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psy324- bio psych > week 10- psychopathy > Flashcards

week 10- psychopathy Flashcards

1
Q

what causes mental illness

A

we don’t know, its complicated

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2
Q

there is ________ distribution among people who experience symptoms of any one disorder

A

normal
see image 9

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3
Q

the onset of schizophrenia is _____ and ____

A

subtle and gradual

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4
Q

what do positive symptoms mean for schizophrenia? give some examples

A

→ Positive (the presence of something)
- Disorganized speech
- Disorganized behavior
- Hallucinations (hearing, seeing something that’s not there)
- Delusions (believing something not true)

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5
Q

what do negative symptoms mean for schizophrenia? give some examples

A

→ Negative (the loss of something)
-Flattened affect and /or anhedonia
- Speech minimized
- Lack of motivation
- Social withdrawal

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6
Q

what are some examples of cognitive symptoms of schizophrenia?

A

→ Cognitive
-Poor sustained attention
- Low psychomotor speed /catatonia
- Poor learning and memory
- Poor abstract thinking/problem solving

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7
Q

what are some examples of complex symptoms of schizophrenia?

A

→ Complex
-Psychosis
- Emotional/Affective Symptoms
- Motivational impairment
- Cognitive impairment

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8
Q

what progression do schizophrenia symptoms take?

A

-symptoms of schizophrenia usually go from positive to negative, then to complex

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9
Q

what are the 5 types of schizophrenia? explain each

A

→ Paranoid- frequent visual and auditory hallucinations /delusions, disorganized speech, trouble concentrating, and significant behavioral impairment.
→ Catatonic- Excessive movement (catatonic excitement), or decreased movement ( catatonic stupor).
- Inability to speak (mutism), mimicking words (echolalia), and mimicking actions (echopraxia).
- Rarest form
→ Disorganized- Disorganized behaviors and nonsensical speech in the absence of delusions and hallucinations.
- Most common.
→ Residual- Previously diagnosed but person is no longer experiencing prominent symptoms (like hallucinations or delusions)
- still exhibited symptoms including a flattened affect, psychomotor difficulties, and disturbed speech.
→ Undifferentiated- symptoms fit into more than one subtype of schizophrenia

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9
Q

what gender is schizophrenia most prevalent in?

A

higher in men than women

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10
Q

what type of country is schizophrenia most prevalent in?

A

-more prevalent in prosperous countries than in 3rd world countries

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11
Q

what is the likelihood of an identical vs. fraternal twin developing schizophrenia? what does this prove?

A

-if one identical twin develops schizophrenia (keep in mind identical twins share 100% of their genes), the other twin has a 48% chance of developing schizophrenia, whereas fraternal twins (share 50% of genes) only have a 17% chance of developing schizophrenia if the other twin has it
-but, this shows that schizophrenia is not just genetics (even though they clearly matter)

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12
Q

what do adoption studies about schizophrenia show?

A

having a genetic risk of developing schizophrenia is high particularly when the environment is severely dysfunctional (gene/environment interactions)

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13
Q

do certain genes greatly increase the risk of one developing schizophrenia?

A

-No common genetic variant produces more than a small increase in the probability of schizophrenia.
-A few rare genes are known to greatly increase the risk of schizophrenia, mostly by disrupting the development of glutamate synapses or by interfering with the immune system.

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14
Q

what is the DISC1 gene?

A

(disrupted in schizophrenia 1 gene) controls differentiation and migration of neurons in brain development (important for neurodevelopment)

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15
Q

what happens if the DISC1 gene is broken or disrupted?

A

people are more likely to develop schizophrenia

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16
Q

describe the DISC1 scottish study and it’s results

A

there was a high prevalence of a “broken copy” of this DISC1 gene in large Scottish family over 5 generations - development of schizophrenia, bipolar & other mood disorders was really high

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17
Q

what is NRG1? what does it do

A

Neuregulin 1, important for brain development

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18
Q

what happens is one’s NRG1 gene is mutated?

A

one is at risk for developing schizophrenia

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19
Q

describe the NRG1 iceland study and it’s results

A

NRG1 risk allele doubles the risk of schizophrenia (a risk allele means that the entire population may have a G allele on the NRG1 gene, but one person may have a C allele – meaning they possess a risk allele)

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20
Q

what is the recent popular hypothesis?

A

not just one gene causes schizophrenia, but new mutations in any one of hundreds of genes

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21
Q

what are microdeletions in the recent popular hypothesis

A

if the population has aabbcc, this individual has abbcc

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22
Q

what are microduplications in the recent popular hypothesus

A

if the population has aabbcc, this individual has aaaabbcc

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23
Q

what is the neurodevelopment hypothesis

A

suggests abnormalities in the neonatal/prenatal development of the nervous system leads to abnormalities in the developing brain that predispose to schizophrenia

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24
Q

how can population density affect schizophrenia onset?

A

one is more likely to develop schizophrenia in a big city than a small city

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25
Q

what is the season of birth effect? why does this happen?

A

Babies born in late winter and early spring months are at higher risk of “positive” schizophrenia
-they found that this is because mothers were more likely to get sick in these months, since they were pregnant that had an influence on the baby

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26
Q

what 2 things can happen if an expecting mother gets a viral infection

A

-Increase cytokines in the mother that impair brain development of fetus
-Cause fever that damages the fetal brain

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27
Q

how can the flu affect schizophrenia onset

A

fetuses exposed to influenza are more likely to get schizophrenia

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28
Q

what are 8 risk factors that can increase the likelihood of the development of schizophrenia

A

-Poor nutrition of the mother during pregnancy
-Premature birth
-Low birth weight
-Complications during delivery
-Extreme stress of mother during pregnancy
-Immunological rejection e.g., Rhesus factor(Rh) incompatible
-Other infections during pregnancy (Toxoplasma gondii)
-Postnatal stressors

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29
Q

what is the two hit hypothesis?

A

Schizophrenia is the result of a combination of a genetic predisposition and impacts from the environment in prenatal/neonatal development, later in life, or both. (this is more about the gene environment interactions)

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30
Q

what are 6 brain abnormalities in people with schizophrenia?

A

-Enlarged lateral ventricle and prominent sulci
-Decreased tissue cerebral gray matter
-Smaller PFC (prefrontal cortex) and hippocampus
-Less gray matter and white matter
-Reduced cortical connectivity and activity
-Glial reductions (glial theory) – less oligodendrocytes and myelin integrity (DISC1), altered microglia in temporal and frontal lobes, less astrocyte glutamate transporters in PFC

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31
Q

what is connectivity like in people with schizophrenia? what is it called?

A

-there is less connectivity between the highly connected regions in the brain (called rich clubs) in people with psychosis
-people with psychosis have less connectivity between rich clubs than healthy controls do
see image 10

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32
Q

looking at image 11, which individual has schizophrenia? why?

A

-the twin on the left has schizophrenia because people with schizophrenia have larger ventricles

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33
Q

what is the dopamine hypothesis?

A

-says that positive symptoms are caused by over-activity of synapses between dopamine (DA) neurons of the ventral tegmental area (VTA) and nucleus accumbens and amygdala (Mesolimbic)

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34
Q

how does the dopamine hypothesis explain delusions and hallucinations?

A

a result of excess dopamine moving through this pathway

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35
Q

how did the dopamine hypothesis come about?

A

-this hypothesis came about by finding out that antipsychotic drugs (like chlorpromazine) block DA receptors (they block D2 receptors, preventing receptor activation (antagonist))

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36
Q

why does amphetamine psychosis resemble schizophrenia?

A

Amphetamine psychosis resembles schizophrenia because amphetamines (and cocaine) block DA reuptake thus increase DA levels (agonist). (amphetamines exacerbate symptoms)

37
Q

what is the glutamate hypothesis

A

-says that schizophrenia is due to excessive glutamate (the primary excitatory neurotransmitter in the brain) and under stimulation of glutamate receptors

38
Q

explain the brain mechanisms of the glutamate hypothesis

A

-in typical people, NMDA receptors (glutamate receptors) would cause excitatory effects, which causes inhibitory transmission of GABA which leads to a moderate release of glutamate BUT in people with schizophrenia, less NMDA leads to less excitation, which leads to less inhibition, which leads to greater glutamate release, causing immediate symptoms and cell damage

39
Q

how do pcp and ketamine relate to schizophrenia

A

-PCP (angel dust) and ketamine (date rape drug) block N-methyl-D- aspartate receptor (NMDA) receptors which creates all symptoms of schizophrenia

40
Q

what drugs reduce positive symptoms of schizophrenia? why?

A

-Antipsychotic drugs (like chlorpromazine) block DA receptors

41
Q

what drugs reduce negative symptoms of schizophrenia? why?

A

-Glycine or D-serine stimulate NMDA receptors and reduce schizophrenic symptoms

42
Q

what drugs reduce all symptoms of schizophrenia?

A

-Atypical antipsychotics (like Clozapine) increases release of DA in PFC and decreases DA in nucleus accumbens

43
Q

what two disorders are within major affective disorder

A

Major Depressive Disorder (MDD) and Bipolar Disorder

44
Q

what is MDD?

A

is unipolar, it’s basically just unremitting depression

45
Q

what is bipolar disorder? what are the two types and what are they characterized by?

A

Bipolar Disorder- cyclical periods of mania and depression
BP I- less depression, severe mania
BP II- severe depression, less mania

46
Q

what is cyclothymic bipolar disorder?

A

cycling between moderate depression and moderate mania – moderate depression and mania

47
Q

what are some common symptoms of major depressive disorder

A

-Hopelessness and helplessness
-Worthlessness, self-hate, guilt
-Agitation/ irritability
-Weight loss
-Concentration
-Fatigue/lack of energy
-Isolation/withdrawal
-Anhedonia
-Sleep
-Suicidal thoughts

48
Q

is mdd more common in females or males?

A

females

49
Q

what are the 4 etiological theories of MDD

A
  1. genetics
  2. chemical imbalance
  3. neurogenesis
  4. neurology
50
Q

mutation of what gene increases the likelihood of MDD? how?

A

-one with a gene mutation of the serotonin transporter gene increases likelihood of MDD development – people with 2 short version of the gene increases likelihood of MDD development ONLY if you are experiencing stressful life events

51
Q

having a low level of what enzyme causes MDD

A

-we have an enzyme called monoamine oxidase (degrades serotonin, norepinephrine, and dopamine) and people predict having a low level of activity in these monoaminergic synapses cause depression

52
Q

degradation of dopamine causes…..

A

anhedonia

53
Q

degradation of norepinephrine causes…..

A

psychomotor symptoms

54
Q

degradation of serotonin causes….

A

rumination and impulsive thoughts

55
Q

why do MAO inhibitors work?

A

they block the degradation of monoamines like serotonin, dopamine, etc.

56
Q

how does neurogenesis cause depression?

A

stress exposure decreases neurogenesis in the dentate gyrus of the hippocampus which causes depression

57
Q

what are 2 pieces of evidence for neurogenesis causing MDD?

A
  1. treatment with anti-depressant meds alleviate symptoms at the same time that they facilitate neurogenesis in the rodent hippocampus
  2. exercise enhances neurogenesis in the hippocampus of both animals and humans and alleviates depressive symptoms
58
Q

in people with depression, what parts of the brain have increased and decreased activity

A

-decreased activity in left and increased activity in right PFC in people with depression

59
Q

there is increased _________ in the amygdala of people with depression

A

blood flow

60
Q

activity in what part of the brain is correlated with severity symptoms in people with depression

A

amygdala

61
Q

what are 3 categories of treatment for people with MDD

A
  1. antidepressants
  2. transcranial magnetic stimulation (tms)
  3. Electroconvulsive Therapy (ECT)
62
Q

what do Tricyclics (TCA’s) do

A

Block transporter proteins that reabsorb serotonin, dopamine, and norepinephrine into the presynaptic neuron after release

63
Q

what do MAOI’s do

A

enhance monoamines by inhibiting MAO.

64
Q

are antidepressants really that better than placebos? use a study to explain

A

-a study on antidepressants vs. placebo drugs showed that if the initial severity of depression was low, there’s no difference between placebo and antidepressants, but if the initial severity of depression was high, there is a big clinically significant difference between placebo and antidepressants

65
Q

how does tms work

A

Pulses of magnetic energy focused over a particular surface along the scalp to deactivate neurons

66
Q

how does ect work?

A

An electrically induced seizure used for the treatment of very severe depression – only used in people with treatment resistant depression and suicidal patients

67
Q

is ect effective?

A

-its applied every other day for a period of 2 weeks, which is effective but has severe side effects such as memory loss (BUT memory loss can be minimized if shock is localized to the right hemisphere)

68
Q

what are the 2 Simplest and Least Expensive Depression Treatments

A
  1. Moderate intensity exercise
  2. Alter the sleep schedule- going to sleep at the same time every day
69
Q

what can sometimes be helpful for seasonal affective disorder?

A

some studies show that if you do periodic sleep deprivation, it can sometimes be helpful in treating seasonal affective disorder, but you have to catch up on your sleep after

70
Q

what are some manic symptoms in people with bipolar

A

-Elevated mood: hyperactive, increased energy, high self-esteem (false), grandiose/delusions
-Racing thoughts
-loud-rapid speech
-Reckless behavior: binging, poor judgment, promiscuity, spending sprees
-Agitated or irritated

71
Q

what gender is most likely to develop bipolar

A

equal for males and females

72
Q

what are the 2 main etiological theories of bipolar

A

→ Genetics
→ Neurobiology
(Overactive Amygdala, Enlarged lateral ventricles)

73
Q

what is the main type of bipolar treatment? what does it do?

A

→ Lithium
-Stabilizes mood and prevents relapse in mania or depression

74
Q

how does lithium work?

A

-Exact mechanism is unknown BUT
Drug shown to work by… Decreasing glutamate activity and decreases inflammation in the brain

75
Q

what is anxiety

A

unfounded, unrealistic, chronic fear

76
Q

what are the 5 common types of anxiety disorders?

A

– Generalized anxiety disorder
– Panic disorder
– Specific phobias
– Obsessive compulsive disorder
– Post-traumatic stress disorder

77
Q

what is Generalized Anxiety Disorder (GAD)? what are the symptoms

A

-Excessive uncontrollable anxiety and worry
-Symptoms: fatigue, muscle tension, restlessness, irritability, sleep disturbances, concentration problems

78
Q

in what gender is most likely to get gad

A

women (onset begins in childhood/early adolescence)

79
Q

what are symptoms exacerbated by for GAD

A

stress

80
Q

what is panic disorder? what are the symptoms

A

-Characterized by repeated and unexpected panic attacks along with worry about future attacks
-Symptoms of panic attacks are similar to those of heart attack and include chest pains, rapid heartbeat, shortness of breath, dizziness, etc.

81
Q

what are the 3 broad categories of phobias? explain each

A
  1. Agoraphobia: fearful of a public place or being outside of the home to the extent that a panic attack or extreme embarrassment is possible
  2. Social phobia: a fear of social activity, especially of being scrutinized and embarrassed
  3. Specific phobias: exaggerated fear of specific objects/situations not covered by the other two
82
Q

what are the 4 risk factors of anxiety

A

→ Genetics
→ Personality Traits
(high in neuroticism = more likely for development of anxiety)
→ Childhood maltreatment
→ Chronic or traumatic stress

83
Q

what brain differences do people with anxiety show?

A

-people with anxiety show increased activation of amygdala and decreased activation of prefrontal cortex (PFC)

84
Q

what is obsessive compulsive disorder

A

-characterized by obsessions and compulsions
Obsessions- thoughts, images, or impulses that are intrusive enough to cause marked rise in anxiety
Compulsions- ritualistic behaviors or mental acts that are designed to lower anxiety

85
Q

for OCD, there is early onset for ________ but late onset for ______

A

females
males

86
Q

dysregulation in what part of the brain is seen in people with OCD

A

the cortico-basal ganglia-thalamo-cortical (CBGTC) loop, 5HT, and dopamine systems

87
Q

in people with OCD, there is hyperactivity in the……., which causes………..

A

-caudate nucleus, which causes compulsivity and impulsivity
-orbitofrontal cortex, which causes obsessive thoughts
-anterior cingulate cortex, involved in emotion regulation

88
Q

in people with PTSD, there is dysregulation in…..

A

the HPA-axis which causes lower than normal cortisol levels and blunted cortisol response to acute stressor

89
Q

what is the hippocampus difference in people with ptsd

A

-people with PTSD have smaller than average hippocampus

90
Q

what is the veteran twin study? what does it show?

A

one twin is a veteran of the war and one isn’t – showed that the one twin who went to war had a smaller hippocampus than the twin that didn’t, which means that the smaller hippocampus was caused by the PTSD

91
Q

there is a higher rate of mental illness in individuals with……. (4 things)`

A

high iq, artists, scientists, and geniuses

psy324- bio psych (11 decks)

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