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Neuro 2 Midterm > Pathology > Flashcards

Pathology Flashcards

1
Q

THE hallmark of all the neurodegenerative diseases

A

Loss of neurons

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2
Q
  • Expanded ventricles (“hydrocephalus ex vacuo”)
  • Narrow gyri and wide sulci
  • Widespread neuronal loss, worst in the hippocampus**
  • Generalized cortical atrophy
A

Alzheimer’s

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3
Q

TAU (gene MAPT) is a component of ____________.

A

microtubules

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4
Q

Taupathies involving neurons and their processes only: (2)

A
  • Alzheimer’s dz / old age

- Chronic traumatic encephalopathy (boxer’s dementia)

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5
Q

Taupathies involving both neurons and oligodendroglia: (5)

A
  • Classic Pick’s dz (i.e., with real tau-based Pick bodies)
  • Progressive supranuclear palsy
  • Corticobasal degeneration
  • The Pick’s-plus-Parkinsonism (FTDP-17) from mutated tau
  • Argyrophilic grain dz
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6
Q

Alpha-synuclein (gene SNCA) pentamers are located in (pre/post)synaptic terminals.

A

PREsynaptic

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7
Q

Synucleinopathies involving neurons: (3)

A
  • Classic Parkinson’s dz
  • Cortical Lewy body dementia
  • Parkinson’s with mutated synuclein
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8
Q

Synucleinopathies involving both neurons and oligodendroglia: (1)

A

Multiple systems atrophy (*Papp-Lantos inclusions)

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9
Q

Amyloid precursor protein may be degraded abnormally to form _______ ____, which is central to 4 major diseases.

A

amyloid beta

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10
Q

Amyloid beta diseases of neurons and vessels: (2)

A
  • Alzheimer’s dz

- Chronic traumatic encephalopathy

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11
Q

Amyloid beta diseases of vessels only: (1)

A

-Some versions of congophilic angiopathy

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12
Q

Amyloid beta diseases of skeletal muscle: (1)

A

-Inclusion body myositis

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13
Q

Diseases of neurons involving TDP-43 (TAR DNA binding protein, TARDBP): (2)

A
  • TDP-related frontotemporal dementia

- Many cases of amyotrophic lateral sclerosis (ALS)

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14
Q

Many (but not all) pts with TDP-43 inclusion-related dz have mutations of: (3)

A
  • TDP-43
  • Progranulin (frontotemporal dementia only)
  • C9orf72
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15
Q

FUS (“Fused in Sarcoma”) diseases involving neurons: (2)

A
  • FUS-related frontotemporal dementia

- FUS-related cases of amyotrophic lateral sclerosis

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16
Q

Polyglutamine inclusions are seen in the nucleus in dz’s caused by genes with long polyglutamine-coding trinucleotide repeat regions: (3)

A
  • Huntington’s chorea
  • Several of the spinocerebellar ataxias
  • Kennedy’s spinobulbar muscular atrophy
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17
Q
  • MC dementia

- Incidence increases with age

A

Alzheimer’s dz

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18
Q

Certain mutations in ___ produce a more amyloidogenic product. The protein is on chr.21 and perhaps this is why Down’s adults usually get Alzheimer’s in their 40’s.

A

APP

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19
Q

Senile plaques are masses of A-beta amyloid in the neuropil, surrounded by neurites containing tau. Seen in:

A

Alzheimer’s

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20
Q

TQ: _______________ _______ stain with silver (binds to the phosphate). In tall neurons, they can look like flames. Seen in:

A

Neurofibrillary tangles

-Alzheimer’s

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21
Q

TQ: Neurofibrillary tangles and neuritic plaques. Silver stain. You think…

A

Alzheimer’s

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22
Q

Granulovacuolar degeneration. You think…

A

Alzheimer’s

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23
Q

Amyloid (congophilic) angiopathy. Almost all pts have amyloid in vessels and bleeding can occur. You think…

A

Alzheimer’s

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24
Q

Tomorrow’s tests for Alzheimer’s dz: (2)

A
  • Diffusion tensor imaging (DTI)

- Serum clusterin

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25
Q

In addition to the selective atrophy of frontal and anterior temporal lobes (sparing of superior temporal gyrus), microscopy often shows balloon neurons.

A

Classic Pick’s dz

Frontotemporal dementia

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26
Q
  • MC illness among a group in which cells are lost from the nigrostriatal system
  • resting tremor (“pill rolling”), rigidity, mask-like face, cogwheel rigidity
  • Alpha-synuclein-rich Lew bodies are found in the substantia nigra and locus ceruleus
A

Parkinson’s dz

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27
Q

Lewy bodies in substantia nigra with only a few neurons remaining. You think…

A

Parkinson’s dz

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28
Q

Clinically, parkinsonism and/or bizarre behavior. Pathologists look for NFT’s.

A

Parkinson’s Variant: Dementia Pugilistica / Chronic Traumatic Encephalopathy

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29
Q

A taupathy involving primarily the substantia nigra and other subcortical structures. Look for globose neurofibrillary tangles.

A

Progressive Supranuclear Palsy (PSP)

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30
Q

A taupathy with tau-containing inclusions in both brainstem and cortex

A

Corticobasal Degeneration

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31
Q
  • Alpha-synuclein inclusions in the glia (esp oligodendroglia) and more damage to the white matter
  • “Hot cross bun” sign on T2 results from selective loss of the pontine raphe nuclei
A

Multiple System Atrophy (MSA)

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32
Q
  • Cerebral cortex tends to be spared
  • Pts have trouble moving their eyes, especially looking down
  • Trucal rigidity and falls are more of a problem than tremor
A

Progressive Supranuclear Palsy (PSP)

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33
Q

“Globose” neurofibrillary tangles in the substantia nigra

A

PSP

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34
Q

Tau “smoke puffs” around an astrocyte - the pathognomonic “astroglial plaque”

A

Corticobasal Degeneration

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35
Q

Tau coils next to neuron nuclei

A

Corticobasal Degeneration

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36
Q
  • Same pathology as striatonigral degeneration with the addition of damage to some autonomic neurons in the cord
  • Cause of orthostatic hypotension
A

Shy-Drager (MSA type A)

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37
Q

Tiny basis pontis

A

MSA-C

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38
Q
  • Relatively common dz that mimics Alzheimer’s but with a faster course, visual hallucinations and paranoia
  • Lewy bodies are seldom numerous, and it’s through that the damage is done by small aggregates of alpha-synuclein
A

Lewy body dementia

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39
Q
  • Autosomal dominant, full-penetrant dz with genetic anticipation
  • Caused by a CAG trinucleotide-repeat mutation at HTT (huntingtin)
  • The polyglutamine protein accumulates in the nucleus and causes loss of neurons, esp in the caudate**
  • Pts present with emotional changes, a curious dance-like movement disorder, and eventually dementia
A

Huntington’s dz

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40
Q
  • The neurons of portions of the hippocampus die off and are replaced by glia
  • Not treatable
  • Younger patients tend to have a history of seizures
A

Hippocampal Sclerosis

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41
Q
  • Striatonigral degeneration

- Putamen takes the worst damage

A

MSA type P

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42
Q
  • Flattening / loss of head of caudate

- Polyglutamine in the nucleus

A

Huntington’s dz

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43
Q
  • Develops around age 10

- Mutation in Torsin A (DYT-1)

A

Dystonia Musculorum Deformans / Torsion Dystonia

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44
Q
  • Caused by mutated frataxin, which allows iron overload within mitochondria
  • Posterior columns and corticospinal tracts are gone
A

Friedreich’s Ataxia

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45
Q
  • Autosomal recessive dz caused by defective ATM (11q22-q23), involved in the repair of DNA breaks and more
  • Purkinje and granular cells are lost from the cerebellum during childhood, esp the vermis
  • Hypoplastic thymus with defective T-cell immunity
  • Prominent arteries (“telangiectasias”) esp on eye surfaces
A

Ataxia-Telangiectasia

“Louis-Bar dz”

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46
Q
  • Involves disappearance of both UMNs and LMNs
  • Fasciculations in the tongue
  • Best-known gene SOD1 - superoxide dismutase
  • Pyramidal motor cells gone
  • Hypoglossal nucleus gone
  • Anterior horns and corticospinal tracts lost
  • Bunina bodies present
  • Many but not all of these pts have mutated germline FUS and an early onset
A

Amyotrophic Lateral Sclerosis

“Motor Neuron dz”

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47
Q
  • X-linked recessive dz with genetic anticipation and polyglutamine causing a toxic product
  • Lesion is in the androgen receptor
  • Both UMN and LMN lost
  • Milder than ALS
A

Kennedy’s spinobulbar muscular atrophy

48
Q

TQ:

  • Autoimmune inflammation and demyelination of CNS
  • Pts can present with optic neuritis
  • Essential lesion = “yellow/jaune plaque”
  • Relapsing and remitting course
  • Most often affects women in their 20s and 30s, more common in whites
  • Periventricular plaques **
  • Link to HLA-B15 and DQ6 **
  • Myelin destroyed, axons spared
A

Multiple Sclerosis (MS)

49
Q
  • Immunity against myelin that tends to follow viral illness
  • Myelin loss is widespread and diffuse
  • “T-cell rampage”
A

Acute disseminated encephalomyelitis

50
Q
  • Immune attack on brain’s myelin and blood vessels
  • Neutrophils ARE involved
  • Outcome is usually death or severe disability
A

Acute necrotizing hemorrhagic leukoencephalitis

51
Q

-Caused by antibodies against glutamic acid decarboxylase

A

Stiff person syndrome

52
Q
  • “Duck foot Purkinje cells”
  • Zebra bodies
  • Deposits in the intima
A

Hurler’s

53
Q

TQ:

  • Lysosomal storage dz, MC due to arylsulfatase A deficiency
  • Accumulation of sulfatides leads to impaired production of myelin sheath
  • Acid cresyl violet stain - stains sulfatides (in histiocytes) brown
A

Metachromatic leukodystrophy

54
Q
  • Myelin gone from white matter
  • Lysosomal storage dz due to deficiency in galactosylceramide
  • Causes accumulation of abnormal lipids within myelin
  • Peripheral neuropathy, developmental delay, optic atrophy, “globoid histiocytes”
A

Krabbe’s leukodystrophy

55
Q

-Can’t break down GFAP

A

Alexander’s

56
Q

-Loss of EIF2B complex, which prevents cell death from minor stress

A

Vanishing white matter dz

57
Q
  • Aspartoacylase deficiency…
  • Causes accumulation of aspartic acid in white matter of the brain, esp right under the cortex…
  • Pulls water in by osmosis, unraveling the myelin and making a bubbly appearance
A

Canavan’s dz

58
Q
  • X-linked genetic disorder typically affecting males
  • Disrupts metabolism of very-long-chain fatty acids…
  • Leads to buildup in nervous system, adrenal gland, and testes
  • Lack gene ABCD1
A

Adrenoleukodystrophy

59
Q
  • Portions of brain are affected by accum of lactic acid, and there is a mild mitochondrial myopathy
  • Little strokes may result
A

MELAS

Mitochondrial Encephalopathy, Lactic Acidosis and Stroke-like episodes

60
Q

-Mitochondrially inherited, often with a tRNA synthetase

A

MERRF

Myoclonic Epilepsy and Ragged Red Fibers

61
Q
  • Result of mutations that prevent proper oxidative phosphorylation
  • Symmetric, widespread destruction of the brain results
A

Leigh’s subacute necrotizing encephalopathy

62
Q

Bleeds in mammillary bodies

A

Wernicke’s (acute)

63
Q

TQ: Shrunken, discolored mammillary bodies.

A

Wernicke’s (old)

64
Q

Hemorrhagic necrosis of the putamen

A

Methanol toxicity

65
Q

Necrosis of the globus

A

Carbon monoxide toxicity

66
Q
  • Miners and foundry workers
  • A movement disorder which combines Parkinson-like symptoms and dystonia
  • Unlike true Parkinson’s dz, the major damage is probably to the globus pallidus
A

Manganese toxicity

67
Q
  • Garlic breath
  • Symmetric CNS necrosis
  • Necrosis of GI epithelium
  • Stocking and glove neuropathy
A

Arsenic poisoning (acute)

68
Q
  • Garlic breath
  • Pigment (neck, armpits, nipples)
  • Muscle weakness
  • Increased keratin on palms
  • Mee’s lines (after 6 weeks)
  • Numbness, worst in legs
A

Arsenic poisoning (chronic)

69
Q

Copper in basal ganglia

A

Wilson’s

70
Q

Caused by pantothenate kinase deficiency

A

Brain iron accumulation type I

71
Q

Indirect bilirubin can cross the newborn’s brain and high levels can cause damage

A

Kernicterus

72
Q

Methotrexate increases the risk of:

A

Radiation necrosis

73
Q

Carboplatin and anti-Hu may cause a ______________ - dorsal root ganglion cells are killed.

A

neuronopathy

74
Q
  • Loss of proprioception and vibration

- “Fall in the dark”

A

Large fiber neuropathies

75
Q

-Loss of pain and temperature, perhaps paresthesias / pain

A

Small fiber neuropathies

76
Q

Mononeuritis multiplex. Think…

A

Vasculitis or vasculopathy

-Lupus, Sjogrens*, and hep C can all produce either a vasculitis or a polyneuropathy

77
Q
  • Autoimmune condition that destroys Schwann cells
  • Causes inflammation and demyelination of peripheral nerves and motor fibers
  • Illness is often preceded by an infection, famously CMV, campylobacter, H. flu
A

Guillain-Barre Acute Inflammatory Demyelinating Polyneuropathy

78
Q
  • Bacteria grow inside the Schwann cells
  • Loss of pain/temp
  • Tendency not to notice injuries is famous
  • Tuberculoid form more likely to see anesthetic, hypopigmented patches*
A

Leprosy (Hansen’s dz)

79
Q

-Produces an axonal neuropathy by molecular mimicry between the microbe and an axonal protein

A

Lyme dz

80
Q
  • MC and most complex of the peripheral neuropathies
  • Attributed to products of non-enzymatic glycosylation but not fully understood
  • Axons, myelin, and vessels are all involved
  • Symmetric sensorimotor neuropathy
  • Starts distally
A

Diabetic neuropathy

81
Q
  • Family of variously-inherited dz’s in which the longest nerve fibers die off first, either from failure of the myelin or the axons
  • Mutations in the essential proteins of myelin
A

Charcot Marie Tooth

82
Q

TQ:

  • In children, most often found in posterior fossa (e.g., cerebellum)
  • Risk factor = neurofibromatosis type I (NF1)
  • Usually feature mutated BRAF
  • Contain Rosenthal fibers
  • GFAP(+)
  • Benign, good prognosis
A

Pilocytic astrocytoma

grade I astrocytoma

83
Q

TQ:

  • Common, highly malignant primary brain tumor
  • Found in cerebral hemispheres
  • Pts usually present with headaches, personality changes and/or seizures
  • 1-year median survival
  • “Pseudopalisading” pleomorphic tumor cells around area of necrosis
A

Glioblastoma multiforme

grade IV astrocytoma

84
Q

____ is amplified or point-mutated in about 50% of primary glioblastomas.

A

EGFR

epidermal growth factor receptor

85
Q

The big new discovery is that most gliomas (90% of glioblastomas) bear a point mutation in __________ ____________.

A

isocitrate dehydrogenase

-Leads to production of 2-hydroxyglutarate, which alters epigenetic controls

86
Q

The MC change in both primary and secondary glioblastomas is loss of heterozygosity on:

A

10q (PTEN)

87
Q

TQ:

  • Most often affects younger adults
  • Grade II tumor
  • Pts with NF1, NF2 or Li Fraumeni are at extra risk
  • Tame-looking cells, lots of fibers
  • These tumors often bear TP53 mutations and/or loss of 17p
A

Diffuse astrocytoma

88
Q

What gene, if knocked out, makes the glioblastoma more vulnerable to the alkylating agent temozolomide?

A

MGMT

methylguanine methyl transferase

89
Q

TQ:

  • Grade III tumors of astrocytes
  • Distinguished by increased cellularity, nuclear atypia, and mitotic activity
  • Risk factors same as diffuse astrocytomas, many have 9p loss
  • Majority of these tumors transform into glioblastoma within two years
A

Anaplastic astrocytoma

90
Q

TQ:

  • Relatively rare, slow growing
  • Grade II tumors
  • Most often in frontal lobes, but usually in cerebral hemisphere (headache, seizure, personality change)
  • “Fried egg” cells**
  • Often calcified
  • Only known risk factor = old radiation
  • Loss of 1p and 19q
A

Oligodendroglioma

91
Q

TQ:

  • Grade II tumors
  • MC primary tumor of spinal cord, but most commonly found in 4th ventricle*
  • Most pts are children and young adults
  • Characteristic perivascular rosettes
  • Rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus
A

Ependymoma

92
Q
  • Grade I tumors
  • On the cortex
  • Seizures
  • BRAF V600E
  • Surgery is curative
A

Ganglioglioma

93
Q
  • Grade I tumors
  • Children with seizures
  • Surgery is curative
A

Dysembryoplastic neuroepithelial tumors

94
Q
  • Grade II tumors

- Walls of ventricles

A

Central neurocytoma

95
Q

TQ:

  • Highly malignant cerebellar (vermis) tumor
  • Grade IV tumor
  • MC aggressive childhood brain tumor (peak age 7 yo)
  • A form of primitive neuroectodermal tumor
  • Can compress 4th ventricle, causing hydrocephalus
  • Can send “drop metastases” to spinal cord, encases spinal cord*
  • Homer-Wright rosettes
  • Solid, small blue cells on histo
  • Molecular target is sonic hedgehog pathway
A

Medulloblastoma

96
Q

TQ:

  • Grade I tumor
  • Common, typically benign primary brain tumor
  • Most often occurs in convexities of hemispheres (near surfaces of brain) and parasagittal region
  • Arises from arachnoid cells
  • Headache, personality change, seizures
  • Spindle cells concentrically arranged in a whorling pattern
  • Psammoma bodies
A

Meningioma

97
Q

Increased mitotic figures** in a meningioma increases the grade from Grade I to Grade __, and is called ________ __________.

A
  • Grade II

- Atypical meningioma

98
Q

-Meningioma featuring obvious anaplasia and/or 20+ mitoses per 10 high power fields

A

Anaplastic meningioma

Grade III

99
Q

TQ:

  • Grade I tumors composed of curious blood vessels that arise sporadically in the cerebellum*
  • Associated with von Hippel Landau syndrome*
  • Can produce erythropoietin leading to secondary polycythemia*
  • Odd vessels, surrounded by big pale benign clear (lipid-filled) cells
A

Hemangioblastoma

100
Q
  • Most hated of all “benign” tumors
  • Arise from notochord remnants on clivus or sacrum
  • “Bubble cells”
A

Chordoma

101
Q

TQ:

  • Benign childhood tumor, may be confused with pituitary adenoma (both can cause bitemporal hemianopia
  • MC childhood supratentorial tumor
  • Derived from remnant of Rathke pouch*
  • Calcification is common* (tooth enamel-like)
A

Craniopharyngioma

102
Q

TQ:

  • Grade I benign subtype of craniopharyngioma, seen in adults*
  • Tumor arises in or just above the sella turcica*
  • Derived from remnant of Rathke pouch*
  • Pts present with visual and/or endocrine and/or emotional disturbances
  • Regions of tumor filled with “machine oil” rich in cholesterol
  • Benign squamous cells, no columnar cells or calcification
  • Mutated BRAF
A

Papillary craniopharyngioma

103
Q

TQ:

  • Most familiar subtype of craniopharyngioma
  • Age peaks among children age 5-15 and adults ages 45-60
  • Rare in US, common in Nigeria and Japan
  • Calcification is common
  • Feature columnar cells bordering more squamous regions, as in a developing tooth
  • Mutated beta-catenin (CTNNB1)
A

Adamantinomatous craniopharyngioma

104
Q
  • Benign (Grade I) brain tumors

- Produce huge amounts of CSF, causing hydrocephalus

A

Choroid plexus papillomas

105
Q
  • Affect 3rd ventricle and are benign but contain mucus
  • Obstruct the foramen of Munro
  • Positional headaches
A

Colloid cysts

106
Q
  • Tumor often seen in young people
  • Present as precocious puberty*
  • Tumors that mimic testicular germ cell cancers are common here for some reason (esp seminoma)
  • Grade 1 and Grade IV varieties
A

Pineocytoma (Grade I)

Pineoblastoma (Grade IV)

107
Q

MC cancer in the CNS

A

Metastatic cancer

108
Q

MC source of metastatic cancer

A

Lung, especially oat/small cell and adenocarcinoma

109
Q

Where do mets begin in the brain?

A

Gray-white junction

where spreading cancer cell gets stuck in a blood vessel

110
Q

TQ:

  • Usually found at cerebellopontine angle
  • Areas with nuclei arranged as zebra stripes (“Verocay bodies”)
  • Often localized to CN VIII
A

Schwannoma

“acoustic schwannoma”

111
Q

TQ:
Genes for tuberous sclerosis: (2)
-Angiomyolipoma of kidney
-Adenoma sebaceum on face

A
  • Hamartin (TSC1)

- Tuberin (TSC2)

112
Q 
TQ:
Gene for von Hippel-Lindau:
-Strange vessels on back of eye
-Hemangioblastoma in cerebellum
-Renal cell carcinoma
A

VHL (Chr. 3)

113
Q 
TQ:
Gene for neurofibromatosis type I:
-Cafe-au-lait spots
-Lisch nodules on iris
-Bilateral optic nerve gliomas
A

NF1, neurofibromin (Chr. 17)

114
Q 
TQ:
Gene for neurofibromatosis type II:
-Bilateral acoustic schwannomas ("neuromas")
-Juvenile cataracts
-Meningiomas and ependymomas
A

NF2, merlin (Chr. 2)

115
Q
  • anti-Yo, anti-PCA-1
  • Destroys Purkinje cells
  • Ataxia and then no movement at all
  • Mostly breast, ovary, uterus cancer
A

Cerebellar degeneration

116
Q
  • anti-Hu, anti-NMDA, others
  • Can destroy amygdala
  • Appalling behavioral changes
A

Limbic encephalitis

117
Q

The 5 MC cerebral paraneoplastic syndromes caused by immunity directed against tumors:

A
  • Cerebellar degeneration
  • Limbic encephalitis
  • Opsoclonus
  • subacute sensory neuropathy
  • Eaton-Lambert myasthenia

Neuro 2 Midterm (5 decks)

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