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Psych 421: The Neural Basis of Behavior > Week 6: Psychopathology > Flashcards

Week 6: Psychopathology Flashcards

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1
Q

Affective Disorders

A

Disorders of the mood; profound alternation of mood

Mania or depression

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2
Q

Depressed Mood

A

Increase or decrease in activity
changes in sleep (insomnia or hypersomnia)
suicidal ideation or thoughts of death

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3
Q

Mania

A

Feelings of gradiosity
Periods of excessive talking
Decreased need for sleep
Risky behavior

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4
Q

Area 25

A

Prefrontal cortex just below the genu of the corpus callosum

Activity (positive or negative) is mostly in this area

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5
Q

VTA to Nucleus Accumbens

A

A major player in reinforcement - changes in reinforcement (bad things seeming worse, good things seeming not as good) is characteristic of affective disorders

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6
Q

Iproniazid

A

Euphoria in TB patients - then used an antidepressant

Enhances MA functioning

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7
Q

Reserprine

A

Depression in hypertensive patients

Affects the vesicles and their ability to package NT to decrease MA functioning

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8
Q

Amphetamines CNS Actions

A
  1. Hampers reuptake of MA’s
  2. Enhances the release of MA’s
  3. Directly stimulates the postsynaptic receptors
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9
Q

Raphe Nuclei

A

huge arousal system

NE increases arousal

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10
Q

Locus Ceoruleus

A

5HT decreases arousal

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11
Q

Medications for Affective Disorders

A
  1. TCA’s
  2. MAO-I’s
  3. SSRI’s
  4. NSRI’s
  5. SNRI’s
  6. Other
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12
Q

TCA’s

A

Hamper reuptake of NE and 5HT, some do one better than the other

desipramine - blocks reuptake of NE better than 5HT

imipriamine - blocks reuptake of 5HT better than NE

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13
Q

MAO-I’s

A

global effect of MA’s

parnate

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14
Q

SSRI’s

A

Zoloft, Prozac

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15
Q

SNRI’s

A

Effexor = Pristiq

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16
Q

NSRI

A

Strattera

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17
Q

Others

A

Wellbutrin(Anti-depressant)/Zyban(quit smoking) - blocks reuptake of DA and NE

Remeron - Histamine receptor antagonist

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18
Q

Monoamine theory of Affective Disorders

A

affective disorders are the result of either underactive monoamine system in the brain or the levels of monoamine NT molecules in the brain are too low

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19
Q

Shortcomings of the MA Theory of Affective Disorders

A

Failst o explain why there is a 10-14 day delay of the onset of taking medication to the onset of clinical improvement

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20
Q

Beta Andrenergic Theory of Affective Disorders

A

Beta Andrenergic receptors are too active and the down regulation of these receptors (which takes 10 - 14 days) helps to treat depression

The down regulation comes with medication that block the reuptake of NE, and also with a variety that do not directly alter NE

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21
Q

Hypericum / St. John’s Wort

A

Helps mild-moderate depression

Inhibits MA’s
Inhibits the reuptake of 5HT, NE

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22
Q

Alternatives to Drug Intervention

A
  1. Electro-shock therapy
  2. Transcortical Magnetic Stimulation (TMS)
  3. Deep Brain Stimulation
  4. Vagus Nerve Stimulation
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23
Q

ETC

A

Current is sent through the patient’s brain

immediately down regulation beta andrenergic receptors
enhances 5HT sensitivity

95% response rate, but also a high relapse rate if nothing else is used.

24
Q

TMS

A

Generates a strong magnetic field over the brain to change behavior, typically depression

data is not entirely convincing

25
Q

Deep Brain Stimulation (DBS)

A

Drop electrodes into area 25 to down regulate activity and depression can be relieved

Some show improvement, some show none

26
Q

Vagus Nerve

A

The relief may be due to its upstream pathway - including the locus ceoruleus, which deals with reward and pleasure

27
Q

Treatment for Mania

A

Lithium

28
Q

Side effects of Lithium

A 
relief of manic symptoms
mental dullness
decreased memory and concentration
headache
fatigue
29
Q

Effects of Lithium on brain functioning

A 
decrease brain calcium levels
enhances reuptake of NE and 5HT
reduces release of NE
Alters Na+K+ATPase Pump
Prevents recycling of IP3 in G-protein system
30
Q

Depression and Cortisol

A

Higher levels of ACTH in depressed patients may raise cortisol levels

May be result of hifh CTRH horomone in the hypothalamus

The feedback look to decrease cortisol may not be working properly (glucorticoid and dexamethasone)

31
Q

Anxiety Disorders

A

Panic Disorder
Generalized Anxiety Disorder
Post-Traumatic Stress Disorder
Obsessive Compulsive Disorder

32
Q

Anxiety Disorders

A

Panic Disorder
GAD
OCD

33
Q

Drugs for Panic and GAD’s

A

first line: Benzo’s
-ativan, Xanax
SSRI
- BuSpar

Second line: antipsychotics

34
Q

Drugs for OCD

A

Antidepressant: clomipramine

35
Q

Motor involvement in OCD

A

The basal Ganglia (Caudate, Putamen, Globus Pallidus)

36
Q

NT used by Basal Ganglia

A
  1. interneurons in the caudate use ACh
  2. Interneruons in putamen use GABA
  3. Striatal projections to globus pallidus use enkepahin and GABA
  4. pars compacta input to the striatum use DA
  5. cerebral cortical input uses glu
  6. output from globus pallidus to substantia nigra uses GABA and substance P
  7. input from raphe to the striatum uses 5HT
37
Q

Psychoses

A
  1. hallucinations
  2. delusions
  3. disturbances of thought, languages and communication
  4. disturbances of emotion
38
Q

Negative signs of Psychoses

A

absence of normal social and interpersonal behaviors

39
Q

Positive signs of Psychoses

A

abnormal behavior

40
Q

Anatomical differences in brains of psychotics

A
  1. reduction in blood flow to the globus pallidus (left side)
  2. frontal cortex does not respond vigorously
  3. the cortex of the medial temporal lobe is thinner and the antereior portion of the hippocampus is smaller
  4. lateral and third ventricles are larger (meaning there is less tissue there)
41
Q

Areas that are prominent in Negative sign of psychoses

A

hippocampus, prefrontal cortex, basal ganglia

42
Q

Hallocinogenic loop

A

Cortex -> basal ganglia -> substania nigra -> thalamus -> Cortex

43
Q

Categories of Antipsychotics

A
  1. First generation antipsychotics - typical antipsychotics
  2. second generation - atypical antipsychotics
  3. third generation - abilify
44
Q

Typical antipsychotics include

A

Thorazine
Prolixin
Haldol

45
Q

Actions of antipsychotic drugs

A

they block DA

Typically induce a tranqulized state without loss of consciousness

46
Q

Actions of antipsychotic drugs on the PNS

A
  1. they block ACh receptors

2. block alpha adrenergic receptors

47
Q

Symptoms of Psychoses that respond well to medication

A 
hallucinations
acute delusions
hostility
flat affect
general withdrawal
48
Q

Effects of blocking Alpha Adrenergic recepotrs

A

increased heart rate
mild decrease in blood pressure
postoral hypertension
mild hypothermia

49
Q

Effects of blocking muscarinic receptors

A

memory difficulties, confusion, delirium

50
Q

DA systems

A
  1. Nigro-striatal DA pathway
  2. meso-limbic and meso-cortical systems
  3. tubero-infundiular sustem
51
Q

DA Theory of Schizophrenia

A

Overactive or too much DA

52
Q

D2 Receptors

A

principle site of action for phenothiazines and butyrophenones

Located in cerebral cortex, limbic structures, striatum (motor area)

53
Q

D3, D4 receptors

A

limbic areas and cerebral cortex, NOT motor areas

Clozapine - Atypical blocks D3, D4 weakly blocks D2

54
Q

Adverse Behavioral Effects of Antipsychotics

A
  1. Acute Dystonia - sustained muscle contractions
  2. Akathesia - compulsion to move
  3. Parkinson syndrome - very similar to Parkinson’s disease, but will recede with stopping on meds.
  4. Tardice Dyskinesia - late-onset motor disorder
55
Q

Challenges to DA Theory

A

DA may not be causal pathway

5HT - Clozaprine, Risperidone, Zyprexa, Abilify
Glu has been suggested - DA may be secondary to Glu, Glu may be secondary to 5HT

Psych 421: The Neural Basis of Behavior (6 decks)

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