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PMHNP > Schizophrenia > Flashcards

Schizophrenia Flashcards

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
Q

1st gen effect on pos and neg sx

A

Treats our positive sx (mesolimbic)
Worsens our negative sx (mesocortical)

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26
Q

when a patient stops their 1st gen

A

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

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27
Q

1st gen effect on nigrostriatal pathway

A

movement dec

pseudoparkinsonism is an AE

28
Q

1st gen effect on tuberoinfundibular pathway

A

dec leads to hyperprolactinemia

29
Q

1st gen AE beyond dopamine changes

A

anticholinergic effects (M1)
sedation (H1)
orthostatic hypotension (alpha)
EPS and hyperprolactinemia (D2)

30
Q

threshold for EPS and hyperprolactinemia in 1st gen

A

close/narrow

31
Q

low vs high potency 1st gen

A

Low: More anticholinergic, antihistamine, more alpha 1, but less EPS

High: Less anticholinergic and antihistamine but more EPS

32
Q

What makes atypical antipsychotics different

A

5HT2A receptor

helps mitigate dopamine antagonism

33
Q

What aytpical antipsychotics do to pathways

A

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
Q

EPS and hyperprolactinemia threshold in 2nd gen

A

not as narrow/close due to 5HT2A mitigating by producing more endogenous dopamine

35
Q

atypical antipsychotics pharmacodynamics

A

complex profiles with many receptors

36
Q

2nd gen rx blocking one or more of 3 receptors responsible for causing sedation

What 3 receptors

A

M1
H1
a1

37
Q

2nd gen that inc sedation (3)

A

clozapine
olanzapine
quetiapine

pine is high

38
Q

2nd gen that dont inc sedation (3)

A

aripiprazole
cariprazine
lurasidone

done pip and rip and low

39
Q

cardiometabolic effects of 2nd gen

1+ of 2 receptors

which receptors

A

H1
5HT2C

40
Q

cardiometabolic effects associated with what sx

A

wt gain
insulin resistance

not as common as 1st gen

41
Q

2nd gen that inc cardiometabolic effect (2)

A

clozapine
olanzapine

pines make worse

42
Q

2nd gen that dont inc cardiometabolic effect (2)

A

aripiprazole
cariprazine
lurasidone
ziprasidone

pip rip and done are low (they can but less common)

43
Q

anticholinergic effect of 2nd gen at what receptor and what are the sx

A

M1

urinary retention
constipation
blurry vision/dry eyes

44
Q

2nd gen that inc anticholinergic effect (3)

A

clozapine
olanzapine
quetiapine

so PINE is high

All others do not effect

Note bowel prophylaxis common with clozapine

45
Q

EPS and hyperprolactinemia sx for 2nd gen at what receptor

A

D2 antagonism

46
Q

How to remember which 2nd gen affect EPS/hyperprolactinemia

A

DONE are high
PINE are low

Risperidone, paliperidone, ziprasidone

Clozapine, quetiapine, olanzapine

opposite of others

47
Q

Hypotension effect of 2nd gen at what receptor

A

a1 antagonism

48
Q

Hypotension effect for 2nd gen
Which rx do and dont effect
harder to remember

A

inc sx: clozapine, quetiapine, risperidone, Iloperidone

dec: Brexiprazole, cariprazine, lurasidone

49
Q

QTC prolongation for 2nd gen activity where

A

HERG potassium channels

50
Q

QTC prolongation for 2nd gen activity rx make worse or not

A

inc: ziprasidone, quetiapine, risperidone, clozapine

dec: aripiprazole, cariprazine, brexpiprazole, lurasidone

Note concern if mult rx are positive

51
Q

2 pips and rip are D2 partial agonists so

A

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
Q

Quetiapine is a NE reuptake inhibitor so

A

good use in mood disorders

53
Q

ziprasidone and lurasidone need

A

to be taken with food

54
Q

the only SL 2nd gen

A

asenapine

55
Q

Pimavanserin

A

5HT-SA inverse agonist
no direct dopamine receptor activity
approved for parkinsons dz psychosis because it doesnt affect underlying dz
research in alzheimers

56
Q

Lumateperone

A

D2 and 5HT-2A antagonist
D1 receptor activity so inc glutamatergic transmission

57
Q

clozapine pros

A

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
Q

clozapine cons

A

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
Q

APA guidelines

A

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
Q

canadian guideline differences

A

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
Q

canadian guidelines for Acute exacerbation/relapse prevention

A

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
Q

Australia/NZ guideline differences

A

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
Q

CATIE

A

Clinical Antipsychotic Trials of Intervention Effectiveness

64
Q

CATIE Efficacy vs effectiveness

A

Efficacy looks at outcome measured on scale (ex: PAN scale)

Effectiveness trial: Real world outcomes

65
Q

CATIE FGA vs SGA conclusions

A

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

PMHNP (24 decks)

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