Schizophrenia Flashcards

1
Q

onset

A

male 19-25

female 24-32

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

causes

A

genetic
dopamine imbalance
virus in 2nd trimester
abnormal neuronal pruning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what neuronal pruning

A

transitioning from infancy to child need to prune some neurons
in schiz too many pruned

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

problems with neuronal ____

A

communication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

dopaminergic excess in

A

mesolimbic and mesocortical areas correlate with psychotic symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

dopaminergic shortfall in

A

frontal lobes correlates with negative and cognitive symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

positive symptoms

A

things that shouldnt be there
hallucination, delusion(false beliefs)
paranoria, agitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

negative symptoms

A

should be there but missing

lack ofpleasure, immobile facial expression, poverty of speech, cognitive impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

functional impairment often related to

A

impact of negative and cognitive symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

first ___ years after diagnosis critical

A

5 years bc impairment corrlated with time and severity of porrly controlled symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

major goals of therapy

A

prevent harm
patient control
restore contact with reality
prevent relapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

components to treatement

A
pharamcotherapy 
vocational therapy 
socail therapy 
support for housing 
substance abuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

initial treatment for psychosis

A

benzos
antipsychotics maybe
positive symptoms are the targets - anxiety, agitation, harm reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

acute agitation medication

A

benzos
potentially FGA and benzo
FGA + benzo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

FGA used in acute agitation

A

haloperidol - works quickly, reliable

zuclopenthixol - sedating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

stabilization phase timeline for improvement of positive symptoms

A

slow erratic and gradual improvement over 6-12 weeks
in 1-3 weeks decreased intensity of hallucinations, paranoria, improved self care, anxiety, and socialization
3-12 weeks further improvement can discharge when safe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

stabilization phase improvement for negative symptoms

A

much slower response compared to positive
more resistant to meds
improvement attained with sustained improvement (keeping someone from becoming acutely ill)

18
Q

which drugs come as depot meds

A

haloperidol, flupheazine, zuclopenthixol
RISPERDONE-microspheres
paliperidone

19
Q

benefit of injection

A

enable adherence

20
Q

first gen antipsychotics block

A

dopamine receptor D2

21
Q

second generation antipsychotics block

A

serotonergic and dopaminergic transmission

22
Q

second gen antipyschotic side effect difference

A

less movement disorders but more metabolic disorders

23
Q

examples of low/med potency first gen antipsychotics

A

chlorpromazine
loxapine
perphenazine

24
Q

examples of high potency first gen antipsychotic

A

haloperidol

fluphenazine

25
Q

what does potency refer to and idicate

A

refers to D2 receptor binding affinity for FGA

all equally effective just require a diff dose

26
Q

first gen antipsychotic AE

A
anticholinergic - muscarinic antagonist
cardiovascular - alpha 1
sedation - histamine antagonist
neurologic - movement disorder from D2 antagonism in nigrostriatum. decreased seizure threshold 
prolactin elevation - D2 antagonism
27
Q

problems with prolactin elevation in males and females

A

men - gynecomastia, sexual disfunction

women - menstrual disturbance, breast enlarged, hirsutism

28
Q

what is neuroleptic malignant syndrome

A

rigid, tachycardia
increased temp, altered consciousness
can be life threatening

29
Q

examples of some extrapyramidal movement disorders

A
dytonic reactions - uncoordinated
akathisia - pacing cant sit still 
akinesia - decreased muscualr movement
rigidity 
pisa syndrome - tilted 
tremor 
tardive (late appearing) dyskinesia
30
Q

drugs to manage EPS

A

anticholinergics - benztropine
propranolol for akathisia
benzo

31
Q

why is PK not that useful for antipsychotics

A

little relevance to antipsychotic effects, these effects due to marinating effect of prolonged presence of the drug in the body not based on levels

32
Q

PK can be useful for detecting

A

side effects

33
Q

problems with FGA

A

treatment resistance
negative and cognitive symptoms porrly respond
EPS and other adverse effects

34
Q

benefits of SGA

A
less EPS 
improved impact on negative symptoms 
different adverse effects
more indications 
no prolactin effects
no upregulation of D2 receptors bc loose binder comes on and off
35
Q

examples of SGA

A
cloazapine 
risperidone 
olanzapine 
quetiapine 
ziprasidone
36
Q

affinity for clozapine

A

high 5HT2 affinity and low D2 affinity
offsets to EPS effect
HI, 5Ht2, alpha1, muscarinic, D4, beta, D1, D2, alpha2

37
Q

short comings of clozapine

A
agranulocytosis 
seizure risk 
weight gain and metabolic issues
weekly blood work 
high cost
38
Q

clozapine agranulocytosis monitoring

A

must have mandatory CBC weekly
reaction is idiosyncratic
reversible if detected early

39
Q

AE of clozapine

A
drowsy 
hypersalivation 
tachycardia
hypotension 
dry mouth 
tremor 
nausea
fever
weight gain
40
Q

is there a therapeutic serum range for clozapine

A

yes

41
Q

role of clozapine

A

not 1st line
NOT FIRST LINE
best results in treatment resistance and suicide risk
try for at least 6 months