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(OMS1) Neuro exam 2 > Cerebral Vasculature and Brain Homeostasis (Karius) > Flashcards

Cerebral Vasculature and Brain Homeostasis (Karius) Flashcards

1
Q

Ventricular system

A

4 ventricles are connected via foramen and apertures, but they are small and can be clogged

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2
Q

Choroid plexus:

A

Located in the floor of the lateral, third and fourth ventricles. Lots of foldings that increase the surface area.
Produces most of the CSF (50-70%)
Rest of CSF produced by blood vessels and ventricular walls

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3
Q

Stage 1 of CSF production:

A

Passive filtration of plasma across the choroidal capillary endothelium out of the capillary into the ECF
Driven by pressure gradient inside and outside the capillary

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4
Q

What types of pressures are responsible for passive filtration at stage 1?

A 
Hydrostatic pressure (blood pressure that pushes the fluid out)
Osmotic pressure inside capillary and pulls fluid into capillary
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5
Q

How exactly is plasma being filtered out of the capillary?

A

Up in the brain, osmotic pressure = 0 since they cancel each other out. So the major force acting on plasma is the blood pressure causing plasma to be filtered out of capillary into the ventricle

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6
Q

Stage 2 of CSF production:

A

Modification of the ionic composition (HCO3, Cl, K)

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7
Q

How is the composition of CSF modified by the choroid plexus?

A

HCO3, Cl and K- entry is controlled by channels on the apical surface of epithelial cells
Aquaporin 1 is expressed on the choroid plexus and allows water to cross

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8
Q

Production of CSF is …

Clinical significance of this concept?

A

Constant over a wide range of intracranial pressures. You continue to make CSF even if you shouldn’t (aka high ICP etc.)

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9
Q

Which ions are the same concentration in CSF and plasma?

A

Sodium (135-150 mEq) and HCO3 (-22.9 mEq)

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10
Q

Which ions are greater in CSF than plasma?

A

Mg++
CO2 (reflects metabolic production of CO2 by the brain due to greater levels of net activity)
Creatinine
Cl-

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11
Q

Which ions are lower in CSF than plasma?

A

K+
Ca2+
Protein
Glucose

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12
Q

Pathway of CSF flow:

A

Ventricle > foramen of Magendie and Luschka (2 different paths) > subarachnoid space

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13
Q

How is CSF absorbed into the blood?

A

Arachnoid membrane is fused to endothelium of the venous sinuses via arachnoid villi. CSF flows into the sinus through the villi (as well as pinocytosis of CSF via mesothelial cells of the villi)). Bulk flow (about 500 - 500 mL/day when CSF pressure is adequate)

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14
Q

CSF pressure

A

99% water so CSF is not compressible and limited space for it so there is pressure generated
Average 112 mm

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15
Q

Absorption of CSF relationship to pressure

When does absorption stop?

A 
Directly proportional (higher pressure pushing out on the villi = more CSF absorbed) 
Absorption stops at pressure below 68 mm CSF
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16
Q

What controls the amount of CSF in the brain?

What is the effect of increased pressure on neurons?

A

Reabsorption stage, NOT production

Increased pressure damages neurons

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17
Q

Protective function of CSF:

A

Gives buoyancy to brain. Apparent weight of brain in CSF is lower. Without it brain is not able to survive normal motion because the nerves etc. are so delicate. Basically CSF is cushioning the brain and its components

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18
Q

Hydrocephalus

A
  • Increased CSF pressure that could be due to decreased absorption by the villi (external or communicating hydrocephalus) or blockage of foramen or somewhere else in the system (internal or noncommunicating hydrocephalus)
  • Brain is trapped between skull and fluid as CSF keeps getting produced
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19
Q

What happens when CSF pressure is too high?

A

Blockage of blood flow and increase pressure on the brain = neuron death.

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20
Q

Blood brain barrier (BBB):

How does it work?

A
  1. Capillary endothelial cells have tight junctions between them
  2. Glial endfeet come in close contact with capillaries, covering them
    So overall result, limited diffusion through BBB
21
Q

Effects of the BBB modifications:

A

Prevent proteins from entering the CSF
Reduce movement of smaller molecules depending on their chemical characteristics

Basically selective permeability

22
Q

Passive diffusion through BBB

A

H2O (via aquaporin 4/AQP4)

23
Q

Other molecules that cross BBB via passive diffusion:

A

O2, CO2, free steroid hormones

24
Q

Why is the BBB important?

A

Controls water homeostasis in the brain and protects against cerebral edema
Impacts neuronal function indirectly

25
Q

How does Glucose get through the BBB?

A

Glut 1, Glut3 and Glut 5 (used by microglia). Cannot passively diffuse in.

26
Q

Glut1:
Function
Kinds and location

A

Moves glucose from blood into CSF, not insulin dependent (works all the time, does not need to wait for insulin)
Glut 1 55K - on capillaries (gets it through the capillary)
Glut 1 45K - on astroglia/podocytes (gets it through the glial endfeet)

27
Q

Glut3:

A

Used to move glucose into the neuron

Also insulin independent

28
Q

Sodium, potassium and chloride and BBB

A

Na/K/Cl transporter moves 1 Na, 1 K and 2 Cl- from CSF to blood
Expression of the transporter is stimulated by release endothelin-1 (ET-1) and 3 (ET-3) from endothelial cells
Seems to be related to controlling concentration of K+ in CSF

29
Q

Major function of the BBB?

Clinical significance?

A

Protect the chemical composition of CSF from blood-borne agents
Some drugs cannot penetrate the BBB.

30
Q

Other functions of BBB:

A

Maintain electrolyte composition (particularly related to K+)Maintain membrane potential
Protect from toxins

31
Q

Drug and peptide transporter

A

P-glycoprotein. Binds to a wide variety of chemicals that cross the BBB and kicks them back to the blood

32
Q

Other transporters into BBB available for which molecules?

A

Thyroid hormone, organic acids, choline, nucleic acid precursors, amino acids

33
Q

What are circumventricular organs?

A

Parts of the brain that do not have tight BBB (these areas need exposure to the blood to work)
Do not have tight junctions between the endothelial cells

34
Q

Examples of circumventricular organs?

A 
Posterior pituitary (has to know what's going on in the blood)
Area postrema - caudal portion of 4th ventricle, trigger zone for vomiting when exposed to chemicals in the blood after eating (bad chemical gotta vomit it out!)
Organum vasculosum (OVLT) and Subfornical organ - both involved in control of body osmolarity (thirst/blood volume etc.)
35
Q

What makes up the cerebral vasculature?

A

Two ICAs
Two Vertebral arteries unite to form the basilar a.
Basilar A. unites with ICAs to form the Circle of Willis

36
Q

How much blood mixing occurs at the Circle of Willis?

A

Very little. Reduced blood flow from any one of the vessels is not corrected by mixture from other vessels. A specific part of the brain will not be getting enough blood, so Very specific neurological signs result from interruption in blood flow rather than general effects due to widespread damage.

37
Q

Postganglionic sympathetic innervation of cerebral vasculature:
Receptors?
When does this occur?

A

Postganglionic sympathetics (Norepinephrine and Neuropeptide Y).
Bind to a-adrenergic receptors.
When systemic blood pressure increases

38
Q

Postganglionic parasympathetic innervation of cerebral vasculature:
What is released at synapse 2?
What receptors receive these?

A

Acetylcholine, VIP (Vasoactive intestinal polypeptide), PMH 27
mAChRs
Innervates large blood vessels, cause vasodilation

39
Q

Afferent (sensory) axons of the cerebral vasculature:

A

These neurons release neurotransmitters back to the vasculature (Substance P, Neurokinin A and CGRP)
All these NTs vasodilate

40
Q

How are sensory afferents activated?

A

Torsion or manipulation of blood vessels leading to pain

Associated with severe headaches

41
Q

How does reduced intracranial pressure activate the sensory neurons?

A

Usually associated with reduced CSF volume. Brain is heavier with less CSF, and puts pressure on the blood vessels when it moves (cushion is gone)
Afferent neuron activation causes vasodilation = increases the blood volume in the brain to make up the difference in lost volume secondary to loss of CSF

42
Q

Local control of cerebrovasculature:

A

Determined by activity levels - which organs need oxygen the most (brain uses so much oxygen so blood flow goes there)

43
Q

How is cerebral blood flow controlled?

A

Strongly autoregulated. Held constant over a wide range of systemic (mean arterial) blood pressures. (brain pressure is still the same even if the body’s BP is changing)

44
Q

How does intracranial pressure influence cerebral vasculature?

A

Increase in intracranial pressure = reduced blood flow due to compression of blood vessels
Decrease in pressure (e.g. lumbar puncture) related to increased blood vessel torsion due to loss of buoyancy, not blood flow

45
Q

Describe the trend in the association of systemic and cerebral blood pressure:

A

<60 mmHg, cerebral and arterial BP are changing proportionally. Between 60 -140 cerebral BP is held constant.
>140 mmHg cerebral and arterial BP are again changing proportionally (mean BP is higher than brain BP)

46
Q

What is the significance of high BP on the BBB?

A

Tight junctions keeping the BBB intact are sensitive to pressure and can be damaged if pressure is too high. This is why keeping the brain pressure constant is protective to the BBB

47
Q

How does sympathetic innervation protect the BBB from high pressure?

A

The sympathetics will vasoconstrict the cerebral blood vessels.This will increase the systemic BP as an expense to keep the pressure to the brain constant.
Extends the range of systemic BPs that keep the cerebral BP constant.

48
Q

How does intracranial pressure affect cerebral arterial blood flow?

A

Increased ICP clogs the venous system outflow which leads to reduced arterial flow through the cerebral vasculature. This reduced blood flow will tell the CV centers in the medulla to increase systemic BP to force the blood through whatever is obstructing the cerebral vasculature.

49
Q

Examples of things that can increase ICP?

A

Hydrocephalus
Cerebral edema
Intracranial bleeding

(OMS1) Neuro exam 2 (24 decks)

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