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NMSP > Demyelinating, Degenerative, Genetic, And Toxic Disease Dr. Martin > Flashcards

Demyelinating, Degenerative, Genetic, And Toxic Disease Dr. Martin Flashcards

1
Q

Multiple Sclerosis (MS)

A

demyelination autoimmune
= neurologic deficit relapsing and remitting episodes, gradual partial recovery
1. unilateral visual impairment (optic neuritis)
2. ataxia, nystagmus, motor and sensory impairment
3. loss of bladder control

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2
Q

MS genetic and environmental factors

A
  1. 1st degree relatives (DR2 gene, IL2 + IL7 receptors gene)

2. higher farther away from equator (VitD association)

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3
Q

MS inflammation is caused by what

A
  1. CD4 Th1 + Th17 cells —-> myelin Ag
    (Th1 —-> INF-g = activate M)
    (Th17 —-> bring leukocytes)
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4
Q

X-ray MS looks like

A

sharp boarders, next to lateral ventricles, corpus callosum, optic nerves*, spinal cord

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5
Q

MS plaques look like

A

gray brown plaques usually around occipital horn and lateral ventricles

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6
Q

how to stain for

  1. active demyelinating plaque :
  2. Complete lack of myelin :
  3. axons are preserved :
A
  1. Active demyelinating plaque : Lipid laden Macrophages seen
  2. Complete lack of myelin : fast blue PAS stain
  3. Axons are preserved : Neurofilament immunostain
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7
Q

if axons are not preserved then what is the cause usually

A

Infarction

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8
Q

stain for Macrophages

A

CD68

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9
Q

active plaque ongoing myeling breakdown

what is going on

A
  1. foamy M, lipid rick
  2. PAS+ (myelin debri)
  3. axons preserved (oligodendrocytes die)
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10
Q

inactive plaque ongoing myelin breakdown

what is going on

A
  1. no inflammation
  2. decrease in axons
  3. astrocytes proliferate and gliosis
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11
Q

shadow plaque

A

boarder between normal and affected white matter (not will circumscribed) = abnormal thinned out myelin sheaths

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12
Q

CSF test for MS

A
  1. mild elevate Protein
  2. Some pleocytosis
  3. increase IgG** oligoclonal
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13
Q

Neuromyelitis Optica (NMO)

A

bilateral optic neuritis + Spinal cord demyelination
= not good recovery from first attack
= many develop MS

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14
Q

Neuromyelitis Optica (NMO) prevalence

A

F > M even more then MS

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15
Q

CSF Neuromyelitis Optica (NMO) looks like

A
  1. high Neutrophils
  2. high opening pressure
  3. turbid looking like bad meningitis
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16
Q

Neuromyelitis Optica (NMO) happens due to what

A

Ag against Aquaporin-4 on astrocyte footprocesses

= breaks BBB

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17
Q

Neuromyelitis Optica (NMO) TX

A

decrease by plasmapheresis

= actue —-> glucocorticosteroids or plasma exchange

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18
Q

Acute Disseminated Encephalomyelitis (ADEM)

A

happens in 1 distinct area in brain unlike MS

= demyelinating after viral or rarely viral immunization

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19
Q

Acute Disseminated Encephalomyelitis (ADEM) SXs AND PROGRESSION

A
  1. 1-2 WEEK SAFTER INFECTION
  2. headache, coma, fatigue
  3. 20% die, survivors recover completely
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20
Q

Acute Disseminated Encephalomyelitis (ADEM) looks like what on the brain and if staining

A
  1. gray discoloration around white matter
  2. preservation of axons
  3. monophasic lesions*
  4. lipid laden macrophages (myelin debri)
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21
Q

Acute Necrotizing Hemorrhagic Encephalomyelitis ANHE

A

CNS demyelination similar to ADEM
= young children and young adults
= after recent upper respiratory infection (from cytokine storm)
= usually fatal

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22
Q

Acute Necrotizing Hemorrhagic Encephalomyelitis ANHE TX

A

intravenous immunoglobulins (giving high dose steroids can increase the infection)

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23
Q

Central Pontine Myelinolysis other name and what happens

A 
Osmotic Demyelination Syndrome
= Myelin loss symmetrically on pontine tegmentum and basis (central pontine)
= axon preservation 
= no inflammation
= paralysis, dysphagia, LOC
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24
Q

Central Pontine Myelinolysis happens due to

A

overly rapid correction of hyponatremia

happens 2-6 days after

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25
Q

how fast should Na be increased

A

no more then 8 mEq/L in 24hrs

no more then 0.5 mEq/L per hour

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26
Q

HD protein aggregate

A

Polyglutamine repeats

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27
Q

Alzhiemers protein aggrugates

A

A B-amyloid, neurofibrillar tangels,

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28
Q

PD protein aggrugates

A

a- synuclein

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29
Q

AD SX and prevalence

A

impaired higher intelligence, mood and behavior changes, memory loss, —-> disabled immobile mute (after 5-10years)
= usually after 50yo,

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30
Q

AD CSF

A

increased phosphorylated TAU

+ decreased A-beta

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31
Q

AD effects what location and what happens

A 
global cortical atrophy
= TEMPORAL
= Frontal 
= parietal  
(most common)

when cortex shrinks —-> Hydrocephalus ex vacuo

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32
Q

degree of dementia in AD is shown by

A

number of Neurofibrillary tangles

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33
Q

Amyloid plaques vs neurofibrillary tangles

A

Amyloid plaques : aggregates of A-beta

Neurofibrillary tangles : aggregates of tau

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34
Q

what is the initial thing causing AD to happen

A

A-beta amyloid deposits

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35
Q

mutation causing frontotemporal lobar degeneration

A

MAPT gene = encoding Tau

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36
Q

gene that as strong association with earlier and more severe AD and what chr

A

CHR 19 ApoE - 4 gene

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37
Q

AD staining neuritic (SENILE) plaques

A

Congo Red for the amyloid core —-> staining the APP (amyloid precursor protein)

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38
Q

AD DIFFUSE PLAQUES

A

no amyloid core

= just early stage plaque development

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39
Q

Down syndrome and AD

A

they have APP gene on Chr 21 so they get AD 2nd and 3rd decade

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40
Q

AD stain neurofibrillary tangles

A

Bielschowsky stain (Silver stain)

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41
Q

2 things seen in AD histology

A
  1. Granulovacuolar degeneration = small vacuoles with granules —-> normal aging however many in AD (hippocompi + olfactory bulb)
  2. Hirano Bodies = glassy eosinophilic bodies (actin stain in hippocampus)
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42
Q

Cerebral Amyloid Angiopathy CAA is what and stain and similar to

A

with AD
- A-beta 40 on vessels walls
congo red

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43
Q

Frontotemporal Lobar degenerations FTLDS is what, looks like, and includes what inclusions causing what diseases

A
  1. frontotemporal dementia
  2. looks similar to AD
  3. FTLD-TAU (no A-beta) = Picks, progressive supranuclear palsy
  4. TDP-43 = ALS
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44
Q

Pick Disease is what and location and what happens

A
  1. early onset behavior and personality changes (F), language changes (T)
    = progressive Dementia
  2. Asymmetric atrophy of frontal and temporal lobe (NOT Post 2/3 of superior temporal gyrus**)
  3. knife edge thin gyri
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45
Q

Picks Disease cells seen

A
  1. Pick cells = swollen cells

2. Pick bodies = cytoplasmic filamentous inclusions stain with silver

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46
Q

Progressive Supranuclear Palsy (PSP)

  1. inclusion
  2. what are sx
  3. what happens
A
  1. FTLD - TAU (4R TAU tangles)
  2. truncal ridgitity, frequent falls, cant move eyes, ,abnormal speech, progressive mild dementia
  3. Globus pallidus, subthalamic nuclei, substantia nigra, dentate nucleus gliosis
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47
Q

