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Block 3 > Path > Flashcards

Path Flashcards

1
Q

most critical exposure period?

A

3-8wks b/c that’s when brain forms

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2
Q

notochord development

A

day 17: notochord secretes signaling molec –> ectoderm becomes neuroderm –> produces neural precursors –> notochord = axis vertebral column

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3
Q

primary vs secondary neurulation vs post neurulation d/o

A

day25-28: Neural tube become brain & spinal cord till S2 –> neural tube separates from ectoderm –> ectoderm becomes epidermis; ant/cranial & post/caudal neuropore close vs day28-wk7: Rod of mesenchymal cells differentiate to neural cells to make neural tube past S2, conus medullaris, filum terminale; post neural tube merges w/ ant neural tube vs herniation d/t disturbance of mesoderm development at cranial (encephalocele) or spinal level (meningocele) –> not considered NTD; CSF pressure –> hydrostatic pressure –> dural hernia

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4
Q

genetic causes of NTDs

A

 MTHFR encodes methylene-tetrahydrofolate reductase –> converts 5,10-methylenetetrahydrofolate to 5-methylthrahydrofolate (5-MTHFA) –> convert homocysteine to methionine
 Homozygosity of C677C–>T variant

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5
Q

Craniorachischisis vs rachisis vs anencephaly

A

anencephaly + open cleft spine –> exposed neural tissue vs entire spinal cord exposed but no skull defect –> chronic infxn, incont, motor/sensory deficits vs cranial neuropore doesn’t close day25; Tunica cerebrovasculosa = dark red nonneural vascular mass attached to abnl skull base

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6
Q

open spina bifida: Myelomeningocele vs myelocele vs Chiari II w/ clinical sxs

A

Sac containing meninges, spinal cord, CSF; neural placode; neurological defects, bladder/bowel, weak LE vs neural plates did not fold edges –> neural placode lying level of skin, incomplete central canal spinal cord; neurological defects, bladder/bowel, paralysis LE vs open spina bifida + small post fossa –> displaced hindbrain

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7
Q

closed spina bifida: lipomyelomeningocele vs hydromyelia vs split cord vs tethered cord vs thick filum

A

Midline lipoma attached to dorsal neural placode extending thru defect vs Dilated, filiform shaped central canal of thoracic spinal cord; fluid cavity lined by ependymal cells, no neuro deficits vs Diastematomyelia & diplomyelia vs anchored by inelastic structure –> taut –> stretched; Abnl conus medullaris below L2-L3 vs >2mm, Incomplete involution of distal spinal cord –> lipoma, cyst in filum

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8
Q

herniation defects: encephalocele vs meningocele

A

sin: glabella, forehead, orbits
bas: nasal cavity, cribriform plate, sphenoid, ethmoid
occ: occ bone
vs
sac w/ CSF, spinal cord, meninges; U shaped –> tethered cord

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9
Q

auto rec primary micro. isolated vs syndromic?

A

mutation in ASPM encoding ASPM protein in mitotic spindle poles of neuronal progenitors –> <3 stdev. no abnilities vs w/ abnlities (holo, liss, polymicrogyria) –> intellectual disability, generalized spasticity, epilepsy, fail to thrive

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10
Q

anatomic vs benign familial vs metabolic megacephaly

A

inc size/number brain cells vs broad gyri, inc white/grey matter, avg or better intelligence vs excess deposits in brain –> lysosomal storage d/o, leukodystrophies

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11
Q

holo: WK5 - pro divides to…via? a vs semi/lobar

A

tele (cerebral cortex, striatum) & di (hypo/thal, caudate/putamen) via sonic hedgehog gene. no separation –> 1 ventricle vs mild midline facial defect –> close set eyes, flat nose, cleft lip

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12
Q

arrhinencephaly

A

no olfactory bulbs, tracts, trigone

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13
Q

agen CC can be sporadic partial (>1 region) or complete (4 regions)

A

Callosal neurons fail to form in cerebral cortex; or callosal neurons form but can’t cross midline –> white matter tracts (Probst bundles) assume anteroposterior position –> separates lat ventricles

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14
Q

cortical development. radial migration vs tangential migration

A

Neuronal progenitors in periventricular zone become neuroblasts –> move to overlying cortical plate –> pial surface –> cerebral cortex. wk12-16 to wk24: Cortical projection neurons from periventricular zone to pial surface guided by radial glial cells vs Interneurons from ganglionic eminence to cerebral cortex –> basal ganglia and amygdala

