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Neuro Part 2 > Week 8.4 > Flashcards

Week 8.4 Flashcards

1
Q

Neurons begin suffering irreversible after what duration of anoxia?

A

5-6 minutes

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2
Q

What are some causes of global brain ischemia?

A
  • suffocation
  • poisoning
  • hypotension
  • cardiac arrest
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3
Q

Which adult brain structures are mot susceptible to ischemia?

A
  • CA1 of hippocampus
  • Purkingje Cells
  • Pyramidal Neurons in layers 3, 5, and 6
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4
Q

What important structure is located within the ACA/MCA watershed zone?

A

the hippocampus

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5
Q

What are four significant causes of focal ischemia?

A
  • thrombosis
  • embolus
  • vasculitis
  • CADASIL
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6
Q

Where in the cerebral vasculature are thrombi most common?

A
  • carotid bifurcation
  • middle cerebral artery origin
  • top and bottom of basilar arter
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7
Q

What are the most common sources of embolus to the brain?

A
  • heart
  • carotids
  • paradoxical
  • fat, tumor, air
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8
Q

Paradoxical emboli travel through a patent ___.

A

foramen ovale

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9
Q

Emboli are most likely to lodge in which cerebral artery?

A

the MCA

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10
Q

What is an hemorrhagic infarct?

A

an ischemic event gets broken up and hemorrhage follows as RBCs leak through damaged endothelial cells causing petechial hemorrhages

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11
Q

What gross changes can you expect following ischemia?

A
  • 0-6 hours: nothing
  • 48 hours: pale, soft, swollen
  • 2-10 days: friable, demarcation
  • 10-21 days: liquefaction
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12
Q

What microscopic changes can you expect following ischemia?

A
  • 12-24 hours: red neurons
  • 12-48 hours: neutrophils
  • 48 hours - 2 weeks: macrophages, necrosis
  • 1 - 4 weeks: astrocytic proliferation
  • chronic: glial scar, cyst, Wallerian degeneration
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13
Q

Name four possible causes of cerebral edema.

A
  • tumor
  • infarct/hemorrhage
  • abscess
  • diffuse axonal injury
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14
Q

Why is subfalcine herniation problematic?

A

it tends to compress the ACA

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15
Q

Why is transtentorial herniation problematic?

A
  • compresses CN III
  • compresses PCA causing occipital lobe infarction
  • causes hemorrhages in brainstem
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16
Q

What is CADASIL?

A

aka cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, an autosomal dominant vascular dementia caused by Notch3 mutation

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17
Q

What causes CADASIL?

A

a notch3 mutation

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18
Q

What are the features of CADASIL?

A
  • onset in 20s-30s with migraine with aura
  • depression
  • recurrent infarcts leading to cognitive decline and dementia
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19
Q

What histologic evidence supports CADASIL?

A

PAS staining of vessels in a skin biopsy

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20
Q

What are lacunar infarcts?

A

small, subcortical infarcts

21
Q

The most common cause of lacunar infarcts is what?

A

hypertensive CV disease and the resulting arteriolar sclerosis

22
Q

Hypertensive CV disease affects predominant which brain structures?

A

deep nuclei and white mater

23
Q

What are the three most common places for lacunar infarcts?

A
  • putamen/globus pallidus
  • thalamus
  • internal capsule
24
Q

The most common cause of intraparenchymal hemorrhage is what?

A

hypertension

25
Q

How does hypertension lead to intraparenchymal hemorrhage?

A
  • hypertension
  • accelerated atherosclerosis
  • hyaline arteriosclerosis
  • increased fragility
  • formation of microscopic aneurysms
  • rupture
26
Q

What are Charcot-Bouchard aneurysms?

A

hypertension induced microaneurysms

27
Q

What are the most common sites of intraparenchymal hemorrhage?

A
  • putamen
  • thalamus
  • pons
28
Q

What is the primary complication of cerebral amyloid angiopathy?

A

cerebral hemorrhage

29
Q

What would cause a fat emboli?

A

long bone trauma

30
Q

What is amyloid?

A

an misfolded protein in a beta-sheet

31
Q

How can we identify amyloid on a stained section of tissue?

A

using congo red stain and polarized light

32
Q

The three most significant vascular malformations are what?

A
  • AVM
  • cavernous angioma
  • capillary telangiectasia
33
Q

What is a cavernous angioma?

A

a venous abnormality in which hyalinized vessels are back-to-back

34
Q

What is capillary telangiectasia?

A

dilated thin-walled vessels separated by normal brain tissue

35
Q

Why are AVMs a problem?

A
  • the strain the heart
  • the are mass-occupying
  • they act as a shunt for oxygen
  • the high pressure input to veins can rupture them
36
Q

What are the two major complications of cavernomas?

A
  • seizures

- cerebral hemorrhage

37
Q

Berry aneurysms cause what kind of hemorrhage?

A

subarachnoid

38
Q

What are major risk factors for subarachnoid hemorrhage?

A
  • hypertension
  • smoking
  • genetics (Marfan’s, NF1, etc.)
39
Q

Where are Berry aneurysms most common?

A
  • anterior communicating artery

- middle cerebral artery (distal and proximal)

40
Q

Subdural hemorrhage is followed by what sort of reorganization?

A

fibroblasts wall off the blood until it can be resorbed

41
Q

Which organisms most commonly cause brain abscesses?

A

staphylococci and streptococci

42
Q

Describe abscess organization.

A
  • center of necrosis and neutrophils
  • rim of granulation tissue and a fibrous capsule
  • surrounded by edema and gliosis
43
Q

Brain abscesses often mimic what other pathology?

A

glioblastoma

44
Q

Taxoplasmosis is transmitted by what species?

A

cats

45
Q

What virus most commonly causes meningitis?

A

enteroviruses

46
Q

What are the typical features of viral encephalitis?

A
  • perivascular chronic inflammation
  • microglial nodules
  • neuronophagia
  • viral inclusions
47
Q

How does rhabdovirus enter the CNS?

A

via intraaxonal retrograde transport

48
Q

Negri bodies are a feature of which CNS infection?

A

rhabies

49
Q

How is a diagnosis of HIV encephalitis made?

A

the presence of multinucleate giant cells in microglial nodules that stain for HIV p24

Neuro Part 2 (18 decks)

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