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HUB paper 2 > When things go wrong part 2 > Flashcards

When things go wrong part 2 Flashcards

1
Q

What is pain?

A

Unpleasant sensory & emotional experience associates with actual or potential tissue damage, described in terms of such damage

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2
Q

Dimensions of pain

A

1 - Sensory/discriminative: sensation of stimulus
2 - cognitive: degradation & evaluation of pain
3 - Motivational aspects of pain: reward or punishment

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3
Q

Physiological pain

A

(fast) Good/acute pain - sudden onset & receded during healing process

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4
Q

Pathological pain

A

(slow) Chronic/bad pain - such as that caused by nerve injury which may be due to toxins, ischemia or diabetes

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5
Q

Classification of nociceptors by modality:

A

1 - mechanical
2 - chemical
3 - thermal
4 - polymodal: responds to combinations of stimuli

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6
Q

Pain stimuli received through usually multimodal receptor such as:

A

Vallinoid receptor (TVRP-1)

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7
Q

Layers of grey matter found in:

  1. layers 1-6
  2. layers 7-9
  3. Layer 10
A
  1. Laminae 1-6 = in the dorsal horn
  2. Laminae 7-9 = in the ventral horn
  3. Lamina 10 = surrounds central canal
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8
Q

Which pathway carries pain?

A

Spinothalamic/anterolateral pathway

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9
Q

The two fibres that bring signals of pain innervate 2nd order neurons in different layers:

A

A. A-delta fibres: laminae 1-5

B. C fibres : laminae 1 &2

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10
Q

What is a stroke

A

a focal neurological deficit due to disruption of regional blood supply. it is a short-term phenomenon & happens suddenly, but typically over hours

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11
Q

Three implications with regards to cerebral blood flow

A
  1. suboptimal cerebral blood flow - neurological dysfunction
  2. cessation of cerebral blood flow for 5-10s - loss of conciousness
  3. cessation of cerebral blood flow for ~5min - irreversible neurological damage
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12
Q

Factors that regulate cerebral blood flow

A
  1. cerebral autoregulation
  2. CO2 (PaCO2)
  3. Oxygen (PO2)
  4. Body temperature
  5. Autonomic system
  6. Local factors
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13
Q

Hypercarbia & Hypocarbia

A 
Hypercarbia = induced cerebral vasodilation when there is too much CO2
Hypocarbia = induced cerebral vasoconstriction when there is too little CO2 dissolved in the interstitial fluid
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14
Q

Stroke risk factors

A
  1. Atherosclerosis - plaque build-up in arteries
  2. Hypertension
  3. Diabetes Mellitus
  4. Smoking
  5. Family history
  6. Cardiac disorders
  7. Obesity
  8. Drugs - alcohol/cocaine/amphetamines
  9. vascular malformations (aneurysms)
  10. Clotting disorders/anticoagulants
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15
Q

Microglia cells functions:

A
  1. resident innate immune cells
  2. 1st line immune defense in the CNS
  3. protect against foreign elements
  4. scavenges the brain for damaged neurons, abnormal proteins & infectious agents
  5. Phagocytes
  6. important role in brain development ==> synaptic pruning
  7. involved in promoting synaptic plasticity
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16
Q

Astrocytes functions

A
  1. structural support (scaffold) of NS
  2. Metabolic support to neurons (lactate)
  3. Neurotrophic factors; NGF, BDNF
  4. Maintain synapses –> regulate ion concentrations in extracellular space
  5. NT uptake & release
  6. Glial scar - brain injury
  7. Support myelin coverage
  8. BBB support
  9. Regulation of blood flow
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17
Q

Both astrocytes & microglial cells have regional heterogeneity - meaning:

A

They have different functions in different brain regions

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18
Q

Cytokines are involved in “house-keeping” functions:

A
  • Memory
  • Behaviour
  • Regulation of sleep
  • Synaptic plasticity
  • Neuronal transmission
  • Intracellular signalling mechanisms
  • Perception of pain
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19
Q

M1 Polarization:

A
  • Neuro-damaging by increased cytokines & oxidative stress
  • reduced scavenging function
  • sustained pro-inflammatory response
20
Q

M2 polarization:

A
  • Anti-inflammatory response

- repair & remodeling of injury

21
Q

A1 Astrocytes;

A
  • Neuro-damaging
  • produce neurotoxic substances
  • decrease new synapses
  • decrease synaptic support
  • decrease glutamate uptake & lead to excitotoxicity
  • decrease glymphatic clearance
  • increase pro-inflammatory cytokines
22
Q

A2 astrocytes:

A
  • increase neurotrophic factors (growth)
  • neuronal protection
  • neuronal repair
  • increase anti-inflammatory cytokines
23
Q

