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67 Cards in this Set
- Front
- Back
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IDH1 |
Isocitrate dehydrogenase I (IDH 1) a metabolicenzyme in the citric acid cycle, is commonlymutated in astrocytomas, oligodendroglioma,and mixed gliomas- low grade (II) and anaplastic(III). |
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Is IDH 1 mutation found in primary or secondary GBM? |
IDH1 and IDH2 are uncommon in primary GBMs(~5%) but can be seen in secondary GBMsarising from lower grade gliomas. |
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Is IDH 1 and 2 mutation good or bad prognosis? |
good |
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MGMT |
O-6-methylguanine-DNAmethyltransferase is a DNA repair enzy that removes ALKYL group thought to predict response to alkylating agents |
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what happens if the MGMT gene is hypermethylated? |
better prognosis |
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cell of origin of meningiomas |
arachnoidal cells |
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what meningioma associated with NF2 |
SPORADIC MENINGIOMAS |
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WHO GRADE I MENINGEOMA? |
fibrous psammomatous classic (meningothelial) secretory microcystic lymphoplasmacytic metaplastic angiomatous |
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WHO GRADE II MENINGEOMA? |
CLEAR CELL CHORDOID |
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WHO GRADE III MENINGEOMA? |
PAPILLARY RHABDOID ANAPLASTIC |
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MENINGIOMA STAINS? |
EMA+ S100+ ck- mib1 > 4% increase recurrence cd34+ fibrous meningioma gfap - cea + secretory |
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what is the most common chromosomal abnormality? |
CH 22 |
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what us the recurrence rate for anaplastic MENINGIOMA? |
50-90% |
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Cerebellar lesion with nidus |
pilocytic astro or hemgioblastoma |
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Kid with medication resistant seizure? |
DNT (dysemberyoplatic neuroeithelioma) |
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what is DNT associated with ? genetic disorder? |
Gorlin syndrome |
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meduloblastoma commonest genetic alteration |
Isochromosome 17 |
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is isochromosome 17 of meduloblastoma a good or bad prognosis |
bad |
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classic autopsy finding in methanol intoxication? |
bilateral (putamen, GP necrosis) |
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when duo see nucleolin in Astrocytomas |
gamistocytic variant |
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who grade 2 astrocytomas? |
gamistocytic granular cell microcystic |
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who grade 3 astrocytomas? |
anaplastic astrocytoma gliomatosis cerebri |
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who grade 4 astrocytomas |
GBM |
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anaplastic astrocytoma of children? |
pontine location |
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in anaplastic astrocytoma what is the microscopic features? |
Increased cellularity Pleomorphism and hyperchromasia Variable mitotic activity |
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Increased cellularity Pleomorphism and hyperchromasia Variable mitotic activity are seen in? |
anaplastic astrocytoma |
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microscopic features of GBM? |
cytologicatypia and mitotic activity, as well as endothelialproliferation and/or necrosis |
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WHAT MOLECULAR MUTATION IN BRAIN STEM GBM OF KIDS |
p53 gene and chromosome 17 p alterations without EGFR geneamplification |
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p53 gene and chromosome 17 p alterations without EGFR gene amplification IS SEEN IN? |
BRAIN STEM GBM OF KIDS |
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MGMT ENZYME, WHAT HAPPENS IF THE GENE GETS METHYLATED? |
MGMT PROTEIN GETS REDUCED AND SO INCREASE RESPONSE TO TEMOZOLIMIDE TREATMENT |
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P53 17P ALTERATION IS FOUND ALSO IN? |
59% ASTROCYTOMAS 65% SECONDARY GBM 84% giant cell gbm 26% gliosarcoma 28% primary gbm |
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small cell GBM |
Primary GBM More common in elderly EGFR overexpression Dismal prognosis Mimic oligodendrglioma |
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gliosarcoma who grade? |
who grade 4 |
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gliosarcoma histology |
Biphasic tissue pattern - GFAP positive astrocytic and - GFAP negative mesenchymalcomponents - Reticulin rich - Bone, cartilage and striated muscle differentiation |
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NF1 gene maps to 17q11.2 |
pilocytic astrocytoma |
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pilocytic astrocytoma microscopic pattern |
bipolar fibrillated astrocytes rosenthal fibers EGB |
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cerebellar cyst with mural nodule? |
Pilocytic astrocytoma |
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childhood astrocytoma |
pilomyxoid astrocytoma |
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location of pilomyxoid astro? |
Hypothalamic/chiasmal region |
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superficial partially leptomeningeal cyst with mural nodule? |
pleomorphic xanthoastro (PXA) |
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location of PXA |
SUPRATENTORIAL USALLY TEMPORAL |
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EGB ARE SEEN IN? |
PILOCYTIC ASTRO PILOMYXOID ASTRP PXA |
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RESTICULIN STAIN IN PXA |
POSITIVE |
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location of SEGA |
WALL OF LATERAL VENT |
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ASSOCIATION WITH SEGA |
TUBEROUS SCLEROSIS |
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SEGA |
- Large cells with abundant, “glassy” cytoplasm to smaller, spindled forms – Largeneuron-like cells with prominent nucleoli |
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EPIDURAL HEMATOMA |
MIDDLE MENINGEAL ARTERY |
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SUBDURAL |
BRIDGING VEINS |
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subfacial (cingulate) herniation
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due to mass effect the cingulate gyrus herniates under the falx cerebri compression of anterior cerebral artery |
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transtintorial herniation |
Anteromedial aspect of parahippocampal gyrus underfree edge of tentorium compreesion of posterior cerebral artery and third crainal n |
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tonsillar herniation |
Downward displacement ofcerebellar tonsils into foramenmagnum compression of medulla |
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lewy bodies |
dense cytoplasmic inclusion with peri-inclusionhalo parkinson disease and aging |
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staining for Lewy bodies |
Ubiquitin (+) α-synuclein (+) Tau protein (−) Actin (−) |
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neurofibrally tangles |
Flame shaped• Pyramidal neurons AD, NORMAL AGING |
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staining for tangles |
Ubiquitin (+/-) Tau protein (+) |
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Granulovacular degeneration? |
Small vacuoles containingsmall, dense, round,basophilic granules present in AD PICK Normal aging present in CA1 region of hippo |
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staining for vascular degeneration |
Ubiquitin (+) Tau protein (+) |
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hirano bodies |
Eosinophilic rod-shaped,refractile inclusions present in AD PICK Normal aging present in CA1 region of hippo |
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staining for Hirano bodies? |
α – Actinin, Actin, Vinculin, Tropomyosin, Tau (+) |
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Bunina bodies |
Small bead – like eosinophilicinclusions Found in motor neuron disease (ALS) |
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Dystrophic neurites |
Abnormally dilated neuronal processes – Pass through amyloid plaques • Alzheimer’s disease |
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ASTROCYTIC INCLUSIONS: |
ROSENTHAL FIBERS EGB CORPORA AMYLACEA |
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ROSENTHAL FIBERS POSITIVE FOR? |
GFAP,αB crystallin and ubiquitin |
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EGB POSITIVE FOR? |
contain α–1– antitrypsin and chymotrypsin Associated with low grade glial tr |
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corpora amylacea |
Composed of glycogen-likecarbohydrates and proteins aging |
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function of oligodendrocytes? |
produce myelin for the CNS |
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where is the inclusions for PML found? |
oligodendroglia Progressive multifocal leukoencephalopathy Homogeneous, eosinophilic inclusion JC virus |
