Neural System 5: Schizophrenia and Bipolar Flashcards

1
Q

what is Schizophrenia?

A

psychotic illness w/periods of psychosis

chronic dysfunction of mood, cognition, and social behavior

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2
Q

Etiology of Schizophrenia

A

Unknown

possible genetic disposition and birth complications

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3
Q

Possible pathophysiology of Schizophrenia

A

Possible cause

reduced prefrontal blood flow during cognitive tasks along with dopamin “dysregulation” (imbalance with overactivity and underactivity in various brain regions)

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4
Q

what are the types of symptoms (categories) that Schizophrenic patients can have?

A
  1. Positive - presence of behaviors
  2. Negative - diminished/absent behaviors
  3. Cognitive - impaired behaviors
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5
Q

what are some positive symptoms of schizophrenia?

A
  1. hallucinations
  2. disturbed reality
  3. abnormal motor behaviors
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6
Q

What are some negative symptoms of schizophrenia?

A
  1. diminished speech
  2. flattened emotions
  3. social withdrawal
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7
Q

what are some cognitive symptoms of schizophrenia?

A
  1. reduced attention
  2. decreased executive function
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8
Q

what is the overall goal for treatment in schizophrenia?

A

reduce symptoms and mediate AE while improving function and QOL

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9
Q

what schizophrenic symptoms are easier/harder to treat?

A

easier = positive symptoms

harder = negative symptoms

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10
Q

what types of medications are typically used to treat schizophrenia?

A

antipsychotics

at a min takes 4-6 weeks to observe changes

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11
Q

what are the classifications of antipsychotics?

A
  1. First generation (FGA) = older, more AE
  2. Second generation (SGA) = newer, less EPS and TD AEs
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12
Q

what is the 1st line trx for schizophrenia and why?

A

SGA = there are less extrapyramidal symptoms and tardive dyskinesia

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13
Q

what are extrapyramidal symptoms?

A

collection of symptoms that are drug induced movement disorders. include:

  1. actue dystonia
  2. akathesia
  3. delayed tardive dyskinesia
  4. acute parkinsonism
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14
Q

what is tardive dyskinesia?

A

repetitive and involuntary movements such as grimicing and eye blinking

*orofacial dyskinesia

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15
Q

T/F: tardive dyskinesia can be irreversible if left untreated and unnoticed?

A

TRUE

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16
Q

what is acute dystonia?

A

spasm of muscles of tongue, face, neck and back

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17
Q

what is akathesia?

A

restlessness and inability to stay still, manifests with finger-tapping, pacing

18
Q

MOA of first generation antipsychotics?

A

block dopamine receptors in mesolimbic tract where excess dopamine may contribute to postive symptoms

19
Q

SGA drugs on our list

A

quetiapine (Seroquel)

20
Q

quetiapine (Seroquel) MOA

A

block D2 receptors but less than FGA; more affinity for 5-HT receptors

*variable effect on histamine, muscarinic and alpha receptors = more variable AE

21
Q

SGA binding to D2 receptors AEs

A
  1. Motor = bradykinesia, and possible EPS
  2. Endocrine (higher risk for metabolic syndromes)
  3. Neuroleptic malignant syndrome
22
Q

if SGAs bind to other receptors what possible AEs can occur?

A
  1. H1 receptors
    • sedation and wt gain
  2. Muscarinic receptors
    1. ABCDs
  3. a1 receptors
    1. hypotension, dizziness
23
Q

Rehab concerns for FGAs

A
  1. CV risks
  2. caution with UV exposure
  3. imapired thermoregulation = caution with overexertion
  4. monitor for EPS
24
Q

Rehab concerns for SGAs

A
  1. wt gain, hyperglycemia, and lipid abnormalities
  2. CV abnormalities risk
  3. risk for heat intolerance
25
Q

what are the types of Bipolar Disorder?

A
  1. Bipolar I disorder
  2. Bipolar II disoder
26
Q

what is Bipolar I disorder (aka manic-depression illness)

A

one manic episode accompanied by history of one or more major depressive episodes

27
Q

what is Bipolar II disoder?

A

major depressive disorder accompanied by at least one hypomanic or milder manic phases

28
Q

what is hypomania?

A

at least 4 days of elevated/irritable mood combined with over-activity

29
Q

Pathogenesis of Bipolar Disoder?

A

Unknown

appears to be dysregulation in dopamine and serotonin systems

30
Q

what regions of the brain are altered in Bipolar disoder and how?

A
  1. limbic-cortical dysfunction
    • hippocampus and prefrontal cortex have diminished acitivty w/smaller volumes
    • amygdala is hyperactivity leading to emotional sensitivity
31
Q

how is Bipolar disorder treated?

A
  1. acute depressive episode = SSRI, bupropion
  2. acute manic episode = lithium
  3. maintenance trx = lithium
32
Q

what is the role of Lithium in treatment of Bipolar Disorder?

A
  1. Management of acute manic or hypomanic episode
  2. prevention of further manic and depressive episodes
33
Q

If lithium is so effective in lots of patients what is the drawback?

A

Lots of AEs

34
Q

Common AEs of Lithium?

A
  1. GI
  2. weight gain
  3. polydipsia and polyuria
  4. CNS issues
    • mental dullness, decreased memory and concentration, fine hand tremor, fatigue and muscle weakness
35
Q

why does lithium require plasma concentration monitoring?

A

can be toxic and toxicity can occur at doses close to therapeutic levels

36
Q

what are signs of Lithium toxicity?

A
  1. persitent diarrhea
  2. vomiting
  3. coarse tremor
  4. mild ataxia
  5. drowsiness
  6. muscular weakness
37
Q

what circumstances can alter lithium concentrations and increase the risk of toxicity?

A
  1. medial illness
  2. crash diets and Na+ restriction diets
  3. strenuous exercise
  4. very hot climate
  5. surgery
  6. advanced age
  7. prenancy and delivery
38
Q

T/F: Lithium is assocaited with many DDIs?

A

TRUE

39
Q

What other medication class can be used in the treatment of Bipolar Disorder?

A

Anticonvulsant medications

  1. Valproic acid (VPA
  2. Carbamazepine
40
Q

what boxed warnings are there for anticonvulsants meds used to treat Bipolar Disorder?

A
  1. Valproix acid = hepatotoxicity
  2. Carbamazepine = Stevens-Johnson Syndrome and toxi epidermal necrolysis (TEN)