Brainscape's Knowledge GenomeTM

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


See full index

week 7 neuro > Mood disorder drugs > Flashcards

Mood disorder drugs Flashcards

1
Q

What are the mechanism of moo disorders?

A
  1. Amine hypothesis

2. Neurotropic hypothesis

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

What is the amine hypothesis?

A

Lack of necessary NT’s for normal mood

  • NE, 5ht, and DA
  • mania if there excess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why is the amine hypothesis incomplete?

A

Mismatch between time course
Postmortum studies show no decrease in amines
Most antidepressants down regulate amine Receptors

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

What is the neurotropic hypothesis?

A

Depression is associated with loss of neurotrophic support

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

What are the factors involved with neurotrophic support?

A

Nerve growth factors like

  • Brain-derived neurotrophic factos
  • which are important for neural plasticity, resilience and neurogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Is the neurotrophic theory accurate if so why?

A

Yes

  • antidepressants increase BDNF
  • effective treatment increase neurogenesis and synaptic connectivity
  • mutations in BDNF lead to increased anxiety and depressive behavior
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the 2 drugs classes to treat mood disorders?

A

Antidepressants and mood stabilizers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the drugs involved with antidepressants?

A
  1. Tricyclic antidepressants
  2. Monoamine oxidase inhibitors
  3. Selective serotonin reuptake inhibitors
  4. dual- mechanisms drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the drugs involved with mood stabilizers?

A
  1. Lithium carbonate
  2. Anticonvulsants
  3. Atypical antipsychotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the mechanism of action of TCA’s?

A

Block reuptake of of NE and or 5HT

  • Desipramine= NE selctive
  • Imipramine = NE and 5HT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the effects of TCA’s?

A

Elevation in mood (2-3 delay)
Sleepiness and light headedness
Antimuscarinic effects
- dry mouth, blurred vision, constipation and urinary retention

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

What are the adverse effects of TCA’s?

A

Orthostatic HoTN
Weight gain
Tachy and arrhythmias
Antimuscarinic effects- more severe in old people

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

What does blocking of histamine receptors cause?

A

weight gains

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

What does blocking of alpha-1 receptor cause?

A

lightheadedness and decreased BP

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

What does blocking NA+ channels cause?

A

Arrhythmias, cardiac arrest and seizures

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

When would you use TCA’s?

A

After first line drugs like SSRI’s and SNRI’s arent working

- of note they are lethal with overdose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some of the pharmakokinetics of TCA’s?

A

long half life
5-10 TI which is low
metabolized by CRP2D6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What should you give if you suspect TCA toxicity?

A

FLuoxetine (Prozac)

- which inhibits CYR2D6 (potent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the mechanism of action of MOA?

A 
Irreversibly blocks MAO-a (NE and 5HT)
Blocks MAO-b (DA) 
- leads to increased mood (2-3) later
- NT change occurs without 24-48hrs 
- low TI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why should you wait 14 days after discontinuation of MAO to start SSRI’s?

A

To prevent serotonin syndrome

21
Q

What is serotonin syndrome?

A

Too much serotonin which leads too:

  • hyperthemia
  • muscle rigidity
  • tremors
  • autonomic instability
  • confusion
  • irritability and agitation
22
Q

What doe MAOI’s potentiate?

A

sympathomimetic amines

  • most specifically Tyramine which is metabolized by MAO’s
  • systemic Tryamine leads to release of NE and EPi (adrenergic)
  • leads to dangerous levels of HTN
23
Q

Name some foods rich in Tyramine?

A

Beer, wine, aged cheese, broad beans, yogurt, avocados, shream, bananas
- cold meds like ephedrine and pseudoephedine

24
Q

What are some SSRI’s?

A 
Fluoxetine 
Sertraline
Paroxetine
Fluvoxamine
Citalopram
Escitalopram
25
Q

What is fluoxetine?

A

Prozac

26
Q

What is Sertraline?

A

Zoloft

27
Q

What is Paraxetine?

A

Paxil

28
Q

What is Fluvoxamine?

A

Luvox

29
Q

What is citalopram?

A

Celexa

30
Q

What is escitalopram?

A

Lexapro

31
Q

How many primary subtpes of serotonin receptors are there?

A

7- which have sever subtypes

32
Q

What is 5HT3?

A

May mediate Gi and sexual adverse effects

33
Q

What is 5HT 2c?

A

May mediate agitation and restlessness

34
Q

WHat is 5HT2a?

A

May be involved in anxiety and mood

35
Q

What are some adverse effects of SSRI’s?

A

N, D, WL, sexual dysfunction, anxiety, nervousness, insomnia

  • Suicide- black box warning
  • should not be taken alone in bipolar disorder
36
Q

What are some atypical (dual/mixed) action antidepressants?

A

Venlafaxine
Duloxetine- Cymbalta
Mirtaxepine
Buproprion

37
Q

What is Venlafaxine and what is the mechanism of action of it?

A

Effexor

It is a NE and 5HT reuptake inhibitor

38
Q

What drug that isnt a TCA has the same mechanism?

A

Effexor

  • doesnt effect adrenergic, histamine or cholinergic receptors
  • dont give to patients on MAOI’s
39
Q

What happens to the NT’s affects by dosing of Effexor?

A

Changes which NT it actions
Low to high dosing
- 5HT–> NE–>DA

40
Q

What is desvenlafaxine (pristiq)?

A

Metabolite of Effexor

- more balanced Ne/5HT reuptake inhibition

41
Q

What is Mirtazapine?

A

Remeron

It affects both adrenergic and and serotonergic neurons

42
Q

What is Buproprion?

A

Wellbutrin

  • Enhances both NE and DA NT (moderate inhibition of reuptake and increased release)
  • also used for smoking cessation
  • AE: agitation, anorexia and insomnia
43
Q

what is the mechanism of action of Ketamine?

A

NMDA receptor antagonist

- nightmares and hallucination

44
Q

what is the mechanism of action of Lithium carbonate?

A

Most likely involved postysynaptic

  • decrease in IP3 and DAG
  • can inhibit sensitive adenylyl clyclase
  • uncouple receptor recognition site fro mGTP by competing with MG
  • ALters gene expression for long-term neuroplastic events
45
Q

What are Lithobid and Eskalith?

A

Lithium drugs

  • 60-80% effecive
  • 5-21 days until you see effects
46
Q

Where is most of lithium excreted?

A

95% from kidneys

- reasopbed about 25% with diuretics

47
Q

What are some adverse effects of lithium?

A

Fatigue, weakness, slurred speech, ataxia, tremor, excessive thirst/urination
Toxic: LOC, coma, regidity, hyperreflexia, Muscle fasciculations
TI is very low

48
Q

what is the mechanism of action of Valproic acid?

A

Anticonvulsant

  • Depakene
  • Depacon–> sodium valproate
  • similare efficacy to lithium
  • if neither work alone use together

week 7 neuro (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions