Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Therapeutics > Exam 5 lecture 1 > Flashcards

Exam 5 lecture 1 Flashcards

1
Q

What is the name of the first antidepressant

A

Imipramine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the types of depression?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Neuroendocrine hypothesis of depression

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

main classes of drugs to treat depression

A

MAOIs
TCAs
SSRIs
SNRIs
5-HT2 antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What do MAO-A and MAO-B do?

A

MAO-A breaks down norepinephrine and serotonin

MAO-B breaks down dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some non selective MAO inhibitors

A

phenelzine
tranylcyclopromine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some MAO-B selective drugs

A

Selegiline
Safinamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are some MAO-A selective drugs

A

Moclobemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

identify structural d/c of MAOI, TCA and SSRIs

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Indication for TCA

A

Depression, panic disorder, chronic pain and enuresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the types of TCAs

A

Tertiary amines
secondary amines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

side effects of tertiary amines

A

These agents cause the most sedation, autonomic side effects and weight gain.

26
Q

What are some tertiary amine drugs

A

Imipramine- Metabolized to desipramine. Enuresis and ADHD

Amitriptyline- metabolized to norttriptamine

Trimipramine

Clomipramine

Doxepin

27
Q

Secondary amine drugs

A

Desipramine
Nortriptyline
Protriptyline
Mapotiline

28
Q

ALL TCAs have which side effects

A

Anticholinergic, CV (elderly), neurological, weight gain

Patients may be suicidal

29
Q

mechanisms of SSRIs

A

SSRIs block serotonin pumps and increase amount of 5 HT in synapse, which activate the 14 serotonin receptors

30
Q

SSRI drugs

A

Fluoxetine
Fluvoxamine
Paroxetine
Sertraline
Citalopram
Escitalopram

31
Q

Uses of SSRIs? Side effects?

A

Uses- depression, alcoholism, OCD, Enuresis, PTSD, Eating disorder, social phobias, panic anxiety, GAD

Side effects- N/V, headaches, sexual dysfunction, anxiety, insomnia

32
Q

symptoms of SSRI dyscontinuation syndorme

A

brain zaps, dizziness, sweating, N/V, confusion, vertigo

33
Q

What is serotonin syndrome? Symptoms? Treatment?

A

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
Q

name a partial serotonin 1A agonist used in anxiety

A

Busperinone

35
Q

What are some SSRI + 5HT1A partial agonists

A

Vilazodone- reduced sexual side effects vs SSRI

Vortioxetine-

36
Q

Name tetracyclic and unicyclic drugs and what receptor they inhibit

A

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
Q

Name 5HT2 antagonists/SERT inhibitors

A

Trazodone- Weak SERT inhibitor, 5HT 2a antagonist

Nefazodone- Weak SERT, 5HT2 antagonist

38
Q

Name SNRI drugs

A

Duloxetine
Milnacipran
Levomilnacipran

39
Q

What receptors do the 4 SNRI drugs act on? What do they treat?

A

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
Q

What are the NSRI drugs? What are they used for?

A

Reboxetine- FDA declined in US

Atomoxetine- uses for ADHD

41
Q

What are the selectivity profiles of amitriptyline vs nortriptyline? Clomipramine? Maprotiline, SSRIs? NSRIs?

A

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
Q

What are some NMDA antagonists

A

Ketamine- subanesthetic doses
Scopolamin (muscarinic and NMDA antagonist)

43
Q

MOA of ketamine

A

blocks NMDA and keeps it in a partially inactive state

44
Q

What percent of pregnant mothers have post partum depression (PPD)> How to treat

A

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
Q

MOA of brexanolone

A

Allopregnanolone levels increase during pregnancy.

GABA receptors get desensitized

Allopregnanolone levels return to normal post partum

Brexanolone resensitizes GABA A receptor

46
Q

What are some new agents in development to treat depression

A

psychadelics (MDMA, psilocybin, LSD)

5HT2C antagonists
metabotropic glutamate receptor agonists
reversible inhibitors of monoamine oxidase A

47
Q

Non-pcol

A

Electroconvulsive therapy
psychotherapy
hospitalization

48
Q

What does filbanserin treat? MOA?

A

hypoactive sexual desire disorder

Agonist as 5HT1A, antagonist at 5HT2A/C

49
Q

Bipolar disorder onset, etiology and how widespread is it?

A

Approximate 1.5-3%
onset<30
Biological, environmrntal and genetic

50
Q

Types of bipolar disorder? symptoms?

A

Bipolar I
Bipolar II
Cyclothymia disorder
Unspecified bipolar and related disorder
Substance-induced mood disorder

Symptoms- mania, hypomania, depression, mixed mania, depression

51
Q

Features of mania

A

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
Q

Treatment of bipolar

A

Hospitalization
Psychotherapy
Pharmacotherapy

53
Q

What is the pharmacotherapy used in bipolar treatment

A

Li, Anticonvulsants, atypical antipsychotics

CCB (verapamil, nimodipine)

combo tx + BZDs

54
Q

MOA of lithium in bipolar tx

A

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
Q

Therapeutic index and onset for effectiveness of lithium therapy

A

small therapeutic index
Lag time for effectiveness

56
Q

Which anticonvulsants are used as mood stabilizers

A

Valproic acid and sodium valproate

Carbamezapine

Lamotrigine

Topiramate

57
Q

MOA of valproic acid as mood stabilizer

A

Multiple MOA- increases GABAergic tone, blocks Na channles
Blocks Ca channels, inhibits histone deacetylase

58
Q

What receptors does carbamazepine act on? Lamotrigine? Topiramate?

A

carbamazepine-Na channels

Lamotrigine- Na and Ca

Topiramate- Na

59
Q

Atypical antipsychotics for mood stabilizing

A

olanzapine
Olanzapine + Fluoxetine
Quetiapine
Risperidone
Ziprasidone
Lurasidone
Aripiprazole

60
Q
A

Therapeutics (38 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions