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Psychology 479 > Chapter 27 - Psychiatric and Related Disorders > Flashcards

Chapter 27 - Psychiatric and Related Disorders Flashcards

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1
Q

What are psychiatric disorders?

A
  • Behavioural disorders characterized by abnormalities in emotional and/or cognitive functioning without obvious brain lesions
  • Treated by psychiatrists and psychologists
  • Biochemical, anatomical, experiential, and genetic basis
  • Affect 1/8 people in the world
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2
Q

What are the 5 major symptoms of schizophrenia?

A

1) Delusions (i.e., beliefs that distort reality)
2) Hallucinations (i.e., altered perceptions)
3) Disorganized speech (i.e., incoherent statements)
4) Disorganized or excessively agitated behaviours
5) Other symptoms that cause social or occupational dysfunction
*Must have 2/5 symptoms over 6 months to qualify for a diagnosis

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3
Q

What are some structural abnormalities in Schizophrenic brains?

A
  • Increased size of lateral and third ventricles (associated with overall decrease in brain volume)
  • Decreased grey matter volume; frontal lobe, temporal lobe (specifically in the superior temporal gyrus, hpc, fusiform gyrus, and planum temporale)
  • Large and extensive reductions in white matter (affects lobes and cerebellum, inter/intrahemispheric connections, lots of individual variability)
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4
Q

What are the cellular abnormalities found in Schizophrenic brains?

A
  • dlPFC cells are simpler in dendritic organization
  • Haphazard orientation of pyramidal neurons in hpc
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5
Q

What are some of the cognitive symptoms of Schizophrenia?

A
  • Premorbid (prodromal) cognitive markers in children can be both general and specific
  • Children and adolescents show premorbid IQ drop of 8-10 points, followed by another equivalent drop once the disorder is evident
  • Verbal deficits, especially in understanding language
  • Executive functions may also be affected: working memory, episodic memory, attention, etc.
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6
Q

What are the general symptoms of depression?

A
  • Prolonged feelings of worthlessness and guilt
  • Disruption of normal eating habits
  • Sleep disturbances
  • General slowing of behaviour
  • Frequent thoughts of suicide
    *Symptoms must be present for at least 6 months
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7
Q

What are the general symptoms of mania?

A
  • Extreme excitement/excessive euphoria
  • Often form grandiose plans (impulsivity)
  • Hyperactivity
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8
Q

What are some of the neurochemical aspects of major depression?

A
  • Reduction in monoamines (part of small-molecule class of NTs, including NE, DA, 5-HT)
  • Don’t really know how antidepressants work
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9
Q

What are some examples of antidepressant actions?

A
  • SSRIs (selective serotonin reuptake inhibitors) = inhibit the reuptake of monoamines into presynaptic neurons, let them sit in the synaptic cleft for longer
  • MAOIs (monoamine oxidase inhibitors) = inhibit the breakdown of monoamines in presynaptic storage vesicles
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10
Q

How do monoamines modulate hormone production and secretion?

A
  • Via the HPA axis (hypothalamic-pituitary-adrenal)
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11
Q

How can excessive cortisol impact the HPA axis?

A
  • Excessive (chronic) cortisol may damage the feedback loop that turns off the stress response
  • Hyperactivity of HPA axis occurs in MDD
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12
Q

How does cortisol interact with the brain?

A
  • Binds with high affinity to mineralocorticoid receptors (MRs) and lower affinity to glucocorticoid receptors (GRs)
  • MRs and GRs expressed highly in HPC, PFC, amygdala
  • Can help explain why disrupted cognition is a feature of depression, affecting memory and executive function
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13
Q

how is excessive cortisol linked to the development of MDD?

A
  • Excessive cortisol is linked to dysregulation of MR and/or GR gene expression/function which may contribute to the development of MDD
  • Excess cortisol + reduced expression of GRs/MRs in the HPC, PFC, and amygdala
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14
Q

What’s the relationship between the HPC and cortisol?

A
  • Prolonged stress (excessive cortisol) appears to kill HPC cells
  • May contribute to depression and anxiety
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15
Q

How do antidepressants affect neurogenesis?

A
  • Brain-derived neurotrophic factor (BDNF) is upregulated by antidepressants, and downregulated by stress (may kill neurons)
  • BDNF can enhance growth and survival of neurons
  • BDNF may also be involved in MDD and/or affecting monoamine levels via loss of neurons/synapses
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16
Q

What’s Prozac?

A
  • A common antidepressant
  • Also called Fluoxetine, works as an SSRI
  • Appears to stimulate BDNF production and neurogenesis in the HPC
  • Prolonged stress may result in a lowered production of BDNF
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17
Q

What was discovered from postmortem hippocampi obtained from suicide victims?

A
  • There were 3 groups: tose with childhood abuse, no abuse, controls (other causes)
  • Abused victims showed decreased gene expression for cortisol receptors
  • Demonstrated how ACEs may alter HPA axis for life
  • Learning and memory may also be affected.
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18
Q

What are other structural abnormalities that are associated with MDD?

A
  • Frontal lobe - reduced grey matter volume, especially OFC
  • Temporal lobe - reduced HPC volume
  • Parietal lobe - reduced volume of posterior cingulate
  • Decreased connections between PFC and temporal cortex; PFC and amygdala/HPC
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19
Q

What are some treatments for MDD?

A
  • Pharmacology
  • Psychotherapy (eg., CBT)
  • Electroconvulsive therapy (ECT)
  • Bright-light therapy (for SAD)
  • Deep brain stimulation (DBS)
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20
Q

How does ECT work?

A
  • Under general anesthesia, electric current is delivered to induce a generalized cerebral seizure
  • Occurs 2-3 times per week; 6-12 treatments total
  • Don’t fully know the mechanism (NTs, gene expression, neuroplastic changes, etc.)
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21
Q

How does DBS work?

A
  • Electrodes implanted in the brain stimulate a targeted area with a low-voltage electrical current to facilitate behaviour (can increase or decrease behaviour)
  • May be used for PD, depression, schizophrenia, OCD, epilepsy, etc.
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22
Q

What brain region is targeted in DBS for depression?

A
  • The subcallosal cingulate cortex (SCC24/25)
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23
Q

When do bipolar symptoms tend to emerge?

A
  • During late adolescence or early adulthood
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24
Q

What neurobiological differences are observed in those with bipolar disorder?

A
  • Decreased gray matter in fusiform gyrus, HPC, and the cerebellum of the left hemisphere
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25
Q

What are some treatments for bipolar disorder?

A
  • Mood stabilizers (e.g., lithium, valproic acid)
  • Atypical antipsychotics (dopamine and/or serotonin receptor antagonists)
  • Antidepressants (in conjunction with other medications)
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26
Q

Typical vs. Atypical antipsychotics?

A
  • Typical - first generation, inhibit only DA
  • Atypical - second generation, inhibit DA and 5-HT
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27
Q

What are some of the anxiety-related disorders listed in the DSM-5?

A
  • Panic disorder
  • PTSD
  • Generalized Anxiety Disorder (GAD)
  • OCD
  • Phobias
    *Together these affect around 4/10 people
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28
Q

What’s the neural control of fear reactions?

A
  • Amygdala sends distress signals to the hypothalamus, which communicates with the rest of the body via the ANS (sympathetic branch via epinephrine/adrenaline)
  • Means there’s a chronic, low level of stress in those with anxiety
29
Q

Which brain structures are involved in controlling fear reactions?

A
  • ACC, vmPFC, OFC, and HPC are involved in controlling fear reactions generated by the amygdala
  • Tends to be poor connections between the amygdala and the PFC in those with anxiety
  • Leads to cognitive inflexibility
30
Q

Provide examples of anxiolytics and sedative-hypnotics used to treat anxiety.

A
  • Anxiolytics - Buspirone (BuSpar), SSRIs
  • Sedative-hypnotics - Benzodiazepines
31
Q

How do sedative-hypnotic drugs work?

