Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 UEA MBBS > Week 1 Stroke and TIAs physiology > Flashcards

Week 1 Stroke and TIAs physiology Flashcards

Physiology of Stroke

1
Q

What are the 3 types of physiological CPP control?

A

Neural, Metabolic, Myogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What nerve paths are used in Neural control?

A

Sympathetic and Parasympathetic innervation.

This neural control is weak and hence loacal metabolic control and myogenic control govern CBF generally.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the metabolic control do?

A

Neural activity leads to ATP breakdown which in turn increases adenosine.
This decrease PO2 and increase PCO2 – CO2 dissolves in water releases H+ ions which decrease pH which causes Vasodilation.
Also the adenosine which is produced in metabolism increases K+ ion conc and so is a vasodilator
Vasodilation causes increased blood flow to one area.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does decrease in mean arterial pressure affect cerebral blood flow?

A

Decrease in MAP picked up by baroreceptor causes increase in sympathetic and decrease in parasympathetic outflow. Increases heart rate and causes vasoconstriction. Causes Increase in MAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does increase in MAP cause?

A

Vasodilation and decrease in Hear rate lowering MAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Cerebral perfusion pressure and how is it calculated?

A

CPP = amount of pressure needed to maintain blood flow to the brain
CPP=MCP-ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is change in intracranial pressure avoided?

A

Vascular volume increase in one region of brain causes vascular volume decrease in another region of brain preventing ICP increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does neurovascular unit match blood flow to local brain activity?

A

Synaptic activity releases glutamate this increases intracellular calcium in astrocytes causing vasodilation and increase in CBF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What changes do Myogenic control cause?

A

Increase in CPP causes vasoconstriction
Decrease in CPP causes vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does blood pressure change after a ischaemic stroke?

A

Body increases blood pressure to force blood through capillary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does the cerebral perfusion pressure change after a haemorrhagic stroke?

A

Ruptured blood vessels cause increase in ICP which causes decrease in CPP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Can cells be kept alive after an ischaemic stroke and how?

A

Cells can be kept alive due to the body supplying cells with collateral circulation but it is insufficient to keep the cells functioning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does a haemorrhagic stroke affect nearby blood vessels?

A

Blood leaking into brain causes Haematoma. Haematoma constricts nearby blood vessels reducing blood flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What changes can be caused to a cell after an ischaemic stroke?

A

Lack of oxygen and nutrients decreases ATP causing Na+/K+ pumps to fail.
Calcium overloads the cells causing enzymes such as protease to be released breaking down neuron
Glutamate over-releases which causes excitotoxicity which causes further calcium overload
Lack of oxygen causes mitochondrial damage and mitochondrial necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens to cells after a haemorrhagic stroke?

A

Direct cell damage from mechanical force
Blood toxicity s haemoglobin and iron form radicals and damage cells
Inflammation as microglia is activated which release cytokine to the site and causes damage to cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What happens after blood brain barrier is disrupted due to a stroke?

A

Blood proteins, immune cells enter brain tissue causing damage to brain cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How heavy is the human brain and how much oxygen does it receive?

A

1.5 kg weight (2% of body mass) but receives 14% of resting cardiac output and uses 20% of resting O2 consumption. The brain is least tolerant of ischaemia. The grey matter uses up 94% of brain’s O2 consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Summarise the reason behind grey matter’s demand for oxygen.

A

Grey matter = close bundle of neuronal cell bodies/soma/. Hence it is the metabolic centre of neurones. neurones have large energy requirement. The neurones must make energy via oxidative phosphorylation (which require oxygen and glucose) Energy deprived neurones die quickly. The grey matter is also packed with mitochondria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the preferred substrate fro brain and how is it transported to the brain?

A

Glucose is transported into brain via glucose transporters on capillary endothelial cells, neurones and astrocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where are glycogen stores found in the CNS?