Progressive Supranuclear Palsy (PSP) other names and prevalence

A
  1. Atypical Parkinsonian Syndrome
    + Parkinson Plus Syndrome
    = PD + Dementia
  2. men , fatal in 5-7 years
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48
Q

vascular Dementia is what and what happens and tx

A

vascular injury causing dementia
= subcortical infarcts like in CADASIL or in HTN
= gait probs, dementia, pseudobulbar sign
= if vasulitis then tx that and pt imporves

49
Q

Basal Ganglia + Brainstem

A

Abnormal posturing + chorea + rigidity

50
Q

Basal Ganglia part that does motor pathway and is effected in parkinsons

A

esp Nigrostriatal pathway

51
Q

Parkinsonism SX

A
  1. decrease facial expressions
  2. slow voluntary movements
  3. Festinating gait (shuffled)
  4. Ridgid
  5. Pill-rolling tremor
52
Q

Damage to Nigrostriatal Dopaminergic system 5 diseases

A
  1. parkingsons Disease
  2. Multiple System Atrophy
  3. Postencephalitic Parkinsonism
  4. {rogressive Supranuclear Palsy
  5. Corticobasilar Degeneration
  6. MPTP : a type of heroin causing this
53
Q

PD happens due to

A
  1. a-synuclein protein accumulation and aggregation + mitochondrial abnormalities + neuronal loss in substantia nigra
  2. Loss of dopamine
54
Q

what do you give PD pt

A

Carbidopa

55
Q

PD gene + chr involved in making lewy body and mit dysfunction from AR or AD

A
  1. SNCA encoding the a-synuclein on chr 4q21
  2. DJ-1, PINK1, PARKIN (AR)
  3. LRRK2 (AD)
56
Q

PD histology

A
  1. pale substantia nigria + locus ceruleus
  2. Lewy bodies : long elongated inclusions that have dense core (a-synuclein) surrounded by a pale halo
  3. some paler cholinergic cells
57
Q

Dementia with Lewy body is what

A

Dementia + PD

  1. hallucinations + frontal lobe problems
  2. Lewy bodies are all over cortex + SN + CL
  3. lewy neurites : have a-synuclein
  4. depigmented SN + CL only
58
Q

Dementia with Lewy bodyvs Alzhiemers

A

preservation of cortex, hippocampus, amygdala (only CL + SN affected)

59
Q

Atypical Parkinsonian Syndromes or Parkinson-plus syndromes 3 types and difference to PD

A
  1. Progressive Supranuclear palsy
  2. Corticobasal degeneration
  3. multisystem atrophy

= have more sx + no response to L-dopa

60
Q

Corticobasal Degeneration CBD

A

progressive taupathy

  1. jerking, cortical impaired (Apraxia), cognitive decline
  2. TAU in cerebral cortex
61
Q

Corticobasal Degeneration CBD histology and cells found

A
  1. Tau+ threads in gray + white matter**
  2. ballooned neurons = gliosis
  3. tufted astrocytes + coiled bodies , astrocytic plaques
62
Q

Multiple System Atrophy causes what 3 things

A
  1. Striatonigral circuit = (parkinsonism)
  2. Olivopontocerebellar circuit = ataxia
  3. Autonomic NS = autonomic dysfunction like orthostatic htn
63
Q

Multiple System Atrophy what happens

A

many brain regions involved

= a-synuclein in oligodendrocytes

64
Q

autonomic sx caused by what brain part

A

medulla, catecholaminergic nuclei

65
Q

HD

  1. inherited how
  2. sx
  3. due to what mutation **
A
  1. AD
  2. progressive movement + dementia problems : jerky, hyperkinetic chorea, slurred speech, behavior changes
  3. Polyglutamine trinucleotide CHR4p16.3 —-> huntington protein = CAG REPEATS **
66
Q

HD effects what part of the brain and neurons

A

Striatal neurons

67
Q

HD common cause of death (Ave 15years after dx)

A
  1. pneumonia
  2. suicide
  3. starvation (they need more food due to many movements)
68
Q

HD onset has to do with

A

CAG repeat extension during spermatogenesis (paternal transmission)

69
Q

neurons that die in HD and normal function of these

A
  1. Spiny neurons of striatal neurons
    = they dampen motor activity
  2. cortex neurons = behavior changes
  3. caudate nucleus + putamen = frontal and cortex
70
Q

brain slice in HD

A

stiatum atrophy + ventricular dilation

71
Q

Spinocerebellar degeneration are what and effects what location and 2 types

A
  1. spinocerebellar ataxia
  2. cerebellum , spinal cord, peripherial nerves
  3. Friedreich ataxia + ataxia telangiectasia
72
Q

Spinocerebellar ataxia mutations and gene involved

A
  1. CAG repeats like in HD

2. SCA genes

73
Q

Friedrich ataxia is inherited how and sx

A
  1. AR

2. progressive ataxia, weakness, sensory probs, cardiomyopathy

74
Q

Friedrich ataxia GENE + repeat

A
  1. GAA

2. CHR9q13 = Frataxin protein = changes mitochondria

75
Q

Friedrich ataxia sx start when and what PE sx do you find

A

1st decade in life

  1. low reflex EXCEPT IN PLANTAR REFLEX
  2. loss of pain, temp
  3. pes cavus + kyphoscoliosis
  4. joint position abnormal
76
Q

Friedrich ataxia COD and increase risk of getting

A
  1. Cardiac arrythmia + CHF + DM

2. COD : pulmonary infections + cardiac disease

77
Q

Ataxia telangiectasia

  1. inheritance
  2. sxs
A

AR

1. telangiectasias : CNS + conjunctiva, skin on face + neck + arms

78
Q

Ataxia telangiectasia mutation and start of sx and death age

A

childhood, death at 2nd decade of life

1. ATM gene CHR 11q22-q23 = cant remove double stranded breaks

79
Q

Ataxia telangiectasia cause of death

A
  1. lymphoid neoplasm, gliomas, carcinoma

2. immunodeficiency —-> recurrent sinopulmonary infections

80
Q

Amyotrophic Lateral Sclerosis what happens and which decade in life `

A
  1. Lower motor neurons loss in spinal cord + brainstem
  2. upper motor neuron loss in cortex

= 5th decade (AD)

81
Q

Amyotrophic Lateral Sclerosis mutation and chr and what happens

A
  1. SOD1 superoxide dismutase on CH21

2. C9orf72 = ALS + FTLD (TDP-43 + FUS)

82
Q

Amyotrophic Lateral Sclerosis what nerves are involved

A
  1. Anterior roots in spinal cord (thin)
  2. Precentral gyrus (Atrophic)
  3. skeletal muscle atrophy
  4. Upper motor neuron
83
Q

Amyotrophic Lateral Sclerosis stain and histology cells

A

PAS+
= Bunina Bodies
= can have TDP-43

84
Q

ALS early sx

A
  1. asymmertric weakness on hands , dropping objects , cramping,
  2. recurrent pneumonia
  3. progressive bulbular palsy

= sclerosis + atrophy of upper and lower neurons

85
Q

Bulbar ALS

A

Progressive bulbar palsy

= progress fast, deglutination+ phonation problems

86
Q

Kennedy Disease other disease other name and what happens

A
  1. X-linked polyglutamine repeat expansion
  2. LMN + brainstem degeneration
    = BOLBAR signs + androgen insensitivity
87
Q

neuronal storage diseases

  • inheritance
  • effects what
  • what happens + SX
A
  1. AR (children get this)
  2. catabolism of sphingolipids, mucolipids —-> enzyme substrates accumulate in lysosomes = cell death
  3. Loss of cognitive function, seizures
88
Q

Leukodystrophies

  • inheritance
  • what happens
  • SXs
  • imaging
A
  1. AR (children get this) X-linked
  2. Myelin problems (lysosome + enzymes)
  3. deterioration of motor skills, spasticity, ataxia, hypotonia
  4. diffuse symmetric in imaging (different then in demyelinating dz)
89
Q

mitochondrial encephalomyopathies include what areas + inheritance + type of disease

A
  1. grey matter + skeletal muscles
  2. mother
  3. heteroplasmy
90
Q

Tay-sachs (neuronal storage disease)

  1. gene involved + enzyme dysfunction
  2. sx and when they start
  3. hallmark finding during PE
  4. what never goes away
A
  1. HEXA gene = Hexosaminidase A
  2. start at 1yo, then mentally + physically degenerate (death at 2yo-3yo)
  3. Cherry red spot in maculae
91
Q

Krabbe Disease (Leukodystrophy)

  1. gene involved + enzyme thats deficient
  2. what accumulates as a result
  3. sx start and sx
A
  1. 14q31 + Galactocerebroside B-galactosidase
  2. galactocerebroside accumulates (not toxic) —-> galactosylphingosine** Toxic to oligodenroglia
  3. 3-6mo (die at 2yo)
    - stiff + weak motor, X feeding
92
Q

Krebbe Disease histology hallmark + TX

A

los of myelin and oligodendroglia in CNS + PNS
(Macrophages called globoid cells** HALLMARK around BVs)

TX : with cord blood pre sxs

93
Q

Metachromatic Leukodystrophy

  1. gene and enzyme and accumulation
  2. sx start when and sx
A
  1. CHR 22q many mutations , Arylsulfatase A deficiency —-> Cerebroside sulfate* accumulation in white matter which inhibits oligidendroglia proliferation
  2. late infant / juvenile : motor problems progress (death 5-10yr)

Adult form : psychiatric + cognitive then motor problems

94
Q

Metachromatic Leukodystrophy

  1. histology
  2. tx
A
  1. BM stem cell trasplant

2. gliosis from demyelination (Metachromasia in mitochondria)

95
Q

Adrenoleukodystrophy

A

X-linked
ABCD1 gene
(ATP -binding cassette transporter family) = VLCFAs accumulate (very long FA chains)
1. myelin loss CNS + PNS
2. adrenal insufficiency
3. behavioral changes (more rapid progression in early onset)

96
Q

Pelizaeus- Merzbacher Disease

A

X-linked (PLP protein and DM20 protein) = same locus as SPG2 spastic paraplegia

= fatal leukodystrophy after birth or early childhood

  1. pendular eye movement, hypotonia, choreoathetosis
  2. spasticity, dementia, ataxia later
97
Q

Pelizaeus- Merzbacher Disease histology sees

A

loss of myelination in patches = TRIGOID PATTERN (tiger looking) when stained

98
Q

Canavan Disease

  1. chr and gene and protein
  2. what happens
  3. Sx
A

CHR17 deacetylating enzyme ASPARTOACYLASE = accumulation of N-acetylaspartic acid

  1. spongy degeneration of white matter (like in CGB)
  2. megalocephaly, severe mental deficits, blindness
    (in infants and die within a few years)
99
Q

Alexander disease

gene+ accumulaiton of and what happens

A
  1. GFAP gene = Rosenthal Fiber accumulation around BVs (in subpial + Subependymal zones) PAS+
  2. white matter loss (fronto-occipital gradient)
100
Q

Vanishing White Matter Leukodystrophy

  1. mutation and protein and what happens
  2. dx
A
  1. EIF2B = white matter injury
  2. ataxia, seizures
    survive only few years
  3. dx by imaging
101
Q

MELAS

  1. mutation
  2. SX
A
  1. MTTL1 : the tRNA leucine
  2. encephalopathy, lactic acid, Stroke like episodes (not corresponding to vascular territories) , weakness, cognitive changes
102
Q

MERRF

  1. mutation
  2. SX
A
  1. tRNA mutation

2. Myoclonic (sudden brief) epilepsy, RAGGED RED FIBERS, ataxia,

103
Q

Leigh syndrome

  1. other name
  2. mutation
  3. SX
A
  1. Subacute Necrotizing Encephalopathy
  2. mito DNA and nuclear DNA
  3. lactic acid, X psychomotor development, feeding probs, seiures, extra-ocular palsies, Hypotonia (death in 1-2years)
104
Q

LEIGH SYNDROME histology

A

Spongiform and vascular proliferation

center and midbrain

105
Q

Spongiform histology is found in what 4

A
  1. CJB
  2. Canavan disease
  3. Subacute necrotizing encephalopathy (Leigh syndrome)
  4. Kearn-Sayre Syndrome (ophthalmoplegia plus)

= B-sheets

106
Q

Kearn-Sayre Syndrome (ophthalmoplegia plus)

  1. mutation
  2. sx
A

large mito DNA deletion

2. cerebellar ataxia, pigmentary retinopathy, cardiac conduction defect, Ophthalmoplegia , RAGGED RED FIBERS

107
Q

Kearn-Sayre Syndrome (ophthalmoplegia plus) histology

A
  1. spongiform in cerebellum gliosis
108
Q

Thiamine B1 def (usually from chronic alcoholism)

A
  1. wernicke encephalopathy : REVERSIBLE, psychosis, ophthalmoplegia, hemorrhage, necrosis, mamillary bodies + 3rd/4th ventricles
  2. Korsakoff : IRREVERSIBLE , memory probs, confabulation
  3. Beriberi : CF
109
Q

Wernicke syndrome casuses what in the brain BOARDS

A

foci Hemorrhage + necrosis of Mammillary bodies (and walls of 3rd + 4th ventricles)

110
Q

B12 def

A

anemia
= defect in myelin formation
= numbness, tingling, ataxia, spastic weakness, —-> paraplegia late course

111
Q

B12 hallmark histologic finding

A
  1. swelling of myelin in midthoracic spinal cord

BOTH ASCENDING POSTERIOR COLUMNS + DESCENDING PYRAMIDAL TRACTS = subacute combined degeneration of spinal cord

112
Q

Hypoglycemia

  1. what part of brain is effected
  2. what happens
A
  1. pyramidal neurons of Sommer’s sector (hippocampus) + Purkinje cells (Cerebellum)

Pseudolaminar necrosis (superficial layer on cortex)

113
Q

Hyperglycemia causes and what it causes

A

ketoacidosis or hyperosmolar coma

= dehydrated, confusion, stupor, coma
= GIVE FLUID GRADUALLY to prevent cerebral edema

114
Q 
Hepatic encephalopathy (impaired liver function)
what happens and what areas in brain it effects
A

high ammonia + inflammation —-> Alzheimer type 2 cells in cortex and BG, and other grey matter like globus pallidus

115
Q

CO poisoning and brain locations and what happens

A

hypoxia

  1. layers 3 and 4 of cerebral cortex, Sommer sector (Hippo), Purkinje cells (Cerebellum)
  2. Bilateral necrosis of GLOBUS PALLIDUM**

+ CHEERY RED COLOR ON SKIN AND ORGANS

116
Q

Methanol

A

degeneration of retina ganglion cells

= bilateral putamenal necrosis

117
Q

ethanol and brain

A

cerebellar dysfunction = truncal ataxia, nystagmus
= atrophy of granule cells (ANTERIOR VERMIS)
= advanced : purkinji cell loss, BERGMANN GLIOSIS (adjacent astrocytes proliferate)

118
Q

Radiation and brain

A

headache + PAPILLEDEMA
= can cause sarcomas, gliomas, meningiomas (effects everything)

= coagulative necrosis, BV HYALINE thickened walls, fibrinoid necrosis + sclerosis
= dystrophic mineralization of axons
= methotrexate and make worse

NMSP (5 decks)

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