A
  • Produce CNS depressant effects, causing sedation (low dose) or hypnosis (higher doses)
  • This effect is achieved through drugs such as Benzodiazepines, barbiturates, etc.
32
Q

What % of people do age-related dementias affect?

A
  • Affects 25-50% of people 80+ years of age
  • Around 1/3 of seniors in the US die with some form of dementia
33
Q

What are Tauopathies?

A
  • A form of dementia caused by the accumulation of tau proteins inside neurons
  • What’s considered Alzheimer disease
  • Also seen in frontotemporal disorders (FTDs): Neuron loss in frontal and temporal lobes
  • Also seen in progressive supranuclear palsy (PSP): Neuron loss in upper brainstem
34
Q

What are Synucleinopathies?

A
  • Accumulation of alpha-synuclein protein in neurons
  • Seen in Lewy body dementia
  • Also seen in PD with dementia
35
Q

What are vascular dementias and vascular cognitive impairment?

A
  • Caused by injuries to cerebral blood vessels
  • Multi-infarct dementia and subcortical vascular dementia (Binswanger’s disease) included
36
Q

What does the term mixed dementias signify?

A
  • Combinations of disorders such as Alzheimer disease and vascular symptoms
37
Q

What’s the difference between frontotemporal disorders and Alzheimer diease?

A
  • For FTDs = usually notice a change in personality first rather than memory loss
  • For Alzheimer = memory loss is first to occur
38
Q

What are some of the first symptoms noticed in progressive supranuclear palsy (PSP)?

A
  • Abnormal body movements
  • Walking and balance issues
  • Eye movement issues
  • Neuron loss is specific to the midbrain
39
Q

How can tau proteins cause issues inside neurons?

A
  • Tau proteins assist in cell microtubule function
  • When misfolded, they clump together and disrupt cell functions
  • Instead they form intracellular aggregates.
40
Q

What are examples of other types of dementias?

A
  • Pron-related dementias
  • Huntington disease
  • Secondary dementias
  • Head injury
  • Infectious dementias
  • Drug-related dementias (ex. chronic alcoholism or ecstasy)
41
Q

What genetic component is likely responsible for early-onset Alzheimer disease?

A
  • Most likely related to variants of amyloid-beta processing
42
Q

What are some risk factors for Alzheimer disease?

A
  • Type 2 diabetes
  • BP variability
  • midlife obesity
  • Cardiovascular diseases
  • TBIs
  • Hearing loss
  • Oral diseases
  • Depression and stress
  • Smoking
  • Air pollution
  • Anticholinergic medication
43
Q

What are some protective factors for?

A
  • High education
  • Cognitive activity
  • Bilingualism
  • Social engagement
  • Marriage
  • Physical activity
  • Moderate alcohol intake
  • Mediterranean diet
  • Vitamins
44
Q

What are amyloid plaques?

A
  • Found in those with Alzheimer disease
  • Found predominantly in cerebral cortex, but spreads
  • Extracellular aggregates of amyloid-beta, fragments of the amyloid precursor protein (APP. “mother” protein)
45
Q

What are other terms for amyloid plaques?

A
  • Neuritic plaques, or senile plaques
46
Q

What are neurofibrillary tangles?

A
  • Found in those with Alzheimer disease
  • First appear in entorhinal cortex; spreads throughout hpc, limbic system, association cortices
  • Intraneuronal aggregates of TAU PROTEIN
47
Q

What are cortical changes observed in those with Alzheimer disease?

A
  • Widespread atrophy
  • Entorhinal cortex affected earliest and most severely
48
Q

What brain regions can decreased brain volume be found in those with Alzheimer disease?

A
  • Entorhinal cortex
  • hpc
  • Posterior cingulate
  • Amygdala
  • Parahippocampal gyrus
  • PFC
49
Q

What cellular changes occur in those with Alzheimer disease?

