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PSYC211 > Mental disorders > Flashcards

Mental disorders Flashcards

1
Q

Why can’t we assume that mental disorders are discrete/unitary diseases

A

-too much heterogeneity within diagnostic categories (ex: 2 ppl with the same disorder can have totally different symptoms)
-too much comorbidity across categories (being diagnosed with more than one mental disorders)
-continuity with normality (because of healthy normal groups variance, it is hard to establish “diagnostic lines”)

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2
Q

Why do gene variants that increase the risk of developing a psychiatric illness persist in the population? Why haven’t they been selected out?

A

Many of the gene variants associated with increased risk of mental illness regulate brain development and neural plasticity.
(neuronal migration in vitro, rules of plasticity, learning, memory, etc etc)

Their expression in the brain gives rise to altered patterns of neural activity throughout the brain. The problematic protein variants slightly alter the dynamic interactions of the thousands of proteins expressed in the brain across different cell types during development and maturation.

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3
Q

What are the components of the theory explaining the persistence of the genes that cause mental disorders? (explain)

A

Mutation-selection balance
→ mental disorder susceptibility genes are continually being selected out through evolution. But NEW mutation keep arising.

Inherited gene mutations
→mutations stick around for a long time. Brain is robust, allowing genetic variations to accumulate in the population if the individual mutations are not too severe

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4
Q

How do bad gene mutations affect the brain?

A

Do not directly cause a disease…they can collectively compromise the evolved interactions of everything in the brain, reducing the overall robustness of brain development and function

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5
Q

Why can identical twins have so much brain differences even if they have the same dna?

A

unavoidable randomness at the molecular level→ impacts how the brain develops
ex: main avec plein de crayons de couleur

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6
Q

What can body symmetry tell us about brain development?

A

Indicative of robustness of the genetic instructions
… clearer instructions

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7
Q

What does not correlate with body symmetry?
a. intelligence
b. physical health
c. physical attractiveness
d. symptom expression in schizophrenia

A

d.

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8
Q

What are the advices to maintain a healthy brain

A

Same as healthy body…(stay active, nutrition, stress and blood pressure reduction, good sleep habits, limit alcohol and avoid tobacco/drugs)

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9
Q

Define schizophrenia

A

Mental disorder characterized social withdrawal, disorganized thinking, abnormal speech, and an inability to understandreality.

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10
Q

Compare the different types of schizophrenia symptoms

A

Negative: the absence of behaviors (lost)
→ex: social withdrawal, reduced emotional expression, poverty of speech, and reduced motivation
Typically emerge 1st…then cognitive…then positive

Cognitive: disorganized and irrational thinking, deficits in learning and memory, poor abstract thinking, and poor problem solving

Positive: the presence of behaviors (not here before) →ex: delusions of persecution/grandeur/control, hallucinations

[Neurological: for example poor control of eye movements and unusual facial expressions]

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11
Q

How can we explain the high percentages of schizophrenia cases in male early adulthood vs female menopause?

A

Seemingly a correlation with hormone signaling.

In men, period associated with the end of myelination.(occipital–prefrontal btw)

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11
Q

How can we explain the high percentages of schizophrenia cases in male early adulthood vs female menopause?

A

Seemingly a correlation with hormone signaling.

In men, period associated with the end of myelination.(occipital–prefrontal btw)
→hypothesis: born with schizophrenia, reveals itself when myelination ends
→other one: pruning is too aggressive, too much synapses are destroyed

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12
Q

What is synaptic pruning?

A

Between early childhood and adulthood, elimination of useless synapses.

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13
Q

Name some believed environmental factors contributing to schizophrenia

A

mother’s nutrition during pregnancy
mother’s stress during pregnancy
certain infections (particularly during pregnancy)
birth month
being raised in a city
childhood trauma
social isolation
perinatal hypoxia / brain damage

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14
Q

What is the cause of schizophrenia?

A

environmental and genetic factors

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15
Q

What does heritability measure?

A

The fraction of phenotype variability that can be attributed to genetic variation
The amount of variation attributed to genetics→ the amount of variation that would be eliminated if everyone had the same genes.
(but even if no genetic variability, there is still the impact of environment )

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16
Q

How does the risk of developing schizo varies as we get further away from family bonds..

A

both parents 50%…one 13%…sibling 8%

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17
Q

Which factor, frequently comorbid with autism and intellectual disabilities, is an alleged cause of schizophrenia

A

rare gene copy number variations (duplicated or missing genes)..around 5% of cases are attributed to this

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18
Q

What is the seasonality effect?