Mechanism of entry of Sars-Cov-2 into CNS:

A 
1 - Olfactory system
2- Paracellular transport
3- Transcellular transport
4 - Adsorptive transcytosis
5 - Receptor-mediated endocytosis
6- Trojan Horse trafficking
24
Q

Astrocyte activation name & charcateristics

A

Astrogliosis - characterized by increase in the number & size of astrocytes during inflammation

25
Q

Astrocyte activation results in:

A
  • regulate BBB integrity
  • Recruit infiltering immune cells
  • activate inflammatory signalling pathways
26
Q

Mechanism of Neuroinflammation

A

1 - pathogens - activate astroycte & microglia
2 - activation - release of cytokines, 2nd messengers, chemokines, ROS
3 - these cause:
- cell responses: proliferation, migration
- gene induction/ upregulation
- impaired BBB functions
- sometimes neurodegeneration

27
Q

Molecular Mechanisms of Neuroinflammation

A
  1. peripheral immune cells activate to release pro-inflammatory cytokines
  2. cytokines travel through blood –> brain
  3. Cross BBB or bind to receptors on endothelium causing glial cells to release cytokines in parenchyma
  4. Cytokines in the parenchyma bind to target cells (other glial cells)
  5. Triggers signalling pathways (multiple steps of molecule activation including activation of TFs)
  6. Inflammatory actions translocate TFs into nucleus of microglial cells
  7. TFs bind to DNA & encode for inflammatory molecules - cytokines, chemokines etc to be released
28
Q

When does cell death occur in the NS:

A
  1. during development of NS
  2. neurodegenerative diseases
  3. after ns injury
29
Q

How is Amyloid Beta protein formed?

A

forms from proteolytic cleavage of APP (amyloid precursor protein)

30
Q

Excitotoxicity - how does it occur?

A

Excitotoxicity = over-excitation of neurons

  • glutamate stimulation
  • neurons could be over excited
  • resulting in excessive Ca2+ influx into the cell
  • triggers cell death (apoptosis)
31
Q

Neuronal Death after injury/stroke

A

1- Necrotic cell death:
- first wave; immediate destruction of cells
2- Apoptotic cell death:
- delayed effects of injury - reperfusion stress
- linked to inflammatory process
- second wave
- prolonged consequences

32
Q

Requirements for functional axon regeneration

A

1) injured nerve cells must be able to survive after lesion & re-express genes required for axon outgrowth (growth cones)
2) The surrounding tissue (mircroenvironment) must be conducive to axon re-growth
3) re-growing axons must be able to find their proper target areas & establish synaptic contact

33
Q

Axon regrowth after injury

A
  1. motoneuron innervating muscle fibre
  2. after cut - wallerian degeneration sets in neuron swelling, chromatolysis, myelin degenerates, schwann cells de-differentiate
  3. Schwann cells form a substrate for axon growth
  4. functional connection is restored
34
Q

How do Schwann cells support axon regeneration?

A
  1. Phagocytose & recycle cellular debris
  2. Provid growth-promoting substrate (cell adhesion molecules - provided by de-differentiated schwann cells)
  3. support neuron survival & axon re-growth - production of neurotrophic factors
35
Q

The 2 hallmarks of AD

A

1 - amyloid beta deposits

2 - neurofibrillary tangles - hyperphosphorylated Tau proteins

36
Q

Neuroinflammation in depression

A
  • activated microglia cells express translocator protein (TSPO) on their mitochondira
  • radio ligand PK11195 binds to TSPO
    (w PET scan)
37
Q

Resident immune cells of the CNS, phagocytic & assume an amoeboid shape when activated

A

Microglia

38
Q

The most numerous glial cells, have star-shaped morphology & immunocompetent

A

Astrocytes

39
Q

Made up of part of BBB & have TJs to control movement of substances

A

Endothelial cells

40
Q

Windows of the brain that have an incomplete or absent BBB

A

Circumventricular organs

41
Q

An inflammatory response within the CNS mediated by cytokines & chemokines

A

Neuroinflammation

42
Q

An irreversible damage to neurons that underlies development of neurological diseases following infection:

A

Neurodegeneration

43
Q

Chemical mediator of immune response released by glial cells for communication during infection

A

Cytokines

44
Q

Mechanism used by toxoplasma parasite, HIV & possible SARS-cov2 virus to enter brain. Characterized by WBCs crossing BBB to parenchyma

A

Trojan Horse Trafficking

45
Q

Mechanism used by Rabies & Polo virus. Characterised by invasion of motoneuron before transport to CNS

A

transneural retrograde transport

46
Q

Misfolded protein molecules which cause Mad cow disease & transported to CNS via the enteric NS which innervates the gut:

A

Prions

HUB paper 2 (6 decks)

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