Chapter 28 part 6 Flashcards

1
Q

Hypoglycemia

A
  • some regions of the brain are more sensitive to it
  • pyramidal neurons of cerebral cortex
  • hippocampus
  • purkinje cells of the cerebellum
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2
Q

hyperglycemia

A

-dehydration, confusion, stupor, coma

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3
Q

hepatic encephalopathy

A
  • impaired liver function
  • elevated ammonia levels and proinflammatory cytokines
  • astrocytes with enlarged nucleus–alzheimer type II cells
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4
Q

carbon monoxide characteristic?

A
  • injury of neurons–layers III and V of cerebral cortex, hippocampus, purkinje cells
  • CO interacts with heme of cytochrome c oxidase–inhibit electron transport in mitochondria
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5
Q

methanol-effects

A
  • retina–degeneration of retinal ganglion cells–can cause blindness
  • bilateral necrosis of putamen and focal white-matter necrosis–when severe exposure
  • illicit liquor (moonshine) contaminated
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6
Q

ethanol effects

A
  • chronic–wernicke-korsakoff syndrome (from thiamine deficiency)
  • cerebellar dysfunction–truncal ataxia, unsteady gait, nystagmus
  • atrophy and loss of granule cells in anterior vermis
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7
Q

radiation effects

A

-coagulative necrosis–edema in surrounding tissue, vascular fibrinoid necrosis, sclerosis

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8
Q

70% of childhood tumors arise in?

A
  • posterior fossa

- tumors of CNS account for 20% of all cancers in childhood

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9
Q

most common group of primary brain tumors

A

-gliomas

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10
Q

gliomas include

A
  • astrocytoma
  • oligodendroglioma
  • ependymoma
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11
Q

2 major categories of astrocytic tumors

A
  • diffusely infiltrating astrocytomas

- more localized astrocytomas (pilocytic astrocytoma–most common)

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12
Q

infiltrating astrocytomas–symptoms? range from?

A
  • 80% of adult primary brain tumors
  • 4-6 decades
  • seizures, headaches, focal neurologic deficits
  • diffuse astrocytoma (grade II/IV)
  • anaplastic astrocytoma (grade III)
  • glioblastoma (grade IV)
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13
Q

glioblastoma occurs in 2 settings

A
  • primary glioblastoma–older patients–new onset of disease

- secondary glioblastoma–progression of a lower-grade astrocytoma-younger patients

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14
Q

glioblastoma–4 molecular subtypes

A
  • classic subtype
  • proneural
  • neural
  • mesenchymal
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15
Q

glioblastoma classic subtype–genes

A

most primary glioblastoma

  • mutation of PTEN tumor suppressor gene
  • deletions of chromosome 10
  • amplification of EGFR oncogene
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16
Q

glioblastoma proneural type–genes

A

most secondary glioblastoma

  • mutation of TP53, IDH1 and 2
  • overexpression of receptor for PDGFRA
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17
Q

glioblastoma neural type genes

A
  • deletions of NF1

- TNF pathway and NFkB pathway–highly expressed genes

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18
Q

most common theme of the subtypes of glioblastomas

A

-most affect 2 cancer hallmarks–sustained proliferative signaling, evasion of growth suppressors

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19
Q

diffuse astrocytoma morphology

A
  • poorly defined
  • cellular density
  • transition bw neoplastic and normal tissue is indistinct
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20
Q

anaplastic astrocytoma–morphology

A
  • more density cellular

- gemistocytic astrocytoma–brightly eosinophilic cell body, stout processes

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21
Q

glioblastoma morphology

A
  • variation in appearance of tumor from region to region
  • some areas are firm/white; others soft/yellow (necrosis); others cystic degeneration and hemorrhage
  • necrosis and vascular/endothelial cell proliferation
  • pseudo-palisading–tumor cells on the edges of necrotic regions
22
Q

gliomatosis cerebri

A
  • diffuse glioma, infiltration of multiple regions of brain

- aggressive–grade III/IV

23
Q

-well differentiated diffuse astrocytoma–outlook

A
  • stable/progress slowly
  • survival more than 5 years
  • clinical deterioration occurs due to emergence of more rapidly growing tumor of higher histologic grade
24
Q

high grade astrocytoma outlook

A
  • abnormal vessels are leaky, permeable BBB

- glioblastoma–prognosis is poor

25
Q

pilocytic astrocytoma–characteristics and morphology

A

(grade 1)

  • children, young adults
  • occurs in patients with NF1 (functional loss of neurofibromin
  • 2 alterations in BRAF signaling pathway also
  • grow very slowly
  • often cystic
  • necrosis is uncommon
  • limited infiltration of surrounding brain
26
Q

brainstem glioma–when? anatomic patterns?

A

clinical subgroup of astrocytomas

  • 1st 2 decades of life
  • pontine gliomas (most common)–aggressive, short survival
  • cervicomedullary jxn tumors–less aggressive
  • dorsally exophytic gliomas–even more benign
27
Q

oligodendroglioma–when? genes?

