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Robbins systemic pathology > Chapter 28: CNS > Flashcards

Chapter 28: CNS Flashcards

1
Q

Differentiate hypoxia and ischemia

A

Hypoxia: low partial pressure of oxygen, or impairment of blood’s oxygen carrying capacity or inhibition of oxygen use in tissue

Ischemia: interruption of normal circulatory flow either from hypotension or obstruction

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2
Q

What are Charcot-Bouchard microaneurysms?

A

-small aneurysms developing as a result of hypertension in the basal ganglia

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3
Q

What syndromes are associated with Berry aneurysms?

A
  • ADPKD
  • Ehlers Danlos type IV
  • NF1
  • Marfan
  • Fibromuscular dysplasia of extracranial arteries
  • Coarctation of aorta
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4
Q

What organisms are seen in neonatal bacterial meningitis? What about adolescents? And the elderly?

A

Neonatal: group B strep, E coli

Adolescents: N. meningiditis

Elderly: S pneumo, Listeria

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5
Q

How does herpes affect the brain?

A
  • encephalitis that is most severe in the inferior and medial temporal lobes
  • necrotizing, hemorrhagic infection with perivascular inflammatory infiltrates
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6
Q

How does CMV affect the brain?

A
  • paraventricular subependymal involvement
  • necrotizing hemorrhagic ventriculoencephalitis and choroid plexitis
  • most often immune suppressed person
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7
Q

What are features of HIV infection in the CNS?

A
  • HIV encephalitis: widespread microglial nodules with multinucleated giant cells often associated with tissue necrosis or gliosis
  • White matter disease with multifocal areas of myelin pallor, axonal swelling and gliosis
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8
Q

Features of CNS toxoplasmosis?

A
  • usually immunosuppressed (especially HIV)
  • multiple ring-enhancing lesions near the gray-white junction
  • necrosis, petechial hemorrhage, with free tachyzoites and encysted bradyzoites at the periphery
  • organisms stain with Giemsa or IHC
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9
Q

What are the pathologic features of CJD?

A
  • spongiform transformation of cortex and deep gray structures
  • Later stages may have neuronal lossa nd reactive gliosis
  • Kuru plaques: extracellular deposits of aggregated abnormal protein that are Congo Red and PAS positive and most often occur in the cerebellum
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10
Q

What is fatal familial insomnia?

A
  • caused by a PRNP mutation
  • results in ataxia and eventually coma
  • does not have spongiform pathology but instead neuronal loss and gliosis most marked in the thalamus
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11
Q

What is the pathogenesis of MS?

A
  • Th1 and Th17 cells reacting against self myelin antigens
  • HLA associations
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12
Q

What are macroscopic and microscopic features of MS?

A

Macroscopic: well-circumscribed gray-tan plaques often adjacent to lateral ventricles, also around optic nerves, brainstem, cerebellum

Microscopic: active plaques have abundant myelin-engulfing macrophages; inactive plaques have a reduction in oligodendrocyte nuclei and astrocyte proliferation and gliosis

-lesions of varying ages (unlike in ADEM)

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13
Q

What are the histologic features of Alzheimer disease and what parts of the brain are most affected?

A

Neuritic plaques: collections of dystrophic neurites around a central amyloid core which stain with Congo Red and are found in hippocampus, amygdala and neocortex; a-beta is found; more specific than tangles

Neurofibrillary tangles: bundles of filaments with a flame shape that are positive for silver staining and made up of hyperphosphorylated tau protein (a microtubule associated protein); found in entorhinal cortex, hippocampus, amygdala

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14
Q

What is present in dopaminergic neurons in Parkinsons disease?

A

-alpha synuclein (Lewy bodies)

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15
Q

What is adrenoleukodystrophy?

A
  • several forms, some X-linked
  • myelin loss from CNS and PNS
  • adrenal insufficiency
  • inability to properly catabolize very long chain fatty acids within peroxisomes
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16
Q

What is Wernicke encephalopathy?

A
  • psychotic symptoms and ophthalmoplegia that develops in thiamine deficiency
  • foci of hemorrharge and necrosis in the mamillary bodies and the walls of the 3rd and 4th ventricles
17
Q

What are features of vitamin B12 deficiency in the CNS?

A

Myelin swelling with vacuolation

18
Q

What neurons are affected first in hypoglycemia?

A

-Selective injury to large pyramidal neurons of cerebral cortex

19
Q

What are toxic effects of carbon monoxide on the brain?

A
  • selective injury to layers III and V of cerebral cortex, Sommer sector of hippocampus and Purkinje cells
  • bilateral necrosis of globus pallidus
  • later, demyelination
20
Q

Where is methanol toxicity manifest?

A
  • degeneration of retinal ganglion cells leading to blindness
  • bilateral putamenal necrosis
21
Q

What are histologic changes in the brain in ethanol toxicity?

A
  • atrophy and loss of granule cells of cerebellar vermis
  • later, loss of PUrkinje cells in the cerebellum and gliosis
22
Q

What molecular alterations are most common in low grade astrocytomas?

A

p53 mutations

Overexpression of PDGFA and its receptor

23
Q

What molecular alterations are assocated with the transition of a low grade to a higher grade glioma?

A

Disruption of RB and p16 as well as an 19q

24
Q

What are features of primary glioblastoma?

A
  • Older individuals
  • More often amplification of MDM2 (which inhibits p53)
  • More often mutations in EGFR genes
25
Q

What is the significance of MGMT promoter methylation in GBM?

A
  • Predicts responsiveness to alkylating agents
  • MGMT required for repair of chemo induced damage so those that are silenced by methylation will respond better to treatment because they can’t repair the damage
26
Q

What genetic alterations are seen in medulloblastoma?

A
  • loss of 17p: most common and associated with poor prognosis
  • MYC amplification: associated with poor prognosis
27
Q

What is the definition for atypical meningioma?

A
  • 4 or more mitoses/10 high power field
  • 3 of: increased cellularity, small cell change, prominent nucleoli, patternless growth, spontaneous necrosis
  • clear cell and chordoid patterns
28
Q

What cytogenetic abnormality is seen most commonly in meningioma?

A

-NF2 loss (22q12): b oth sporadic and syndromic

29
Q

What is the function of NF1?

A

Neurofibromin stimulates the activity of a GTPase that inhibits RAS activity

30
Q

What is the function of NF2?

A

Merlin is a structural cytoskeletal protein that may regulate membrane receptor signalling and inhibit growth

31
Q

What are clinical features of NF2?

A

Bilateral 8th nerve schwannomas

Multiple meningiomas

Gliomas, typically spinal cord ependymomas

Must less common than NF1

32
Q

What is the function of TSC1 and TSC2?

A

Hamartin (9q34) and Tuberin (16p13)

  • both proteins form a complex that inhibits mTOR which is a key regulator of protein synthesis
  • mTOR controls cell size, which may be why tumors in TS have abundant cytoplasm
33
Q

What are clinical features of tuberous sclerosis?

A

Cortical subers and subependymal nodules

Subependymal giant cell astrocytomas

Epilepsy from tubers

Renal angiomyolipomas

Retinal glial hamartomas

Cysts of liver, kidneys and pancreas

Pulmonary LAM

Cardiac rhabdomyomas

Angiofibromas

Shagreen patche

Ash-leaf hypopigmented patches

Subungual fibromas

34
Q

What are clinical features of VHL?

A

Hemangioblastomas especially of cerebellum and retina

Cysts of pancreas, liver, kidneys

Renal cell carcinoma

Pheochromcytoma

35
Q

What is the function of VHL (3p25)

A

Component of a ubiquitin ligase complex that downregulates HIF1

HIF1 normally regulates expression of VEGF, erythropoeitin, etc

Dysregulation of erythropoietin is responsible for polycythemia seen in hemangioblastomas

Robbins systemic pathology (17 decks)

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