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Pathoma > Ch 17 - CNS Pathology > Flashcards

Ch 17 - CNS Pathology Flashcards

1
Q

Neural crest cells become:

A

Peripheral Nervous System – includes DRG

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2
Q

NEURAL TUBE DEFECTS are associated with low levels of:

A

LOW FOLATE levels PRIOR TO CONCEPTION

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3
Q

DETECTION of NEURAL TUBE DEFECTS

A

ELEVATED ALPHA-FETOPROTEIN (AFP) in amniotic fluid and maternal blood

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4
Q

ANENCEPHALY

A

ABSENCE OF SKULL & BRAIN – disruption of the cranial end of neural tube

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5
Q

FETAL Appearance in ANENCEPHALY

A

FROG-LIKE appearance – eyes appear predominant with absence of skull and brain

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6
Q

MATERNAL Condition in ANENCEPHALY

A

MATERNAL POLYHYDRAMINOS – fetal swallowing of amniotic fluid is impaired (brain centers not developed)

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7
Q

SPINA BIFIDA

A

Failure of the posterior vertebral arch to close – disruption of the CAUDAL end of neural tube

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8
Q

Physical appearance of SPINA BIFIDA OCCULTA

A

DIMPLE or PATCH OF HAIR overlying the vertebral defect

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9
Q

MC cause of HYDROCEPHALUS in NEWBORNS

A

CEREBRAL AQUEDUCT STENOSIS – blocks draining from 3rd ventricle → 4th

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10
Q

Clinical Presentation of CEREBRAL AQUEDUCT STENOSIS in NEWBORNS

A

Enlarging head circumference – due to dilation of the ventricles

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11
Q

DANDY-WALKER MALFORMATION

A

FAILURE OF CEREBELLAR VERMIS to develop

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12
Q

CLINICAL FEATURES of DANDY-WALKER MALFORMATION

A

Massively DILATED 4TH VENTRICLE, ABSENT CEREBELLUM, often hydrocephalus

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13
Q

ARNOLD-CHIARI MALFORMATION

A

EXTENSION of CEREBELLAR TONSILS through the FORAMEN MAGNUM

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14
Q

CLINICAL FEATURE OF ARNOLD-CHIARI MALFORMATION

A

HYDROCEPHALUS – from obstruction of CSF flow

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15
Q

ARNOLD-CHIARI MALFORMATION is ASSOCIATED with:

A

MENINGOMYELOCELE and SYRINGOMYELIA

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16
Q

SYRINGOMYELIA – pathophys, assoc, location

A

CYSTIC DEGENERATION of spinal cord assoc with TRAUMA or ARNOLD-CHIARI MALFORMATION; usually occurs at C8-T1

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17
Q

CLINICAL FEATURES OF SYRINGOMYELIA

A

DEGENERATION OF ANTERIOR WHITE COMMISSURE → SENSORY LOSS OF PAIN/TEMP in UPPER EXTREMITIES (cape-like distribution)

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18
Q

SYRINX Expansion in SYRINGOMYELIA

A

May expand to involve LATERAL HORN OF HYPOTHALAMOSPINAL TRACT (HORNER SYNDROME) and LOWER MOTOR NEURONS in ANTERIOR HORN (muscle atrophy, weakness, decreased tone, and impaired reflexes)

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19
Q

CLINICAL FEATURES of HORNER SYNDROME

A

PTOSIS (droopy eyelid), MIOSIS (constricted pupil), and ANHIDROSIS (decreased sweating)

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20
Q

POLIOMYELITIS

A

Damage to anterior motor horn due to POLIOVIRUS infection → LMN signs

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21
Q

WERNDIG-HOFFMAN DISEASE

A

INHERITED DEGENERATION OF ANTERIOR MOTOR HORN; floppy baby – death within few years

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22
Q

AMYOTROPHIC LATERAL SCLEROSIS

A

DEGENERATION of ANTERIOR MOTOR HORN CELLS & LATERAL CORTICOSPINAL TRACT

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23
Q

ALS – UMN or LMN?