A
  • infiltrating gliomas, resemble oligodendrocytes
  • 4-5 decades
  • neurologic complaints, seizures
  • mutations of IDH1 and IDH2 (better prognosis)
  • survival 5-10 years
28
Q

oligodendroglioma–morphology

A
  • well circumscribed, cysts, focal hemorrhage, calcification
  • anastomosing capillaries
  • grade II
29
Q

anaplastic oligodendrogliomas

A

higher cell density, necrosis, mitotic activity

30
Q

ependymoma–where? when? gene?

A
  • ofern arise next to ependyma–lined ventricular system, central canal of spinal cord
  • first two decades–near 4th ventricle
  • in adults–spinal cord–NF2
31
Q

ependymoma–morphology

A
  • in 4th ventricle–well demarcated, but near vital pontine and medullary nuclei
  • intraspinal tumors–sharp demarcation
  • cells–regular, round to oval nuclei, chromatin
  • perivascular pseudorosettes–tumor cells arranged around vessels, thin ependymal processes directed toward wall of vessel
32
Q

ependymoma clinical features

A
  • posterior fossa ependymomas–hydrocephalus (obstruction of 4th venricle)–worst outcome (5yr survival=50%)
  • CSF dissemination is common
33
Q

subependymomas-what are they?

A
  • solid, sometimes calcified, slow-growing nodules attached to ventricular lining and protrude into ventricle
  • usually asymptomatic
  • can cause hydrocephalus
  • mostly found in lateral and 4th ventricles
34
Q

choroid plexus papillomas

A
  • most common in children–lateral ventricles
  • adults–4th ventricle
  • exactly looks like structure of normal choroid plexus
  • present with hydrocephalus
35
Q

colloid cyst of 3rd ventricle

A
  • non-neoplastic enlarging cyst
  • young adults
  • attached to roof of 3rd ventricle, can obstruct foramina of monro–cuases noncommunicating hydrocephalus–rapidly fatal
  • headache
  • cyst–thin, fibrous capsule, cuboidal epithelium
36
Q

neuronal tumors–when?

A

far less common than glial tumors

-seen in young adults–presents with seizures

37
Q

gangliogliomas–what are they?

A
  • mix of mature neuronal and glial cells
  • superficial lesions–seizures
  • most common neuronal tumors of CNS
  • slow growing, but glial component can become anaplastic (then progresses rapidly)
  • mutation in BRAF gene
  • most often–temporal lobe-cystic component
38
Q

dysembryoplastic neuroepithelial tumor–what are they?

A
  • rare, low grade (I) tumor of childhood–seizures
  • good prognosis after resection
  • most often in superficial temporal lobe
39
Q

central neurocytoma–what is it?

A
  • low grade II in ventricular system

- evenly spaced, round, uniform nuclei and often islands of neuropil

40
Q

medulloblastoma

A
  • malignant embryonal tumor, grade IV
  • exclusively in cerebellum
  • most common- 20% of brain tumors in kids
41
Q

medulloblastoma–4 groups of genetics

A
  • Wnt type (older children–prognosis is best!)
  • SHH type (infants, young adults)
  • group 3 medulloblastoma (MYC amplification, isochromosome 17-infants/children–worst prognosis)
  • group 4 (isochromosome 17; without MYC amplification; some MYCN amplification–intermediate prognosis
42
Q

medulloblastoma–morphology where?

A
  • kids–midline of cerebellum
  • adults-lateral
  • hydrocephalus
  • well circumscribed, densely cellular
43
Q

nodular desmoplastic variant

A

-areas of stromal response–collagen, “pale islands” that have more neuropil and neuronal markers

44
Q

large cell variant

A

-large irregular vesicular nuclei, mitosis, apoptotic cells

45
Q

drop metastases

A

-form linear chains of cells that infiltrate through cerebellar cortex–spread to subarachnoid space
-dissemination through CSF–common complication!
gives rise to nodular masses some distance from primary tumor

46
Q

atypical teratoid/rhabdoid tumor–when? where?

A
  • highly malignant tumor–young children–grade IV
  • posterior fossa, supratentorial compartments
  • divergent differentiation with epith, mesenchymal, neuronal, glial components, often includes rhaboid cells
47
Q

apical teratoid/rhabdoid tumor–genes, hallmark??

A
  • alterations in chromosome 22–hallmark

- hSNF5/INI1

48
Q

apical teratoid/rhabdoid tumor–morphology/ clinical?

A
  • large, soft
  • rhabdoid cells
  • highly aggressive–very young–before 5-live 1 year
49
Q

primary CNS lymphoma

A
  • most common CNS neoplasm in immunocompromised patients (infected by EBV)
  • multifocal in brain parenchyma
  • most are B-cell origin
  • aggressive, bad outcomes
50
Q

characteristic of primary brain lymphoma

A

-hooping–infiltrating cells separated from 1 another by silver staining material

51
Q

intravascular lymphoma

A
  • large cell lymphoma
  • grows within small vessels
  • instead of presenting as a mass lesion, the occlusion of vessels by malignant cells and results in infarcts