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PATHOLOGY 120 > Module 4 (Disorders of the Nervous System) > Flashcards

Module 4 (Disorders of the Nervous System) Flashcards

1
Q

What is the role of glial cells in the nervous system?

A

Help neurons communicate with each other
(regulating environment around neurons, maintain position of neurons, repair neurons)

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2
Q

Explain the process of nerve signalling in the nervous system

A

RECEPTION at dendrites
ACTION POTENTIAL
Signal at SYNAPSE triggers release of neurotransmitter
TRANSMISSION to next neuron

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3
Q

Explain the process of neurotransmission

A

At rest neurotransmitters stored in vesicles
Action potential releases them
Neurotransmitters bind to receptors on adjacent cells to initiate action potential
After signal complete, neurotransmitters unbind

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4
Q

The role of Schwann cells

A

Support and insulate neuron, form and maintain myelin sheath

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5
Q

The role of oligodendrocytes

A

Produce and maintain myelin sheath

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6
Q

The role of microglial cell

A

Immune system in brain
Clear damaged neurons and cellular debris
Pruning synapses in development

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7
Q

The role of astrocytes

A

Provide growth factors and nutrients to neurons
Maintain cells that make up blood brain barrier
Help in tissue repair

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8
Q

What is mental illness?

A

Diagnosable and treatable medical condition
Does not involve identifiable structural brain abnormalities
Reduced ability for a person to function effectively

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9
Q

Explain the concept of ACEs

A

Traumatic events in first 18 years
High ACE scores = high risk for disease
Used to help identify children and risk

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10
Q

Individual factors to prevent and manage ACE

A

Strong identity
Self regulation
Sense of purpose
Effective coping skills
Problem solving skills

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11
Q

Family/relational factors to prevent and manage ACE

A

Stable supportive relationships
Adequate housing/income
Stimulating home environment
Role model
Connection to positive social network

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12
Q

Community factors to prevent and manage ACE

A

Safe and connected communities
Access to services
Mentorship
Positive relationship with peers
Access to activities
Positive school environment
Quality child care

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13
Q

What does Alzheimer’s disease affect?

A

Hippocampus and cerebral cortex

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14
Q

What does Parkinsons and Huntingtons disease affect?

A

Neurons in basal ganglia

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15
Q

Overview of Spinocerebellar Ataxias

A

Group of disorders affecting spinal cord and cerebellum
Results in impairment of balance and coordination of movement

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16
Q

Overview of Charcot Marie Tooth disease

A

Several genetic disorders affecting PNS

17
Q

Explain the pathogenesis of neurodegenerative diseases

A

INCREASING AGE (defects in mitochondrial metabolism, increased production of reactive O2 species, cell injury, cell death)
PROTEIN MISFOLDING (abnormal protein folding/clumping)
SYNAPTIC DYSFUNCTION (disturbance of structure/function)
NEURONAL CELL DEATH

18
Q

Explain dementia

A

Decline in cognitive function (memory, thinking, reasoning, motor skills)
Incurable
Symptoms result of neurodegeneration

19
Q

Risk factors for dementia

A

Increasing age
Health (genetics, diabetes, high BP/cholesterol)
Diet/Lifestyle (smoking, inactivity, obesity, substance abuse, poor diet)
Mental health (PTSD, depression, schizophrenia)

20
Q

Explain the medicine wheel for dementia prevention

A

NORTH
- attend ceremonies, use prayer, express gratitude
EAST
- eat healthy, prevent head injuries, exercise, stay away from contamination
SOUTH
- laugh, sing/dance, read, seek therapy, stay connected to community, be kind
WEST
- use original language, storytelling, craft, puzzles, be educated on dementia

21
Q

Give an overview of Alzheimers. Who was it named after?

A

Progressive neurodegenerative disease
Named after Dr. Alois Alzheimer who reported autopsy results of cognitive disorder in 1207

22
Q

Risk factors for Alzheimers

A

Genetics
Sex (women more than men)
Lifestyle

23
Q

What are the microscopic changes associated with AD?

A

Alterations of Amyloid beta and tau protein cause misfolding and aggregations, resulting in injury and death of neurons

24
Q

Explain the process of amyloid beta oligomers and plaques

A

Small oligomers (fragments concentrate and synapse and disrupt function
Aggregation of oligomers making AB plaques
Plaques activate microglia-> neural injury
Aggregations can also damage walls of brain-blood vessels

25
Q

Explain the process of tau oligomers and neurofibrillary tangles

A

Proteins misfold/bind less strongly with microtubules
Oligomers further aggregate inside neuron as tau tangles (both toxic to neurons)
Misfolded tau can also pass through synapses spreading to other neurons leading to more misfolding

26
Q

What is tau’s regular function?

A

Binds to microtubules helping stability

27
Q

Explain the process in the Amyloid Cascade Hypothesis

A

Amyloid beta PRODUCED by cleavage in APP in cell membrane
Oligomers DISRUPT function in synapse in space between neurons
Oligomers AGGREGATE into plaques outside cell disrupting neuron function
Amyloid beta DEPOSITS outside cell activating microglial (triggering harmful inflammatory response)
Misfolded TAU tangles collect in neuron
Misfolded tau pass through synapse CATALYZING further misfolding

28
Q

What does the Amyloid cascade hypothesis suggest?

A

Neurofibrillary tangles occur later to further disease

29
Q

Describe the early stage of AD

A

Begins near hippocampus (involved in encoding/retrieval of memory, spatial navigation)

30
Q

Describe the middle stage of AD

A

Large areas of cerebral cortex
Amyloid plaques and neurofibrillary tangles cause death of neurons

31
Q

Describe the late stage of AD

A

Increasing amount of amyloid and tau aggregations

32
Q

What is the different roles of marking disease progression in the microscopic changes?

A

Amyloid Beta
- mark start of disease
- may precede diagnosis by 10-15 years
Tau tangles
- accumulate closer to onset of symptoms/ neurodegeneration

33
Q

What are the macroscopic changes associated with AD?

A

Cerebral Cortex atrophy
Enlarges Ventricles
Hippocampal atrophy

34
Q

Describe Charcot Marie Tooth Disease

A

Most common inherited neurological disorder
Usually onset in childhood
Progressive weakness and atrophy in legs
Slow progressing
Does not impact patient lifespan

35
Q

Describe type 1 CMT

A

Primarily impacts Schwann cells
Slow progressing weakness in lower legs
Later in life there is hand weakness and loss of sensation

36
Q

Describe type 2 CMT

A

Primarily in axon
Mutation causes degeneration of neuronal axon (loss of nerve supply)
Same symptoms as CMT1 but milder with less disability and sensory loss

PATHOLOGY 120 (7 decks)

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