A

LMN SIGNS – from anterior motor horn degeneration and UMN SIGNS – from degeneration of corticospinal tracts

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24
Q

EARLY sign of ALS

A

ATROPHY & WEAKNESS OF HANDS

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25
Q

What distinguishes ALS from SYRINGOMYELIA?

A

NO SENSORY IMPAIRMENT IN ALS

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26
Q

CAUSE OF FAMILIAL ALS

A

ZINC-COPPER SUPEROXIDE DISMUTASE (SOD1) MUTATION → free radical injury in neurons

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27
Q

FRIEDREICH ATAXIA

A

Degenerative disorder of the cerebellum (→ataxia) and spinal cord

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28
Q

ETIOLOGY OF FRIEDREICH ATAXIA

A

EXPANSION of unstable TRINUCLEOTIDE REPEAT (GAA) in FRATAXIN GENE - FRiedrich FRataxin

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29
Q

FRATAXIN protein – function and loss

A

ESSENTIAL for MITOCHONDRIAL IRON REGULATION; Loss results in Fe buildup → free radical damage

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30
Q

FRIEDREICH ATAXIA is assoc with:

A

HYPERTROPHIC CARDIOMYOPATHY

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31
Q

MC Causes of MENINGITIS in NEONATES

A

GBS, E. coli, Listeria monocytogenes

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32
Q

MC Cause of MENINGITIS in CHILDREN & TEENAGERS

A

Neisseria meningitidis

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33
Q

How does N. meningitidis spread to MENINGES?

A

Enters nasopharynx → blood → meninges

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34
Q

MC Cause of MENINGITIS in ADULTS & ELDERLY

A

Strep pneumo

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35
Q

MC Cause of MENINGITIS in NONVACCINATED INFANTS

A

H influenza

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36
Q

MC VIRAL CAUSE of MENINGITIS – population affected and transmission

A

COXSACKIEVIRUS – children via fecal-oral transmission

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37
Q

MC Cause of MENINGITIS in IMMUNOCOMPROMISED Pts

A

FUNGI

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38
Q

CLINICAL FEATURES OF MENINGITIS

A

TRIAD OF HA, NUCHAL RIGIDITY & FEVER; also photophobia (esp virus – Coxsack), vomiting, altered mental status

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39
Q

How is MENINGITIS DIAGNOSED?

A

Lumbar Puncture

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40
Q

What LEVEL is the needle placed in a LUMBAR PUNCTURE?

A

between L4 and L5

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41
Q

What LAYERS are crossed during a LUMBAR PUNCTURE?

A

SKIN, LIGAMENTS, EPIDURAL SPACE, DURA & ARACHNOID – NOOOOT THE PIA

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42
Q

WHAT LAYER is NOT crossed during a LUMBAR PUNCTURE?

A

PIA

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43
Q

CSF FINDINGS in BACTERIAL MENINGITIS

A

NEUTROPHILS w/ DECREASED CSF GLUCOSE

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44
Q

CSF FINDINGS IN VIRAL MENINGITIS

A

LYMPHOCYTES w/ NORMAL CSF GLUCOSE

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45
Q

CSF FINDINGS IN FUNGAL MENINGITIS

A

LYMPHOCYTES w/ DECREASED CSF GLUCOSE

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46
Q

Complications of BACTERIAL MENINGITIS

A

Cerebral edema (pus, exudate) → herniation → death; Also fibrosis → hydrocephalus, hearing loss, and seizures

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47
Q

Repeated Episodes of HYPOGLYCEMIA (insulinoma) can produce what type of CEREBROVASCULAR DISEASE?

