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Psych 421 > Week 6 > Flashcards

Week 6 Flashcards

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1
Q

Affective Disorders

A

disorders of MOOD (depression & mania)

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2
Q

Depressed mood symptoms

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

Mania symptoms

A
  • feelings of grandiosity
  • excessive talking
  • decreased need for sleep
  • distractibility
  • engaging in risky behavior
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4
Q

Areas 25

A

Frontal Cortex & Cingulate Gyrus

*important in mood disorders
depression = over or under activity

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5
Q

Nucleus accumbens and anhydonia

A

GABA and dynorphin pathway

  • decreases VTA activity
  • ->decreased reinforcement
  • ->decreased pleasure
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6
Q

Iproniazid origins

A

used to treat TB originally

-increased mood to point of euphoria

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7
Q

Reserpine origins

A

when hypertensive patients given reserpine

caused depression

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8
Q

Chlorpromazine origin

A

antihistamine that had antipsychotic effects

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9
Q

imipramine origin

A

antidepressant activity

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10
Q

iproniazid mechanism

A

MAO-I (monoamine oxidase inhibitor)

  • ->enhanced NT functioning
  • ->elevated mood
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11
Q

Reserpine mechanism

A

binds to vesicles in Monoamine terminals

  • ->prevents NT from entering/binding
  • ->decrease NT functioning
  • ->depressed mood
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12
Q

amphetamines mechanisms

A

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
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13
Q

Raphe nucleus projections

A 
*unilateral
projects to:
-hypothalamus
-thalamus
-hippocampus
-MFB
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14
Q

Locus Coeruleus projections

A 
*unilateral
projects to:
-hypothalamus
-amygdala
-hippocampus
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15
Q

Monoamine pathways tend to be…

A

unilateral

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16
Q

5HT-1A receptor locations

A 
cerebral cortex
hippocampus
septum
amygdala
raphe nucleus
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17
Q

5HT-2A receptor locations

A

cerebral cortex & basal ganglia

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18
Q

5HT-2C receptor locations

A

hippocampus, cerebral cortex

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19
Q

NE receptor locations

A

hippocampus

cerebral cortex

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20
Q

Ways drugs can change neural activity

A
  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
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21
Q

1st generational antidepressants (traditional)

A
  • TCA’s
  • MAO-I
  • lithium
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22
Q

Atypical antidepressants (newer)

A
  • SSRI
  • SNRI
  • Buproprion
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23
Q

