54
MOA of lithium in bipolar tx
Li leads to depletion of PIP2 enzyme for PLC GQ activates PLC, PLC cleaves PIP2 into IP3 and DAG, IP3 gets recycyled back as PIP2 lithium blocks recycling of IP3 to PIP2.
55
Therapeutic index and onset for effectiveness of lithium therapy
small therapeutic index Lag time for effectiveness
56
Which anticonvulsants are used as mood stabilizers
Valproic acid and sodium valproate Carbamezapine Lamotrigine Topiramate
57
MOA of valproic acid as mood stabilizer
Multiple MOA- increases GABAergic tone, blocks Na channles Blocks Ca channels, inhibits histone deacetylase
58
What receptors does carbamazepine act on? Lamotrigine? Topiramate?
carbamazepine-Na channels Lamotrigine- Na and Ca Topiramate- Na
59
Atypical antipsychotics for mood stabilizing
olanzapine Olanzapine + Fluoxetine Quetiapine Risperidone Ziprasidone Lurasidone Aripiprazole
60

Therapeutics (38 decks)

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