DK/not in FA: BBB: Sweatman and Dr. J Flashcards

1
Q

Where do CN VII and VIII enter/exit skull?

A

enter: internal acoustic meatus
exit:
VII: stylomastoid foramen
VIII: external auditory meatus

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2
Q

What creates the sagittal and lateral sinuses in the brain?

A

separated dura layers

  1. outer dura: periosteal layer
  2. inner dura: meningeal layer
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3
Q

falx cerebri

A

separates left and right hemispheres of brain

formed from meningeal layers

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4
Q

tentorium cerebelli (tentorium)

A

separates cerebellum from cerebral hemispheres

formed from meningeal layers

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5
Q

falx cerebri

A

separates left and right hemispheres of brain

formed from meningeal layers

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6
Q

tentorium cerebelli (tentorium)

A

separates cerebellum from cerebral hemispheres

formed from meningeal layers

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7
Q

Meningeal spaces: potential

A

spaces do not exist under normal circumstances
head trauma can cause bleeding into spaces
1. epidural space (bleeding: middle meningeal a.)
2. subdural space (bleeding: venous)

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8
Q

subarachnoid space

A

true meningeal space
between arachnoid and pia mater
contains CSF, blood vessels

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9
Q

What meninges continue on peripheral nerve as

  1. epineurium
  2. perineurium
A
  1. dura

2. arachnoid

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10
Q

How many dura layers are there

  1. surrounding brain
  2. surrounding spinal cord
A
  1. 2

2. 1

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11
Q

What does the external carotid supply?

A
  1. face
  2. scalp
  3. meninges
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12
Q

What are the branches of the internal carotid?

A
  1. first branch: ophthalmic a. (near apex of hairpin turn)
  2. anterior cerebral a.
  3. middle cerebral a.
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13
Q
  1. Where do the vertebral arteries originate?
  2. At what level do they enter the vertebral foramen?
  3. Where do they enter the calvaria?
  4. Where do they join? To form what?
A
  1. subclavian arteries
  2. C6
  3. foramen magnum
  4. junction of medulla and pons to form basilar artery
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14
Q

CSF composition compared to blood

A

protein: 1/100
glucose: 2/3 glucose

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15
Q

foramen of Monro

A

btwn lateral ventricles and third ventricle

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16
Q

aqueduct of Sylvius

A

same as cerebral aqueduct: btwn third and fourth ventricle

MIDLINE

17
Q

foramina of Magendie and Luschka

A

fourth ventricle to subarachnoid space

18
Q

Where is CSF reabsorbed?

A
  1. spinal cord: egress point of nerve roots

2. brain (get to it through opening in tentorium cerebelli): venous sinuses via arachnoid granulations

19
Q

obstructive hydrocephalus

A
physical block (tumor or clot) of ventricular system 
btwn lateral and third, third and fourth, and at foreman magnum
20
Q

arachnoid/ pacchionian granulations

A

one way valve for CSF to flow out of ventricular system (but not back in)

21
Q

non-obstructive or communicating hydrocephalus

A

obstruction of arachnoid granulations

22
Q

choroid plexus

A

secretion of CSF into ventricles

made from outpouching of capillaries and pia mater into ventricular space with lining of choroid epithelium

puts capillary btwn pia mater and arachnoid membrane

23
Q

choroid epithelium vs ependymal cells

A

contiguous with one another

choroid: line choroid out pouching; tight junctions
ependymal: line ventricular walls; normal fenestrations

24
Q

blood CSF barrier

A
  1. fenestrated capillaries
  2. tight junctions of choroid epithelial cells and between arachnoid villus cells
    prevent back flow of substances from venous sinuses into CSF
25
Q

blood brain barrier

A

prevent free-passage of molecules from periphery to CNS and vice versa

  1. tight junctions between endothelial cells (req. transcellular transport)
  2. BM
  3. astrocytes

also: enzymes, P-gp (efflux, influx, bidirectional) pumps

26
Q

list of circumventricular organs

A

brain areas that lack BBB and typically line ventricular system

  1. pineal gland
  2. OVLT
  3. median eminence
  4. posterior pituitary
  5. area postrema
  6. subfornical organ
27
Q

glymphatic system

A
  1. clears waste in CNS
  2. exchange of solutes between CSF and interstitial fluid driven by arterial pulsation
  3. regulated during sleep by expansion and contraction of brain extracellular space
  4. facilitated by astrocyte aquaporin 4
28
Q

What can break down the BBB 1. progressively

2. temporarily

A
  1. disease, age

2. post MI leading to cerebral edema, marked rise in BP, injection of hypertonic solutions

29
Q

adherens junctions

A

stabilize cell cell interactions in junctional zone

30
Q

What can

  1. pass BBB
  2. not pass BBB unless use regulatory transport pathways
A
  1. lipophilic, water, CO2, O2; drugs that are free (not bound), non-ionized, lipophilic
  2. polar, large; drugs that are proteins, polypeptides, ions (ex. quaternary amine)
31
Q

Factors that increase BBB disruption

A
  1. comorbidity
  2. age
  3. inflammation
  4. neurodegenerative disease
  5. medications
  6. concussions (increase of S100B in blood leading to Ab)
32
Q

AE of BBB disruption

A
  1. vulnerability to stroke
  2. white matter disease
  3. delirium
  4. adverse drug reactions
33
Q

octanol/water partition coefficient

A

experimental measurement of lipophilicity

octanol (more lipid soluble): right on X-axis

increase brain uptake: up on Y-axis

34
Q

lipophilic drugs in CNS: duration of action vs. elimination

A
  1. short duration: lipid soluble drugs: get into CNS quickly but redistribute quickly
  2. long elimination: can be stored in adipose but isn’t at active site anymore
35
Q

P-gp role in CNS drugs and cancer

A
  1. many CNS drugs (antidepressants/ antipsychotics) are P-gp substrates and are ineffective
  2. many anticancer drugs are substrates
  3. can compromise diagnostic tests against micro-metastases (have to wait until tumor big enough to disrupt BBB)
36
Q

P-gp inhibitors

A
  1. amiodarone
  2. cyclosporin
  3. nifedipine
  4. quinidine
  5. verapamil

none clinically useful because of AE

37
Q

factors that effect individual drug responsiveness to anti-depressants

A

polymorphism of

  1. CYP: can overcome by dose adjustment
  2. P-gp: req. selection of another non-substrate drug
  3. possible up-regulation of P-gp in depressed patients
  4. drug is substrate of other active pump substrates
  5. antidepressants might be competitive inhibitors of concurrent substrates of P-gp: (allow more of other substrate into CNS)
38
Q

How can antidepressants effect cortisol levels thru P-gp?

A
  1. in depressed patients: P-gp prevents cortisol from getting into brain for neg. feedback mechanism: increase plasma cortisol, hyperactive HPA axis
  2. antidepressants might be competitive inhibitors of concurrent substrates of P-gp
  3. antidepressants inhibit P-gp: allows cortisol access to hypothalamus: reestablish neg. feedback to HPA axis