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NEUR 1203 > Midterm - Review > Flashcards

Midterm - Review Flashcards

1
Q

Necrosis

A

Premature cell death where cells rupture, spilling their content into extracellular space

Results in inflammatory response

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2
Q

Apoptosis

A

Programmed cell death

Cells are dismantled into membrane-bound vesicles

‘Cell Suicide’

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3
Q

Traumatic Brain Injury

A

ABI which includes on damage to the brain caused by an external mechanical force

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4
Q

Cause of TBI

A

When a blow to the head is sufficiently forceful the CSF is unable to protect the brain resulting with a collision of the brain and skull

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5
Q

Coup TBI

A

Brain collides with skull on same side of impact

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6
Q

Contrecoup TBI

A

Brain collides with skull on opposite side of impact

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7
Q

TBI severity depends mostly on degree of _______

A

Rotational Force - skull rotates and brain is to slow to catch up

Can result in sheared corpus callosum or torn bridging veins

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8
Q

Site of Contact with skull in TBI

A

Swelling (edema) or Bleeding (hematome) which can lead to Intracranial Pressure (ICP)

Necrotic Death due to direct impat (causing cells to rupture)

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9
Q

Generalized Damage in TBI

A

Possible infection from penetration or open trauma

Diffuse injury throughout brain due to different density of white and gray matter

Diffuse Axonal Injury (DAI) - twisting and shearing forces cause axon to be torn from cell body (axotomy)

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10
Q

Energy Crisis faced in TBI

A

Disrupted blood flow leads to:

Lack of Oxygen (hypoxia) - causes switch to anaerobic metabolism which leads to overproduction of lactic acid (acidosis) which damages BBB

Lack of Glucose (Hypoglycemia) - leads to cognitive deficits and further reduction in ATP production

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11
Q

Excitotoxicity

A

Excess Glutamate

Glu continously binds to and activates post-synaptic receptors leading to Ca2+ influx, resulting in depolarization, Ca2+ get sequestered in Mitochondria which disrupts production of ATP

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12
Q

Causes of Excitotoxicity

A

TBI - Necrosis (Excess Glu due to rupturing cells)

Stroke - Neuronal Depolarization

HD & ALS - Decreased Glu reuptake

AD - Due to Atrophy

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13
Q

Immune Activation in TBI

A

Microglia secrete pro-inflammatory cytokines

Environmental stress increased toxic Reactive Oxygen Species (ROS) production which leads to Oxidative Stress

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14
Q

Oxidative Stress

A

Result of = ROS > AntiOX

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15
Q

Immune Privilege

A

Sites of body able to tolerate introduction of foreign substances without eliciting inflammatory response

Brain is NOT immune privileged due to interaction with peripheral immune system

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16
Q

Concussion

A

Mild TBI - a head injury with a temporary loss of brain function

  • Upper brainstem & RAS* - Alterations of consciousness
  • Corpus Callosum & Ant. Commissure* - Altered neurological function
  • Vascular Injuries* - Headache, dizziness, fatigue
  • Hippo. & Frontal Lobe* - memory, attention, concentration
  • Amyg. & Basal Forebrain* - mood and emotion
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17
Q

Chronic Traumatic Encephalopathy (CTE)

A

Progressive degenerative disease found in an individual with a history of multiple concussions

Brain Changes: Decreased brain weight, enlarged ventricles, neuronal death, tau aggregates, beta-amyloid plaques

Symptoms: Memory impairment, erratic behavior, impulsivity, depression, suicidal thoughts

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18
Q

Neurocirculation

A

Brain’s blood supply comes from Common Carotid and Vertebral Arteries (form Circle of Willis)

Main arteries which rise to brain - ACA, MCA, PCA

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19
Q

Stroke

A

Interruption of blood flow to the brain

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20
Q

Ischemic Stroke

A

Blockage in blood vessels

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21
Q

Ischemia

A

Lack of blood flow to tissue or organ

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22
Q

Hemorrhagic Stroke

A

Rupture in blood vessels

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23
Q

Ataxia

A

Reuslt of Cerebellar stroke

Motor impairments, difficulty walking, balance and coordination problems

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24
Q

Brain’s Energy Supply

A

Brain relies on blood supply to get Glucose and Oxygen (energy supply)

