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Neuro > Lecture 6 > Flashcards

Lecture 6 Flashcards

1
Q

neuron

A

primary communication/information cell type of the nervous system

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2
Q

glial cells

A

supportive cells of the nervous system

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3
Q

neuron structures

A

cell body (soma)
dendrite
axon
terminal axon

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4
Q

neuron function

A

responsible for neurotransmitter signaling in the nervous system

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5
Q

cell body

A

production factory for all components of the neuron: enzymes, proteins, membrane structures, organelles

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6
Q

cell body clinical application

A

abnormal protein synthesis, assembly and clearance associated with neurodegenerative diseases

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7
Q

dendrites

A

sensory input
narrowed extension of cell body that results in huge synaptic surface area - 30x’s surface area of cell body

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8
Q

axons

A

conduct action potentials for signaling
myelinated= nodes of ranvier: located between myelin sheaths allow faster transmission of action potential, internode: segment that is covered in myelin
unmyelinated = slower transmission of AP

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9
Q

anterogade transport

A

cell body to terminal axon

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10
Q

retrograde transport

A

terminal axon to cell body

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11
Q

microtubular highway

A

transports molecular components necessary for cell function and structure
consists of microtubules and neurofilaments

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12
Q

microtubules

A

hollow tubes made of protein molecules

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13
Q

motor proteins

A

transport cellular substances to/from cell body along the microtubule

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14
Q

terminal axon and synapse

A

neurotransmitter synapse with a dendrite
terminal axon releases neurotransmitter -> terminal end is responsible for re-uptake of neurotransmitter -> neurotransmitter is broken down/recycles in terminal axon

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15
Q

presynaptic side

A

contains synaptic vesicles filled with neurotransmitters -> AP signals calcium influx to facilitate neurotransmitter release -> also responsible for re-uptake of neurotransmitter from synaptic cleft

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16
Q

post synaptic side

A

target dendrite or cell
neurotransmitters binds to receptors (proteins) -> after recognized by post-synaptic receptor is released back into the synaptic cleft

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17
Q

types of glial cells

A

astrocytes
oligodendrocytes
microglial cells (microglia)
ependymal cells
schwann

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18
Q

astrocytes

A

fill the space between neurons
dynamic and significant role in CNS signaling, function and health
damage/dysfunction leads to CNS pathology

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19
Q

astrocytes processes

A

surround the blood vessels in the brain/CNS
form synapses with other neurons and other glial cells

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20
Q

astrocyte functions

A

regulate the BBB
transport nutrients = rapid removal of excess glutamate, maintain extracellular potassium
regulates synapses
remodeling = neuron recovery and scar formation after neuron injury

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21
Q

gliosis

A

glial cell reaction or responses to CNS injury/damage

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22
Q

astrogliosis

A

reactive defense response that minimizes/repairs damage to the CNS and plays a role in scar formation

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23
Q

astrocyte dysfunction

A

acute injury/trauma/stroke
neurodegenerative diseases: Alzheimer’s, Parkinson’s, MS
psychiatric: disrupted signaling

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24
Q

oligodendrocytes function

A

myelinating axons of the CNS

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25
Q

oligodendrocytes pathology

A

there will be demyelination

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26
Q

microglial cells function

A

clear toxic materials

27
Q

ependymal cells

A

specialized epithelial cells that line the ventricles, central canal of the spinal cord, and choroid plexus of the CNS

28
Q

schwann cells function

A

only in PNS
responsible for myelinating axons in the nerves of the PNS
also provide connective tissue support and have a phagocytosis role in the peripheral nerve

29
Q

proteinopathies

A

develop from abnormal protein production or excess accumulation of cellular proteins within and/or around neurons
excess accumulation of proteins eventually leads to neuron cell death

30
Q

different types of proteinopathies

A

α-synuclein
Tau protein
beta amyloid plaque
TDP-43

31
Q

neurodegenerative disease

A

Alzheimer, pick’s disease, chronic traumatic encephalopathy (CTE), Huntington, Parkinson, Lewy body dementia, ALS

32
Q

Alzheimer

A

α-synuclein
Tau protein
beta amyloid plaque

33
Q

Pick’s disease

A

Tau proteins (Pick bodies)

34
Q

chronic traumatic encephalopathy (CTE)

A

Tau proteins

35
Q

Parkinson’s disease

A

α-synuclein

36
Q

Alzheimer’s disease

A

progressive onset of symptoms that range from small memory loss to severe memory loss, cognitive loss, and personality changes
*most common form of memory loss
*prevalence increases with age

37
Q

Alzheimer’s pathology

A

progressive widespread atrophy of the cerebral cortex
*begins in the temporal lobe
astrocyte dysfunction=disrupted glutamine and protein clearance, reduction of blood flow and damage to BBB
proteinopathy= impaired protein clearance and abnormal protein accumulation leading to formation of neuritic plaques, neurofibrillary tangles

38
Q

neuritic plaques (amyloid plaques)

A

abnormal accumulation of beta amyloid
healthy CNS = protein constantly produced from cell membrane and removed from the brain
alzheimer’s CNS = promotes excess amyloid and accumulation of beta amyloid proteins form neuritic plaques that surround and damage axon
intracellular protein accumulation

39
Q

neurofibrillary tangles

A

abnormal accumulation of Tau proteins within the axon forming neurofibrillary tangles
healthy CNS = tau proteins equilibrium are regulated by phosphorylation of Tau proteins
alzheimer’s CNS = excess tau phosphorylation disrupts the microtubule structure/function causing abnormal tau protein accumulation creating neurofibrillary tangles
extracellular protein accumulation

40
Q

trauma and AD

A

traumatic brain injury can increase risk of developing alzheimer’s disease
trauma disrupts cell function, causes abnormal protein clearance pathways and may form a proteinopathy that leads to Alzheimer’s disease

41
Q

Alzheimer’s Disease: Clinical Features

A

visuospatial deficits
memory deficits
impairment with planning and performing familiar tasks
judgement, safety, and a problem solving impairments
personality changes
language decline
motor impairments = posture, gait, bradykinesia

42
Q

Pick’s Disease

A

frontotemporal dementia (FTD)
Pick Body Dementia

43
Q

Pick’s Disease: Signs and Symptoms

A

apathy
poor insight into consequences of behavior
repetitive behaviors
loss of personal hygiene
loss of social graces
impulsive behaviors
disinhibition

44
Q

Pick’s Disease Pathology

A

mutations of the tau gene causing abnormal Tau protein accumulation that lead to neuron death
pick’s disease neurofibrillary tangles are round (Pick bodies)

45
Q

Multiple Sclerosis

A

demyelinating disease that damaged oligodendrocytes and disrupts the nerve signaling

46
Q

UMNL

A

location: injury to the CNS
muscle tone: hypertonia
reflexes: hyperreflexia, + Babinski
weakness: spastic paralysis
atrophy: slow/disuse atrophy

47
Q

LMNL

A

location: injury to the PNS
muscle tone: hypotonia
reflexes: hyporeflexia, - Babinski
weakness: flaccid paralysis
atrophy: quick atrophy

48
Q

MS pathology

A

impairment of BBB/astrocytes
promote inflammation responses that target oligodendrocytes and cause damage to the myelin sheath and potentially the axons of the CNS neurons
episodes of acute inflammation = MS flare

49
Q

MS proteinopathy

A

MS plaques (scarring) develop from prolonged or severe episodes of immune/inflammation attacks
astrogliosis = reactive defense response and scar formation in immune/inflammation attack
fibrous scars (plaques) replace may permanently damaged neurons
TDP-43
synaptic protein bassoon (Bsn) proteinopathy

50
Q

MS: Exacerbations

A

vary in frequency and duration
triggers may include = viral or bacterial infections, stress, heat, poor health

51
Q

acute concussion

A

absence of gross CNS damage = result is a functional loss and not structural damage
neurological imaging = no structural abnormalities are demonstrated in standard neurological imaging studies

52
Q

acute concussion pathology

A
  1. initial injury causes transient microscopic disruption “neuron gets dinged” = stretch/deform the cell membrane, alter axonal transport, abnormal neurotransmitter glutamate release and electrolyte imbalance
  2. astrocytes work overtime and are unable to maintain CNS homeostasis from the excess release of intracellular and extracellular glutamate, potassium, calcium, and glucose
  3. mismatch of cerebral blood flow is inadequate for metabolic demands of the jolted neurons = astrocytes are unable to maintain adequate blood flow to the area
53
Q

Chronic Traumatic Encephalopathy

A

progressive neurodegenerative pathology associated with any form of repetitive mind brain trauma

54
Q

symptoms of CTE

A

memory loss, depression, suicidal, aggressive affect, cognitive loss and sometimes motor impairments

55
Q

CTE pathology

A

repetitive trauma disrupts protein clearance pathways

56
Q

CTE proteinopathy

A

abnormal accumulation of tau proteins form neurofibrillary tangles, similar to AD but has a different regional distribution pattern in the brain
does NOT have amyloid accumulation
CTE often not diagnosed until after death = no current diagnostic markers for living individuals

57
Q

structure of peripheral nerve

A

epineurium = outer most layer, surrounds one peripheral nerve
perineurium = surrounds one fascicle or group of nerve bundles
endoneurium = surrounds a single axon

58
Q

schwann cells

A

specialized glial cells located only in the PNS
function = myelinating axons in the nerve of the PNS, also provide connective tissue support and have a phagocytosis role in the peripheral nerve

59
Q

mechanism of injuries to peripheral nerves

A

stretch/traction force injuries
laceration injuries
compressive force injuries (entrapment neuropathies)

60
Q

wallerian degeneration

A

process of degeneration that provides opportunity for regeneration to occur
phase 1 = acute nerve injury
phase 2 = degeneration (immune response)
phase 3 = regeneration

61
Q

neuropraxia

A

least severe nerve injury with good prognosis
focal demyelination, but no axonal loss
wallerian degeneration does not occur
complete recovery in 3 to 6 weeks

62
Q

axonotmesis

A

variable severity nerve injury
disruption of axons with perineurium and epineurium remaining intact
wallerian degeneration occurs
variable progress and may require many months

63
Q

neurotmesis

A

most severe nerve injury
complete transection of all components of the nerve
wallerian degeneration occurs
requires surgical repair or no chance for improvement

64
Q

peripheral nerve recovery

A

rate of recovery = slow
1-2mm/day
0.04 to 0.08 inches per day
1 - 2 inches per month
motor recovery = approximate window of 12-18 months before irreversible motor end plate degeneration occurs
sensory recovery = time frame for sensory reinnervation is longer than motor but eventually plateaus/stops

Neuro (21 decks)

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