A
  • Loss of dendritic arborization
  • This contributes to cortical atrophy
  • This is observed in cortical pyramidal cells and hippocampal cells
50
Q

T/F: Most cases of Alzheimer disease are sporadic.

A
  • TRUE
51
Q

Which susceptible gene is linked to Alzheimer disease?

A
  • The APOE4 variant of the APOE gene (codes for apolipoprotein E)
  • May promote A-beta plaque formation and impair A-beta clearance
52
Q

What percentage of cases does familial AD account for?

A
  • Less than 5% of all cases
53
Q

Mutations in which three genes are known to cause AD (i.e., deterministic genes)?

A
  • APP (amyloid-beta precursor protein) on chromosome 21
  • PSEN1 (presenilin 1)
  • PSEN2 (presenilin 2)
54
Q

Why are people with Down syndrome at an increased risk of developing AD?

A
  • Since they have two copies of chromosome 21, they are at an increased risk of containing APP, which is found on chromosome 21
  • This is a deterministic gene for AD
55
Q

How can immune reactions be linked to AD?

A

Aging negatively impacts the immune system:
- Reduced efficacy (immunosenescence, meaning less effective)
- Autoimmunity arising from dysregulated self-tolerance = neuronal death

56
Q

How can blood flow contribute as a cause to AD?

A
  • Healthy individuals have a 20% decline in cerebral blood flow between 30-60 years
  • PET studies show reduction in CBF and glucose metabolism in AD patients
  • Appears early in disease progression and correlates with severity of cognitive impairment
57
Q

Which medications are often used to help mitigate cognitive decline in those with AD?

A
  • Acetylcholinesterase inhibitors (mild - moderate cases) (prevent breakdown of ACh at the synapse)
  • Drugs targeting A-beta (mild cases only)
  • NMDA-R antagonists (moderate - severe cases)
58
Q

Why is exercise such a good preventative measure for AD?

A
  • Increased hpc volume
  • Increased neurogenesis
  • Brain-derived neurotrophic factor
    *All help slow cognitive decline
59
Q

What’s a prion?

A
  • Shorthand for “proteinaceous infectious particle”
  • A misfolded protein that induces misfolding of normal variants of the same protein and triggers apoptosis
60
Q

What’s Prion Theory?

A
  • Several progressive neurodegenerative disorders may be caused by prions
61
Q

What are transmissible spongiform encephalopathies (TSEs)?

A
  • Progressive, neurodegenerative disorders characterized by tiny holes in the brain
  • May also occur sporadically, or as hereditary diseases
62
Q

What are some symptoms of TSEs?

A
  • Personality changes
  • Neuropsychiatric problems
  • Lack of motor coordination
  • Memory problems
  • Confusion
63
Q

What type of proteins are prions?

A
  • They’re cell surface proteins
64
Q

Where’s the highest level of PrP expression found in the body?

A
  • In the CNS, often associated with synaptic membranes
  • Encoded by the PRNP gene
65
Q

Which is the infectious variant of the PrP gene?

A
  • PrP^Sc (scrapie isoform of the prion protein) is the infectious variant
  • PrP^C (cellular prion protein) is the normally-folded variant
66
Q

What’s the prion disease mechanism of transmission?

A
  • Transmission via altered protein conformation, not genetic material
  • PrP^Sc causes PrP^C to adopt the abnormal conformation
  • Elicits a chain reaction by which more and more normal proteins are converted to the infectious type
  • There are no immunologic or inflammatory reactions to defend against it.
67
Q

What specific structural differences are found between PrP^C and PrP^Sc?

A
  • Issues with secondary structures
  • PrP^Sc has beta sheets when it should have alpha helices
  • Makes it resistant to enzymatic degradation
  • Prone to aggregation
68
Q

What other neurodegenerative disorders (non-transmissible) may be classified as prion-like diseases?

A
  • Alzheimer disease - A-beta may spread in a prion-like manner
  • Parkinson disease - Alpha-synuclein may spread in a prion-like manner

Psychology 479 (13 decks)

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