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Pumps Pipes and Electrics > Lecture 8 > Flashcards

Lecture 8 Flashcards

1
Q

what are the two routes of cerebral blood supply and what supplies them

A
  1. anterior / posterior cerebral

2. vertebral artery and ICA

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2
Q

Describe the route of the anterior cerebral artery

A

extends forwards and upwards from the ICA

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3
Q

Describe the middle cerebral artery

A

largest branch of the ICA

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4
Q

where does the posterior cerebral artery stem from

A

basilar artery

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5
Q

what does the ACA supply

A

Frontal lobe

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6
Q

what does the MCA supply

A

portion of frontal lobe and lateral region of parietal and temporal lobe

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7
Q

what does the PCA supply?

A

temporal and occipital lobe

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8
Q

what is the rate of cerebral blood flow?

A

constant

to allow neural activity not be compromised

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9
Q

what is the role of the ANS on cerebral blood flow?

A

very small –>global / acute / protective effect

SNS does’nt affect intracerebral pressure

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10
Q

can brain cells store energy?

A

no, they must be supplied with oxygen and glucose at the rate at which they expend energy

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11
Q

what percentage of cardiac output is supplied to the brain?

A

20%

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12
Q

what factors protect the brain’s blood supply?

A
  • metabolic factors
  • cerebrovascular autoregulation
  • endothelial function
  • BBB
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13
Q

what do astrocytes do?

A

important role in coupling blood flow and neural activity

-superimposed between neurons and blood vessels

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14
Q

what 3 things form the microvascular bundle?

A
  • neurone
  • astrocyte
  • microvessel
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15
Q

role of astrocytes in neurovascular coupling?

A

astrocytes transmit chemical messages causing the cerebral vessels to constrict or dilate in relation to neural activity

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16
Q

How does neurovascular coupling works?

A

Astrocytes respond to signals released from neurons

  • Neurons release glutamate
  • Glutamate acts on NMDA / mGluRs receptors on astrocytes
  • This produces Ca2+ spikes
  • Which leads to the release of vasoconstrictor / dilator substances such as prostaglandins / arachadronic acid
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17
Q

What is hyperaemia?

A

an excess of blood in the vessels supplying an organ or other part of the body.

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18
Q

What is the role of NO?

A

vasodilator

cerebral vessels causes relaxation of vascular smooth muscle in the arterioles supplying cerebral microvessels

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19
Q

what does NO released by?

A

neurons and endothelial cells to dilate blood vessels

20
Q

when is endothelial NO released?

A

in response to Ach released by cholinergic neurons

21
Q

When is neuronal NO released?

A

co-released from interneurons with NPY

22
Q

What is NPY

A

a powerful vasoconstrictor

23
Q

what does chronically increased pressure do to the brain?

A

overwhelms the cerebral regulatory mechanism and cerebral perfusion pressure rises

24
Q

What causes cerebral artery obstruction?

A
  • deposition of atherosclerotic plaques
  • Increase in wall thickness by inflammatory process and oxidative stress leading to hypertrophic remodelling of smooth muscle cells in response to increased pressure
25
Q

Describe the steps in neurodegeneration

A
  • remodelling causes disurption of BBB
  • vessel leakage
  • toxic products enter the brain parenchyma
  • e.g amyloid B in alzheimers
26
Q

describe the steps in a stroke occurring ?

A
  • reduced CBF
  • CBF no longer matches neural activity
  • focal ischaemia
  • stroke
27
Q

What are the three types of stroke?

A

Ischaemic - 85% of cases - lack of oxygen supply to an area
Haemorrhagic - 15% of cases - rupture of blood vessel causing bleeding
TIA- mini stroke - symptoms dissappear after 48hr

28
Q

what is thrombolysis?

A

clot breaking treatment using tPA

restores blood flow in ischaemic stroke

29
Q

what are the limitations of thrombolysis?

A
  • must be treated within 4.5hr
  • must have a CT scan to rule out haemorrhagic stroke
  • patients may not response and 5% can have haemorrhagic stroke
30
Q

What is neuroprotection

A

drugs with interfere with the ischaemic casade

no clinical use so far

31
Q

What are the 3 severities of the ischaemic casade

A
  1. autoregulation
  2. TIA with recovery
  3. permanent damage
32
Q

What are the main events in autoregulation?

A
  1. Ischaemia –> loss of glucose and oxygen supply + build up of C02 / lactic acid
  2. Failure of membrane pumps ( Na+ K+ ATPases) leads to oedema and failure of glutamate reuptake
33
Q

What are the main events that occur in TIA with recovery?

A
  1. disrupted membrane action potentials –> consistent action potential firing
  2. build up of glutamate causes overexcitation of glutamate receptors
34
Q

what are the main events that occur in permanent stroke damage?

A
  1. Ca 2+ influx into cells and activates intracellular enzyme systems
  2. breakdown of cellular structure and free radical production
  3. apoptosis and necrosis
35
Q

what are the role of pericytes in BBB dysfunction?

A

regulate the movement of substances between lumen of cerebral blood vessels and cerebral interstitial space

36
Q

What happens to pericytes during disease

A

damaged by inflammatory cytokines in diseases affecting CNS such Alzheimers/ stroke / ALS / AIDS
BBB becomes leaky

37
Q

what is the role of pericytes in health?

A

release molecules to brain endothelial cells in order to maintain the BBB integrity. Pericytes also secure normal perfusion and vasoregulation

38
Q

What happens when pericytes are loss?

A

With pericyte loss, vessels regress and loose their vasoreactivity, leading to hypoperfusion and hypoxia. The BBB breaks down, resulting in leakage of neurotoxic substances leading to neuronal damage

39
Q

What is the role of white matter?

A

50% of brain volume

transmit signals from one half of the cerebrum to another and lower brain centers

40
Q

What is white matter made from?

A

mostly glial cells
axons –> myelinated and unmyelinated
bloods vessels

41
Q

what are the causes of white matter ischaemia

A
  • stroke / cardiac arrest
  • neurodegnerative diseases
  • Periventricular leukomalacia
42
Q

what are oligodendrocytes

A

myelin-forming cells of the CNS

-most susceptible parts of white matter to ishaemic injury

43
Q

role of cerebral white matter changes

A

major role with the onset of alzhiemers

44
Q

PVL pathogenesis in neonates

A
  • loss of immature and fully differentiated neonates

- myelin disturbances

45
Q

What is PVL

A

The most common form of white matter damage in human neonates and often results in neonatal death

46
Q

key features of PVL

A

5-10% of surviving premature infants develop cerebral palsy (a condition that affects muscle control and movement)

Also associated with intellectual impairment or visual disturbances.

Much more common in premature infants than in full-term infants.

White matter damage is due to changes in blood flow to areas around the ventricles which contain nerves affecting motor control.

Pumps Pipes and Electrics (12 decks)

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