2. Cerebral Vasculature and Brain Homeostasis Flashcards

1
Q

what is the amount and flow of CSF

how is it made

A

Thru the ventricles and around the brain & spinal cord ==> flow is one way and reabsorbed by arachnoid villi at the end

~150 mL at any given time & not recirculated –> so make ~550 mL/day

made primarily by choroid plexus (esp in lateral & 4th ventricle) & rest by tissue that lines the ventricles

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2
Q

How are the 4 ventricles connected

A

Intraventricular Foramen –> Lateral ventricles - 3rd ventricle

Cerebral Aquaduct–> 3rd ventricle - 4th ventricle

Median Aperture –> 4th ventricle - cisterna magna

Lateral Apertures –> 4th ventricle - arachnoid space

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3
Q

What happens if the ….

  1. intraventricular foramen
  2. cerebral aquaduct
  3. median aperture
  4. lateral aperture

are blocked?

A

CSF build up in…

  1. lateral ventricles
  2. 3rd ventricle
  3. 4th ventricle
  4. 4th ventricle

and the ones prior?*?*?*?*?*

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4
Q

What is stage 1 of making CSF

A

Step 1: Passive filtration of serum (Dependent on two pressures)

  1. Hydrostatic pressure (BP in capillaries = tissue hydrostatic P)
  2. Oncotic Pressure (cancel each other out)

–> fluid moves from blood vessel into ventricle

*RMR: production of CSF is constant over wide rances of ICPs*

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5
Q

What is hydrostatic pressure

A
  • In capillary = blood pressure –> Pushes fluid out. = large force on capillaries (= net Pressure bc oncotic cancel out!)
  • Surrounding the capillary = Tissue hydrostatic pressure –> Pushes fluid into capillary = small force on brain/body
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6
Q

what is oncotic pressure

A

= osmotic pressure (dep. on solutes in blood)

  • In capillary => “pulls” fluid into the capillary.
  • Surrounding capillary =>“pulls” fluid out of the capillary
  • At the choroid plexus, these two are equal and opposite.
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7
Q

What is step 2 of formation of CSF

A

Modification of ion composition:

  • HCO3, Cl, and K concentrations controlled by channels on epithelial cells. •Aquaporin 1 allows H2O to cross.
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8
Q

Does production of CSF fluctuate with pressure?

A

NO! its CONSTANT!!!

= so even if a lot of CSF or increased ICP –> STILL make more & get build up

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9
Q

what molecules/ions in the CSF will be in similar in concentration as plasma

A
  • Na+ (range overlaps with average concentration in plasma
  • HCO3
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10
Q

CSF contains more ________ than plasma

A

Mg++ (interact w/ channels in brain)
Cl-

CO2 (brain metabolic rate makes it ==> CSF is 1st step of getting it out and into blood)

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11
Q

Plasma contains higher concentrations of which molecule/ions, compared to CSF?

A

K+ (bc metabolic rate, dont need much bc cells push it out)

Ca++ (can be toxic for cells)

Protein (low oncotic P –> no buffer for H+ ==> pH diff from plasma as well)

Glucose

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12
Q

How does absorption by arachnoid villi occur

A

endothelium of sinus & membrane on villi are fused => bulk flow of CSF (one way flow)

absorption proportional to ICP

-at ICP < 68 mm - no absorptions ==> BUILD UP

at normal pressure ~ 112 mm = normal absorption

*control of amount of CSF based on reabsorption NOT production*

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13
Q

What will occur if the arachnoid villi fibrose

A

decrease reabsorption –> increase pressure –> damage neurons!

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14
Q

primary role of CSF

A

protect brain!

brain weighs: 1400 g in air BUT w/ CSF it weighs 50 g

(bc high lipid concentration)

=bouyancy & protection

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15
Q

What is the blood brain barrier (BBB) and what is its fxn?

A

Capillaries that limit exchange bc tight jxn btn endothelial cells & Glial endfeet in contact with BVs (add lipid bilayers- restrict things coming)

Fxn = protect chemical composition of CSF, maintain electrolyte composition (esp K+ & Vm), protect from toxins

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16
Q

what substances can cross the BBB via passive diffusion

A

H2O- via AQP4 (either direction)

CO2 (very lipid soluble)

O2

free steroid hormones (highly lipophilic)

17
Q

How does glucose enter the brain

A

Glut-1 transporters (not insulin dependent! aka work at all times)

two types: 45K for astroglia & 55K for capillaries (one to cross membrane of endothelial cell and other to cross end plate)

glucose imp for neuron fxn (=energy source) -

18
Q

what transporter do neurons use to move glucose into cell

A

glut 3

19
Q

what controls the expression of the Na/K/2Cl transporter ?

what does this transporter do?

A
  • endothelin 1 & 3 from endothelial cells of blood vessels (BVs)
  • all moves ions from CSF to blood (seems to be related to [K+] in CSF, so if too high, then all 3 ions are kicked out of cell)

=electro-neutral movement)

20
Q

what is the role of P-glycoprotein

A

pump glycoprotein

-bind to variety of substances (move drugs that cross BBB back out)

21
Q

What are the areas in the BBB that lack tight jxn btn endothelial cells?

A

=places where we want brain exposed to blood (circumventricular organs)

  1. Posterior Pituitary - aka Neurohypohysis (= modified neural tissue, release hormones in response to blood)
  2. Area Postrema: vomiting (chemotoxic trigger zone)
  3. Organum Vasculosum of the Lamina Terminalis (OVLT)- control body water/thirst/blood volume (body osmolarity)
  4. Subfornical Organ- control body water/thirst/blood volume (body osmolarity)
22
Q

What are characterisitcs of cerebral circulation

A

requires 750 ml/min (14% of blood from heart/min)

  • 2 internal carotid A and the basilar A join & form Circle of Willis
  • little mixing of blood from diff sources
  • disruption of 1 input –> localized areas of ischemia (other areas continue to get enough blood)
23
Q

What is the sym innervation of the cerebral circulation

A

Neurotransmitters: Norepi & Neuropeptide Y (NPY)

Receptors: alpha-adrenergics

Leads to constriction when ONLY when systemic cardiac output/blood pressure increase

24
Q

what is the parasym innervation of cerebral circulation

A

•Innervation of larger blood vessels

  • NT =-Ach
  • =Vasoactive intestinal polypeptide (VIP)
  • =PHM-27 (derived from pre-pro-VIP (vasoactive intestinal polypeptide)

–> cause vasodilation

25
Q

what is the sensory innervation of the cerebral circulation

A

sensory innervation in distal blood vessels

NTs = Substance P, Neurokinin A & CGRP (all cause dilation!)

-extremely sensitive to torsion/manipulation –> cause pain (headaches!)

*these neurons release NT back onto vasculature!*

26
Q

What is the role of sensory innervation of cerebral circulation

A

-reduced CSF volume (like after lumbar puncture) –> brain = heavier –> ‘torsion’ of the blood vessels & simple motion = pain! via….

==> Activate afferent fibers –> sense torsion & manipulation –> same neuron release NT –> vasodilation and increase blood flow

27
Q

How is cerebral circulation controlled?

A
  • Local control - O2 consumption dictates blood flow –> flow to places that are active
  • Autoregulated: flow is constant over wide range of systemic (mean arterial) BP
  • Influenced by ICP- hydrocephalus, cerebral edema, intracranial bleeding
28
Q

what happens to cerebral circulation if you have high blood pressure

A

high BP –> sym innervation cause vasoconstiction –> increase systemic vascular resistance but protects capillaries in the brain and BBB from damage

29
Q

How is ICP related to systemic BP

A

as ICP increases, venous outflow is obstructed –> decrease arterial flow –> activate cardiovascular control centers in medulla –> increase systemic BP

*–> ICP increased by hydrocephalus, cerbral edema, intracranial bleeding) <–*

30
Q

What is the reason flow is constant thru a wide range of mean arterial BP?

A

-protect BBB b/c capillaries get damaged with high pressure, this keeps things level

31
Q

when is blood flow dependent on mean arterial blood pressure

A

low BP (<60 mm Hg)

high HP (>140 mm Hg)

32
Q

how does sympathetic stimulation influence cerebral circulation

A

alpha-adrenergic receptors –> constrict vessels –> extend range (where flow & BP are unrelated)

==> mechanism to protect BBB