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NEURO 0010 > mental illness > Flashcards

mental illness Flashcards

1
Q

what is the difference between neurological disorders and psychiatric disorders?

A

neurological
- nervous system disorders

psychiatric
- disorders affecting mind/phsyche

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2
Q

what is comorbidity?

A

if diagnosed with one illness, there is an increased risk of being diagnosed with another

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3
Q

what is are anxiety disorders?

A
  • inappropriate expression of fear
  • encompasses generalized anxiety disorders, OCD, phobias and more
  • most common psychiatric disorder
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4
Q

what are symptoms of anxiety?

A
  • increased vigilance
  • sympatheic response
  • HPA axis activation
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5
Q

how is anxiety treated?

A
  • benzodiazepines
  • SSRIs
  • cognitive behavioral therapy
  • tricyclic antidepressants
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6
Q

what do benzodiazepines do?

A
  • have an immediate response
  • activate GABA channels, but can be addictive
  • ethanol also binds to these channels
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7
Q

what do SSRIs so?

A
  • have a delayed response
  • therapeutic effect may instead be bs nervous system adapts to chronically elevated brain serotonin
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8
Q

what does cognitive behavioral therapy do?

A
  • delayed response
  • experience dependent plasticity to rewire learned responses
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9
Q

what do tricyclic antidepressants do?

A

block serotonin and NE reuptake
- delayed response (weeks)
- experience-dependent plasticity

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10
Q

what is cortisol?
what does it do?

A

a glucocortorid
- increases blood concentration of glucose

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11
Q

what is HPA regulated by?

A

amygdala

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12
Q

what is the amygdala involved in?

A

emotional and stress response

amygdala controls our stress response in stressful and potentially dangerous situations

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13
Q

what does too much activity in the amygdala do?

A

cause anxiety

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14
Q

what does the hippocampus do?

A

inhibits HPA axis

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15
Q

what are the types of affective disorders?

A
  • major depressive disorder and bipolar disorder
  • mood disorders
  • may have genetic component
  • somewhat more common in women than men
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16
Q

what are symptoms of major depressive order?

A

No longer responds to surroundings but persists in a state of low mood or inability to feel joy (“anhedonia”)
■ Sleep (too much or too little)
■ Weight/appetite (might eat too much or not enough, lose or gain weight)
■ Self-esteem (sense of worthlessness, guilt)

○ Depressive episodes can come and go but major depression only diagnosed when symptoms have been present for 2 weeks

17
Q

major depressive disorder treatments?

A

Antidepressants:
a. MAO inhibitors ⇒ blocks enzyme that breaks down NE & 5-HT b. Tricyclics ⇒ block reuptake of NE and 5-HT
c. SSRIs ⇒ block reuptake of 5-HT only (more precise)
2. CBT
3. Ketamine
4. Electroconvulsive Therapy (ECT)
- Very effective in altering mood
- Immediate effect, specific reservations
5. Stimulations:
a. Deep Brain Stimulation in ventral caudate nucleus
b. Vagus Nerve Stimulation: interaction of viscera-brain, can help with
symptoms, also for seizures
c. TMS: reversibly stimulate or depress cortical areas lying just below the
skull

18
Q

what contributes to mood disorders?

A
  • dysfunction of monoamine systems
  • HPA axis
  • anterior cingulate cortex
  • gonadal hormones and stress
19
Q

describe dysfunction of monoamine systems?

A

Dysfunction can happen at multiple possible levels: Synthesis, release, reuptake, breakdown, receptors, 2nd messenger systems

20
Q

describe treatment for monoamine systems?

A

○ Treatment: drugs that potentiate monoamine systems (MAOIs, tricyclics, SSRIs)
■ MAO inhibitor: Inhibits monoamine oxidase (enzyme that breaks 5-HT and
NE)
■ Tricyclic antidepressants: Inhibit reuptake of 5-HT and NE from cleft
■ SSRIs (Fluoxetine/Prozac): more precise b/c affects reuptake of 5-HT
preferentially
○ BUT takes several weeks to have effects → mood disorder therapies probably
promote long-term adaptive changes in the brain

21
Q

how might the HPA axis contribute to mood disorders

A

Depression increases cortisol release and adrenal gland size, and CRH can induce
depression-like symptoms
○ May explain comorbidity with anxiety b/c HPA axis affects both
○ Diathesis-stress hypothesis of affective disorders: genetic predisposition for an
illness (diathesis) compound with stressful events and conditions (stress)

■ Genes and early childhood experiences influence the number of HPPC
cortisol receptors

22
Q

how is the anterior cingulate cortex contribute to mood disorders?

A
  • increased resting-state metabolic activity in depressed patients
  • connects frontal cortex, hippocampus, amygdala, hypothalamus, and brainstem
  • may link our internally-generated emotional state and the HPA axis
23
Q

how might gonadadal hormones and stress contribute to mood disorders?

A

puberty: estrogen levels are usually higher
- estrogen may modulate mood systems

menopause: estrogen levels drop
- associated with decreased severity and frequency of depressive events

24
Q

describe bipolar disorder?

A

unusual shifts in mood, energy, activity levels, and ability to carry out day-to-day tasks
- people can cycle between feeling normal, deperession, hypomanic and manic

25
Q

what is type 1 bipolar disorder vs. type 2 bipolar disorder?

A

type 1
- more common, mania with or without depression

type 2
- less common, hypomania and always depression

26
Q

how can bipolar disorder be treated?

A
  • lithium stabalizes mood and stops mania-depression cycle
27
Q

what are the positive components of schizophrenia?

A

pos
- phsychosis
- disorganization
- catatonic behavior

28
Q

what are the negative components of schizophrenia?

A
  • lack of emotion, engagement, interest, speech and goal directed behaviour
  • mood instability
29
Q

does schizophrenia impact memory?

A
  • poor performance on wisconsin card sorting
  • MRI studies demonstrate progressive loss of gray matter over 5 years in schizophrenia, medication can slow this and reduce symptoms
30
Q

what are the contributing factors of schizophrenia?

A

dopamine hypothesis: overactive dopamine system
- treatment by blocking DA receptors using neuroleptic drugs may take a while but help
- neuroleptic drugs block DA receptors
- affects prefrontal cortex
- neuroleptics cause tardive dyskinesia/involuntary movements

glutamate hypothesis: underactive glutamate system
- NMDA receptors in particular
- drugs like PCP and ketamine which block NMDA channels produce behaviors in individuals that are difficult to distinguish from schizophrenic phenotype

31
Q

how does estrogen influence schizophrenia?

A
  • estrogen may play a protective role: schizophrenia is less prevalent and less severe in women and has a later onset
  • neuron communication mylenation and metabolism

NEURO 0010 (22 decks)

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