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Flashcards in Week 6 Deck (81)
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1

Affective Disorders

disorders of MOOD (depression & mania)

2

Depressed mood symptoms

1. profound changes in activity (increase or decrease)
2. changes in sleep (insomnia or hypersomnia)
3. suicidal ideation or thoughts of death

3

Mania symptoms

-feelings of grandiosity
-excessive talking
-decreased need for sleep
-distractibility
-engaging in risky behavior

4

Areas 25

Frontal Cortex & Cingulate Gyrus

*important in mood disorders
depression = over or under activity

5

Nucleus accumbens and anhydonia

GABA and dynorphin pathway
-decreases VTA activity
-->decreased reinforcement
-->decreased pleasure

6

Iproniazid origins

used to treat TB originally
-increased mood to point of euphoria

7

Reserpine origins

when hypertensive patients given reserpine
caused depression

8

Chlorpromazine origin

antihistamine that had antipsychotic effects

9

imipramine origin

antidepressant activity

10

iproniazid mechanism

MAO-I (monoamine oxidase inhibitor)
-->enhanced NT functioning
-->elevated mood

11

Reserpine mechanism

binds to vesicles in Monoamine terminals
-->prevents NT from entering/binding
-->decrease NT functioning
-->depressed mood

12

amphetamines mechanisms

increases monoamine functioning in 3 ways
1. blocks reuptake of all 3 monoamines
-->NTs stay in synapse longer
2. enhances release of monoamines
*probably due to MAO-I activity (package more NT)
3. directly stimulate post-synaptic receptors

13

Raphe nucleus projections

*unilateral
projects to:
-hypothalamus
-thalamus
-hippocampus
-MFB

14

Locus Coeruleus projections

*unilateral
projects to:
-hypothalamus
-amygdala
-hippocampus

15

Monoamine pathways tend to be...

unilateral

16

5HT-1A receptor locations

cerebral cortex
hippocampus
septum
amygdala
raphe nucleus

17

5HT-2A receptor locations

cerebral cortex & basal ganglia

18

5HT-2C receptor locations

hippocampus, cerebral cortex

19

NE receptor locations

hippocampus
cerebral cortex

20

Ways drugs can change neural activity

1. alter synthesis
2. interfere with vesicle storage
3. directly stimulate receptors
4. block enzyme breakdown of NT (MAO-I's)
5. interfere with reuptake

21

1st generational antidepressants (traditional)

-TCA's
-MAO-I
-lithium

22

Atypical antidepressants (newer)

-SSRI
-SNRI
-Buproprion

23

TCA

some block/hamper reuptake of NE more efficiently than they block reuptake of serotonin

others block reuptake of serotonin more efficiently than they block reuptake of NE

24

MAO-I

inhibit MAO enzyme
-->more NT packaged
-->release of more NT molecules with each AP

25

SSRI

block reuptake of serotonin
very little blocking of NE

26

SNRI

serotonin and NE reuptake inhibitors

27

buproprion

blocks reuptake of DA (and NE)

28

Monoamine theory of affective disorders

disorders are result of underactive monoamine systems in the brain
OR levels of monoamine molecules are too low

29

failure of monoamine theory of affective disorders

fails to explain why there is a 10-14 delay from onset of meds to clinical improvements

30

Beta adrenergic theory of affective disorders

disorders result of too many beta adrenergic receptors (NE receptors)