Exam 3 Flashcards

(63 cards)

1
Q

4 major symptoms of Parkinson’s

A
  • Tremor: in hands, arms, legs, head, and jaw
  • Stiffness: of the limbs, trunk
  • Bradykinesia: slowed movement/ Brady: slow kinesia: motion/movement
  • Impaired balance and coordination
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2
Q

Parkinson’s non-motor deficits:

A
  • Impaired sleep
  • Fatigue
  • Depression
  • Memory difficulties
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3
Q

5 stages of progression in Parkinson’s:

A

1: tremor and movement symptoms on one side of the body, changes in facial expression, posture, and walking.
2- symptoms worsen and affect both sides of the body
3- slowness of movement, loss of balance, frequent falling
4- walker required, help with daily activities required
5- wheelchair, bedridden, hallucinations, delusions, nurse required

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4
Q

What typically causes death in Parkinson’s

A

Pneumonia or infection from falling or in the lungs

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5
Q

Risk factors in Parkinson’s

A

Genetics: 5-10% causes are early-onset <50 years old
Age: typically in older age but could happen at a young age
Sex: affects 50% more men than women.
Exposure to toxins

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6
Q

Parkinson’s: Parts of the basal ganglia

A
  • The striatum: caudate and the putamen
  • Subthalamic nucleus
  • Substantia nigra: release dopamine. Where the dopaminergic neurons are degenerating. Not producing or releasing dopamine causing a shortage.
  • Globus pallidus interior/ exterior
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7
Q

Direct pathway

A

Central cortex, striatum , globus pallidus internal, thalamus

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8
Q

Indirect pathway

A

Central cortex, striatum, Globus pallidus external, subthalamic nucleus, globus pallidus internal, thalamus

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9
Q

Braak’s hypothesis in Parkinson’s

A
  • hyposmia- loss of smell
  • Sleep disorder
  • Constipation
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10
Q

How L-dops, MAO/COMT, dopamine agonists work

A
  • L-dopa: converts into dopamine
  • MAO/COMT: prevents the breakdown of dopamine
  • Dopamine agonists: substitute for dopamine.
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11
Q

Explain what multiple, sclerosis and autoimmune refer to

A
  • multiple: affects various regions of optic nerve, brain, spinal cord
  • sclerosis: hardening or scarring from damaged myelin
  • autoimmune: antibodies produced against healthy tissues=inflammation
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12
Q

Multiple sclerosis symptoms:

A
  • Double vision, partial or complete blindness
  • Dizziness
  • slurred speech
  • numbness or tingling in limbs
  • weakness or fatigue
  • tremor, spasms, stiffness, or paralysis
  • lack of coordination balance
  • bladder and bowel dysfunction
  • depression, memory/concentration loss
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13
Q

Multiple sclerosis: 4 patterns of progression

A

-Clinical- isolated syndrome: single episode > 24 hours, 50% have lesions found on MRI and likely progress to RRMS
-relapsing-remitting (RRMS): 85%, new or increasing symptom attacks with partial or complete recovery
-Secondary-progressive(SPMS): steady progression/ worsening after 20+ years of RRMS
-Primary-progressive (PPMS): 10-15% steady
progression/worsening from symptom onset, shows up later in life (40’s-50’S), equal numbers of men and women.

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14
Q

Multiple sclerosis risk factors:

A
  • Regions of temperate climate
  • Northern European descent
  • More women than men
  • Onset usually mid-20s
  • Family history
  • Other autoimmune diseases( type 1diabetes, thyroid disease, IBD)
  • Epstein-Barr virus (mono)
  • smokers
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15
Q

What is myelin, which cells make it ?

A

Produced by oligodendrocytes and is made up of glial cells

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16
Q

What is tolerance in relation to the thymus

A

Healthy tissue

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17
Q

Role of T-cells, B-cells

A
  • T-cells: secret cytokines to signal other cells

- B-cells: secrete antibodies against antigen

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18
Q

Apoptosis:

A

The death of cells, normal

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19
Q

APC’s:

A
  • Antigen-presenting cells

- dendritic cells

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20
Q

Self-antigens:

A

Antigen that comes from yourself, can be a healthy tissues protein that is supposed tO be there but us causing an immune response, causing the T-cells to react to the wrong thing

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21
Q

BBB

A

Blood-Brain barrier: t-cells can re-enter the bloodstream and eventually gain access to the CNA

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22
Q

Blood Cerebrospinal fluid barrier

A

BCSFB

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23
Q

Plaques, where they can occur in CNS? (3 general areas)

A
  • Optic nerve
  • Brain
  • Spinal cord
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24
Q

How Ocrevus work?

A

Immunoglobulin/antibody medication against B cells. Block them from releasing antibodies attacking against yourself antigen

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25
Two defining groups of symptoms + examples in autism
- Repetitive/ Stereotypes behaviors * Arm flapping * Rocking * Twirling * excessive interest in a particular topic - Social interaction/communication * Avoiding eye contact * Failing to respond to name * delayed, flat or awkward speech echolalia(repeating what you are saying) * Difficulty understanding body language, gestures, emotions * Only interacting with others to achieve goal
26
risk factors for Autism
- Included both genetic and environmental contributions - Over 100 genetic loci * Family history- 5 times as likely if parent or sibling has it * Sex- 4.5 boy to every 1 girl - Older parental age (>35 years) - Premature birth (<26 weeks), low birth weight, birth trauma with ischemia(lack of blood supply) or hypoxia (lack of oxygen, under oxygenated)
27
Atypical brain development (too rapid then stunted and ages when each happens)
- 2-4 years, larger head circumference and brain volume than typical - 6-8 years, arrested growth compared to typical - Volume becomes similar to typical by adolescence/adulthood, but opportunity for environment to shape brain may have been missed
28
Lobes and structures affected by autism
Temporal and frontal lobes
29
Language-processing - Typical vs. autism
Language is typically processed in the frontal temporal cortices of the left hemisphere vs in autistic children who show an increase in activity of these areas in the right hemisphere, contributing to language-processing deficits.
30
Wernicke's
In charge of understanding languages and is in temporal lobe
31
Fusiform gyrus
located on the medial side of the temporal lobe, is less active in autistic children, which may contribute to facial and emotion-processing deficits.
32
Cingulate gyrus
located on the medial side of each hemisphere, is involved in self-awareness, empathy, and response-inhibition, and also shows decreased activation in autistic children. In the limbic lobe/system
33
Amygdala
situated deep within the temporal lobe, undergoes this atypical pattern of development, which may contribute to difficulties with socio-emotional processing and anxiety.
34
Caudate
the production of stereotypical behaviors is fronto-striatal circuitry involving the caudate nucleus, which also undergoes this atypical development pattern
35
Purkinje cells: Where are they and how are they different in typical vs. an autistic brain?
Purkinje cells are located in the cerebellum. In autistic brains they are smaller and less densely packed, impairing language, imitation and attention processes.
36
Dendrites, long and short-range connections in typical vs. autistic brain
Increase in short range connections but decrease in long range connections between cortical areas, these areas are not talking to each other and not being coordinated, not as much activity connecting them together.
37
Describe the hypothesized role of glutamate and GABA and its relation to seizures in 30% of autistic cases.
Too much glutamate is creating too much citation and GABA is not creating enough inhibition, causing too much electrical activity leading to seizures.
38
Two neuropeptides that regulate affiliative/bonding behaviors
- oxytocin | - vasopressin
39
How does Balovaptan work?
It is supposed to improve social interactions and communication by easing anxiety. It is a vasopressin antagonist.
40
4 symptom domains in schizophrenia
``` Postive: Hallucinations Delusions Disorganized thoughts Affective: Depression Dysphoria Anxiety Suicidality Negative: Blunted affect abolition anhedonia alogia Asociality Cognitive: Attention Learning Working memory Executive functioning ```
41
Risk factors of schizophrenia
- Advanced paternal age - Famine while in utero - Prenatal complications (preeclampsia) - obstetrical complications - Birth location (urban) - Birth season(early spring) - Migration - Cannabis use
42
Gene location
Chromosome 22 right arm 22q 11.2 deletion
43
What happens to brain volume, ventricles, temporal lobe, cortical gray matter, and gyrification
- Brain volume: decreased - Ventricles: enlarged lateral and third ventricles - Temporal lobes: smaller medial - cortical gray matter: decreased - gyrification: altered
44
Latent inhibition in typical vs. schizophrenia
- prepulse inhibition in typical: they will be primed and the startled response will be less - in schizophrenia, no matter how much prepulse you give them they can't regulate their responses and it will be the same.
45
Dopamine role in schizophrenia:
Blocking receptors ameliorates symptoms
46
Glutamate role in schizophrenia:
Blocking receptors exacerbates symptoms
47
GABA role in schizophrenia:
is not activated when glutamate is blocked, doesn't inhibit=disinhibition
48
PV interneurons role in schizophrenia
regulate gamma oscillations, critical to working memory, and other cognitive functions impaired in schizophrenia. Alterations in gamma band activity are associated with multiple symptom domains
49
4 dopaminergic pathways and functions
- Meso-cortical: Cause some of the cognitive and negative symptoms - Miso-limbic: hyper function causes some of the positive symptoms - Nigro-striatal: negative side effects on the nitro-striatial pathway - Tubero-infundibular: negative side effects on the tubers-infundibular pathway.
50
1st vs 2nd generation D2 antagonists
- 1st generation: block d2 receptors, typical, chlorpromazine and haloperidol, high risk EPS - 2nd generations: blocks D2 and 5HT2A, atypical, clozapine, high risk metabolic issues
51
Animal model used by Allen
a mouse
52
Scientific question/ area of research for Allen
visual system/ approach behavior/ primary visual cortex
53
behavior studied
pray detection and freezing or approaching
54
Brain areas studied
superior colliculus (SC)
55
Differences in behaviors and brain areas activated between subject age groups
Different ages: Younger: approaching more older: freezing more
56
Human subjects in scurry
Early deaf people and normal hearing
57
What happens to the auditory cortex in deaf people
it adapts and is used for other functions. Starts processing new information, visual, tactical, and other sensories
58
ED
early deaf
59
NH
normal/ healthy hearing
60
AC
auditory cortex
61
S1:
Primary somatosensory cortices
62
S2:
secondary somatosensory cortices
63
STS:
SUPERIOR TEMPORAL SULCUS