TCA

A

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

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24
Q

MAO-I

A

inhibit MAO enzyme

  • ->more NT packaged
  • ->release of more NT molecules with each AP
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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)
31
criticism of Beta adrenergic theory of affective disorders
too animal based
32
long term consequences of chronic antidepressant medications
down regulation of beta adrenergic receptors (takes 10-14 days)
33
Beta adrenergic receptors and SSRI/MAO-I's
will down regulate Beta adrenergic receptors
34
TCA antidepressants and serotonin
influence 5HT-1A serotonin receptor sensitivity
35
serotonin and NE interaction
down regulation of beta adrenergic receptors | and increased 5HT receptor activity
36
St Johns Wort mechanism
Treatment of patients with mild-moderate depression combined effect of several mechanisms: -inhibits both 5HT and NE uptake in dose dependent manner (stronger for NE) -upregulation of 5HT-1A & 5-HT2A -down regulation of Beta adrenergic receptors -weak MAO & COMT inhibition
37
Alternatives to pharmacotherapy
1. ECT 2. TMS 3. DBS 4. VNS
38
ECT used for patients who
need immediate relief critical for suicidal patients *down regulates beta adrenergic receptors
39
2 concerns with ECT
1. induce confusion & loss of memory - ->more severe with increased sessions 2. without addtnl medication support there is a high relapse rate
40
TMS mechanism
strong magnetic field over brain - limits to how deep into brain it can go - some success but not super convincing
41
DBS
some success with parkinsons | -->depression is frequent side effect
42
VNS treatment
offers relief from several disorders including depression | *may be due to upstream pathway that projects to locus coeruleus
43
Lithium responses
- relief of manic sx's (normalize cycles) - mental dullness - decreased memory and concentration - headache - fatigue
44
lithium effects on brain (many)
- decrease brain calcium levels - enhances reuptake of NE and Serotonin - reduces release of NE - alters Na+/K+ pump * inhibits inositol G protein system (reduced responsiveness of neuron)
45
Depression and cortisol
abnormally high ACTH-->oversecretion of cortisol | -may be result of high levels of CTRH in hypothalamus
46
non-depressed vs depressed people cortisol
non-depressed: have negative feedback loop that will respond to synthetic glucocorticoid to stop secretion of more cortisol depressed patients: do not respond and cortisol level remains high
47
rat anxiety experiment
rats will normally stay in covered areas, explore a little - when given anti-anxiety meds they will explore a lot more - when given an antagonist to induce anxiety, never leave the covered area
48
1st line drugs of Panic Disorder or GAD
- Benzodiazapenes | - SSRI's
49
2nd line drugs for Panic or GAD
antipsychotics
50
OCD
persistent thought persistent behaviors *motor and anxiety disorder
51
Basal ganglia structures
1. caudate nucleus 2. putamen 3. globus pallidus
52
Basal ganglia receives input from | and outputs to
``` frontal cortex (glutamate) substantia nigra (dopamine) raphe nucleus (serotonin) ``` outputs GABA to substantia nigra
53
SSRI, clomipramine, and behavioral therapy treatment
decrease hyperactivity of caudate nucleus and frontal cortex
54
non-invasive treatment (psychotherapy)
can modify dysfunctional neural circuitry associated with anxiety disorders
55
psychoses symptoms
1. hallucinations 2. delusions 3. disturbances of thought, language, communication 4. disturbances of emotion
56
1st generation antipsychotic drugs
- produced parkinsons like side effects (stiffness, tremor, difficulty initiating movements - some block serotonin receptors - drugs that increase dopamine can produce psychotic symptoms
57
Negative signs of psychosis
absence of normal social behaviors
58
positive signs of psychosis
presence of distinctly abnormal behavior
59
anatomical differences in psychoses
1. reduction in blood flow of globus pallidus (basal ganglia) 2. frontal cortex in general doesn't respond as vigorously 3. cortex of temporal lobe is thinner AND hippocampus is smaller 4. ventricles are larger (less tissue)
60
important cognitive areas of brain
hippocampus frontal cortex basal ganglia
61
loop of cognitive functioning
cortex-->basal ganglia-->substantia nigra-->thalamus--cortex
62
false theory of psychotic episodes
theory that psychotic episodes may leave behind weakened neurons/apoptosis is WRONG *medications are more detrimental
63
1st generation antipsychotics
block dopamine receptors
64
1st generation antipsychotic effects on PNS
1. block ACh receptors | 2. block NE receptors
65
Behavioral effects of blocking PNS ACh receptors
- produces 'artifical hibernation' (tranquilized state without loss of consciousness) - relief of psychotic symptoms
66
Effects of blocking PNS NE receptors
- increased heart rate - decreased blood pressure - ->postural hypotension - mild hypothermia
67
effects of blocking CNS ACh receptors
- memory difficulties - confusion - maybe even delerium
68
Hormonal/behavioral effects of antipsychotics
decreased libido lactation decreased menstruation
69
Important dopamine systems
1. nigro-striatal pathway 2. meso-limbic and cortical pathway 3. tubero-infundibular pathway
70
DA theory of schizophrenia
caused by too much Dopamine
71
Traditional antipsychotic DA receptor types
D2 receptors - in cerebral cortex - in limbic structures - in striatum
72
D2A
post synaptic surface
73
D2B
inhibitory auto receptors (pre-synaptic) | and also post-synaptic
74
D3
on pre-synaptic terminals
75
D3 and D4 locations in brain
found in limbic areas and cerebral cortex but NOT in motor areas like striatum
76
Clozapine (Atypical antipsychotic)
blocks D3 and D4 best | also binds to serotonin and histamine receptors
77
Adverse behavioral effects of antipsychotics
1. acute dystonia (sustained muscle contractions) 2. akathesia (compulsion to move) 3. parkinsons syndrome 4. tardive dyskinesia (late onset motor disease) 5. tourrettes
78
Atypical antipsychotics
block D2 receptors but primarily serotonin receptors
79
Abilify
``` agonist of D2 antagonizes serotonin (decrease activity) ```
80
Glutamate theory of psychoses
hypofunctioning of NMDA in frontal cortex may actually regulate Dopamine serotonin can regulate glutamate, that regulates dopamine
81
CB1 receptors and psychoses
marijuana can be therapeutic

Psych 421 (8 decks)

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