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15
Q

liss. Classical LIS vs cobblestone

A

Too few neurons reach cortex –> 2-4 layer cortex –> abnl longitudinal band of thick grey matter deep to cerebral cortex separated by thin white matter. loss of fxn mutation in LIS1, DCX, TUBA1A encoding cytoskel microtubules –> abnl neuronal migration vs mutation in POMT1/2, FKPR encoding glycosyltransferases for glycosylation –> hypoglycosylation of dystroglycan –> disrupt glia limitans under pia mater –> neuronal overmigration –> dec sulcation –> bumpy/pebbly cortical surface

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16
Q

polymicrogyria. bil sylvian PMG sxs

A

excess small and partly fused 2-3mm gyri separated by shallow sulci; either unlayered for 4 layered, thick 8-12mm cortex. developmental delay, mild spastic quadriparesis, impaired language development, epilepsy

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17
Q

neuronal heterotropia. periventricular nodular heterotropia vs subcortical laminar heterotropia

A

grey matter in abnl locations d/t failed radial migration. Loss of fxn X-linked dom mutation in FLNA at Xq28 encoding filamin A crosslinking actin to cell membrane for mig –> interrupted radial migration –> sz, mild intellectual disability vs X-linked dom mutation in DCX at Xq23 for doublecortin for cytoskel microtubules for migration –> developmental delay, spastic quadriparesis, sz, fine motor deficits

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18
Q

focal cortical dysplasia

A

Germline or somatic mutations in genes regulating PI3K/Akt/mTOR pathway –> loss of horizontal lamination of cerebral cortex –> epilepsy

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19
Q

congenital vs acquired aqueduct stenosis

A

X-linked mutation in L1CAM on Xq28 encoding L1 cell adhesion molec for neuronal migration –> hydrocephalus, AS stenosis, ventriculomegaly, mental retard, spastic paraplegia (absence of corticospinal tracts), adducted thumbs vs intraut infxn, perinatal intraventricular hemorrhage d/t prematurity

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20
Q

cerebellar malformations: cerebellar agen vs cerebellar hypoplasia vs Dandy Walker vs Joubert

A

brains develops w/o cerebellum but sm remnants remain –> poor movement, clumsy, intellectual & emotional problems vs dec cerebellar w/ small but nml shaped vermis, folia, fissures –> ataxia, dec muscle tone/hypotonia, developmental or language delay, nystagmus vs cystic dil of 4th v –> hydrocephalus, macrocephaly, irritability, emesis, developmental delay, hypotonia, bal & coordination vs auto rec mutation in AHI1 encoding jouberin in basal bodies of primary cilia –> block forming primary cilia –> hypoplasia of vermis –> episodic tachypnea and/or apnea, hypotonia, delay in motor, ataxia, oculomotor apraxia, nystagmus, intellectual disability

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21
Q

Chiari 1 vs 2 vs 3

A

caudally placed tonsils + sm occ bone & post cranial fossa –> impacted vs inf brainstem displacement + myelomeningocele vs inf brainstem displacement + occ encephalocele

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22
Q

spinal cord malformations: syringomyelia vs syringobulbar vs hydromyelia

A

CSF-filled gliosis-lined tubular cavitation of spinal cord; congenital = Chiari 1, tethered cord; acquired = hydrocephalus, meningitis, MS, post trauma, spinal cord tumors vs syrinx w/in brainstem that’s not lined by ependymal cells but lined by CSF; asx but if destroys spinothalamic tracts –> loss pain & temp; or destroys dorsal column –> loss fine touch, vibration, proprio; or destroys pyramidal tracts –> spastic paraparesis of UE or LE vs you know this

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23
Q

Cerebral edema: gross vs micro appearance

A

inc fluid in brain –> enlarged brain, wide/flat gyri, narrow sulci, compressed ventricles; micro enlarged perivascular/neuronal spaces —> intracranial pressure –> brainstem herniation, HA, emesis, altered state of consciousness

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24
Q

cytotox vs vasogenic edema

A

neural/glial cell injury –> early phase of anoxia/ischemia –> loss ATP –> inhibit Na/K ATPase, GluE also binds to neuronal & astrocyte receptors –> Na+, Cl-, H2O enter cells –> CNS cells swell –> intracellular fluid accumulation vs influx of fluid & blood solutes into brain –> dmg tight jxns & basement membrane by proteases & free radicals –> endothelial “permeability pores” –> incompetent BBB; MRI shows affecting white matter only

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25
Q

what’s inc ICP and caused by?

