Blood flow to the brain and regulation Flashcards

1
Q

Flow rate to the brain

A

55ml/100g tissue/min

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

what reduction of blood flow causes impaired brain function?

A

> 50%

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

syncope

A

interruption of blood flow for 4 seconds will knock someone unconscious

a few minutes and irreversible brain damage occurs

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

glucose usage of the brain

A

the brain uses a vast majority of glucose

it can’t store, synthesise or utllitilise other sources of energy except ketones at times of starvation

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

what glucose levels causes unconsciousness?

A

2mM

eventually into coma and then death

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

what is the MABP range that CBF is auto regulated at (total control)?

A

60-160 mmHg

below and above this range, auto regulation is not possible

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

How does vascular smooth muscle affect BP?

A

higher BPs due the SM contraction

lower BPs due the SM relaxation

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

why is blood supply changed locally?

A

the brain activity determines the oxygen consumption and glucose demands. Local changes in flow are required

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

what enables local auto-regulation to the brain?

A

1) neural control

2) chemical control

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

how can local changes to blood flow be visualised?

A

PET scans

fMRI (functional)

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

what are the features are involved in the local neural auto regulation of CBF?

A
  • sympathetic nerve
  • PNS facial nerve
  • central cortical neurones
  • dopaminergic neurones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

effect of sympathetic nerve on neural control of CBF?

A

Vasoconstriction when MABP is high

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

effect of PNS facial nerve on neural control of CBF?

A

slight vasodilation

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

effect of central cortical neurones on neural control of CBF?

A

release vasoconstrictors

e.g. catecholamines

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

effect of dopaminergic neurones on neural control of CBF?

A

local vasoconstrictive effects

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

what cause the contraction of pericytes (Brain macrophages)?

A

aminergic and serotininergic receptors

17
Q

vascularisation of CNS

A
arteries from Pia mater 
go into brain tissue 
branch to form capillaries 
they drain into veins --> pial vessels 
no neurone is more than 100 micrometers from a capillary
18
Q

what features are involved in the chemical control of CBF?

A
  • CO2 (indirect)
  • pH
  • NO
  • K+
  • Adenosine
  • Anoxia
  • Kinins, prostaglandins, histamine

all vasodilators

19
Q

the effect of CO2 on cerebrally arterial vasodilation?

A

H+ increase in blood due to CO2 (decreases pH)
VSMC constrict to cause vasoconstriction

H+ is derived from CO2 reacting with carbonic anhydrase and water to form bicarbonate and H+. It can also come form neural metabolic activity

20
Q

what produces CSF?

A

choroid plexus (modified ependymal cells lining the ventricles)

21
Q

flow pathway of CSF

A
  • choroid plexus lining ventricles
  • secrete into lateral ventricles
  • into 3rd ventricle via interventricular foramen
  • into 4th ventricle via aqueduct
  • into subarachnoid space via central canal
  • or into cerebellar space via medial and lateral apertures
22
Q

what is the volume of CSF produced in a day?

A

80-150 ml

23
Q

what are the functions of CSF?

A

protective
nutritional
transport

24
Q

CSF compared to plasma

A

similar pH and osmolarity
very low protein levels
different potassium, magnesium , calcium ion and AA concentrations to plasma

25
Q

how is protein concentration in CSF used to identify possible bacterial infection?

A
  • normally very low protein content in CSF

- infection is indicated with higher concentration of protein present in CSF

26
Q

what are the 3 types of capillaries based on cell wall?

A

continuous, fenestrated, sinusoidal (e.g. hepatocytes)

27
Q

characteristics of BBB capillaries?

A
  • extensive tight junctions at endothelial cell-cell contact zones (reduce leakage)
  • as you get deeper, the less permeable it gets up to the BBB proper
  • uses transcellular vesicular transport
  • pericytes closely adherent to capillaries to maintain function and integrity of the capillaries
  • covered in “end feet” form astrocytes to help maintain its properties
28
Q

what do the tight junctions of the BBB enable it to do?

A
  • control the exchange of large or hydrophilic solutes e.g. glucose, AA, antibiotics
  • It uses specific transporters for these
  • prevents infectious agents entering CNS tissue (infections tend to infect the meninges instead whose vessels aren’t part of the BBB)
  • lipophilic molecules freely pass the brain

meninges vulnerable to infection as vessels are not protected by BBB

29
Q

how are lipophobic molecules transports across BBB?

A

water via aquaporins
glucose via GLUT-1
amino acids via 3 transporters
electrolytes via specific transporters

30
Q

examples of circumventricular organs (CVOs)

A
area postrema (CTZ)
subfornical organ
pituitary stalk
median eminence
pineal gland (SCN input)
31
Q

what are circumventricular organs?

A

places where the capillaries lack BBB properties as a necessity.

32
Q

circumventricular capillaries, why are they fenestrated?

A

fenestrated

required as CVOs need to sample blood or secrete molecules into the blood itself

33
Q

example of CVOs that sample blood or secrete into blood

A

posterior pituitary secretes

area postrema samples

34
Q

clinical importance of BBB

A

some drugs can’t enter the brain at all whilst others enter very readily causing unwanted effects

“old fashioned” H1-channel blockers were hydrophobic so entered the brain readily and caused drowsiness

second gen antihistamines are hydrophilic/polar so do not cross to BBB so no drowsiness occurs

35
Q

how is Parkinsons Disease treated?

A

treatment of PD involves raising dopamine levels in the brain: LEVODOPA (+ carbidopa)
- dopamine itself ,however, does not cross the BBB so can’t be administered peripherally so its precursor is used

36
Q

how is the problem of dopamine administration in PD overcome

A

L-Dopa can cross the BBB
- but it is broken down peripherally so Carbidopa is co-administered (a DOPA-decarboxylase inhibitor)

L-Dopa therefore “survives” and crosses the BBB while Carbidopa doesn’t cross the BBB itself

37
Q

treatment of PD (drugs)

A

L-dopa

carbidopa