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Physiological Psychology > Last Lecture > Flashcards

Last Lecture Flashcards

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1
Q

What is a mass of cells whose growth is uncontrolled and that serves no useful function?

A

Tumor

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2
Q

What determines whether a tumor is malignant or benign?

A

Whether the tumor is encapsulated or not (Benign: encapsulated)

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3
Q

How does malignant and benign tumors damage brain tissue?

A

Malignant: compress and infiltrate
Benign: compress

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4
Q

How are primary and secondary brain tumors differ?

A

Primary: tumor starts in CNS
Secondary: tumor has metastasized to brain

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5
Q

T/F: Benign tumor is more common in women, and malignant tumor is more common in men.

A

True

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6
Q

T/F: Most common brain metastases are from lung and breast cancer.

A

True

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7
Q

What is the most common primary brain tumor type?

A

Gliomas; (astrocytoma and meningioma are types of gliomas)

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8
Q

What is Glioblastoma Multiforme?

A
  • A grade 4 astrocytoma
  • most aggressive tumor form
  • can spread in months, prognosis is 2 year
  • high incidents in white individuals
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9
Q

What are some characteristics of meningioma?

A
  • tumor of the meninges
  • usually benign (encapsulated)
  • slow growing (could take up to 10 years for symptoms to be noticed)
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10
Q

What are the three main treatments of brain tumor?

A
  • surgical resection (debulking)
  • radiation
  • chemotherapy
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11
Q

What is a challenge with brain tumor radiation?

A

Damage to the hippocampus (but now they have hippocampus sparing, which prevents radiation from targeting hippocampus)

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12
Q

What is a period of sudden, excessive activity of cerebral neurons?

A

Seizure

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13
Q

What are the two types of partial/focal type seizure and how are they different?

A
  • Simple partial: no major change in consciousness
  • Complex partial: cause a loss of consciousness
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14
Q

What are the three types of generalized type seizure?

A
  • Tonic-Clonic (aka Grand mal; most severe)
  • Absence (aka petit-mal)
  • Atonic
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15
Q

What happens in each of the stages of the Grand Mal seizure?

A
  • Aura stage: hallucination, confusion, dizziness, etc
  • Tonic stage: stiffening of muscle, incontinence, arched back
  • Clonic stage: jerky movement, frothy saliva
  • Postictal stage: exhausted, sleepy
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16
Q

What are some symptoms of Petit Mal seizure and how long do they last?

A
  • Sudden lapse in consciousness
  • Staring blankly into space
  • Eyelid fluttering
  • Lip smacking
  • Involuntary hand movements
  • Last less than 15 seconds
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17
Q

What are the characteristics of Atonic seizure?

A
  • Aka “drop seizures”
  • Sudden loss of muscle control, which results in collapse or fall
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18
Q

How are cataplexy in narcolepsy and a fall in atonic seizure different?

A

Cataplexy: they are aware
Atonic: they are unaware (loss of consciousness)

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19
Q

What are some problems that may come with seizure?

A
  • 50% show damage to the hippocampus
  • Falling
  • Drowning
  • Car accidents (unable to drive for 1 year post seizure event)
  • Pregnancy complications
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20
Q

What are some common mental/emotional health issues associated with seizure?

A
  • Most common: ADHD, Anxiety, aggression
  • 6-10% experience post-ictal psychosis
  • Epilepsy increases risk of schizophrenia by 2.5x
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21
Q

T/F: Neurodegenerative disorders continue to cause degeneration in your CNS.

A

True.

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22
Q

What are the two common types of prion disease?

A

Creutzfeldt-Jakob disease and Kuru disease

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23
Q

Prion disease

A
  • When prion protein, found throughout the body, begins folding into an abnormal three-dimensional shape.
  • Damaged prion protein destroys brain cells, leading to a rapid decline in thinking and reasoning.
  • Also called Transmissible Spongiform Encephalopathies
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24
Q

Creutzfeldt-Jakob disease

A
  • Most common TSE
  • Can be sporadic or familial
  • Causes severe mental deterioration and dementia
  • Prognosis: about 8 month
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25
Q

Kuru Disease

A
  • From eating contaminated human brain tissue
  • A part of traditional practice in Papa New Guinea
  • Can have 10-50 year incubation period
  • Leads to total loss of muscle control and dysphagia
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26
Q

Parkinson’s disease

A
  • Caused by the degeneration of dopamine-secreting neurons in the substantia nigra that send axon to the basal ganglia
  • Causes a deficiency of automatic, habitual motor responses
  • 95% cases are sporadic
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27
Q

What are some symptoms of Parkinson’s disease?

A
  • Dystonia (rigidity)
  • Bradyskinesia & Slowed reaction times (resulting in falls)
  • Shuffling gait
  • Face Masking (lack of facial expression)
  • Tremors
  • Pill Rolling Tremor (75%)
28
Q

What are some treatments for Parkinson’s disease?

A
  • L-Dopa (only works for a period of time; side effects of hallucinations and delusions)
  • Deprenyl (slows Parkinson’s progression)
  • lesioning of the pathway
  • Deep Brain Stimulation (75% see relief of symptoms, but not good for those with cognitive/memory impairments)
29
Q

Huntington’s disease

A
  • Inherited (chromosome 4 mutation)
  • degeneration of the basal ganglia
  • In DNA, CAG repeats more than normal
  • Typical onset ages 30-50
  • 10-15 year prognosis following symptom onset
30
Q

What are the CAG counts in Huntington’s disease?

A
  • 27 to 35: no symptom but can pass on genetically
  • 36 or more: HD
31
Q

What are some symptoms of Huntington’s disease?

A
  • Chorea: involuntary jerking movements (almost like dancing movements)
  • Dystonia
  • Slurred speech and swallow difficulties
32
Q

Amyotrophic Lateral Sclerosis (ALS)

A
  • degenerative disorder that attacks spinal cord and cranial nerve motor neurons (supports brainstem), which results in brain and muscle connection loss
  • Average onset age in late 50’s
  • 10% inherited (mutation of chromosome 21 in inherited cases)
33
Q

What are some symptoms of ALS?

A
  • Progressive weakness and muscular atrophy
  • eventual loss of speech, swallow, paralysis
  • Eye movements are spared
  • Death typically caused by respiratory failure (typically within 24 months)
34
Q

Multiple Sclerosis

A
  • an autoimmune demyelinating disease
  • body attacks its own myelin sheaths and leave behind sclerotic plaques
  • Onset in late 20’s to 30’s
  • Damage occurs in white matter
35
Q

What are some risk factors of MS?

A
  • Females > Males
  • Living far from the equator
  • Black or white race
  • Smoking
36
Q

What are some symptoms of MS?

A
  • Fatigue
  • Vision problems
  • Bladder/bowel dysfunction
  • Spasms
  • Slowed Processing Speeds
37
Q

What are the four types of MS?

A
  • Relapsing-Remitting
  • Secondary Progressive
  • Primary Progressive
  • Progressive-Relapsing
38
Q

What are some causes and etiology of meningitis?

A
  • Virus (most common)
  • Bacteria, fungus, parasite
  • spread of middle-ear infection to the brain
  • head injury
  • embolus that has dislodged from bacterial infection in the heart
  • *increased risk for IV drug users
39
Q

What are some symptoms of meningitis?

A
  • stiff neck
  • headache
  • altered mental status
  • fever
    -photophobia
40
Q

What are the two meningitis tests?

A
  • Brudzinski’s sign: flexion of the hips and knees in response to neck flexion
  • Kernig’s sign: resistance to extension of leg while the hip is flexed
41
Q

What is dementia and what are the five types?

A
  • Umbrella term for loss of memory and other thinking abilities severe enough to interfere with daily life
  • Alzheimer’s
  • Lewy body dementia
  • Vascular dementia
  • Frontotemporal dementia
  • Mixed dementia
42
Q

What is dementia and what are the five types?

A
  • Umbrella term for loss of memory and other thinking abilities severe enough to interfere with daily life
  • Alzheimer’s
  • Lewy body dementia
  • Vascular dementia
  • Frontotemporal dementia
  • Mixed dementia
43
Q

Alzheimer’s

A
  • accumulation of neuritic plaques (beta amyloid) and tau tangles
  • exposure to toxins, TBI, infections may trigger
    abnormal beta amyloid formation
  • estrogen lowers risk of developing Alzheimer’s
  • memory loss is core symptom (ask: have you ever gotten lost in a familiar place?)
  • onset later in life (70+)
44
Q

Vascular dementia

A
  • accumulation of small mini-strokes (lacunar infarcts)
  • associated with brain damage due to ischemic injury and anoxia
  • risk factors are same as stroke risk factors
  • typical age of onset 65
45
Q

What is the difference between mild cognitive impairment and dementia?

A

In mild cognitive impairment, ADL is generally okay.
In dementia, ADL becomes more difficult/impaired.

46
Q

T/F: For Alzheimer’s and vascular dementia, the patient is unaware that they have dementia.

A

False. In Alzheimer’s, they are unaware they have dementia. In vascular dementia, they are aware that something is off about them.

47
Q

How are impairments in Alzheimer’s and vascular dementia similar and different?

A

Similar: Deficit in Executive/Attentional Functioning
Alzheimers: Impairments in Episodic Memory, Language, and Cuing/Recognition does not help
Vascular dementia: Impairments in Semantic Memory, Visuo-spatial/Perceptual Skills, Slowed processing speed, and With cuing/recognition paradigm can recall information

48
Q

Dementia with Lewy body

A

Characterized by the abnormal build up of alpha-synuclein proteins into masses (lewy bodies)

49
Q

What are the symptoms of Lewy body dementia?

A
  • Visual hallucinations (one of the first symptoms)
  • Falls & Dysautonomia (autonomic functions like blood pressure and body temp regulation is off)
  • Movement issues
  • Sleep problems (REM sleep disorder common)
  • Fluctuating cognition
  • Mood and behavior changes
50
Q

T/F: with frontotemporal dementia, you can see the brain damages through imagining.

A

True

51
Q

Frontotemporal dementia

A

Accumulation of Tau protein overwhelms the brain and causes tissue death

52
Q

What are the three types of frontotemporal dementia?

A
  • Behavioral Variant: most common, changes in personality and behaviors
  • Primary Progressive Aphasia: communication progressively worsens
  • Movement Disorders
53
Q

Schizophrenia:

A
  • 46% heritability rate
  • 10x risk of African and Caribbean migrants
  • Men > Women
  • Mutation in 21 of the 23 chromosomes
  • Older Paternal Age
  • Atypical prenatal development
  • Poor social adjustment and academic performance
  • Deficient psychomotor functioning
  • 20% reduction in life expectancy
54
Q

What are some extrapyramidal antipsychotic med side effects for schizophrenia?

A
  • Tardive Dyskinesia: tongue moves around alot; caused by too much antipsychotic medication
  • Akathisia: subjective unpleasant feeling of
    restlessness (kinda like a kiddo with ADHD)
  • Pseudo-Parkinsonism
  • Acute Dystonia
55
Q

What is anti-cholinergic?

A

Antipsychotic med side effect that causes dry mouth, urinary retention, blurred vision, and constipation

56
Q

T/F: Families of persons with affective disorders are 10x more likely to develop MDD or BMD.

A

True

57
Q

What are some facts about neuropathology of depression?

A
  • Hedonic Tone: trait or genetic predisposition that affects one’s baseline range and lifelong ability to feel pleasure
  • Dysfunction of mesolimbic and mesocortical pathways
  • Loss of 40-90% of glial cells
58
Q

Low hedonic tone can increase the risk of which diagnoses?

A
  • anhedonia
  • depression
  • dysthymia
59
Q

hippocampal neurogenesis

A
  • the brain getting used to the presence of SSRI
  • explains 3-6 week lag in tx response time
60
Q

Maternal emotional distress during the first trimester can result in which symptoms in the child?

A
  • Internalization of sxs and negative emotionality in MALES in childhood
  • Increase risk of autism, Tourette’s, OCD, and ADHD
61
Q

Maternal emotional distress during the third trimester can result in which symptoms in the child?

A

Internalizing sxs in FEMALE adolescence

62
Q

T/F: Elevated milk cortisol levels during lactation is associated with more fearful and reactive bx in all infants.

A

False. Elevated milk cortisol levels during lactation is associated with more fearful and reactive bx in FEMALE infants as compared to male infants

63
Q

What are some brain mechanisms in GAD?

A
  • Reduced connections between amygdala and PFC
  • Activation of the vmPFC does not result in reduction of amygdala activation
  • Lowered GABA presence in amygdala
64
Q

What are some brain mechanisms in social anxiety?

A

Disproportionate activation of amygdala when viewing negative expressions and neutral ones

65
Q

What are some brain mechanisms during panic attack?

A
  • Increased activation of amygdala & periaqueductal grey
  • Can be induced by the breathing of CO2 and injection of lactic acid
66
Q

How are “Anxious Apprehension” and “Anxious Arousal” different?

A
  • Anxious Apprehension: related to cognitive thoughts and ruminative thinking; increased internal dialogue due to L Frontal lobe activation
  • Anxious Arousal: related to physiological anxiety and increased sensitivity to environmental sounds and noises; increased activation in right temporal lobe
67
Q

What’s the difference between partial/focal and generalized seizures?

A

Partial/focal: specific part of the brain is affected
Generalized: both hemispheres of the brain is affected

Physiological Psychology (3 decks)

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