A

> /= 20mmHg pressure inside skull, brain tissue, CSF caused by intracranial mass; cerebral edema from acute ischemia/ischemic stroke/hepatic encephalopathy/traumatic brain injury; hydrocephalus; obstruct venous flow; idiopathic

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26
Q

clinical pres of ICP (5)

A

o HA, N/V
o Vision probs from papilledema (axon flow impeded by inc pressure around optic nerve)
o Abnl posturing (decerebrate/corticate)
o Impaired consciousness from pressure on midbrain reticular formation
o Cushing reflex (late sign of ICP, warning sign of brain herniation)

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27
Q

what if ICP > cerebral arterial perfusion?

A

no cerebral perfusion –> destroyed axons in periventricular pyramidal tracts & CC –> brain death

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28
Q

ICP: subfalcine vs transtentorial vs tonsillar vs extracranial

A

Mass in frontal/parietal/temp lobe –> pushes ipsi cingulate gyrus under falx cerebri –> focal necrosis of cingulate gyrus; compressed CC/contralat cingulate gyrus/A2 pericallosal a –> contralat LE wk, abulia, dec verbal fluency vs uncal: uncus moves below tentorial notch –> midbrain & contralat cerebral peduncle against Kernohan notch –> oculomotor paresis, loss of consciousness, hemiparesis. central: thal & both temp lobes herniate thru tentorial notch –> compressed reticular activating system –> coma; Duret hemorrhage of basilar a vs tonsils herniate thru foramen magnum into cervical cord –> fora mag compromises resp/circ centers –> stiff neck, head tilt, resp/cardiac depression vs Comminuted skull fx –> swollen brain tissue herniating thru surgical defect/lacerated dura –> mushroom cap –> venous infarct

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29
Q

what causes hydrocephalus?

A

CSF obstructed flow (obstructive/noncommunicating), inadeq CSF absorption, CSF overprod (nonobstructive/communicating) –> dil ventricles, inc ICP

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30
Q
  • CSF prod
  • CSF circ
  • CSF absorption
  • CSF pressure
A

-by choroid plexus in ependyma lining of ventricles (mostly lat ventricles)
-ventricular system
-into cerebral venous system by arach gran adjacent to sup sag sinus via pressure-dependent grad
-7-13mmHg when pt on side, 15-22mmHg when pt sitting

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31
Q

how does inadeq CSF absorption vs CSF overprod cause hydrocephalus?

A

o Immature arach gran/villi –> can’t absorb CSF continuously
o Inflamm/scar of arach villi, meningitis, subarach hemorrhage –> clog CSF reabsorption
o High venous pressure sinus –> impair CSF translocation to venous circ
vs
from choroid plexus papilloma

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32
Q

congenital vs acquired hydrocephalus

A

o Aqueduct stenosis: X linked mutation in L1CAM encoding L1 cell adhesion molec
o Chiari II
o Dandy Walker –> atresia of apertures
o Arachnoid cysts: meningeal maldevelopment –> split arachnoid membrane –> intraarach sacs filled w/ CSF –> Asx unless too big –> mass effect
o CSF overexcretion –> choroid plexus papilloma/carcinoma –> communicating hydrocephalus
o Intraut infxns
vs
o meningitis –> obstructed CSF flow in Syl or 4th –> block subarach spaces –> impede CSF absorption
o Traumatic brain injury: posttraumatic intraventricular hemorrhage, subdural hematoma –> block CSF flow at Syl, 4th; or obliterated arach gran d/t inflamm or RBCs –> hemorrhage in subarach space or ventricular system

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33
Q

clinical pres of hydrocephalus in infants vs older kids/adults

A

sutures haven’t closed; CSF accumulation –> enlarged head, ant fotanelle bulge, splay cranial sutures, Setting Sun eyes vs no enlarged head; inc ICP –> HA, N/V, drowsy, sunsetting eyes; blurred vision from papilledema & optic n atrophy; unsteady gait, dementia

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34
Q

hydrocephalus ex vacuo vs benign external hydrocephalus

A

Alzheimer’s –> degen brain vol loss –> compensatory enlarged ventricles & subarach spaces; nml ICP vs infants w/ inc head circumference + enlarged subarach spaces or ventricles –> immature arach gran/villi –> can’t absorb CSF continuously

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35
Q

nml pressure hydrocephalus. how to dx?

A

nml LP but enlarged ventricles
o Form of communicating hydrocephalus caused by intraventricular hemorrhage, subarach hemorrhage, meningitis
o Triad: gait disturbance, dementia, urin incont
o MRI: ventriculomegaly w/ maintained cerebral parenchyma
-
o Imging: US for infants if ant fontanelle = open  mono/bi/tri/panventricular hydrocephalus
o LP: assess CSF pressure & presence of biochemical abnlities but risk cerebral herniation

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36
Q

mild vs mod vs severe traumatic brain injury sxs

A
  • Mild = loss of consciousness <1hr or amnesia <24h; GCS 13-15
  • Moderate = loss of consciousness 1-24h or amnesia 1-7d; GCS 9-12
  • Severe = loss of consciousness >24h or amnesia >1wk; GCS 3-8
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37
Q

linear vs depressed vs basilar vs ring skull fx

A

single fx going thru entire calvarium –> little to no clinical sxs unless going thru middle meningeal groove or venous sinus –> epidural hematoma or venous thrombosis vs part of skull = displaced below adjacent skull –> dmg brain parenchyma –> CNS infxn, sz, death vs linear fx at base of skull w/ dural tear –> retroauricular or mastoid ecchymosis/Battle sign; periorbital ecchymosis/raccoon eyes; CSF leaks like clear rhinorrhea/otorrhea; hemotympanum vs fall –> cervical spine move up to foramen magnum & occ bone –> basilar fx of skull –> fatal

38
Q

cerebral concussion vs contusion

A

direct blow to head –> quick rotational accel to brainstem –> temporary paralysis of brainstem reticular formation neurons –> GCS 13-15; transient loss of consciousness <30min; amnesia; HA, N/V confusion, dizzy vs mechanical force dmg blood vessels, neurons, glial cells of brain parenchyma –> bruise brain

39
Q

mild vs mod vs greater contusion locations

A
  • Mild force = outer layer cortex & gyri crests
  • Moderate force = large areas of cortex, confluent hemorrhagic lesion in subcortical white matter & subarach space
  • Greater force = tear cortex –> intraparenchymal hemorrhage; bruised necrotic tissue phag by macs; astrocytosis –> scar
40
Q

cerebral contusion clinical pres (know the lobe). CT?

A

o Unconscious for few min or longer, drowsy, vomit, sz, impaired bal
o Ant temp lobe –> delirium; orbitofrontal –> disinhibited behavior, impulsiveness; med temp lobe –> mem loss; convexity –> focal defects (aphasia, hemiparesis). patchy hyperdense hemorrhagic foci w/ hypodense edema (salt & pepper)

41
Q

diffuse axonal injury

A

unrestricted head movement from injury –> rotation accel or brain shaking –> shear effect –> stop fast axonal flow –> mito & vesicles build up –> dmg axons –> coma, veg state, contusion, lesion

42
Q

Axonal varicosities vs Axonal swellings

A
  • Axonal varicosities = axonal elongation w/ rupture; enlargements then shrunken areas
  • Axonal swellings = round/elliptical eos masses
  • Both found via immunostain w/ ab to beta-amyloid precursor protein
43
Q

Chronic traumatic encephalopathy. gross vs micro?

A

degen dz d/t rpt concussions & traumatic brain injury –> bal, Parkinson’s sxs, behavior/mood changes, mem loss. Reduced brain wt, enlarged ventricles, front & temp lobe atrophy v Neuronal loss & gliosis in hippo, sub nigra, cerebral cortex, accumulation of phosphorylated tau protein; neurofibrillary tangles in layers 2/3

44
Q

sxs of epidural hematoma. characteristics of acute vs subacute vs chronic subdural hematoma

A

initial unconsciousness, transient complete recovery –> neuro deterioration (N/V, contralat hemiparesis, brady, arterial HTN, apnea, death. 3d, fresh & jelly clot, loss of consciousness vs 3-21d, blood clot & fluid d/t fibrinolysis, altered mental state/hemiparesis vs >21d, fluid, altered mental state/hemiparesis

45
Q

Spinal cord injury caused by? lower thoracic vs cervical vs C1-C4

A

from vertebral fx/dislocation, tearing lig, disrupt/herniate intervertebral discs. paraplegia vs quadriplegia vs paralyzed diaphragm

46
Q

4 cause mechanisms for spinal cord injury

A

o Vert fx: impact + compression injury
o Neck hyperextension injury: impact + transient compression
o Distraction injury: 2 adjacent vertebrae pull apart –> spinal column stretches and tears
o Laceration & transection injuries from sharp bone frag, severe dislocation, missile injuries

47
Q

complete cord injury vs incomplete cord injury vs central cord syndrome vs ant cord syndrome vs transient paralysis & spinal shock

A

spared sensation & motor above not below v various motor fxn below injury, sensation preserved below injury v motor deficits UE > LE, blad & sensory loss below v : dmg to ant spina a by retropulsed disc or bone frag –> spare DCML v loss spinal cord fxn above injury –> flaccid paralysis, anesthesia, blad/bowel incont, loss reflexes

48
Q

hypoxic ischemic encephalopathy vs perinatal stroke vs encephalopathy prematurity

A

placenta/ut abrupt, prolonged labor w/ transverse arrest, cord prolapse –> dec O2, CO2, lactic acidosis –> nec of neocortex, hippo, thal, basal ganglia; infarcts b/w MCA & PCA –> sz, hypotonia, poor feeding, dec consciousness 7-14d vs lg cyst in R MCA –> meningitis + arteritis or phlebitis, trauma, congenital arterial malformation or heart dz, hypercoag, placental thrombosis –> sz vs in premies <32wks w/ birth wt <1500g; maternal chorioamnionitis, neonatal resp distress syndrome –> perinatal inflamm/infxn, hypoxia-ischemia –> necrosis in white matter w/ loss of cellular elements => periventricular leukomalacia –> sz, weak LE, inc tone in neck extensor muscles, apnea, brady

49
Q

germinal matrix hemorrhage. what is germinal matrix?

A

no cerebral autoreg –> fluctuation in cerebral blood flow –> vessels rupture –> hemorrhage b/w thal & caudate –> ruptures into ventricles –> subarach hemorrhage –> sz, resp depression, apnea, abnl posturing, bulging fontanelles. layer of primitive neuroectodermal cells under ependyma b/w thal & caudate –> migrate & melt away by wk36-37

50
Q

origin sites of CNS primary tumors. 4 major types of tumors?

A

brain, spinal cord, meninges. gliomas, neuronal tumors, meningiomas, embryonal tumors

51
Q

most common brain tumors in adults vs children

A

gliomas, meningiomas vs embryonal tumors/medullobastoma, high grade glioma, pilocytic astrocytoma

52
Q

where can gliomas arise from?

A

multipotent progen –> astrocytes, oligodendrocytes, ependymal cells

53
Q

describe astrocytes

A

multipolar, star like cells w/ eos cyto; has glial fibrillary acidic protein for cytoskel

54
Q

astrocytomas: diffuse astrocytic tumors

A

invades subcortical white matter & can progress into higher grades: diffuse astrocytoma II (inc cell density) anaplastic astrocytoma III (inc cells density + nuclear pleomorphism & atypia), glioblastoma IV (anaplastic + necrosis, glomeruloid microvasc prolif)

55
Q

clincal pres of diffuse astrocytic tumors?

A

dull constant HA, sz, muscle wk/vision/lang deficit, personality change; mass effect, edema if big enough

56
Q

genetic causes for diffuse astrocytic tumors

A

hetero point mutation in IDH1>2 –> can’t turn isocit to alpha ketoglutarate –> makes 2-HG –> inc expression of ca genes. ATTR mutation –> mutation in TP53 gene –> no reg in transcpxn. TERT promoter mutation –> cell prolif by oncogenes

57
Q

astrocytomas: circumscribed astrocytic tumors

A

don’t invade brain; pilocytic astrocytoma, pleomorphic xanthoastrocytoma, subependymal giant cell astrocytoma

58
Q

pilocytic astrocytoma

A

cerebell > optic n/chiasm > hypothal. biphasic appearance of compact pilocytic w/ microcystic areas; dense piloid astrocytes w/ long bipolar processes; thick long eos rosenthal fibers; eso granular bodies

59
Q

clinical pres of pilocytic astrocytoma. genetic causes?

A

depends on location: HA, N/V, ataxia > bad vision. BRAF mutation (fusion gene) –> activate Ras –> activate MEK then ERK –> MAPK; or val to glu point mutation –> activate MEK w/o Ras. both lead to prolif & tumorigenesis

60
Q

how to dx astrocytic tumors?

A

GFAP stain: stronger in circumscribed but dec w/ higher tumor grade –> anaplastic & glioblastomas = neg GFAP

61
Q

oligodendroglioma II vs anaplastic oligodendroglioma III

A

hyperchromatic nuclei/fine chromatin pattern w/ small nucleoli; perinuclear haloes; in sheets & lobular groups surrounded by vasc like “chicken wire”. GFAP neg vs more cellular & nuclear pleomorphism and atypia, more mitotic activity & vasc prolif

62
Q

clinical pres of oligodendrogliomas. genetic cause?

A

sz, HA. IDH1>2 mutation + whole arm chrm del of 1p & 19q

63
Q

ependymomas

A

glial tumors from ependymal cells in ventricles & central canal; also from fetal ependymal cell crest mig from periventricular areas

64
Q

classic ependymomas II

A

circumscribed. true ependymal rosettes = elongated tubules lined by ependymal cells around empty lumen like ependymal canals; perivascular pseudorosette = spoke wheel of ependymal cells w/ central processes around blood vessel

65
Q

classic ependymomas II: subependymoma vs myxopapillary ependymoma

A

slow growing pearly white nodules on wall of lat/4th ventricle –> can cause hydrocephalus vs slow growing cuboid cells surrounding basophilic mucus in con med, cauda equina, filum terminale

66
Q

anaplastic ependymoma

A

hypercellular, cellular & nuclear pleomorphism, freq mitosis, necrosis; perivascular rosettes

67
Q

clinical pres of ependymoma. genetic cause?

A

depends on location. in ventricle –> HA, N/V, ataxia, papilledema, vertigo; in spinal cord –> back pain, paraparesis. hypermethylation in CpG-rich promoters –> in post fossa; fusion of RELA & C11orf95 –> supratentorial; NF2 somatic mutation –> intramedullary spinal

68
Q

choroid plexus papilloma I vs choroid plexus carcinoma III

A

circumscribed pink cauliflowers from ventricle; cuboid cells w/ fibrovasc stalk in finger like projections vs lobulated cystic & necrotic areas w/ loss of papillary architecture; hypercellular, pleomorphic, inc mitosis, necrosis

69
Q

clinical pres of choroid plexus tumors

A

nonspecifc & depends on location. hydrocephalus & ICP

70
Q

gangliocytoma I. clinical pres? tx?

A

benign & slow growing, GFAP neg tumors in supratentorial, frontal, temp lobes. depends on locaton; sz, ICP, focal sxs. surgical removal

71
Q

gangliogliomas I. genetic cause? clinical pres?

A

mix of lg dysplastic multipolar neurons + lg/sm dysplastic glial cells in temp > front > occ > par; GFAP & chromogranin A pos. BRAF activating mutation. chronic intractable epi

72
Q

dysembryoplastic neuroepithelial tumor I

A

mixed neuronal-glial tumor in cortical grey matter in temp > front/par-occ; Alcian blue pos mucin

73
Q

embryonal tumors

A

high mal/undifferentiated tumors of neuroepithelial origin in peds; most common = medulloblastoma

74
Q

medulloblastoma IV. how to tx?

A

soft pink/gray tumors w/ hemorrhage & nec in vermis > cere hemi; hypercellular, basophilic hyperchromatic nuclei, little cyto, mitosis. radiosensitive –> multi modality therapy

75
Q

3 variants of medulloblastoma IV: classic vs desmoplastic nodular vs lg cell/anaplastic variant

A

small round blue cells w/ mito & apop, Homer Wright rosettes vs pale nodules, reticulin-rich undifferentiated cells w/ hyperchromatic & mild pleomorphic nuclei vs lg anaplastic cells w/ hyperchromatic nuclei, prominent nucleoli, brisk mito, apop, nec

76
Q

4 genetic causes of medulloblastoma IV

A

overactive sonic hedgehog pathway; upreg of Wnt pathway; amp MYC protooncogene; amp MYCN & CDK6 protooncogene

77
Q

what are lymphomas? primary vs secondary?

A

neoplasms from lymph nodes or lymphocytes. originate from CNS (brain, spinal cord, leptomeninges, eye) vs from systemic lymph nodes

78
Q

primary CNS lymphoma. risk factor? clinical pres? tx?

A

subcortical white matter in front lobe, periventricular white matter, cerebellum, basal ganglia; most from B cells w/ hemorrhage & nec. immunodefic. HA, focal neuro deficits, behavior changes. chemo then whole brain radiotherapy

79
Q

meningioma

A

benign from meningothelial cells of arachnoid attached to inner surface of dura –> intracranial but extraaxial neoplasms. in convexity & parasagittal regions of brain; tent cerebelli, sphenoid wings, olf groove, tuberculum sellae

80
Q

risk factors of meningioma: genetics vs radiotherapy

A

NF2 mutation –> abnl merlin in actin-cytoskel organization –> abnl tumor suppressor protein –> auto dom d/o leading to mult neoplasm; TRAF7 mutation –> E3 –> MAPK –> NFkB –> tumor at skull base; chrm losses vs from tx of other brain tumors

81
Q

key features of meningioma

A

yellow/tan globular rubbery tumor w/ whorls, concentric lamellated calcified psammoma bodies, intranuclear pseudoinclusions (target-like nuclei w/ central clearing & periph chromatin margination)

82
Q

4 variants of meningiomas: meningothelial vs fibroblastic vs transitional vs psammomatous meningiomas

A

epith cells w/ indistinct cell borders –> syncytial appearance surrounded by collagen or fibrous septa vs spindle shaped cells in parallel bundles w/ collagen & reticulin vs mixed meningothelial & fibroblastic features vs excess whorls w/ psammoma bodies in centers

83
Q

meningioma I vs II vs III

A

benign tumors w/ any 4 variants & no anaplastic vs atypical growths w/ inc cellularity & prominent nucleoli –> surgery and/or radiation vs malig de novo or from lower grade meningiomas –> invade brain, inc mito & nec

84
Q

clinical pres of meningioma (7)

A

depends on location: convex –> HA, sz, motor/sensory deficits; parasagittal –> mem & behavior change; middle –> wk legs, urin incont; posterior –> homonymous hemianopsia; parasellar & orbital –> vision; cerebellopontine angle –> hearing; spinal –> cord compression

85
Q

imging vs tx for meningioma

A

CT/MRI showing calcification + prominent vasc; dural tail sign to show it’s really extraaxial vs surgery resection, rad if can’t do resection; II/III do resection but incomplete –> adjuvant external beam rad + stereotactic radiosurg

86
Q

metastatic brain tumors

A

more common than primary CNS tumors. from pulm > br > skin melanoma > GI > renal via hematogenous route –> HA, sz, focal neuro sxs, ataxia

87
Q

most common sites for brain metastasis generally vs in cerebrum. meningeal carcinomatosis

A

cerebrum > cerebellum > brainstem; usually at GW jxn vs front > par > temp > occ. when metastasis infiltrate meninges –> subarach, ventricles –> CSF

88
Q

paraneoplastic neurologic syndromes

A

autoimmune affect any part of nervous system not caused by metastasis; from sm cell lung ca, lymphoma or mal myeloma

89
Q

paraneoplastic cerebellar degen w/ ab

A

loss Purkinje; from sm cell lung ca (anti Hu), ov/ endomett/br ca (anti Yo), Hodgkin lymphoma (anti Tr)–> gait ataxia, truncal & limb ataxia, dysarthria/phagia, nystagmus

90
Q

paraneoplastic limbic encephalitis w/ ab

A

involve limbic system –> behavior change, short term mem, complex-partial sz, cog dysfxn; from sm cell lung ca (anti Hu), testes ca (anti Ta), br ca, Hodgkin lymphoma, thymoma (CV2/CRMP5)

91
Q

Paraneoplastic opsoclonus-myoclonus with ab

A

chaotic syncrhonus eye movments, spont muscle jerks, ataxia; from sm cell lung ca, br/gyn ca, neuroblastoma in kids; sometimes w/ encephalitis in cerebell or brainstem; anti Ri for br/gyn ca against Nova proteins for reg synaptic proteins

Block 3 (23 decks)

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