A

A disproportionately large number of schizophrenic patients being born in February, March, April, and May

→suggests that something is happening in the womb few months earlier (ex: colder, ppl go inside and are more likely to get infections)

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19
Q

Name some factors affecting development in utero and leading to schizophrenia.

A

Season of birth, viral epidemics, population density, parental smoking

→Higher number of schizophrenic births in late winter and early spring if the temperature was lower than normal during previous autumn (keeps people indoors and favors transmission of viral illnesses)
→Three times more prevalent large cities >rural areas (transmission of infectious illnesses is facilitated by increased population density)

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20
Q

Monochorionic vs dichorionic twins

A

share one placenta vs individual placenta (identical twins either way)

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21
Q

How can prenatal environments of identical twins affect schizophrenia rates

A

Prenatal environments of monochorionic twins + similar than di
Concordance rate for schizophrenia ↑ for monochorionic twins

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22
Q

Name the behavioral and anatomical evidence indicating that abnormal prenatal development is associated with schizophrenia

A

Behavioral: Children who go on to develop schizophrenia display less sociability and deficient psychomotor functioning as kids.

Anatomical: Minor physical abnormalities are often seen in children who go on to develop schizophrenia →ex: partial webbing of the two middle toes and a high-steepled palate.

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23
Q

What is the main treatment for schizophrenia

A

Medication, often combined with psychological and social supports

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24
Q

How do antipsychotics/neuroleptics work?

A

Block dopamine D2 receptors
→relieve positive symptoms

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25
Q

In contrast with neuroleptics, what are the effects of dopamine receptors (ex: crystal meth)

A

Temporary activation on the positive symptoms of schizophrenia in ppl who do not have the disorder

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26
Q

What is the Dopamine Hypothesis

A

Excessive dopamine D2 receptor activity, particularly in the nucleus accumbens (striatum), underlies the positive symptoms of schizophrenia.

*some aspects of reinforcement learning is disrupted in schizophrenic ppl

*too much dopamine in the basal ganglia

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27
Q

What is the presumed cause of the negative symptoms of schizophrenia?

A

Hypo frontality: decreased activity of frontal lobes (+ dorsolateral prefrontal cortex, may relate to hypoactivity of local dopamine D1 receptors)

*too little dopamine prefrontal cortex

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28
Q

What are the effects of atypical antipsychotic clozapine

A

(in monkeys) simultaneously decrease dopamine levels in the striatum and increase dopamine levels in the prefrontal cortex

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29
Q

What are the goals of atypical antipsychotic

A

[made after 1990]. Do more than block D2 receptors

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30
Q

What are the effects of atypical antipsychotic aripiprazole

A

Partial agonist at the dopamine D2 and D3 receptors. It is thought to reduce dopamine receptor activity in the striatum (nucleus accumbens) but boost it in the prefrontal cortex.

31
Q

What is a partial agonist?

A

Drug with very high affinity for a receptor but it activates it less than the normal ligand does.
can act as an agonist in regions of low concentration of normal ligand and as antagonist in regions of high concentrations

32
Q

What is the autistic spectrum disorder?

A

Wide range of developmental disorders that are characterized by troubles with social interaction and communication, and by restricted and repetitive behavior.

33
Q

What are the categories of symptoms that characterize autism

A

1st: trouble with social interactions and communication (verbal/nonverbal)

2nd: restricted/obsessive and repetitive behavior.

34
Q

Autism is often a comorbid disorder. Name some common disorders diagnosed with autism

A

Intellectual disabilities, seizure disorder, sensory processing issues

35
Q

Name some “typical” behaviors of autistic children

A

Not caring whether they are held or not; arch their backs when picked up
Call the kid’s name, does not consistently turn to look at you
Does not look in the eyes

36
Q

What is the cause and heritability of autism?