A

GLOBAL CEREBRAL ISCHEMIA – probably mild (give glucose and pt promptly recovers)

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48
Q

ETIOLOGIES of GLOBAL CEREBRAL ISCHEMIA

A

Low perfusion (atherosclerosis), Acute decrease in blood flow (cardiogenic shock), chronic hypoxia (anemia), or REPEATED EPISODES OF HYPOGLYCEMIA (insulinoma)

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49
Q

What type of NECROSIS occurs in PYRAMIDAL NEURONS of the CEREBRAL CORTEX following MODERATE GLOBAL ISCHEMIA?

A

LAMINAR NECROSIS – lines of necrosis in layers 3, 5, 6

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50
Q

What areas are affected by MODERATE GLOBAL ISCHEMIA?

A

WATERSHED AREAS – pyramidal neurons of the cerebral cortex (→ LAMINAR NECROSIS), pyramidal neurons of the hippocampus (affects long-term memory), Purkinje layer of the cerebellum (sensory perception with motor control)

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51
Q

THROMBOTIC STROKE – etiology, where, type of infarct

A

Due to RUPTURE OF ATHEROSCLEROTIC PLAQUE; develops at BRANCH POINTS (bifurcations); results in PALE infarct at periphery of cortex

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52
Q

EMBOLIC STROKE – etiology, where, type of infarct

A

Due to THROMBOEMBOLI; usually involves MIDDLE CEREBRAL ARTERY; results in HEMORRHAGIC INFARCT at periphery of cortex

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53
Q

MC Source of EMBOLI

A

Left Side of the heart (ex: Afib) –> EMBOLIC stroke

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54
Q

LACUNAR STROKE – etiology, where, findings

A

Occurs secondary to HYALINE ARTERIOSCLEROSIS (complication of HTN); MC involves LETINCULOSTRIATE VESSELS → SMALL CYSTIC AREAS OF INFARCTION

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55
Q

ISCHEMIC STROKE leads to what type of NECROSIS?

A

Liquefactive

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56
Q

MICROSCOPIC FINDINGS after ISCHEMIC STROKE

A

Early 12hrs RED NEURONS; 24hr COAG NECROSIS; days 1-3 Neutrophils; days 4-7 Microglial cells; weeks 2-3 granulation tissue; end result is GLIOTIC CYST (fluid-filled cystic space surrounded by gliosis)

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57
Q

EARLY MICRO FINDING after ISCHEMIC STROKE

A

RED NEURONS 12hrs after

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58
Q

ISCHEMIC STROKE – END RESULT MICRO FINDING

A

GLIOTIC CYST

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59
Q

INTRACEREBRAL HEMORRHAGE – etiology, MC site

A

Due to RUPTURE OF CHARCOT-BOUCHARD MICROANEURYSMS OF LENTICULOSTRIATE VESSELS; MC site is BASAL GANGLIA

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60
Q

Clinical Features of INTRACEREBRAL HEMORRHAGE

A

Severe HA, N/V, Eventual coma

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61
Q

SAH – ETIOLOGY, MC SITE

A

Most due to RUPTURE OF BERRY ANEURYSM; MC located in ANTERIOR CIRCLE OF WILLIS BRANCH POINTS OF ACOM ARTERY

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62
Q

BERRY ANEURYSMS

A

LACK A MEDIA LAYER increasing risk for rupture → SAH

63
Q

SAH is associated with what conditions

A

MARFAN SYNDROME & ADPKD (autosomal dominant polycystic kidney disease)

64
Q

CLINICAL Presentation of SAH

A

Sudden HA (worst HA of all time) w/ NUCHAL RIGIDITY

65
Q

LP Findings in SAH

A

XANTHOCHROMIA – yellow hue due to bilirubin breakdown

66
Q

EPIDURAL HEMATOMA – ETIOLOGY, CT FINDINGS

A

Blood between dura and skull due to FRACTURE OF TEMPORAL BONE WITH RUPTURE OF MIDDLE MENINGEAL ARTERY; LENS-SHAPED LESION on CT

67
Q

CLINICAL FEATURES OF EPIDURAL HEMATOMA

A

TALK & DIE SYNDROME – lucid interval may precede neuro signs; Herniation is lethal complication

68
Q

SUBDURAL HEMATOMA – ETIOLOGY, CT FINDINGS

A

Blood underneath dura and covering surface of the brain due to TEARING OF BRIDGING VEINS btwn dura and arachnoid usually with trauma; CRESCENT-SHAPED LESION ON CT

69
Q

CLINICAL FEATURES OF SUBDURAL HEMATOMA

A

Progressive neuro signs and herniation as lethal complication

70
Q

TONSILLAR HERNIATION and its Clinical Features

A

Displacement of cerebellar tonsils into the foramen magnum → compression of brain stem → CARDIOPULMONARY ARREST

71
Q

SUBFALCINE HERNIATION and its Clinical Features

A

Displacement of CINGULATE GYRUS under FALX CEREBRI → compression of anterior cerebral artery → infarction

72
Q

UNCAL HERNIATION and its Clinical Features

A

Displacement of TEMPORAL LOBE UNCUS under TENTORIUM CEREBELLI → compression of CN3, posterior cerebral artery (infarct), and rupture of paramedian artery (Duret Hemorrhage)

73
Q

METACHROMATIC LEUKODYSTROPHY

A

DEFICIENCY OF ARYLSULFATASE (autosomal recessive) → MYELIN CANNOT BE DEGRADED → MYELIN ACCUMULATES IN LYSOSOMES OF OLIGODENDROCYTES

74
Q

MC LEUKODYSTROPHY

A

METACHROMATIC LEUKODYSTROPHY

75
Q

KRABBE DISEASE

A

DEFICIENCY OF GALACTOCEREBROSIDE β-GALACTOSIDASE → GALACTOCEREBROSIDE accumulates in macrophages

76
Q

ADRENOLEUKODYSTROPHY

A

IMPAIRED ADDITION OF COENZYME A TO LONG-CHAIN FAs (X-linked) → accumulation of FAs damages adrenal glands and white matter

77
Q

MS

A

AUTOIMMUNE DESTRUCTION OF CNS MYELIN & OLIGODENDROCYTES

78
Q

MC POPULATION with MS

A

Young WOMEN (20-30yo)

79
Q

MS – HLA and Environmental Trigger

A

HLA-DR2 and regions AWAY FROM EQUATOR

80
Q

CLINICAL FEATURES OF MS

A

Blurred vision unilateral, Vertigo, SCANNING SPEECH, INTERNUCLEAR OPHTHALMOPLEGIA (affected MLF), hemiparesis or U/L loss of sensation

81
Q

Dx of MS

A

MRI – plaques (areas of white matter demyelination) and LP – Lymphocytes, INCREASED IMMUNOGLOBULINS with OLIGOCLONAL IgG BANDS, myelin basic protein

82
Q

Tx of Acute MS Attacks

A

High-dose steroids

83
Q

Long-term Tx of MS

A

IFN-β

84
Q

Subacute Sclerosing Panencephalitis (SSPE) – Etio and Population affected

A

Slowly progressing, persistent infection of the brain by MEASLES VIRUS – infection occurs in INFANCY and neuro signs arise years later

85
Q

Subacute Sclerosing Panencephalitis (SSPE) Micro findings

A

Viral inclusions within neurons (gray matter) and oligodendrocytes (white matter)

86
Q

Progressive Multifocal Leukoencephalopathy (PML) – Etio

A

JC VIRUS infection of oligodendrocytes; Immunosuppression (AIDS or leukemia) leads to reactivation of the latent JC virus

87
Q

CLINICAL FEATURES of PML

A

Rapidly PROGRESSIVE neuro signs – visual loss, weakness, dementia

88
Q

CENTRAL PONTINE MYELINOSIS – Etio

A

Focal demyelination of the pons due to RAPID IV CORRECTION OF HYPONATREMIA – in severely malnourished pts (alcoholics and pts with liver disease)

89
Q

CLINCAL FEATURES of CENTRAL PONTINE MYELINOSIS

A

Acute B/L paralysis - “LOCKED IN” syndrome

90
Q

DEGENERATION difference between DEMENTIA & MOVEMENT DISORDERS

A

DEMENTIA – degeneration of CORTEX; MOVEMENT DISORDERS – degeneration of BRAINSTEM and BASAL GANGLIA

91
Q

MC Cause of DEMENTIA

A

Alzheimer disease

92
Q

CLINCAL FEATURES of ALZHEIMER DISEASE

A

FOCAL NEURO DEFICITS NOT SEEN IN EARLY DISEASE, slow-onset memory loss, progressive disorientation, loss of learned motor skills and language, changes in behavior/personality, mute/bedridden

93
Q

MC Cause of death in Alzheimer pts

A

Infection

94
Q

Which ALLELE is associated with HIGHER or LOWER risk of ALZHEIMER DISEASE?

A

ε2 is associated with DECREASED RISK; ε4 is associated with INCREASED RISK

95
Q

EARLY-ONSET ALZHEIMER DISEASE is seen in:

A

Familial Cases – PRESENILIN 1 & 2 mutations; DOWN SYNDROME – by age 40

96
Q

ALZHEIMER DISEASE is assoc with which TRISOMY DISORDER

A

DOWN SYNDROME – amyloid precursor protein is also on chromosome 21 → increased Aβ amyloid

97
Q

MORPHOLOGIC FEATURES of ALZHEIMER DISEASE

A

DIFFUSE CEREBRAL ATROPHY, NEURITIC PLAQUES, NEUROFIBRILLARY TANGLES

98
Q

In ALZHEIMER DISEASE, what is a complication of DIFFUSE CEREBRAL ATROPHY?

A

HYDROCEPHALUS EX VACUO – the ventricles are able to expand

99
Q

How is Aβ AMYLOID DERIVED in ALZHEIMER DISEASE?

A

AMYLOID PRECURSOR PROTEIN (APP) normally undergoes alpha cleavage but in AD it undergoes BETA CLEAVAGE → Aβ AMYLOID

100
Q

AMYLOID COMPLICATION in ALZHEIMER DISEASE

A

CEREBRAL AMYLOID ANGIOPATHY – AMYLOID may deposit around vessels → increased risk of hemorrhage

101
Q

What is a NEUROFIBRILLARY TANGLE COMPRISED of in ALZHEIMER DISEASE?

A

Intracellular aggregates of fibers composed of HYPERPHOSPHORYLATED TAU PROTEIN → can no longer organize microtubule → tangles

102
Q

Dx of Alzheimers

A

Made clinically after excluding other causes; Confirmed by histology at autopsy

103
Q

VASCULAR DEMENTIA

A

2nd MC cause of dementia; multifocal infarction and injury due to HTN, atherosclerosis, or vasculitis – consequence of moderate global cerebral ischemia to layers 3,5,6 (gray) and hippocampus of temporal lobe (memory)

104
Q

PICK DISEASE – location

A

degenerative disease of FRONTAL & TEMPORAL CORTEX

105
Q

PICK DISEASE – morphology

A

ROUND AGGREGATES OF TAU PROTEIN (Pick bodies) in neurons in cortex

106
Q

CLINICAL FEATURES of PICK DISEASE

A

Behavioral (Frontal) and Language (Temporal) Sx arise early → progresses to dementia

107
Q

PARKINSON DISEASE – Pathophys

A

DEGENERATIVE LOSS of DOPAMINERGIC NEURONS in the SUBSTANTIA NIGRA PARS COMPACTA of basal ganglia

108
Q

What Drug can CAUSE PARKINSONS?

A

MPTP

109
Q

CLINICAL FEATURES OF PARKINSONS

A

TRAP – Tremor (pill rolling), Rigidity (cogwheel), Akinesia/bradykinesia (slowing of voluntary movement, expressionless face), Postural instability (shuffling gait)

110
Q

PARKINSON DISEASE – histo findings

A

LOSS OF PIGMENTED NEURONS IN SUBSTANTIA NIGRA and round eosinophilic inclusions of α-SYNUCLEIN (LEWY BODIES)

111
Q

What are LEWY BODIES COMPRISED of?

A

round eosinophilic inclusions of α-SYNUCLEIN

112
Q

DIFFERENCE between LEWY BODY DEMENTIA and PARKINSONS

A

LEWY BODY DEMENTIA – EARLY onset dementia; PARKINSONS – LATE onset dementia

113
Q

HUNTINGTON DISEASE – etio

A

Autosomal DOMINANT disorder characterized by EXPANDED TRINUCLEOTIDE REPEATS (CAG) IN HUNTINGTON GENE (Chromosome 4) → DEGENERATION of GABAergic neurons in CAUDATE NUCLEUS

114
Q

HUNTINGTON DISEASE – pathophys of chorea

A

Degeneration of GABAergic neurons in CAUDATE NUCLEUS → disinhibition → random firing → random muscle movements

115
Q

HUNTINGTON DISEASE – further nucleotide expansion

A

Further expansion of CAG repeats DURING SPERMATOGENESIS leads to ANTICIPATION – Grandfather Dx at age 60, father at age 55, son at 50, etc

116
Q

CLINICAL FEATURES OF HUNTINGTON DISEASE

A

Presents with CHOREA, can progress to dementia and depression, ATHETOSIS (slow writhing movements of fingers)

117
Q

NORMAL PRESSURE HYDROCEPHALUS – pathophys

A

INCREASED CSF → dilated ventricles → STRETCHING OF CORONA RADIATA NERVE FIBERS → classic triad

118
Q

CLINICAL FEATURES of NORMAL PRESSURE HYDROCEPHALUS

A

Wet, Wobbly, Wacky – URINARY INCONTINENCE, GAIT INSTABILITY, DEMENTIA

119
Q

LP in NORMAL PRESSURE HYDROCEPHALUS

A

IMPROVES Sx

120
Q

Tx in NORMAL PRESSURE HYDROCEPHALUS

A

Ventriculoperitoneal shunting

121
Q

SPONGIFORM ENCEPHALOPATHY – Pathophys

A

Degenerative disease due to prion protein; Disease arises with conversion to a β-pleated conformation (PrPsc) which is not degradable → converts normal (PrPc) to pathologic form

122
Q

SPONGIFORM ENCEPHALOPATHY – Morphologic features

A

Damage to neurons and glial cells is characterized by intracellular vacuoles (spongy degeneration)

123
Q

MC SPONGIFORM ENCEPHALOPATHY

A

CREUTZFELDT-JAKOB disease (CJD)

124
Q

CREUTZFELDT-JAKOB DISEASE (CJD) – Etio

A

usually sporadic – rarely can arise due to exposure to prion-infected human tissue (HGH or corneal transplant)

125
Q

CLINICAL FEATURES of CJD

A

RAPIDLY PROGRESSIVE DEMENTIA assoc with ATAXIA and STARTLE MYOCLONUS (little stim); death usually <1 yr

126
Q

EEG findings of CJD

A

SPIKE-WAVE COMPLEXES

127
Q

VARIANT CJD

A

Related to exposure to bovine spongiform encephalopathy (mad cow) – younger pts and consumption of meat

128
Q

FAMILIAL FATAL INSOMNIA

A

Inherited form of prion disease characterized by severe insomnia and exaggerated startle response

129
Q

METASTATIC CNS TUMORS

A

make up 50% of CNS tumors, present as multiple, well-circumscribed lesions at gray-white junction; LUNG, BREAST and KIDNEY are common sources

