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Schizophrenia Flashcards

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1
Q

psychosis

A

syndrome associated with a variety of illnesses

set of sx in which a person’s mental capacity, affective response, capacity to recognize reality, communicate, and relate to others is impaired.

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2
Q

DSM dx Schizophrenia 6 main sx

A

Delusions
hallucinations
disorganized speech
grossly disorganized or catatonic behavior
negative symptoms
signs of disturbance for at least 6 months

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3
Q

positive symptoms

A

delusions
hallucinations
agitation
disorganization

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4
Q

negative symptoms

A

asociality
affective flattening
alogia
avolition
anhedionia

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5
Q

affective sx

A

depressed mood
inappropriate
blunted

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6
Q

cognitive sx

A

poor attention
problems with learning
impaired fluency

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7
Q

5 As

A

asociality
affective flattening
alogia
avolition
anhedionia

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8
Q

avolition

A

lack of motivation

kinda looks like depression which is why some dx with depression first

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9
Q

alogia

A

poverty of speech

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10
Q

4 pathways

A

mesocortical pathway
mesolimbic pathway
nigrostriatal pathway
tuberoinfundibular pathway

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11
Q

dopamine hypothesis

A

mesocortical dec D2
mesolimbic inc D2
Nigrostriatal and tuberoinfundibular not affected

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12
Q

mesocortical pathway

A

Innervates the prefrontal cortex

Which is responsible for personality, executive function

Dec dopamine means behavioral deficits like impaired cognition

this is whats affected in prodromal phase before psychosis

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13
Q

mesolimbic pathway

A

Brain tries to compensate with excess in mesolimbic

this leads to Psychosis: Hallucinations, delusions, misinterpret our environment

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14
Q

Nigrostriatal pathway

A

Responsible for movement

normal function but untreated you see tardive dyskinesia etc

But for simplicity we will say its normal

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15
Q

Tuberoinfundibular pathway

A

Controls hypothalamus, adrenal, pituitary

We know dysregulation including temp and psychogenic polydipsia

But for simplicity we say its kind of normal there

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16
Q

Glutamate

A

Involved in mult dx and is a key target for rx (esp newer rx) in schizophrenia and depression

Works tandem with dopamine

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17
Q

glutamate requires what to function

A

Co-transmitter

Needs glycine and D-serine

required on the NMDA receptor for glutamate to function

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18
Q

key glutamate pathways

A

Prefrontal cortex
Nucleus accumbens

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19
Q

Glutamate hypothesis

A

Glutamate activity at NMDA receptors is hypofunctional

so you get:
Neurodevelopmental abnormalities
GABA interneurons in the PFC
Glutamate becomes hyperactive

Also glutamate regulates dopamine in the mesolimbic and mesocortical pathways

It innervates the pathways differently

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20
Q

typical antipsychotics started when and with that

A

1950s

with thorazine

caused neurolepsis but was originally an antihistamine

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21
Q

neurolepsis

A

Slowness, absence of motor movements, affective indifference

Neuroleptics AKA antipsychotics

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22
Q

typical antipsychotics aka

A

1st gen
conventional

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23
Q

typical antipsychotic binding sites

A
  1. M1 antag
    a. muscarinic
  2. H1 antag
    a. histamine
  3. Alpha 1 antag
  4. D2 antag
    a. Block the activity of a ligand, stays resting
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24
Q

typical antipsychotic changes to pathways

A

dec mesocortical pathway MORE
dec mesolimbic which was elevated
dec nigrostriatal and tuberoinfundibular which were unaffected

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25
1st gen effect on pos and neg sx
Treats our positive sx (mesolimbic) Worsens our negative sx (mesocortical)
26
when a patient stops their 1st gen
their neg sx improve they can navigate the world better Motivation, organization, processing etc are a prob for these pt and so coming off those may improve and we have to be cautious about worsening these sx
27
1st gen effect on nigrostriatal pathway
movement dec pseudoparkinsonism is an AE
28
1st gen effect on tuberoinfundibular pathway
dec leads to hyperprolactinemia
29
1st gen AE beyond dopamine changes
anticholinergic effects (M1) sedation (H1) orthostatic hypotension (alpha) EPS and hyperprolactinemia (D2)
30
threshold for EPS and hyperprolactinemia in 1st gen
close/narrow
31
low vs high potency 1st gen
Low: More anticholinergic, antihistamine, more alpha 1, but less EPS High: Less anticholinergic and antihistamine but more EPS
32
What makes atypical antipsychotics different
5HT2A receptor helps mitigate dopamine antagonism
33
What aytpical antipsychotics do to pathways
mesocortical: less of a decrease and some actually increase mesolimbic: still dec pos sx Nigra and tubero: does not affect much which mitigates EPS and hyperprolactinemia
34
EPS and hyperprolactinemia threshold in 2nd gen
not as narrow/close due to 5HT2A mitigating by producing more endogenous dopamine
35
atypical antipsychotics pharmacodynamics
complex profiles with many receptors
36
2nd gen rx blocking one or more of 3 receptors responsible for causing sedation What 3 receptors
M1 H1 a1
37
2nd gen that inc sedation (3)
clozapine olanzapine quetiapine pine is high
38
2nd gen that dont inc sedation (3)
aripiprazole cariprazine lurasidone done pip and rip and low
39
cardiometabolic effects of 2nd gen 1+ of 2 receptors which receptors
H1 5HT2C
40
cardiometabolic effects associated with what sx
wt gain insulin resistance not as common as 1st gen
41
2nd gen that inc cardiometabolic effect (2)
clozapine olanzapine pines make worse
42
2nd gen that dont inc cardiometabolic effect (2)
aripiprazole cariprazine lurasidone ziprasidone pip rip and done are low (they can but less common)
43
anticholinergic effect of 2nd gen at what receptor and what are the sx
M1 urinary retention constipation blurry vision/dry eyes
44
2nd gen that inc anticholinergic effect (3)
clozapine olanzapine quetiapine so PINE is high All others do not effect Note bowel prophylaxis common with clozapine
45
EPS and hyperprolactinemia sx for 2nd gen at what receptor
D2 antagonism
46
How to remember which 2nd gen affect EPS/hyperprolactinemia
DONE are high PINE are low Risperidone, paliperidone, ziprasidone Clozapine, quetiapine, olanzapine opposite of others
47
Hypotension effect of 2nd gen at what receptor
a1 antagonism
48
Hypotension effect for 2nd gen Which rx do and dont effect harder to remember
inc sx: clozapine, quetiapine, risperidone, Iloperidone dec: Brexiprazole, cariprazine, lurasidone
49
QTC prolongation for 2nd gen activity where
HERG potassium channels
50
QTC prolongation for 2nd gen activity rx make worse or not
inc: ziprasidone, quetiapine, risperidone, clozapine dec: aripiprazole, cariprazine, brexpiprazole, lurasidone Note concern if mult rx are positive
51
2 pips and rip are D2 partial agonists so
so there is a ceiling affect. High affinity for receptor but doesnt impact as much so you can add aripiprazole to risperidone when patients have hyperprolactinemia
52
Quetiapine is a NE reuptake inhibitor so
good use in mood disorders
53
ziprasidone and lurasidone need
to be taken with food
54
the only SL 2nd gen
asenapine
55
Pimavanserin
5HT-SA inverse agonist no direct dopamine receptor activity approved for parkinsons dz psychosis because it doesnt affect underlying dz research in alzheimers
56
Lumateperone
D2 and 5HT-2A antagonist D1 receptor activity so inc glutamatergic transmission
57
clozapine pros
Gold standard in terms of efficacy Proven to reduce suicidality Associated with lowest risk of all cause mortality DOC for side effects caused by D2 blockade AKA people with risk for parkinsonism and NMS Glutamatergic activity
58
clozapine cons
Hits many receptors so big AE profile Agranulocytosis Needs blood monitoring Seizures DKA Myocarditis/ Cardiomyopathy Needs baseline lab Constipation Abrupt withdrawal has been associated with psychosis and cholinergic rebound
59
APA guidelines
Tx with antipsychotic and monitor for effect and AE Continue if sx improve Clozapine for tx resistant (2 failed mono) Also if suicidality remains despite other rx Tx acute dystonia with anticholinergic Tx mod to sev tardive dyskinesia with VMAT2 inhibitor
60
canadian guideline differences
1st episode use low dose and titrate trial 2-4 wks and switch if no response cont for at least 18 mo if pos sx resolution
61
canadian guidelines for Acute exacerbation/relapse prevention
inc or change rx reassess at 4-8 wks maintenance: 300-400mg CPZ equivalents 4-6 mg risperidone Duration 2-5 yrs LA injection if poss
62
Australia/NZ guideline differences
a. Start low go slow b. Consider diff dx c. Specific rx and dosing d. CBT should be offered e. Monitor for metabolic syndrome f. Recc for combining antipsychotic meds Note US asks for 3 mono before polypharmacy
63
CATIE
Clinical Antipsychotic Trials of Intervention Effectiveness
64
CATIE Efficacy vs effectiveness
Efficacy looks at outcome measured on scale (ex: PAN scale) Effectiveness trial: Real world outcomes
65
CATIE FGA vs SGA conclusions
This was 2005 when 2nd gen coming out No significant diff in effectiveness Poss small sway toward olanzapine but lots of wt gain No significant diff for neg sx or cognitive impairment High rate tx d/c Diff is more in AE rather than therapeutic effects so good to figure out patient preference

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