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MedSci 206 Module C > Pathogenesis of Perinatal Brain Injury > Flashcards

Pathogenesis of Perinatal Brain Injury Flashcards

1
Q

What are cystic lesions?

A

Large ‘holes’ in the brain.

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2
Q

Where do infants typically have brain injury?

A

In the deeper structures of the brain rather than the cortical structures.

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3
Q

What happens when white matter dies in the brain?

A

Ventricles compensate by increasing in size.

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4
Q

Where do focal lesions occur?

A

In the grey matter.

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5
Q

Which disease is likely to occur more than cancer?

A

Cerebral Palsy.

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6
Q

What are two main forms of acidosis?

A

Hypercapnia and metabolic acidosis. Both can be caused by umbilical cord occlusion.

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7
Q

What is hypercapnia?

A

High levels of carbon dioxide in the blood which makes H2CO3, lowering the pH of the blood.

“Respiratory Acidosis”.

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8
Q

What is metabolic acidosis?

A

An accumulation of lactic acid in the blood. Anaerobic metabolism occurs during hypoxia.

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9
Q

What is apoptosis?

A

Programmed cell death

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10
Q

What is asphyxia?

A

A condition arising when the body is deprived of oxygen, causing unconsciousness or death; suffocation.

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11
Q

After asphyxia occurs, what does the BP in the body do?

A

It increases to compensate for the decrease in BP. We require a certain BP for good perfusion for oxygen and glucose delivery.

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12
Q

How much ATP in our body is produced from ion channels/pumps?

A

About 1/3

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13
Q

What does adenosine do in the brain?

A

It is a neurotransmitter that shuts down brain function. It is a protective mechanism.

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14
Q

What do adenosine blockers do?

A

Inhibit adenosine so that there is an increase in brain function (speeding it up).

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15
Q

What are the 3 types of neural regeneration?

A

Peripheral Nerve Regeneration
Restoration of damaged central nerve cells
Wholesale genesis of new neurons.

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16
Q

In terms of oxygen, what is a stimulus for apoptosis to occur?

A

Hypoxia - HIF-1

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17
Q

What is prophylaxis and when is it applied?

A

It is treatment given or action taken to prevent disease. It is applied in the “pre-insult” phase.

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18
Q

What are the 4 main strategies of the evolution of injury treatment?

A

Pre-insult, insult, recovery and reorganisation.

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19
Q

What are the 3 phases in the recovery strategy?

A
  1. Reperfusion
  2. Latent
  3. Secondary
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20
Q

What is the time frame of the Reperfusion phase in recovery?

A

0 - 30 mins

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21
Q

What is the time frame of the Latent phase in recovery?

A

30 min - 6 hours

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22
Q

What is the time frame of the Secondary phase in recovery?

A

6 hrs - 2/3 days

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23
Q

What phase comes under the reorganisation strategy?

A

Tertiary phase (weeks, months, years)

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24
Q

When does neuroprotection occur?

A

During the recovery strategy

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25
Q

When does neurorepair and augmentation (increase in size) occur?

A

During the reorganisation strategy

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26
Q

What triggers necrosis to occur?

A

Factors that are external to the cell or tissue, such as infection, toxins, or trauma. Results in inflammation.

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27
Q

What is reperfusion injury?

A

Reperfusion injury is the tissue damage caused when blood supply returns to the tissue after a period of ischaemia or lack of oxygen.

Free radicals are generated by the return of oxygen.

Blood pressure needs to be maintained.

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28
Q

What is hyperaemia?

A

The increase of blood flow to different tissues in the body.

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29
Q

How is the latent phase of recovery characterised?

A

By the absence of seizures (pre seizures) and

reduction in early cytotoxic edema. (Presence of this would be secondary phase).

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30
Q

What happens in the latent phase in hypoxic conditions?

A

The depletion of ATP and the reduction of resting membrane potentials in neurons and glia.

Potassium leaks out of cells and
depolarizes neurons leading to a massive release of glutamate (excitotoxicity). Act via
NMDA receptors, glutamate permits the intracellular influx of calcium, which triggers a number of potentially harmful enzymes.

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31
Q

What happens in the secondary phase of recovery following hypoxia?

A

The secondary phase of energy depletion coincides with the onset of cytotoxic edema and seizures.
An accumulation of excitotoxins, increased production of NO, and a fall in brain electrical
activity.

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32
Q

True/false: Most cells die after insult.

A

True.

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33
Q

True/False: Damage does not increase during recovery.

A

False, it does increase.

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34
Q

When is the best time to treat cerebral hypothermia with the cooling of the head?

A

1.5 - 5.5 hrs delay of cooling (latent phase).

NOT secondary phase as too many neurons have been lost. If there has been more than about 65% lost, no efficacy.

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35
Q

What is easy to monitor in a newborn?

A

Cardioresp function, other organs, etc.

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36
Q

What is not so common to monitor in a newborn?

A

Brain activity and blood flow
Brain oxygenation
(EEG, NIRS)

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37
Q

With reperfusion and restoration of blood flow/oxygen after insult, what happens?

A

Recovery of oxidative metabolism (latent phase)

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38
Q

In hypoxic conditions, how is energy produced to maintain oxidative phosphorylation?

A

PCr donates it’s phosphate group to ADP, producing ATP so that oxidative phosphorylation may occur.

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39
Q

What does focal cystic necrosis involve?

A

All cellular elements.

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40
Q

Brain injury in the preterm infant predominantly involves damage to what?

A

White matter.

41
Q

Which structures are relatively spared in preterm infant brain injury?

A

Cerebral cortex and grey matter structures.

42
Q

What four things can MRI imaging of white matter show?

A

Cavitary white matter lesions
Diffuse white matter lesions
Ventriculomegaly
Decreased volume of white matter tracts (white matter atrophy)

43
Q

What is ventriculomegaly?

A

The dilation of the lateral ventricles.

44
Q

Do preterm babies have smaller brains?

A

Yes.

45
Q

In a term infant, what time of lesions would predominantly occur?

A

Widespread grey matter lesions.

This is selective neuronal death (smaller insults - hippocampus, cortex and striatum) and Laminar cell death (more severe espec. in striatum and cortex).

Also focal grey matter lesions.

46
Q

What is the main difference between brain injury in preterm and term infants?

A

Preterm: white matter lesions
Term: grey matter lesions

47
Q

True/false. Neurons in the preterm brain are mores susceptible to injury.

A

FALSE. Neurons in the term brain are more susceptible to injury.

48
Q

What is pseudolaminar necrosis?

A

Superficial layers of cortex are almost separated from the deeper layers.

49
Q

How likely is Cerebral Palsy to occur?

A

10 times more likely than cancer.

50
Q

How often is a child born with Cerebral Palsy?

A

Every 20 minutes.

51
Q

What are common symptoms of Cerebral Palsy?

A
  • arm and leg weakness
  • if they walk, it’s abnormal
  • curvature of spine
  • swallowing/eating problems
  • learning disabilities
  • social alienation
52
Q

When do babies typically get brain injury?

A

With new imaging technologies, have determined that injuries occur well BEFORE birth.

53
Q

What are 4 causes of Perinatal brain injury?

A
  • Hypoxia-ischemia
  • Infection
  • Accident/trauma
  • Teratogens (drug use, alcohol, smoking…)
54
Q

What are causes of fetal hypoxia-ischemia?

A
  • placental abruption
  • tight umbilical cord knot (severe)
  • twisted umbilical cord knot and meconium staining (moderate)
  • prolonged birth
  • CV instability or heart disease (cerebral hypoperfusion)
  • cardiorespiratory arrest
  • preterm lung development
55
Q

What is hypoxemia?

A

Low oxygen in arterial blood.

56
Q

What is the driving force for oxygenation in the body?

A

Partial pressure of oxygen.

57
Q

What pressure does hypercapnia look at?

A

PCO2

58
Q

If there is impaired waste removal, what happens to cause brain injury?

A

Accumulation of CO2 -> Respiratory acidosis -> hypoxia and acidosis = impaired CV system -> reduced brain blood flow and O2 = hypoxia-ishemia -> brain injury.

59
Q

If there is fetal hypoxia, what happens to cause brain injury?

A

Anaerobic metabolism and lactate production -> metabolic acidosis -> hypoxia + acidosis = impaired CV system -> reduced brain blood flow and O2 = hypoxia-ischemia -> brain injury.

60
Q

Define cellular homeostasis.

A

Ability of cell to maintain its normal function over a range of different conditions. The loss of this causes cell damage.

61
Q

What are 4 key homeostatic mechanisms?

A

– i. Maintenance of intra/extracellular ionic gradients by ion pumps

– ii. Production of ATP (energy) under aerobic and anaerobic conditions

– iii. Delivery of oxygen/energy to brain cells (blood perfusion to brain)

– iv. Matching of cellular metabolic activity (demand) to energy supply

62
Q

Ion pumps require how much energy in order to maintain homeostasis?

A

1/3 of all ATP produced.

63
Q

What is the equation for oxidative phosphorylation?

A

Glucose + 6O2 -> 38 ATP +6CO2 + 6H2O

64
Q

True/False. The brain has a limited store of ATP.

A

True.

65
Q

At what partial pressure will no more ATP be produced?

A

Below PO2 of 1mmHg. (thus very low oxygen available)

66
Q

What is the limiting factor to maintaining cellular energy?

A

The amount of oxygen. NOT glucose.

67
Q

During hypoxia, metabolism becomes…?

A

Anaerobic.

68
Q

What is the equation for anaerobic metabolism?

A

Glucose -> 2ATP + lactate

less effective and ACIDOSIS

69
Q

What happens when there is ATP exhaustion?

A

Failure ATP ion exchangers -> DEPOLARISATION -> repeated/uncontrolled -> injury processes begin.

70
Q

With decreasing BP, what happens to the rate of cell death?

A

It increases. Cell survival requires good perfusion.

71
Q

What is asphyxia?

A

A condition when the body is deprived of oxygen.

72
Q

Why does the fetal HR initially decrease in asphyxia?

A

To preserve energy.

73
Q

What 4 main responses occur in a fetus during asphyxia?

A
  • Dec. HR
  • Early inc. BP
  • Peripheral vasoconstriction
  • Reduced brain blood flow
74
Q

What protective response does the brain undergo during a reduced energy supply?

A

The brain tries to reduce its activity. Partly adenosine mediated.

75
Q

Cell lysis is caused by what?

A

Excessive osmosis or hyperhydration (oedema). The cell membrane can’t handle the osmotic pressure of the water inside so lyses.

76
Q

In apoptosis, what can you see in the early apoptotic and late apoptotic cell?

A

Early: membrane blebs
Late: apoptotic bodies and nuclear fragments

77
Q

Is there an inflammatory response with apoptosis?

A

No.

78
Q

Is apoptosis energy dependent?

A

Yes.

79
Q

Is apoptosis upregulated with injury?

A

Yes.

80
Q

Is injury an evolutionary process?

A

Yes. Cell loss is not only during insult, but afterwards as well.

81
Q

Is post-asphyxial hypoperfusion to the brain a common response? What happens to the EEG amplitude?

A

Yes.There is a decrease in the EEG amplitude.

82
Q

What does reduced cerebral blood flow (CBF) reflect?

A

Reduced brain metabolism - not damaging.

83
Q

Hypoperfusion is controlled by which nervous system?

A

The sympathetic nervous system.

84
Q

How does Phentolamine effect the SNS?

A

It blocks the SNS receptors thus preventing hypoperfusion.

85
Q

How does phentolamine effect brain injury?

A

It blocks EEG suppression in the latent phase and increases EEG spiking, increasing brain injury. SO EEG is partially neuroprotective.

86
Q

How can NMDA receptor inhibitors effect brain injury?

A

NMDA receptor inhibitors can block EEG spiking activity, reducing brain injury. SO EEG transients are mediated by glutamate and trigger cell injury.

87
Q

How do glutamate receptors trigger cell death?

A

Over-activation of glutamate receptors can trigger intracellular Ca2+ levels and trigger cell death.

88
Q

Explain glutamate excitotoxicity.

During insult and after insult

A

During: Energy low -> glutamate transporters fail. Accumulation of extracellular glutamate and excessive glutamate receptor activation.

After: cerebral energy normal, thus glutamate levels normal. BUT:

  • glutamate receptors hypersensitive to normal glutamate.
  • SO during latent phase, excessive glutamate receptor activity triggers lots of intracellular Ca2+ and apoptosis.
89
Q

What signal in the apoptosis pathway is the final executor of cell death?

A

Caspase-3

90
Q

Pathways leading to caspase-3 activation require what?

A

Time.

91
Q

True/False. Dead cells in the latent phase can come back.

A

FALSE.

92
Q

Is hypoperfusion related to BP?

A

No.

93
Q

True/False: Secondary phase of energy failure is NOT driven by deficits in brain oxygenation or nutrient supply.

A

True.

94
Q

Secondary oxidative metabolism failure will cause what in the mitochondria?

A

Mitochondrial failure.

95
Q

Does the EEG recover in the secondary phase?

A

Yes.

96
Q

Does blocking seizures improve brain injury?

A

No.

97
Q

When does edema recover?

A

In the latent phase. It increases again during the secondary phase of cell death.

98
Q

What are the 4 main characteristics of secondary phase of injury?

A
  • secondary failure of oxidative metabolism
  • Stereotypic evolving seizures (big seizures)
  • Hyperaemia (increased CBF and volume)
  • Secondary edema – necrosis/lysis ongoing

MedSci 206 Module C (6 decks)

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