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25
What causes a stroke?
Narrowing of arteries in neck or brain (cholesterol deposits) Genetic mutations which increase risk of hypercholesterolemia, damage blood vessel walls, or cause clotting disorders Environmental/Experiental factors which increase inflammation of vessel walls (High BP, smoking, obesity, alcoholism)
26
Intracerebral Hemorrhagic Stroke
Blood vessel ruptures Blood leaks into surrounding brain tissue and creates swelling (edema) and ICP Necrosis Causes: High BP and aging blood vessels
27
Subarachnoid Hemorrhage
Bleeding in subarachnoid space Cause: Brain Aneurysm (blood-filled bulge in weakened blood vessel wall) Prognosis not good - 40-50% mortality rate
28
Transient Ischemic Attack (TIA)
Mild Ischemic Stroke (Mini Stroke) Similar to stroke - only lasts minutes-hours Leads to more severe attack 15-30% of time Could be adaptive (prepares brain for more severe attack) Treatment - Anti-coagulants (blood thinners)
29
Core of Stroke
Area directly fed by occluded vessel Less than 20% normal blood flow Necrosis and Apoptosis
30
Penumbra of Stroke
Outskirts of lesion, receive blood flow from other vessels 20-40% of normal blood flow Apoptosis - Ripple Effect
31
Stroke Necrosis
Lack of oxygen → switch to anaerobic glucose metabolism → Acidosis → decreased membrane permeability → Ions and water rush into cell → cells swell and rupture
32
Stroke Apoptosis
Lack of Glucose → no fuel for Na/K pumps → Cells Depolarize → flooding of Glu leads cells to initiate self-destruct
33
Damaged BBB in a Stroke
During Ischemia, epithelial cells are weakened (due to hypoxia and resulting acidosis) → during reperfusion peripheral immune cells can leak through and exacerbate immune response and inflammation
34
Increase Ca2+ in Stroke
Result of Neuronal depolarization Triggers release of Glu Excess Calcium results in production of ROS - as a result Mitochondria can't deal with stress and release signals to induce apoptosis
35
Collateral Circulation
Blood flow through secondary pathways after the obstruction to the principle pathway occurs
36
Neuroplasticity
Ability of the brain to reorganize and form new connections
37
Neuroplasticity after a Stroke
Following neuronal death and removal of death tissue, nearby undamaged neurons can migrate to affected area and take over some lost functions
38
Regrowth after a stroke
Endogenous Repair: Axonal sprouting - new connections from surviving neurons Angiogenesis - vascular growth, restores flow of nutrients to affected area
39
DNA
Packaged into Chromosomes in the cell's nucleus Can be copied - which allows for cell division and reproduction
40
Genes
Segments of DNA that code for the production of specific proteins (Recipes for proteins)
41
Chromatin
DNA + Histones DNA gets wrapped around proteins called Histones This controls activity - if a gene is needed DNA qill unfrul to expose segments of DNA that must be processed (to mRNA then to Protein)
42
Alleles
Variants (alternative forms) of a gene Dominant - only need one to produce a phenotype Recessive - need two to produce a phenotype
43
Epigenetics
Changes in gene expression related to experience The environment can cause certain genes to be turned on or off by changing accessibility via epigenetic markers Acetylation - On, loosen Methylation - Off, tighten
44
Huntington's Disease
Neurodegenerative genetic disorder Follows autosomal-dominant pattern of inheritance HD Gene located in Chromosome 4
45
Symptoms of HD
Motor - chorea, occular movements, clumsiness, dystonia, athetosis Cognitive - restlessness, agitation, irritability, lack of concetration, memory problems Emotional - depression, apathy, anti-social behaviors, aggression
46
Dystonia
Persistent and intermittent muscle contractions causing abnormal and repetitive movements or postures
47
HD symptoms later in disease
