Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2: Neurobiology II > Lecture 10: Psychopathology > Flashcards

Lecture 10: Psychopathology Flashcards

1
Q

epidemiology of mental illness in US adults; who is most at risk

A

21% of adults; 4% have severe impairment
higher in females
higher in younger adults
highest in LGBTQ
racial background results in cultural factor

*drug abuse doesn’t count

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

most common types of mental illness

A

anxiety is most common = 19%

depression is next = 4%

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

types of mental illness

A

emotional - related to limbic system
- internalizing = anxiety/depression
- externalizing = drugs/conduct disorder

psychotic - more association areas involved
- i.e. bipolar or schizophrenia

**mental illness is a spectrum

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

examples of primary vs secondary mental illness

A

autism pt develops mental illness = secondary

cannabis abuse (primary) causes psychosis (secondary)

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

characteristics of mental illness in adolescents

A

most start to show in adolescence

50% of adolescents have some kind of mental illness; 11% have severe impairment

prevalence peaks at 17-18 years

no obvious difference in prevalence with sex BUT females do have different S&S than males

major increases in substance abuse in those with mental illness

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

how does the cerebral cortex develop/mature

A

matures from posterior to anterior and right to left

posterior portion of the brain is like the gas pedal (contains limbic system); everything based on emotion

anterior portion (prefrontal lobe) is like the brake; more sound/logic decision; stop impulses

L dorsolateral prefrontal cortex (last to develop) = working memory and executive functions

ratio of gray matter to white matter increases?

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

3 critical stages of synaptogenesis

A

1st: sensorimotor, 2 months before birth and peaks 1 month after

2nd: frontal, parietal, temporal association cortex; peaks around 8 months of age

3rd: prefrontal cortex develops last, peaks around 2 years of age

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

which critical stage is the fastest

A

1st/sensorimotor

fastest in utero

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

all 3 critical stages peak by what age

A

2 years

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

frequency of firing at peak synaptogenesis vs peak pruning

A

peak synpatogenesis = 4.3 million per min

peak pruning = 0.072 million per minute (lasting longer = maturation)

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

describe the functional connections and myelination of the brain during critical stages

A

whole brain has less gray matter and more white

prominent in adolescent period

males have 20% more brain mass than females; not necessarily a good thing

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

describe what happens to the brain with marajuana

A

increase in non functional connections

more connections but they are not useful and inhibit the good connections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

describe the stages of brain development from 1 month to 9+months

A

1 month = internal capsule, projection fibers (coordination with different body parts)

2 months = long association fibers (inter regional?)

5-6 months = long association fibers (inter regional?)

7-9 months = commissure and short association fibers (regional functioning and cross talking)

over 9 months = all fibers start to mature

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

pathophysiology of ASD

A

altered functional connections

decreased long distance/subcortical connections = compromised integration functions

increased short distance association fibers (focus a lot on details but not the context of the whole situation)

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

core diagnostic criteria for ASD

A

loss of social cognition
increase of repetitive behavior

females - different S&S (more depression like)

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

prevalence of ASD

A

1-3%

17
Q

prevalence of different mental illnesses secondary to ASD

A

10-50% = depression
80% = anxiety
30% = bipolar
28-39% = childhood onset schizophrenia

over 75% of ASD pts have one or more mental illness

18
Q

what is a phenotype and what is the implication of this

A

universal formula

gene(s) + environmental factor(s) = phenotype(s)

some diseases are genetically predisposed; some can be managed (PKU) but some cannot (HD)

environments can promote activation or inhibition of certain genes

genetic component varies from 0-100%; decides how much of it you can manage/control

19
Q

describe the types of onset of ASD

A

congenital = mainly prenatal and during critical development stage I (genetic/environmental)

postnatal = trauma to amygdala, temporal lobe, cerebellum, etc (environmental)

20
Q

diagnosis of schizophrenia

A

2 of the following:
- delusion (thoughts)
- hallucinations (perception)
- disorganized speech

21
Q

pathology implications of those with schizophrenia

A

enlarged lateral and 3rd ventricles

atrophy of frontal lobe association cortex
- frontal eye field problems; can’t smooth track
-delusion
- disinhibition function
- trouble with working memory (LDLPFC)

22
Q

what S&S of schizophrenia are caused by temporal lobe atrophy

A

auditory hallucinations

disorganized speech; fluent aphasia/talking to the hallucination

loss of frontal temporal synchrony

loss of sensory gating (reactions are not decreased after 1st sensory stimuli is perceived)

23
Q

how much of schizophrenia is genetic vs environmental

A

50% for both

24
Q

congenital vs postnatal

A

congenital
- lacking nutrition
- drug abuse
- viral/bacterial infection of embryo/fetus

postnatal
- drug abuse (i.e. MJ)
- trauma to frontal/temporal lobe

25
Q

types of mental illness with critical stage III

A

control of emotion

internalizing = depression and anxiety

externalizing = drug abuse and behavior

antisocial personality disorder = 3.5% in US

adolescents highly vulnerable to drug abuse due to brains not being fully developed yet

26
Q

describe the mechanism of drug abuse and addiction

A

2 dopaminergic pathways initiated in middle brain
- substantia nigra/caudate and putamen = motor/cognition/emotion
- ventral tegmental/nucleus accumbens = reward seeking path

almost all addictive drugs affect the reward seeking path

27
Q

what happens in the brain with binge drinking

A

decreases corona radiata contents (all axonal bundles of brain)

affects cognition, emotion, and behavior

compromises temporal lobe functions; 10% volume decrease in gray AND white matter

28
Q

describe the negative effects of cannabis on the brain

A

compromises frontal lobe development
- decision making
- increases connections = false memory (emotional and psychotic mental illness)

29
Q

describe the negative circuit of marajuana use

A

abuse = delay in prefrontal development = controls emotional development = decides future orientation = leads to more future abuse

30
Q

features of depression and clinical presentation

A

chronic feelings of sadness and hopelessness; loss of interest in activities

clinical presentation:
- can’t accept negative feedback
- ruminating on negative results

31
Q

describe the loss of functional connections with depression/ areas of the brain affected

A

cingulate gyrus - negative emotions

L dorsolateral prefrontal cortex - decreased inhibition function

Amygdala - decreased aversion to neg stimulus

32
Q

medication management for depression

A

SSRIs

incidental findings

tryptophan metabolism

33
Q

purpose of cognitive behavior therapy for depression

A

reconnection of ACC and L DLPRC

34
Q

non-invasive vs invasive treatment for depression

A

repetitive transcranial stimulation: rTMS activates L DLPFC

deep brain stim: DBS inhibits neg circuitry

vagus n stim: balance HPA axis stress and improve alertness/arousal

35
Q

what can PT do for depression pts

A

30 min daily high intensity exercise is better than meds and cognitive behavior therapy

36
Q

describe the longitudinal impairment from early life stress and how it relates to depression

A

through hypothalamus pituitary gland pathway (HPA axis)

“double crush theory”

increased cortisol and sympathetic nervous system activates: sensitization

recall SNS and sleep cycle; depression is worse in winter due to decreased sunlight exposure

37
Q

describe pathophysiology of HD and the implications

A

100% genetic predisposition

degeneration of basal nuclei and cortex (caudate is worst) = subcortical dementia

impairments of cognitive, sensorimotor, and emotional functions

38
Q

prefrontal lobe injury results in what

A

psychopathological presentation

i.e. Phileus gage L DLPFC; compromised with psychopathology but still functional

can happen with stroke, viral infections, etc

39
Q

effects fo physical activity/PT on mental illness

A

large effects on depression and schizophrenia

moderate effects on aerobic capacities

small effects on anthropometry

Year 2: Neurobiology II (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions