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Social And Behavioral 2 > Schizophrenia > Flashcards

Schizophrenia Flashcards

1
Q

What is the central deficit/key symptoms in schizophrenia?

A

cognitive impairment - the disorganized thought

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2
Q

What percentage of the population will be affected? gender?

A

less than 1% - more so in males

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3
Q

Which comes firsst? THe cognitive impaitment or the psychosis with hallucinations and delusions?

A

the cognitive impairment

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4
Q

What are some of the affective or “negative” symptoms of SD?

A

apathy, flat affect, withdrawal, social avoidance, poor motivation, self neglect

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5
Q

What are the “positive” symptoms of SD?

A

hallucinations (auditory more often than visual), delusions, paranoia, odd behaviors, poverty of thought

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6
Q

What were the 4 schizophrenia subtypes that are now not used?

A

disorganized, paranoid, catatonic, undifferentiated

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7
Q

Is SD more prevalent in urban or rural settings?

A

urban

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8
Q

Is SD more severe in low SES or high SES?

A

low SES - the “social drift downward”

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9
Q

When is the peak onset for men and for women?

A

men: 17-27
women: 17-37

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10
Q

When during the year are births more associated with SD?

A

late winter/early spring - maybe infection?

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11
Q

Where in the US does more SD occur?

A

higher lattitues - northeast and west

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12
Q

How are the uses of illicit drugs related to SD?

A

They seem to be able tot rigger symptoms in predisposed individuals

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13
Q

What is the life expectancy for people with SD?

A

generally 20 years less than age-matched controls

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14
Q

What NT is increased in SD?

A

DA

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15
Q

Where in the brain does significant brain mass occur in SD?

A

the dorsolateral prefrontal cortex and temporal lobes (note you also lose brain connections)

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16
Q

What is the concordance rate for SD?

A

40-50% in monozygotic twins!

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17
Q

What are four candidate gnes for SD?

A
  1. dysbindin
  2. neuregulin 1
  3. COMT
  4. genes for NMDA and DA receptors in general
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18
Q

Exposure to influenza during what trimester especially increases risk for SD?

A

2nd trimester

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19
Q

Besides influenza, what other viruses may incur a higher risk for SD?

A

borna disease virus, borrelia, toxoplasmosis, retrovirus

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20
Q

Why might SD disease courses be more mild in rural areas?

A

maybe less demand for individual performance, maybe less isolation (counterintuitive but true), more social support etc.

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21
Q

Describe the “expressed emotion” observation for SD course.

A

People do better if their families have low expressed emotion - so they have a calmer environment in the face of disease in compariosn than people who live in a family that has high levels of expressed fear or anger or confusion aboutt he disease

22
Q

Which dopamine receptors are mainly affected by the first gen antipsychotics?

A

D1 and D2

23
Q

Which dopamine receptor mediates most of the side effects like the extrapyramidal effects?

A

D1

24
Q

How is 5HT likely involved in SD as well?

A

it is increased and it stimulates further DA release

25
Q

How is glutamate likely affected in SD?

A

It is decreased, so you have an increase in DA release as well (PCP blocks Glu)

26
Q

How is GABA likely affected in SD?

A

it’s probably decreased in frontal lobe and hippocampus, so it can’t modulate DA and Glu

27
Q

How is Ach affected in SD and what does this result in?

A

nicotinic receptors decreased in frontal, hippocampus, thalamus and striatum - affects memory?

28
Q

What percentage of people with SD smoke? WHy might this be?

A

80-90%

  • could be that it stimulates the nicotinic receptors that are there to decrease symptoms
  • or…the people who hate the side effects of the antipsychotics smoke because it induces metabolism of these drugs
29
Q

How is NE affected in SD?

A

probably lower - may worsen negative symptoms

30
Q

How might the brain’s development lead to SD?

A
  1. early lesion in DA or Glu tracts
  2. loss of gABA function
  3. abnormal apoptosis
  4. reduced synaptic connection formation
  5. decreased BDNF in frontal cortex and increased in hippocampus
31
Q

What symptoms of SD is loss of the superior temporal gyrus (esp on left) associated with?

A

auditory hallucinations

32
Q

What set of symptom s are in part mediated by a dorsolateral prefrontal and limbic system “disconnect”

A

the negative symptoms

33
Q

What group of symptoms is in part mediated by disturbances of the cortex, thalamus, or cerebellum?

A

the positive symptoms

34
Q

An SD brain is more or less adaptable than a normal control brain?

A

less

35
Q

How many of the complex psychotic symptoms and for how long must they be present for the diagnosis of SD?

A

at least 2 (hallucinations, delusions, speech disorganization, idsorganized behavior, neg sx) for over 6 months

36
Q

What should you keep on your differential diagnosis with SD?

A
  1. other psychiatric disorders: mood disorders, autism, etc
  2. substance use disorder
  3. general medical disorder
37
Q

Why should you keep mood disorders on your DD with SD?

A

because 20% of mood disorders have hallucinations

38
Q

What substances should you keep in your DD in particular with D?

A

esp amphetamines and other stimulants, but also cannabinoids, hallucinogens, marijuana and PCP

39
Q

What are some general medical disorders that could present in a similar fashion as SD?

A

brain tumor, metabolic, endocrine, infectious, neurologic issues, drugs - steroids, anticolinergics, disulfiram, or dementia with psychosis

40
Q

When during steroid use is the risk for psychosis greatest?

A

during the taper

41
Q

When do dementia patients look like potential SD?

A

early stages when they develop paranoida

42
Q

What are some other psychotic disorders you should consider with SD?

A 
schizophreniform disorder (when it's less than 6 months)
Schizoaffective disorder
delusional disorder
brief psychotic disorder
schizotypal personality
43
Q

What common endocrine disorder should you rule out for SD?

A

hypo or hyperthyroidism (also adrenal disorder)

44
Q

What was the first antipsychotic created?

A

chlorpomazine (thorazine)

45
Q

Are the first gen antipsychotics more effective against the positive or negatie symptoms?

A

positive only really - the FGAs may actually cause negative symptoms

46
Q

Besides the negative symptoms, what other set of syptoms can be made worse by the FGAs?

A

the cognitive symptoms - sedation and slowing

47
Q

Describe the adverse motor side effects of the FGAs.

A

the acute parkinsons-like symptoms or extrapyramidal symptoms: tremor, gait impairment, slowed movement, rigidity, akathisia
then later on, choreiform movements, tardive dyskinesia, tardive dystonia, etc.

48
Q

What are some non-motor FGA side effects?

A

sedation, GI issues, sexual side effects, urinary retention, weight gain and diabetes

49
Q

What is the only antipsychotic that will work for both the positive and negative symptoms without causing motor side effects?

A

clozapine (clozaril) - it’s a SGA developed in the 90s

50
Q

What’s the rare, but severe side effect you need to be careful of for clozapine?

A

less than 1 % get agranulocytosis

51
Q

Beside agranulocytosis, what are the side effects for clozapine?

A

increased risk for seizures, weight gain and diabetes

52
Q

Why don’t the SGAs cause the extrapyramidal effects?

A

they have a lower D2 blockage and more of a 5HT blockade

Social And Behavioral 2 (18 decks)

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