Bradykinesia, rigidity, difficult initiating and maintaining voluntary movement Unable to function independently Cognitive issues worsen - progressive dementia
48
HD Prognosis
Death within 15-20 years of symptom onset
49
Cause of HD
HD Gene codes for htt (huntingtin) HD Gene has a section containing repeat of the codon CAG, when there are more than 40 repeats this results in mutant htt which leads to HD CAG codes for AA Glutamine (Gln) - long stretches of Gln result in misfolding and toxic protein aggregates in cells
50
HD Pathology cause
Increased mhtt function + Loss of WThtt function = HD pathology
51
Where does neurodegeneration occur in HD?
Basal Ganglia: Striatum → Medium-Spiny Neurons (MSNs) of caudate nucleus and putamen Cerebral Cortex → Pyramidal Projection Neurons + Neurons with projections to motor cortex and limbic structures
52
Mutant htt in HD
Mutant htt accumulates in the nucleus of neurons (this is correlated with length of CAG repeats)
53
How do mhtt aggregates form?
When mhtt is produced, cell knows this is an irregular protein and releases factors to cut these proteins and dispose → some fragments end up sticking together and creating protein aggregates
54
GABA and HD
Upregulated in early stages, followed by marked reduction Increased upregulated GABA activity + dysfunctional Glu activity in corticostriatal circuit → disruption of integrative processes by MSNs GABA may initially by upregulated to deal with excess Glu
55
Glutamate and HD
Evidence of excitotoxic neuronal death in HD brains Increased Glu receptor stimulation → symptoms of HD Excitotoxcity due to decreased reuptake of Glu
56
Upper Motor Neurons
Originate in either the motor cortex or brainstem → axons extend to synapse onto LMNs Bring motor commands to LMNs May act directly or through interneurons Release Glutamate
57
Lower Motor Neurons
Originate in brainstem or spinal cord → axons leave CNS and synapse onto muscles Receive signals from UMNs and bring messages to muscles Can pass through spinal nervs (limbs and trunk) or cranial nerves (head and neck) Release ACh at NMJ
58
Corticospinal Tract
UMNs from motor cortex → Spinal Cord Control muscles of limbs and trunk Most axons decussate at medulla
59
Corticobulbar Tract
UMNs from motor cortex → LMNs brainstem Contols muscles of head and neck Some decussate and some remain ipslilateral
60
Upper Motor Neuron Damage
Failure to inhibit LMNs Without inhibition LMN keeps telling muscles to contract → sustained contraction → stiffness and rigifity of muscles (spasticity) and hypertonia Hyperreflexia - increase in muscle stretch reflexes No muscular atrophy
61
Damage to Lower Motor Neurons
Unable to tell muscle to start contracting Result is no contraction of muscles → flaccidity, hypotonia, fasciculations (twitching) Hyporeflexia - decrease in muscle stretch reflex Muscle atrophy
62
Amyotrophic Lateral Sclerosis
Degeneration of upper and lower motor neurons controlling voluntary movements Use it or lose it → muscles that do not get ussed will atrophy (waste away) Muscles are NOT dying first → wires connecting brain to muscle are degenerating and muscles are receiving signals
63
ALS Symptoms
Weakness in arms (sporadic) and legs (familial) first Eventually - loss of control of all voluntary muscles in arms, legs, trunk, neck, and head
64
ALS prognosis
Fatal 3 years - 50% 5 years - 80% only 10% live longer than 8 years
65
Riluzole
Treatment for ALS which increases life expetancy 2-3 months Slows loss of muscles by blocking sodium channels and decreasing glutamate
66
LMNs and UMNs in ALS
LMN degeneration → muscle atrophy and fasciculations UMN degeneration → spasms, increased muscle tone, abnormal reflexes
67
Astrocytes in ALS
Release toxins which lead to motor neuronal death Necroptosis (programmed necrosis)
68
Glutamate and ALS
Decreased Glu transporters → Excitotoxicity
69
Action Potential
1. Depolarization

NEUR 1203 (9 decks)

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