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Brain and Behaviour > Week 6- Emotion and Personality > Flashcards

Week 6- Emotion and Personality Flashcards

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1
Q

What sensations is the hippocampus informed of?

A

ALL of them. It has input from the amygdala, sensory association areas (therefore sensations go to the cortex first) and the entorhinal cortex (which is like bc in the parahippocampal gyrus

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2
Q

How many nuclei does the amygdala have and which one regulates social behaviour and which one regulates cortisol

A

4 nuclei (medial, central, lateral and basolateral)

Central does Cortisol

Medial does social behaviour (the face you present to the media)

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3
Q

Which nuclei in the hypothalamus do diurnal cycles, ADH response, melatonin and the final common pathway for cortisol release?

A

SCN: diurnal cycles (makes sense, it’s right above the optic chiasm)

SON: ADH response

MB: melatonin

PVN: final common pathway for cortisol release. lies next to the ventricle but is still protected by the BBB

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4
Q

What are the acute and chronic sequelae of the panic response?

A

This comes back to cortisol

  • mobilize energy–> myopathy, DM
  • increase vascular tone –> HTN
  • suppress digestion —> ulcers
  • suppress reproduction–> amenorrhea
  • suppress immune system–> increase infection risk
  • sharpen cognition–> eventual neuronal cell death
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5
Q
A

Appearance/ Assessment (Attention, LOC, orientation

Speech

Emotion (mood and affect)

Perception (hallucinations, illusions)

Thought

  • content: obsessions, delusions
  • form: circumstantiality, tangentiality, perseveration

Insight and Judgement

Cognition (MMSE)

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6
Q

What are the DSM IV axes?

A
  1. Major psych conditions
  2. Personality and intellectual disability
  3. The medical problems
  4. Psychosocial and environmental stressors
  5. Global assessment of function (WHODAS)
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7
Q

SIGECAPS

A

Sleep

Interest

Guilt

Energy

Cognitive changes

Appetite

Psychomotor changes

Suicide

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8
Q

What are the criteria for major depressive episode, manic episode, hypomania?

What combination of these mood episodes give MDD, bipolar 1 and bipolar 2?

A

Major depressive episode (lasts 2 wks or more):

  • decreased mood OR ahedonia
  • AND
  • 4 of SIGECAPS

Mania ( lasts 1 wk or greater and causes distress/impairment/hospitalization)

  • 1 wk of elevated/expansive/irritable mood AND
  • 3 of:
    • decreased need for sleep
    • racing thoughts
    • pressure of speech
    • distractability
    • grandiosoty
    • increased goal-directed activity
    • increased involvement in pleasurable but risky activities

Hypomania (lasts less than 4 days and does not cause impairment)

  • all of the above

MDD:

  • At least one major depressive episode

Bipolar I

  • MDD + at least one mania

Bipolar II

  • MDD + at least one hypomania
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9
Q

How long does dythymia have to last for to be diagnosed?

A

2 yrs of chronic low grade depressive sx

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10
Q

What are the 5 factors of personality

A
  1. emotional stability/neuroticism
  2. Extroversion
  3. Openness to experience
  4. Agreeableness
  5. Conscientiousness
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11
Q

What is a personality disorder? When is the usual onset?

A

An enduring pattern of inner experience that deviates markedly from expectations of a person’s culture. Manifests in (>2) cognition, impulse control, affectivity, interpersonal functioning. It is inflexible and pervasive across situations. Causes functional impairment or distress.

Onset is usually in adolescence/young adulthood.

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12
Q

What are the three clusters of personality disorders?

A

A: odd & eccentric

  • paranoid (Mad-Eye Moody)
  • schizoid: detached, does not connect **(arelational) **(Professor Snape)
  • schizotypal: relational discomfort, cognitive/perceptual distortions, eccentricities (…Luna Lovegood)

B: dramatic & erractic

  • histrionic: excessive emotionality + need for attention (Professor Trelawney)
  • boderline: unstable relationships, unpredictable, impulsive (Moaning Myrtle)
  • antisocial: disregard for others, superficially charming but hostile when confronted (Voldemort)
  • narcissitic: need for attention, lack of empathy (Gilderoy Lockhart)

C: Anxious & fearful (much ADO about nothing…)

  • Avoidant: social inhibition, hypersensitive (but has desire to be close to others vs. schizoid)
  • Dependant (Merope)
  • Obsessive-Compulsive (Percy)

Tx is behavorioural therapy and perhaps antipsychotics for schizotypal

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13
Q

What is anxiety vs. fear? What are the common features of anxiety disorders?

A

Anxiety: anticipation of future threat

Fear: emotional response to perceived threat

Unwanted emotion, thoughts and actions

Panic attacks are a feature of all anxiety disorders

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14
Q
A
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15
Q

Lifetime prevalence for GAD, social anxiety and specific phobia?

A

GAD: 55%!!!!

Social anxiety disorder: 5-15%

Specific phobia: 7-10%

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16
Q

How long does a panic attack usually last for?

A

less than 20, peaks at 10

17
Q

How long do you have to have unexpected recurrent panic attacks to have Panic Disorder? How to differentiate from agoraphobia, specific phobia, GAD

A

At least one month, with persistent concern of further attacks or maladaptive behaviour.

Agoraphobia duration is 6 months, there is a fear of a particular situation AND there is avoidant behaviour. Agoraphobia the fear is loss of control.

Specific phobia can be to an object or situation, the person recognizes the fear is unreasonable.

GAD: excessive anxiety and worry with restlessness, fatigue, difficulty concentrating, muscle tension etc… for 6 months

18
Q

PTSD features

A

reexperiencing

avoidance

negative changes in mood and cognition

hyperarousal

19
Q

What brain circuits are dysregulated in OCD

A

frontal striatal: there is dysregulation in the circuit that does error monitoring (the person gets a persistent error message)

20
Q

What is the cognitive model of panic attacks?

A

trigger–> perceived threat–> apprehension–> body sensation–> body sensation perceived as catastrophic–> percieved threat –>apprehension etc…..

21
Q

What are the monoamines? What terminates the action of monoamines? What is the monoamine hypothesis and what does it pertain to?

A

5-HT, NE, Dopa

  • MOA (all), COMT (NE and dopa), SERT (5-HT)

Monoamine hypothesis: depressed state due to upregulation of monoamine receptors

Bipolar disorder is more like dopaminergic dysregulation

22
Q

Which symptoms are 5-HT, NE and dopa involved in the pathopathysiology of depression?

A

All three: Sleep, mood, apathy, psychomotor

NE/dopa: concentration and fatigue

5-HT: guilt, weight, suicidal ideation

23
Q

What are the different classes of anti-depressants and what do they block? What are mood stabilizers and what are anxiolytics?

A

SSRIs: block SERT

  • fluoxetine, escitalopram, paroxetine

SNRIs (5-HT, NE): block SERT and NERT

  • venlafaxine, duloxetine

NDRI (NE, dopa): weakly blockes dopa and Ne reuptake. doesn’t block SERT or MAO

  • bupropion only

NaSSA (NE and serotonin specific antidepressant)

  • antagonizes alpha-2 (presynaptic) causing more NE and 5-HT release.
  • blocks 5-HT 2A and 2C…thought to increase 5-HT1 transmission
  • mirtazapine

SARI’s (5-HT antagonist, reuptake inhibitor):

  • blocks 5-HT 2A, 2C
  • trazadone

TCA’s

  • based on chemical structure, not mechanism SNRI, SRI, NRI

Mood stabilizers are some AED + lithium and are used in bipolar disorder

Anxiolytics are 1st line SSRI/SNRI at lower dose +/- short term benzos and are used in anxiety disorder

24
Q

What are the various blockades possible with TCAs

A

Histamine: weight gain, fatigue

anti-cholinergic: blurred vision, dry membranes, urinary retention

alpha-adrenergic blockade: orthostatic hypotension

Na channel blockade: arrhythmia in overdose

25
Q

What are mood stabilizers?

A

Most of them are ALSO anticonvulsants:

  • carbamazepine
  • valproate
  • lamotrigine

And lithium, which is not an AED

26
Q

What are the important/memorable side effects of:

SSRIs

NDRI

SARI

A

SSRIs:

  • wt gain
  • sexual DFx
  • bleeding (5-HT is a platelet activator…don’t use with warfarin!)

NDRI (bupropion):

  • can cause insomnia if dosed too close to bed
  • less sexual effects

SARI (trazadone)

  • priapism

TCAs can have a blockade of

  • histamine
  • ACh
  • alpha adrenergic
  • sodium channels

MAO

  • hypertensive crisis…have to watch tyramine in diet
27
Q

What is the reason for the time to clinical effect gap with SSRIs? (autoreceptors and stuff)

A

SSRIs block SERT. This increases 5-HT concentrations. This tells the presynaptic neuron to downregulate the number of 5-HT1A receptors in the presynaptic terminal. Normally these receptors (like most auto-receptors) DECREASE the amount of sertonin release. So if you decrease the number of 5-HT1A receptors, you increase the amount of serotonin released

28
Q

In CBT, automatic thoughts are….

A

thoughts on the periphery of awareness…

29
Q

Does the presence of GAD increases the risk of other mood disorders or anxiety disorders? Or both?

A

Both.

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