Module 4 Flashcards

1
Q

What are the functions of the nervous system?

A

creating motor response, interpreting sensory info, maintaining internal enviro, emotion, learning, memory, high level cognitive function

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2
Q

What is the CNS?

A

brain and spinal cord

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3
Q

What is the PNS?

A

All nerve tissues outside of the CNS including motor and sensory nerves

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4
Q

What are neurons?

A

cells responsible for the transmission of info

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5
Q

What are glial cells?

A

help neurons communicate, maintain positions of neurons, regulate enviro around neurons, and help repair neurons

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6
Q

What is the cell body?

A

nucleus, mitochondria, and other organelles

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7
Q

What are dendrites?

A

protrusions of membrane for receiving incoming signals

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8
Q

What are axons?

A

extensions of cell body that transmit signals away from cell body

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9
Q

What are myelin sheaths?

A

fatty coating around some axons which insulates neuronal signals allowing for increased transmission speeds

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10
Q

What are axon terminals?

A

Point where signal is transmitted into adjacent neurons

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11
Q

What are nerve impulses?

A

transmitted signals

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12
Q

What type of process is signal transmission?

A

electrochemical

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13
Q

What are the steps of neuronal transmission?

A

reception, action potential, synapse, transmission

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14
Q

What is reception?

A

signal from outside the neuron is received at its dendrites

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15
Q

What is action potential?

A

dendrite stimulation generates an electrical signal which propagates through cell body, down its axons

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16
Q

What is synapse?

A

when ECS reaches exon terminal, NT release is triggered into EC spare where they are received by dendrites. The site between adjacent neurons is called the synapse

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17
Q

What is transmission?

A

Nts trigger new action potential and process repeats until final purpose is fulfilled

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18
Q

How is neurotransmission regulated?

A

highly

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19
Q

Where are NTs stored?

A

secretory vesicles in the axon terminal

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20
Q

What happens when action potentials reach axon terminal?

A

NTs are released into synaptic cleft

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21
Q

Where do NTs bind?

A

receptors on adjacent neurons to initiate new action potential

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22
Q

What happens once signalling is complete?

A

NTs unbind from receptors, vesicles are recycled, neurons return to a resting state

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23
Q

How does an action potential travel in myelinated neurons?

A

action potential jumps between nodes of ranvier

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24
Q

What are Schwann cells?

A

cells that wrap around the entire length of the axon in a spiral extension of their cell membrane, supporting and insulating neurons. Responsible for the formation and maintenance of myelin sheaths in PNS, starting in fetal life and accelerating in infancy

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25
What are Oligodendrocytes?
Glial cells that produce and maintain myelin sheaths around axons in the CNS. Each typically myelinates multiple axons
26
What are microglial cells?
Immune system in brain. responsible for clearing dmg neurons, pruning synapses in development, removing cellular debris
27
What are astrocytes?
star-like cells that provide growth factors and nutrients to nerves. maintain the cells that make up the brain-blood-barrier
28
What cells are many diseases often linked to?
Glial cells rather than neurons
29
What is the ratio of glial cells to neurons in the brain?
1:1
30
What elaborate functions are the nervous responsible for?
memory, encoding, recall, complex emotions, decision making, spatial navigation, fight/flight, rest/digest
31
What is mental health?
a state of psychological and emotional wellbeing that is necessary for overall health
32
What kind of interventions may impaired mental health require?
behavioural therapy, medication, etc..
33
What is mental illness?
diagnosable and treatable mental conditions that don't involve structural brain abnormalities
34
How does mental illness affect an individual?
reduces ability of a person to function. causes feeling of isolation, loneliness, or sadness
35
What causes mental illness?
changes in thinking, mood, behaviour, or stress
36
What does mental illness include?
anxiety, depression, ED, schizophrenia
37
What are determinants of mental health?
factors that contribute to or detract from mental health (can be physical, social, etc...)
38
What is ACE score?
assesses negative experiences from the first 18y of life
39
What is a high ACE score associated with?
increased risk for mental physical social problems in adulthood. can disrupt healthy brain development, social development, and can compromise the immune system
40
What are ACEs?
Adverse childhood experiences
41
What are examples of ACEs?
traumatic events (i.e. neglect, instability, abuse)
42
How do programs typically work to counteract ACEs?
They work to increase resilience in children.
43
What are ACE scores used for?
Used to determine most effective interventions and treatments, identify at risk children to help build resilience early
44
What are resilience factors?
positive coping strategies, asking for help, developing healthy, trusting relationships
45
What are individual factors?
strong cultural identity, self-regulation, sense of meaning and purpose, effective coping skills, problem solving skills
46
What are family and relational factors?
stable and supportive relationships, adequate housing and income, stimulating household environment, role modelling, connection to positive social network
47
What are community factors?
safe and connected communities, access to services, mentorship, positive relationship with peers, access to extracurriculars positive school environment, quality childcare
48
What are neurodegenerative disorders?
A heterogenous group of slowly progressing diseases of the nervous system caused by loss of cell function and death
49
What are the ways to slow and cure neurodegenerative disorders?
none
50
What does treatment of neurodegenerative diseases focus on?
managing comorbidities
51
How are neurodegenerative disorders diagnosed?
Based on clinical/pathologicl features
52
What part of the nervous system is AD associated with?
hippocampus and cerebral cortex
53
What part of the nervous system is huntington 's and Parkinson's disease associated with?
basal ganglia
54
What part of the nervous system is spinocerebral ataxias associated with?
spinal cord and cerebellum, impairing balance and coordination
55
What part of the nervous system is charcot-marie-tooth disease associated with?
PNS
56
What themes are common in the pathogenesis of neurodegenerative diseases?
age, protein misfiling, synaptic disfunction, neuronal cell death
57
How is age associated with NDDs?
increased age is a risk factor. defects in mitochondrial metabolism, increased ROS, cell injury, and cell death
58
How is protein misfolding associated with NDDs?
abnormal protein folding causing aggregation
59
How is synaptic disfunction associated with NDDs?
disturbance in structure/function of the synapse is likely an important event in early disease development
60
How is neuronal cell death associated with NDDs?
neurons in most affected regions die. They have usually been maladapted or stressed for months or years beforehand, so treatment on them is limited
61
What is dementia?
A general term for a decline in cognitive function (memory, thinking, reasoning, complex motor skills) due to neurodegenration
62
Is dementia a normal part of aging?
No
63
What are the financial and societal implications of dementia?
As the population ages, dementia prevalence will increase
64
What health factors increase the risk of dementia?
genetics, diabetes, BP, cholesterol
65
What lifestyle and dietary factors increase the risk of dementia?
smoking, physical activity, obesity, drug and alcohol abuse, poor access to a good diet
66
What mental health factors increase the risk of dementia?
PTSDm depression, schizophrenia
67
What is the burden of dementia on Indigenous communities?
increased incidence, up to 10 years earlier onset, not diangnosed fast enough too benefit from care and support
68
What is the Indigenous view of dementia?
considered normal and deeply rooted in culture, many terms for it that are humorous and gentle like 2nd childhood, closer to creator. considered circle of life and since it is not associated with illness, less access care
69
What is I-CAARE?
Indigenous cognition and aging awareness research exchange
70
What are the spiritual cares related to dementia?
attend ceremonies and use medicine for wellness, use prayer, maintain health holistically, attend ceremony/church, express gratitude
71
What are the physical cares related to dementia?
eat healthy, unprocessed foods, prevent head injuries, exercise, don't abuse substances, stay away from contaminants in food/medecine, grow/gather own food
72
What are the mental cares related to dementia?
laugh, sing and dance, read, seek therapy, stay connected, be responsible and accountable, practice kindness
73
What are the emotional cares related to dementia/
speak/listen/learn original languages, participants[pate in storytelling/singing, craft/bead/knit/crochet/sew, carry and share songs/teachings/ceremonies, do puzzles and crosswords, be aware of aging nd dementia, use internet
74
Who is pearl?
a 73yo woman in generally good health but with memory lapses
75
What did Charlie's letter say?
Mother is beginning to not care about family or friends or gardening
76
What was performed at Pearl's appointment?
Cognitive tests to evaluate judgement reasoning, memory and problem solving
77
What was the result of Pearl's test?
Couldn't draw a clock at a specific time, couldn't follow a pattern
78
What do cognitive tests assess?
oral, written, listening to test short term memory, orientation, and visuoconstructive skills
79
How is orientation assessed?
Asked about current date, address, city
80
How is ST memory assessed?
given 5 words, told to repeat them. asked to perform a separate task, repeat again
81
How is visuoconstructive tested?
asked to draw a clock showing a given time (called the Montreal Cognitive Assessment)
82
What is AD?
progressive neurodegenerative disease that is the most common cause of demetia
83
What is the life expectancy after an AD diagnosis?
4-8y, but outliers can hit 20y
84
Who is AD named after
Alzheimer, a German psychiatrist who reported autopsy results of Auguste Deter in 1907
85
How much is the incidence of Alzheimer's expected to increase?
2x by 2030, and >3x by 2050, increasing the burden on the health care system
86
How does AD affect indigenous pops?
Scarce info, making responding to emerging info difficult. No validated screening tool that is First Nations sensitive and take SDH into account. 4x increase by 2030
87
What are the risk factors for AD?
Genetics, Sex, Lifestyle
88
How does genetics affect AD risk?
1% of cases are caused by inherited mutation affecting amyloid b processing, with other mutations increasing the risk of the more common sporadic form
89
How does sex affect AD risk?
incidence in women is 2x that of men
90
How does lifestyle affect AD risk?
Modifiable risk factors like diabetes obesity, depression, smoking, low education increase risk
91
What are the two proteins associated with AD?
tau and amyloid b
92
What is amyloid b?
A small protein fragment from cleavage of amyloid precursor protein found in the neuronal membrane
93
What occurs is APP is cleaved improperly?
aggregation into oligomers concentrated at synapse and outside of the neuron forming plaques
94
What happens once a plaque is formed?
microglial activating, inflammatory molecules released, causing neuronal injury, dmg walls of brain blood vessels leading to cerebral amyloid angiopathy
95
What is tau?
a protein that bind to microtubules, promoting stability?
96
What happens if tau misfolds?
oligomers form which aggregate as neurofibrillary n=tangles, which are toxic to neurons and can spread through synapses, causing further misfolding
97
What is the amyloid cascade hypothesis/
the most accepted model for AD development, proposing that accumulation and deposition of AB is primary cause of AD and tau tangles come later, exacerbating.
98
What is the first step of the ACH?
AB is produced by APP cleavage in cell membrane?
99
What is the second step of the ACH?
AB oligomers disrupt synaptic function
100
What is the third step of the ACH?
AB oligomers aggregate into plaques outside cell, disrupting function
101
What is the fourth step of the ACH?
Ab deposits outside of the cell activate microglial, leading to harmful inflammation
102
What is the fifth step of the ACH?
misfiled tau aggregates. displacing intracellular organelles
103
What is the sixth step of the ACH?
Misfiled tau can go through synaptic transmission leading to further misfolding
104
Where does early stage AD affect?
begins in/near hippocampus on the medial surface of each temporal lobe of the brain, involved in memory retrieval/encoding, and spatial recognition
105
Where does middle stage AD affect?
increased areas of cerebral cortex, causing neuronal death
106
How long does it take for middle stage AD to progress to late stage?
several years
107
How long before diagnoses does AB plaque begin to form?
10-15 years
108
When do tau tangles form?
close to the onset of symptoms
109
What is an abnormal decline in cognition called?
MIld Cognitive Impairment (AD precursor)
110
What macroscopic changes are associated with AD?
cerebral cortex atrophy, enlarged ventricles, and hippocampal atrophy
111
What is cerebral cortex atrophy?
atrophy of outermost ;ayer of cells, decreasing size and weight of brain
112
What is vertical enlargement?
fluid-filled spaces enlarge due to tissue degeneration (exvacuohydrocephalus)
113
What is hippocampus atrophy?
hippocampus shrinks as result of neuronal cell death
114
How is AD diagnosed?
examining mental history, mental exam, bloodwork, brain imaging, cog. testing, insidious onset, examine function, look for no other red flags, diagnose dementia
115
What are next steps for AD?
education, support, family planning, future planning, some medications
116
How is life with AD?
Requires care from a team, daily care with caretakers participating in decision making
117
How is a caretaker affected by AD?
Increased work, increased stress
118
What are the benefits of an early AD diagnosis?
appropriate care, accurate diagnosis, patient is more involved in decisions, better treatment options, can set priorities in life, access to resources, advocacy for Alzheimers awareness and wellness
119
Who Is Jack?
18yo Hsc student on QU soccer team who has difficulty walking to and from class, trips easily, has a decrease in soccer abilities, and has intermittent pain in outer calf for 20 min or more at a time
120
What is the suspected cause of Jack's problems?
Nerve Damage
121
What neurological examinations were performed on Jack?
Nerve conduction study, Electromyopgraphy test, and genetic testing
122
What is a nerve conduction study?
tests function of electrical signals in nerves electrical charge through electrodes on skin. Weak response may indicate weak signal transmission
123
What is an electromyography test?
inserts thin needle into muscle, attached to wire, connected to machine, flex/relax muscles, monitors electrical activity
124
What was Jack's genetic test?
A blood sample to check for hereditary neuropathies
125
What is CMT?
most common inherited neurological disorder In NA characterized by progressive weakness and atrophy beginning in the legs that, as it progresses, can lead to diminished or absent muscle stretch reflexes and sensory deficits
126
When is CMT onset?
Childhood, with a slow progression that doesn't impact lifespan
127
How is living with CMT?
discouraging, frustrating, overwhelming, sadness, loneliness, guilt, anger, fear
128
How is CMT a spectrum?
it is an umbrella term for a genetic disease that affects the PNS. There are o er 100 genes linked to the disease
129
What is CMT type 1?
demylinating neuropathy that affects Schwann cells, slowing conduction
130
How does CMT type 1 affect an individual?
It is slowly progressive, beginning in legs and spreading to hand, etc..
131
What is CMT type 2?
Axonal neuropathy caused by the degeneration of axons, leading to loss of nerve supply to muscles and the atrophy of skeletal muscle
132
How does CMT type 2 affect an I individual?
milder symptoms than CMT1 with less disability and sensory loss
133
What did Jack's test result show?
slower than normal nerve impulses, and duplication on chromosome 17 of PMP22 gene, which functions in PNS myelin
134
How is exercise used in CMT management?
physiotherapthy is standard of care for muscle maintenance to prevent further atrophy
135
What is Jack's diagnosis?
CMT type 1
136
What is Jack's prognosis?
limited to Lowe rlimbs, so it will not affect his studies, no more competitive sports, training with team where he does adaptive exercises, 2-3h of aerobic exercise and 2-3 hours of standing and walking time per week, with follow ups every 3-4 months