130
Q

Location of PRIMARY CNS TUMORS in KIDS vs ADULTS

A

KIDS – INFRAtentorial; ADULTS – SUPRAtentorial

131
Q

MC Primary MALIGNANT CNS TUMOR

A

GBM

132
Q

GLIOBLASTOMA MULTIFORME (GBM) – cell type, location

A

Malignant, high grade tumor of astrocytes; arises in CEREBRAL HEMISPHERE and CROSSES CORPUS COLLOSUM (butterfly lesion)

133
Q

GLIOBLASTOMA MULTIFORME (GBM) – morphologic features

A

PSEUDOPALISADING – regions of necrosis surrounded by tumor cells, ENDOTHELIAL CELL PROLIFERATION; tumor cells are GFAP POSITIVE (intermediate filament in glial cells)

134
Q

MENINGIOMA – population affected

A

WOMEN (EXPRESSES ESTROGEN RECEPTORS), rare in children

135
Q

CLINICAL PRESENTATION of MENINGIOMAS

A

May present as seizures – tumor compresses but does not invade the cortex

136
Q

MENINGIOMA – histo features

A

WHORLED PATTERN, PSAMMOMA BODIES (whorled pattern → calcify → psammoma)

137
Q

SCHWANNOMA – clinical presentation

A

most frequently involves CN VIII at cerebellopontine angle → hearing loss and tinnitus

138
Q

SCHWANNOMA – tumor marker

A

S-100 positive

139
Q

BILATERAL SCHWANNOMAs are assoc with:

A

NEUROFIBROMATOSIS TYPE 2

140
Q

CAs assoc with NF2

A

MISME – Multiple Inherited Schwannoma, Meningioma, Ependymoma

141
Q

OLIGODENDROGLIOMA – morphologic features and location

A

CALCIFIED tumor in white matter usually involving FRONTAL LOBE; FRIED EGG appearance of cells

142
Q

PILOCYTIC ASTROCYTOMA – location, morphology, marker

A

Usually arises in CEREBELLUM – CYSTIC LESION w/ MURAL NODULE, ROSENTHAL FIBERS; GFAP POSITIVE

143
Q

MC BENIGN CNS tumor in ADULTS

A

Meningioma

144
Q

MC CNS tumor in CHILDREN

A

Pilocytic astrocytoma

145
Q

What are ROSENTHAL FIBERS?

A

thick eosinophilic processes of astrocytes seen in PILOCYTIC ASTROCYTOMA

146
Q

MEDULLOBLASTOMA – population and derivation

A

Children; malignant tumor derived from GRANULAR CELLS of CEREBELLUM (NEUROECTODERM)

147
Q

MEDULLOBLASTOMA – histo

A

small, round blue cells; HOMER-WRIGHT ROSETTES – blue cells surrounding neuritic processes

148
Q

MEDULLOBLASTOMA – mets

A

Tumor grows rapidly and SPREADS VIA CSF; DROP METASTASIS – mets to cauda equina

149
Q

EPENDYMOMA – population, location

A

Children – MC arises in 4th ventricle

150
Q

EPENDYMOMA – clinical presentation and morphologic findings

A

Present with HYDROCEPHALUS (obstructed 4th ventricle); PERIVASCULAR PSEUDOROSETTES

151
Q

CRANIOPHARYNGIOMA arises from

A

EPITHELIAL REMNANTS of RATHKE’s POUCH; tends to recur after resection

152
Q

CRANIOPHARYNGIOMA – clinical presentation

A

Presents as SUPRATENTORIAL MASS in CHILD or YOUNG ADULT; may compress optic chiasm leading to BITEMPORAL HEMIANOPSIA

153
Q

BILATERAL HEMIANOPSIA is assoc with which tumors?

A

Pituitary tumors (adenomas) but in children think Craniopharyngioma

154
Q

CRANIOPHARYNGIOMA – morphologic findings

A

CALCIFICATIONS seen on imaging

Pathoma (3 decks)

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