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Neurosciences > Exam3Lec1PsychiatricDisorders > Flashcards

Exam3Lec1PsychiatricDisorders Flashcards

1
Q

Are there behaviors that are universally abnormal?

A

NO

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2
Q

What are three topics together that contribute to the definition of “abnormal”

hy

A

Infrequency
Norm violation
Personal suffering

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3
Q

What is infrequency?

hy

A

Those behaviors displayed by the greatest number of people are considered normal. Statistical infrequency considers behaviors that is atypical or rare to be abnormal

some behaviors that is rare such as high IQ, but is not dysfunctional, therefore, statistical infreq alone is not adequate

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4
Q

What is norm violation?

hy

A

People who behave in ways that is bizarre, unusual, or disturbing enough to violate social norms or cultural rules termed abnormal

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5
Q

What is personal suffering?

hy

A

Psychological problems causing distress require treatment. Because some people with disorders may not experience distress, personal suffering cannot be the only criterion for abnormality

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6
Q

How are psychological disorders diagnosed?

on study guide

A

Mental disorders are diagnosed according to the DSM-V (diagnostic and statistical manual of mental disorders)

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7
Q

What is the goal of diagnosing?

A
  • Help identify appropriate treatment for clients
  • To accurately and cosistently group pts with similar disorders (for research)
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8
Q

What is the definition of psychologcal disorders?

A

Significant disturbances that affect cognition, emotion regulation, or behavior that results in a dysfunction

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9
Q

What are 3 limitations of diagnosing mental disorders?

A

Validity and Interrater reliability and cofounders

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10
Q

Nearly ____ US adults live with a mental illness.

A

1 in 5

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11
Q

What is the diathesis-stress model?

hy

A

It is diathesis (vulnerability) + stressors = a neuropsychiatric output (disorder)

stres and vulnerbaility go hand in hand, With a low stress level, you typically have a low degree of disorder. With increasing stress level and diathesis present you start to see more degree of disorder

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12
Q

What can be classified as diathesis (vulnerability)?

hy

A
  • Genetic factors
  • Biological characterisitcs
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13
Q

What can be classified as stressors?

hy

A
  • Traumatic life events
  • negative family life
  • economic
  • environment
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14
Q

What is a mood disorder?

ly

A

A distortion or inconsistency of ones emotional state or mood with their circumstances that interferes with normal fxns.

Mental illness results from the combo of biology and experience

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15
Q

What is Major depressive disorder?

ly

A

A mood disorder characterized by at least one major depressive episode

absence of mani or hypomanic states (bipolar disorder)
absence of happiness is a more reliable symptom than increased sadness

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16
Q

What four things is MDD is linked to?

A
  1. Corticolimbic system (amygdala and PFC)
  2. Serotonin
  3. Dopamine
  4. Norepi
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17
Q

What are the risk factors for depression?

study guide

A
  1. Biological differences: physical changes in the brian (corticolimbic circuit)
  2. Brain chemisitry: regulation of NT and their effect on mood stability
  3. Hormones: changes in the body’s balance of hormones may be involved on causing or triggering depression
  4. Inherited traits: depression is more common in ppl whose blood relative also have this condition
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18
Q

What is hyperactive in MDD and what does it predict?

A

Amygdala is hyperactive and it predicts symptom severity

you see higher amyg activity

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19
Q

The connectivity between the amygdla and the mPFC for MDD is increased or decreased?

A

decrease in functional activity between the amy and the mPFC

as we have lower connectivity we see more symptoms

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20
Q

What is the monoamine hypothesis for MDD ?

hy

A
  1. Drugs used for other purposes, like reserpine for hypertension, can cauuse depression-like symptoms. These drugs deplete serotonin, dopamine, and norepinephrine.
  2. Drugs that inihibit MAO, like isoniazid for TB can relieve depression symptoms

this hypotheiss was reionforces by successes of using monoamine targeting drugs for the treatment of depression

21
Q

Explain then serotonin hypotheisis for depression

A

When given an antidepressant drug it was discovered that there was increasing serotinin levels outside the cell and decreasing depressive symptoms

depleted levels of serotonin at the synaptic cleft can lead to incr depressive sympotms, Treatment with SSRIs/SNRIs can reverse this (incr serotonin lvls)

22
Q

What is the serotonin gene linked to depression?

A

SERT: a gene indentified through candidate studies to have variants that incr susceptibility for depression.

controls the serotonin transporter proteins
contols the ability for the axon to reabsorb the NT after its release

23
Q

____ of the SERT gene are associated with an incr likehood of depression after stressful events

hy for exam

A
  • 2 short forms

s/s

incr vulnerability to experience depression w/ that gene environment and after stressful events

24
Q

Do SSRI’s have high or low efficacy and why?

A

Low because 50% of ppl show a good response within weeks after use of antidepressant drugs and 30% respond to a placebo

depression isnt just the result of low serotonin lvls, bc depressed ppl can have normal lvls of serotonin

25
Q

True or false: Antidepressants alter synpatic acitivity quickly but the effects on behavior are not derived until weeks later.

A

True

26
Q

How can SSRIs for MDD restore balance to the corticolimbic system?

A

SSRIs can decr amygdala hyperactivity and incr functional connectivity between amygdala and mPFC

evidence where pt are getting biological changes not just neurological changes

27
Q

What is schizophrenia?

A

Loss of executive control of emotional responses and information processing

28
Q

What are the symptoms of schiz?

A

They have both positive and negative symptoms in addition to cognitive impairment.

include severely disturbed thinking, emotion, perception, and behavior which impairs a persons ability to communicate and function on a daily basis.

29
Q

Definition of positive sympotms and examples

A

Positive symptoms: “Positive refers to overt symptoms that should not be present

EX: hallucination, delusion, disorganized thought

30
Q

Definition of negative symptoms

A

Negative symptoms: “negative” does refer to a person’s attitude but instead to a lack of characteristcs that should be present.

31
Q

What are examples of negative sympotoms with their respective medical terms.

A
  1. reduced speech (alogia)
  2. social withdrawl (asociality)
  3. lack of facial and emotional expression (affective flattening)
  4. decr ability to find pleasure (anhedonia)
  5. no ability to begin and sustain activities (avolition)
32
Q

Definition of Cognitive deficits and examples

A

Cognitive deficits: difficulties with following aspects of cognition can make it hard to live a normal life or earn a living
EX:memory, atttention, planning, decision making

33
Q

What is schiz linked to?

A

Linked to changes in spine density in Glu/GABA neurons in the corticolimbic system (dIPFC).

neurotransmission of Glu/GABA and dopmane have been shown to be impt
dont confuse with mPFC

34
Q

What are the risk factors for schiz?

study guide

A
  1. Genes
  2. Environment ( exposure to viruses, problems during birth)
  3. Different brain chemistry and structure
  4. Imbalance in dopamine and glu/GABA
35
Q

What gene controls the rate of generation of new neurons in the hippocampus and is disrupted in Schiz?

A

DISC1

other genes are imp for synaptic plasticity and brain developmemt (AMPA, NMDA, and mGLU receptos)

36
Q

What two things contribute to changes in the corticolimbic system with schiz?

hy

A
  1. Lower working memory capacity
  2. Structural abnormalities in the DiPFC
37
Q

At low and high levels of working memory, how is the dIPFC activity affected for schiz?

hy

A

At low levels of working memory: increased dIPFC activity
At high levels of working memory: decreased dIPFC activity

38
Q

What are the structual abnormalities in the diPFC that is linked to schiz?

A
  • Reduced spines that connect b/w glutamatergic and GABAergic neurons
  • Defects in dopaminergic signaling
  • Abnormal development of the dIPFC
39
Q

Do you have overt or reliable neuron death with schiz?

A

NO, you have reduced spine density, especially on Glu and GABA neurons in the diPFC.

nnumber of neurons are the same but the communication is difff b/c you have reduced spine density

40
Q

Explain the neurodevelopment hypothesis for schiz

hy

A

Abnormalities in the prenatal development of the nervous system can lead to subtle abnormalities of brain anatomy and major abnormalities in behavior
1. Abnormalities from genetics, trouble during prenatal development, birth, or early postnatal development
2. Several kinds of prenatal or neonatal difficulties are linked to later schiz
3. ppl with schiz have minor brain abnormalities that originate early in life

41
Q

What are the limitations of the neurodevelopmental hypothesis for schiz?

hy

A
  • Evidence suggests more than one “hit” required
  • Does not account for genetic and environmental effects that clearly influence the disorder
42
Q

Explain the glutamate hypothesis for schiz

hy

A
  • Genetic link: genetics variants of many genes associated with glutamatergic neurotransmission
  • Postmortem studies show abnormalities in the connections between glutamateric and gabergic neurons in the dIPFC and b/w dIPFC and other cortical regions
  • Schiz is associated with lower than normal release of glutamate and fewer receptors in the prefrontal cortex and hippocampus
43
Q

Explain the dopamine hypothesis for schiz

hy

A
  • Genetic link: genetic variant DRD2 (dopamine receptor) identified
  • Substance-induced psychotic disorder characterized by hallucinations and delusions resulting from large repeated doses of amphetamines and cocaine prolonging activity of dopamine
  • Antipsychotics block dopamine receptor
44
Q

What are the limitations of the dopamine hypothesis for schiz?

hy

A
  • Does not explain cognitive defects or psychomimetic effects of activation of other neurotransmitter pathways.
  • Levels of dopamine and its metabolites are relatively normal
  • Antispsychotc drugs block dopamine within minutes but effects on behavior gradually build over 2-3 weeks, Not all patients respond
45
Q

What symptoms does the 1st generation (typical), 2nd generation (atypical), and 3rd generation (atypical) treat?

said we dont need to know drugs/recep but just incase

A

1st gen: positve symptoms
2nd gen: postive sympotms and have some benefit for negative symptoms
3rd gen: postive sympotms and have some benefit for negative symptoms

46
Q

1st gen (typical) antipsychotics (FGA) are what class of drugs?

ly

A

Dopamine D2 antag

47
Q

2nd gen (atypical) antipsychotics (SGA) are what class of drugs?

ly

A

Serotonin (5-HT) receptors

48
Q

3rd gen (atypical) antipsychotics are what class of drugs?

A

Dopamine partial agonists (system stabilizer)

49
Q

Match the geneeration of antipsuchotics with the description

A. Can cause EPS (extra pyramidal symptoms)-spasms/motor issues
B. Lower risk for EPS and has a higher risk for metabolic side effects
C. Lower risk of EPS and metabolic side effects

ly

A

A. 1st gen
B. 2nd gen
C. 3rd gen

Neurosciences (28 decks)

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