A

genetic and environmental factors,
heritability around 70%
Many cases linked to spontaneous rare gene mutations that have severe effects
→ chromosomal abnormalities (ex: deletions, duplications or inversions)

Other cases associated with rare multigene interactions
→ ex: neurons don’t migrate to the right spot, cell types do not have the same numbers, synapses are different in terms of excitatory/inhibitory balance

Some cases linked with viral infections during pregnancy

37
Q

How are the mild forms of autism called and what are the typical symptoms

A

deficient or absent social interactions and repetitive and stereotyped behaviors along with obsessional interest in narrow subjects.
don’t understand social cues and do not know what they are doing wrong

38
Q

Explain the sex differences in autistic disorder

A

-heterogametic sexes tend to have more variance/variability in different aspects
-2:1 when autism + intellect disability
-7:1when high-functioning

39
Q

Hypotheses for the cellular and molecular bases of early brain overgrowth include the following

A
  • Altered neuronal migration during early gestation
  • Abnormal formation of synapses and dendritic spines
  • Overconnectivity in key brain regions
  • Unbalanced excitatory–inhibitory neural networks
40
Q

What do fMRI studies show in the brains of people with autism

A

marked abnormalities in brain activity, ex: little to no activity in the fusiform face area of autistic adults looking at human faces

41
Q

How can autism be treated

A

goals: lessen impacts

  • Intensive, sustained special education programs , behavior therapy early in life (self-care, communication, and life skills)
    -Medications generally do not address the core symptoms, but often help reduce the irritability, inattention, and repetitive behaviors. comorbidity
    examples
    anticonvulsants (↑ GABA receptor activity)
    antidepressants (↑ serotonin receptor activity)
    antipsychotics (↓ dopamine receptor activity)
    stimulants (↑ dopamine receptor activity)
42
Q

Define affect and mood disorder

A

Affect: feelings/emotions

mood disorder: 1.bipolar 2.major depressive disorder

43
Q

What is the difference between bipolar and major depressive disorder.

A

difference in mania

bipolar→ cyclical periods of mania and depression

MDD→ unremitting depression (or periods)..no alternation with mania

environmental factors

44
Q

What is mania

A

[Episodes] characterized by sense of euphoria that does not seem to be justified by circumstances→ usually nonstop speech and motor activity

45
Q

What can we use to treat bipolarity?

A

Lithium.
Once mania is eliminated, depression usually does not follow.
Unknown mechanism

46
Q

What are the biological treatments for MDD

A
  • Drugs that increase serotonin and/or norepinephrine signaling by inhibiting their enzymatic breakdown (e.g., monoamine oxidase inhibitors, MAOi) or by blocking their reuptake (e.g., tricyclics and serotonin specific reuptake inhibitors, SSRIs).
  • Ketamine (NMDA glutamate receptor blocker)
  • Electroconvulsive therapy (ECT)
  • Deep brain stimulation
  • Transcranial magnetic stimulation
  • Vagus nerve stimulation
  • Bright-light therapy (phototherapy)
  • Sleep deprivation
47
Q

How do tricyclic antidepressants work ?

A

Inhibits reuptake of serotonin and norepinephrine but also affects other neurotransmitters

48
Q

How do SSRI work ?

A

Inhibit the reuptake of serotonin without affecting the reuptake of other neurotransmitters.

49
Q

How do SNRI work ?

A

Specifically inhibits reuptake of norepinephrine and serotonin without affecting reuptake of other neurotransmitters.

50
Q

What is the monoamine hypothesis?

A

Idea that depression is caused by insufficient monoamine receptor activity (serotonin, ne, dopamine)

(depression symptoms are generally not relieved by

51
Q

What is the monoamine hypothesis?

A

Idea that depression is caused by insufficient monoamine receptor activity (serotonin, ne, dopamine)

(depression symptoms are generally not relieved by strong dopamine agonists–>research focus on ne and serotonin)

52
Q

What could happen to someone with a low-tryptophan diet?

A

low-tryptophan diet and then a tryptophan-free amino acid “cocktail” lowers brain tryptophan levels and consequently decreases their synthesis of serotonin (5-HT). This tryptophan/serotonin depletion procedure can elicit a depressive episode in people susceptible to depression
(susceptible people )

53
Q

What did functional imaging scans tell us about the role of the prefrontal cortex in depression?

A

One area of the anterior cingulate cortex (the subgenual region known as area 25) becomes less active after successful treatments

54
Q

DBS

A
55
Q

Describe the electroconvulsive therapy (ECT)

A

Used therapeutically to alleviate severe depression and bipolar disorder.

Seizures are electrically induced by applying brief electrical shocks to the head

In contrast to the delayed therapeutic effects seen with monoamine related treatments, the effects of other treatments (including ECT, lithium, DBS, VNS, and sleep deprivation) are more rapid. The seizures induced by ECT often reduce symptoms within days

56
Q

What can explain the fact that total sleep deprivation has an antidepressant effect

A

a chemical builds up during waking hours that has some antidepressant effect, and it gets cleared away during sleep.

REM sleep deprivation also works, although more slowly, over the course of several weeks (similar to SSRIs)

57
Q

Describe the sleeping habits of a depressed individual

A

Shallow, fragmented sleep. They tend to awaken frequently, especially toward morning.

In general, they spend more time in stage 1 sleep and less time in deep, slow-wave sleep (stages 3 and 4).

They also enter REM sleep soon after falling asleep, much earlier in the night in comparison to other people

58
Q

Describe the types of anxiety disorders

A

General anxiety disorder: excessive anxiety and worry serious enough to cause disruption of their lives

Social anxiety disorder: excessive fear of being exposed to the scrutiny of other people that leads to avoidance of social situations in which person is called on to perform

Panic disorder: episodic periods of severe and unremitting terror. Includes symptoms such as shortness of breath, irregularities in heartbeat, and other autonomic symptoms, accompanied by intense fear

Agoraphobia: Fear of being away from home or other protected places

→ ((((Anticipatory anxiety: Fear of having a panic attack promotes anticipatory anxiety that sometimes leads to the development of agoraphobia)))

59
Q

Describe anxiety disorder prevalence

A

12% people…around 2x more in females

60
Q

What are the causes of anxiety disorders?

A

genetic + environmental (ex: childhood history) factors.

61
Q

What parts of the brain are involved in anxiety disorders?

A

amygdala and prefrontal cortex
ex: Adolescents with generalized anxiety→ +activation amygdala, - activation ventrolateral prefrontal cortex when looking at angry faces

62
Q

What is used to treat anxiety disorders

A

-Lifestyle change
- CBT
- Medication →ex: benzodiazepines

63
Q

What are the 4 main groups of OCD symptoms

A

symmetry, cleaning, hoarding (every possession is valuable, cant throw things away ), forbidden thoughts (deviant nature, intrusive thoughts)

64
Q

Compare compulsions vs obsessions

A

obsessions: recurrent, unwished thoughts

compulsions: behaviors seeking obsession-related anxiety

most adults realize that their behaviors do not make sense

65
Q

What is the incidence of OCD cases

A

2%
Higher rates for women, but later diagnostic for them

66
Q

What are the causes of OCD

A

genetic (50% of variability) and environmental factors (ex: child abuse, adverse events, even infections)

67
Q

How is OCD treated

A

counseling, CBT, exposure-prevention

pharmacology : SSRIs

68
Q

OCD can appear after brain damage. In what parts,,,ok tu comprends

A

basal ganglia, cingulate gyrus, prefrontal cortex

69
Q

What brain activity particularity can we see in OCD patients

A

+ act frontal lobes and striatum

70
Q

what is cingulotomy

A

cutting fiber bundle between PFC and anterior cingulate

71
Q

What is ADHD

A

characterized by problems paying attention, hyperactivity, or difficulty controlling (inhibiting) behavior in an age-appropriate manner.

72
Q

What are ADHD symptoms

A

reckless and impetuous behavior
act without reflecting
let interfering activities intrude into ongoing tasks
have difficulty withholding a response

73
Q

How can we treat ADHD

A

counseling and ++ medication.
often stimulants that raise dopamine levels by blocking or reversing the dopamine reuptake transporter
+ dopamine-→this is important ok focus

74
Q

What are the 2 branches of stress activation

A
  1. sympathetic branch of the ANS
  2. adrenal glands activation
75
Q

What are the stress hormones

A

→→Glucocorticoids
Help to break down and convert proteins into glucose, make fats available for energy, increase blood flow, suppress secretion of sex hormones and stimulate behavioral responsiveness
Glucocorticoids have other physiological effects, too, some of which are not well understood. Almost every cell in the body contains glucocorticoid receptors, which means that few of them are unaffected by these hormones.

→→Cortisol

76
Q

secretion of glucocorticoids is controlled by the hypothalamus. what are the steps leading to secretion

A

In response to stress, the hypothalamus starts a chain of events by releasing CRH/CRF (corticotropin-releasing hormone/factor).

CRH stimulates the pituitary to secrete ACTH (adrenocorticotropic hormone).

ACTH stimulates the adrenal gland to produce glucocorticoids.

PSYC211 (5 decks)

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