A

Astrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Outline role of Neurones and why they demand oxygen

A

They carry out the receiving, processing and sending of info. Thus they require huge amounts of energy load needed to maintain action potentials inside and outside of the neuron. Energy needed to pump ions against electrical and chemical gradient.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

When food not eaten for 24 hrs, what happens to muscle?

A

Gluconeogenesis and muscle breaks down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What type of metabolism of glucose is brain dependent on?

A

Oxygen dependent

24
Q

Which role/part of neurones is most oxygen requiring?

A

Synaptic transmission

25
Q

How much glucose is metabolised by brain each day?

A

100gm

26
Q

Outline how collateral circulation arises from the C.O.W

A

C.O.W safeguards oxygen supply form interruption due to arterial blocks. If a stenosis develops in one artery, other branches of the the C.O.W can still transport O2 to the brain. This idea is collateral circulation.

Complete C.O.W aids in resisting neurological impairment to humans.

Blood reaches the brain through two source arteries ( x2 internal carotid and x2 vertebral arteries).

27
Q

What are the three enveloping and distributing bilateral arterial pairs around the cerebral hemisphere?

A

Anterior, middle and posterior cerebral arteries.

28
Q

Where is the site of microcirculation in brain?

A

Brain capillaries

29
Q

What does 1-3 weeks of chronic hypoxia exposure cause in brain tissue?

A

Brain capillary density nearly doubles

30
Q

What does hypertension do the amount of brain capillary density?

A

Decreases the capacity

31
Q

Outline effects of chronic hypoxia and hypertension on brain capillary density.

A

BCD decreases in hypertensive state.
BCD increases in chronic hypoxia exposure.
Hence hypertension can impair vascular resistance.

32
Q

What is primary task of cerebral circulation?

A

Maintain oxygen and nutrient delievry to brain

33
Q

Outline the structure of the cranium and how the volume remains constant inside.

A

The cranium or skull encloses all cerebral vasculature, along with brain and the CSF. The cranium has a RIGID fixed total volume. Increase in one part of the cranium means there must be corresponding change elsewhere to compensate for this increase.

34
Q

Outline how cerebral oedema, haemorrhages or brain tumours can cause neurological deficits

A

They restrict blood flow due to vascular compression.

35
Q

How does brain regulate mean arterial pressure (MAP)?

A

Through a feedback loop.

If baroreceptors detect increased arterial pressure, they pass on this info via afferent pathway to the medulla. The medulla then dials down/slows down the heart into a bradycardiac state. The vessels’ smooth muscle layer relax and so combined, vasodilation and bradycardia decrease mean arterial pressure.

36
Q

What is the difference between afferent and efferent pathways?

A

Afferent and efferent pathways are two types of nerves in the peripheral nervous system.

Afferent pathways bring information from the body to the central nervous system, and efferent pathways bring information from the central nervous system to the body

37
Q

Outline how parasympathetic and sympathetic nervous pathways are used to regulate blood pressure if the arterial BP is low

A
38
Q

Discuss Cushing’s reflex

A

Increased ICP (due to haemorrhages etc) can compress blood vessels leading to the brain. Increased ICP means decreased Cerebral pressure, leading to cerebral ischaemia, leading to sympathetic activation. Sympathetic nervous pathway increases systemic blood pressure in an effort to restore cerebral perfusion.

39
Q

What is the required cerebral blood flow?

A

50ml/min per 100gm of brain tissue

40
Q

What is the constant CPP required for adequate cerebral vasculature and constant cerebral blood flow?

A

CPP is major determinant of CBF. Through autoregulation, cerebral vasculature maintains a CPP of between 50-150 mmHg

41
Q

What is CPP?

A

Cerebral perfusion pressure is the amount of pressure required to maintain blood flow to brain. CPP regulated by MAP and intercranial pressure (ICP) . ICP is the force that keeps blood out of the brain due to rigidity of cranium. MAP is the force that pushes blood into brain on average.

42
Q

What should ICP be?

A

0-10 mmHg

43
Q

Formula for CPP?

A

MAP-ICP

44
Q

In hypotension, what happens to CBF (cerebral blood flow)?

A

Remains the same as cerebral vascular resistance is now higher.

45
Q

In hypotension, what happens to vascular resistance?

A

It falls/decreases

46
Q

What happens to cerebral autoregulation post stroke episode?

A

Dramatic impairment

47
Q

What happens if there is a collapsed vein in CNS?

A

Collapsed vein decreases CPP to decreased blood flow and MAP, whilst also increasing ICP as more blood is leaving the cranium and brain. Cerebral blood flow (CBF) is a balancing act between the two opposing MAP and ICP forces!

48
Q

Outline the role of astrocytes

A

Astrocytes regulate CBF.
Upregulate tight junction proteins
Contribute to ion and water homeostasis.
Interfere directly with neurons.
Store glycogen in CNS.

49
Q

What is NVU (Neurovascular unit)?

A

The neurovascular unit is composed by neurones, astrocytes, endothelial cells of blood-brain barrier (BBB), myocytes, pericytes and extracellular matrix components. These cells, through their intimate anatomical and chemical relationship, detect the needs of neuronal supply and trigger necessary responses (vasodilation or vasoconstriction) for such demands.

It is a component of BBB
Both astrocytes and neurons cooperate in NVU coupling through glutamate signalling, which in turn increase CBF.
NVU is thus a regulator of CBF and blood flow to neurons.
A Stroke, increased BP, spinal chord injury in NVU lead to astrocyte coupling.

50
Q

Outline myogenic activity

A

Independent of nerve supply and depends on PERFUSION PRESSURE.
Myogenic activity or control is due to direct changes in vascular resistance, which itself is dependent on changes in perfusion pressure.

Increased pressue -> smooth muscle stretched -> opening of stretch activated channels-> Na + and Ca2+ influx depolarisation-> voltage gated Ca2+ channels open-> Ca2+ influx-> vasoconstriction.

Increased pressure means more blood flow which leads to dilution of vasodilating factors-> inhibition of vasodilation overtime-> constricition favoured

51
Q

How does myogenic activity combat against increased blood flow

A

Increased pressue -> smooth muscle stretched -> opening of stretch activated channels-> Na + and Ca2+ influx depolarisation-> voltage gated Ca2+ channels open-> Ca2+ influx-> vasoconstriction.
OR
Increased pressure means more blood flow which leads to dilution of vasodilating factors-> inhibition of vasodilation overtime-> constricition favoured

52
Q

How does the NVU cause vasodilation?

A

Neurons release glutamate-> intracellualr Ca2+ conc increases in atsrocyte-> This stimulates the release of vasodilatory factors like Nitrous oxide, prostaglandin E2 and vasoactive intestinal peptides etc

53
Q

What is ultimate goal of NVU coupling?

A

Neurovascular coupling is mainly regulated by neuron-astrocytic interactions in the NVU. Neurons release glutamate to activate metabotropic glutamate receptors on astrocytes and release Ca2+, leading to the activation of downstream Ca2+-dependent enzymes and the generation of vasodilatory substances. In addition, ionotropic NMDA glutamatergic receptors activate NOS and release NO to regulate blood flow

54
Q

What is the Blood brain barrier? (BBB)

A

The blood vessels that vascularize the central nervous system (CNS) possess unique properties, termed the BLOOD BRAIN BARRIER, which allow these vessels to tightly regulate the movement of ions, molecules, and cells between the blood and the brain.

55
Q

What are the two types of cells in blood vessels?

A

Blood vessels are made up of two main cell types: Endothelia Cells that form the walls of the blood vessels, and Mural cells that sit on the ablumenal surface of the EC layer. T
he properties of the BBB are largely manifested within the ECs, but are induced and maintained by critical interactions with mural cells, immune cells, glial cells, and neural cells, which interact in the neurovascular unit

Year 2 UEA MBBS (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions