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NE2 > Cerebral Vasculature > Flashcards

Cerebral Vasculature Flashcards

1
Q

What happens to action potential in hyperkalemia

A

Depolarization. More excitability

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2
Q

What happens to action potential in hypercalcemia

A

Alter permeability to Na+ leading to hyperpolarization leading to muscle weakness

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3
Q

Where is the synapse between the pre- and post- ganglionic cell

A

In a ganglion

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4
Q

Where is BP most carefully regulated

A

At carotid and aortic baroreceptors. Afferents synapse on solitary tract nucleus. Increase stretch=increase BP.

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5
Q

What happens to parasympathetics and sympathetics when BP is high

A

Parasymp. in depressor region are EXCITED and symp. in pressor region are INHIBITED

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6
Q

Where is CSF made

A

on the choroid plexus in lateral, 3rd, and 4th ventricles. Remaining CSF is made by tissue that lines the ventricles and blood vessels.

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7
Q

What are the 2 stages to CSF production

A
  1. Passive filtration of serum

2. Modification of CSF composition

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8
Q

Describe passive filtration of serum in CSF production

A
  1. Hydrostatic pressure: in the capillary BP pushes fluid out, surrounding the capillary tissue hydrostatic pressure pushes fluid into capillary
  2. Oncotic pressure: in the capillary, fluid is pulled into the capillary. Surrounding the capillary, fluid is pulled out of the capillary.
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9
Q

Production of CSF is ____ over a wide range of ICP

A

CONSTANT. Even if we have a high ICP, will continue to make CSF.

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10
Q

Ion concentrations in CSF same as plasma

A

NA+

HCO3-

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11
Q

Ion concentrations higher in CSF than plasma

A

Mg2+
pCO2 due to higher metabolic activity and O2 consumption
Creatinine
Cl-

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12
Q

Ion concentrations lower in CSF than plasma

A 
K+
Ca2+
Protein (changes oncotic pressure. good buffer for H+, making pH of CSF lower than that of blood)
Glucose 
Urea
Urate
Cholesterol
Inorganic PO43-
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13
Q

Intraventricular foramen

A

lateral ventricles to 3rd ventricle

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14
Q

Cerebral aquaduct

A

3rd ventricle to 4th ventricle

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15
Q

Median Aperture

A

4th ventricle to cisterna magna

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16
Q

Lateral Apertures

A

4th ventricle to arachnoid space

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17
Q

What is the flow of CSF

A

Ventricle-> Either foramen of magendie and Luschka-> subarachnoid space-> arachnoid vili-> flows across arachnoid membrane into cerebral sinuses by BULK FLOW

pinocytosis of CSF by mesothelial cells of arachnoid vili seen too

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18
Q

What happens with arachnoid granulations

A

Fibrosing causes less fluid to leave the space and enter the sinus, so there is less resorption of CSF and thus higher ICP.

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19
Q

Cause of External or communicating hydrocephalus

A

Arachnoid villi decrease the absorptive capacity

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20
Q

Cause of Internal or noncommunicating hydrocephalus

A

Foramen or ventricular blockage

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21
Q

What’s the relationship between CSF absorption and intracranial pressure

A

Directly proportional

<68 mm CSF, no absorption
normal pressure is 112 mm CSF

22
Q

What happens to blood flow when CSF pressure increases

A

Decrease blood flow or increase pressure on brain

23
Q

What 2 things limit exchange in brain capillaries

A
  1. Tight junctions (prevent fluid motion out of capillary, anything that comes thru must be somewhat lipid soluble)
  2. Glial endfeet
24
Q

What crosses BBB via passive diffusion

A

H20 via AQP4
CO2
O2
free steroid hormones (hormones not attached to a protein)

25
Q

What does AQP4 do

A

Helps water cross. Protective against cerebral edema. Indirect effect on neuronal function by changing H20 levels to impact K+ homeostasis.

26
Q

How does glucose, the main fuel for the brain, cross the BBB

A

GLUT-1

27
Q

Where are GLUT-1 transporters found? Are they insulin dependent?

A

55k on capillaries. 45k on astroglia. NO.

28
Q

What do neurons use to move glucose inside?

A

GLUT-3. This is insulin dependent and may be impacted by polymorphisms.

29
Q

What happens when CSF glucose is low?

A

Neurons cannot make enough ATP to maintain the membrane potential. Leads to seizures. Can fix with a low carb/hi fat (ketogenic) diet so neurons can use ketone bodies for fuel.

30
Q

What do microglia use to move glucose inside?

A

GLUT-5

31
Q

How are ions taken out of the CSF and into the blood?

A

Transport 1 Na+, 1K+, 2 CL-. Using endothelin 1 and 3 which are expressed due to factor being released by astrocytes, thought to keep CSF [K+] low.

32
Q

what does P-glycoprotein do

A

Helps limit brain exposure to systemically derived drugs. Takes drugs that cross the BBB and moves them back to blood. Binds to lots of stuff.

33
Q

How do we handicap the BBB

A

Get rid of tight junctions. Make it fenestrated.

34
Q

What are the 4 circumventricular organs

A
  1. Posterior Pituitary
  2. Area Postrema
  3. OVLT (organum vasculosum of lamina terminalis)
  4. Subfornical region
35
Q

Posterior pituitary

A

AKA Neurohypophysis. It is modified neural tissue. Hormone release in the blood in response to blood-derived signals.

36
Q

Area Postrema. Where is it? What does it do?

A

Located at caudal 4th ventricle.

Initiates vomiting from blood-borne chemicals, like food that has been ingested.

37
Q

OVLT and Subfornical Region. What are they and what does it do?

A

Both involved in control of body water/thirst/blood volume control. ADH osmoreceptors act at OVLT. Angiotensin acts at subfornical region to initiate thirst.

38
Q

Which arteries join to help form CoW

A

Internal carotids and basilar artery (formed from the 2 vertebral arteries)

39
Q

What is unique about the CoW

A

There is little mixing of blood. No anastomotic connections. So, disruption of one of the inputs creates localized, discrete areas of ischemia. Specific neurological signs rather than widespread effects.

40
Q

Post ganglionic sympathetic.

What does it do? Neurotransmitters? Receptors?

A

Innervate larger arteries. Leads to constriction when systemic cardiac output/BP increases.

NT: norepinepherine and Neuropeptide Y
Receptors: alpha-adrenergics

Not a normal regulatory mechanism

41
Q

Post ganglionic parasympathetic.

What does it do? Neurotransmitters? Receptors?

A

Innervates large blood vessels. Causes vasodilation.

NT: ACh and VIP (vasoactive intestinal polypeptide)
and PMH-27 (derived from pre-pro-VIP)

Receptors: ACh binds to muscarinic receptors

42
Q

Afferents

What does it do? Neurotransmitters? Receptors?

A

Innervates smaller, distal arteries. Sensitive to vasodilation and torsion. Sensory nerves that detect torsion release NTs to trigger vasodilation and an increase of blood flow to return the ICP volume back to normal.

NT: Substance P, Neurokinin A, CGRP

43
Q

How is low CSF volume and torsion related?

A

Low CSF=heavier brain=simple motion causes pain and torquing of blood vessels

why you might get a HA after an LP

44
Q

What dictates where in the brain blood goes to?

A

Cerebral blood flow is under LOCAL control. O2 consumption and metabolite production influences arterioles.

45
Q

How is cerebral blood flow regulated?

A

It is AUTOREGULATED. Held constant over a wide range of systemic (MAP) blood pressures.

46
Q

Which innervation is activated when systemic BP is high?

A

Activation of the cerebral sympathetics increases resistance and is used when systemic BP is high.

47
Q

What happens to blood flow with increased ICP

A

Increase ICP = obstructed venous outflow = reduced arterial flow

48
Q

Describe the pathway of MAP-Autoregulation

A

High systemic BP -> Increase cerebral vasculature sympathetic innervation activity -> releases more norepi -> norepi binds to alpha-adrenergics -> causes VASOCONSTRICTION of cerebral vasculature -> protects BBB by preventing pressure from being transmitted to capillaries

49
Q

What will be activated when there is a decrease in brain perfusion?

A

Activates the cardiovascular centers in the medulla to try to increase brain perfusion. Does so by increasing systemic BP, sometimes dramatically.

50
Q

What can increase ICP?

A

Hydrocephalus of any kind.
Cerebral edema.
ICH

NE2 (12 decks)

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