Path Flashcards
autoregulation at this level makes brain special
capillary level
marker of astrocytes
GFAP
lewy bodies are
synuclein accumulation
chromatolysis
in nissl preps, nissl granules disappear; sign of retrograde degeneration
herpes encephalitis has____ inclusions
cowdry type a
wallerian degeneration
degen of axon distal to injury; if axon is myelinated the myelin sheat will fragment as secondary effect
dying back
degeneration of the most distal segments of an axon due to inability of the cell body to maintain adequate axoplasmic flow or produce needed nutrients
gliosis
astrocytes responding to stimulus by first enlarging then retracting when injuries process subsides–>form a network called glial scar
microglia
specialized monocyte/acrophage which arise in bone marrow and populate the CNS before birth; not glial derived from mesoderm
vasogenic edema
when the BBB is compromised, as in with some neoplasms or infections, allowing excess fluid to escape from intravascular space the intercellualr spaces of the brain parenchyma
-vessels damaged, increased vascular perm, plasma filtrate
cytotoxic edema
when glia or neurons enlarge due to change sin their cell membranes and ion/h20 flux
inflammatory myopathies
polymyositis
dermatomyositis
inclusion body myositis
buzzword neuropathic myopathy
fiber-type grouping of atrophic fibers
neuropathic myopathies are
tDP43-opathies
upper neurons
Betz cells and axonal extensions into corticospunal tracts
lower neurons
anterior horn cells and cranial motor nerves
s/s neuropathic myopathy
degen of upper nad lower motor neurons
death due to neuropathic myopathy
results frm resp failure due to involvment of cervical cord
mitochondrial myopathies
ragged red fibers; lots of red, big cracks, not specific for mito dz
ratings of glasgow coma scale
13 or above- mild
9-12 moderate
8 or less severe
three proponents of glasgow scale
eye response
verbal response
motor response
concussion
totally reversible, transient cerebral malfunction which may be associated with a brief loss of consciousness or postural tone
contusion
physical damage to the surface of the brain; path finding
diffuse axonal injury
widespread damage to axons within the CNS that results frm severe acceleration or deceleration of the head
DAI comes from ___ not ____
rotation NOT blow to the head
most patients with DAI
go comatose immediately after injury and do not experience a lucid interval, remain unconscious, vegetative, or at least severely disabled until death
common distribution of DAI
white matter corupus callosum walls of third ventricle dorsolateral surface brainstem peraqueductal gray area
indicators of shaken baby syndrome
retinal hemorrhages
parental risk factors
subdural and subarachnoid hem
DAI
grade 1
benign, unlikely to recur, spread, or infiltrate brain extensively
grade II
slow grwoing but will probs come back
cant totally resect- follow/watch
grade 3
aggressive, requires therapy more than just surgery alone
grade IV
anaplastic, malignant, lethal
treat aggressively
subfalcine herniation
cingulate gyrus forced under falx–>impinge cerebral arteries–>infarcted cortex
transtentorial
mesencephalon/thal/hypothal pushed through tentorium
uncinate
unicated process on medial temporal lobe pushed over free edge tent–>pinch nerves, vessels–>infarct medial temporal
defect
surgery–>brain swells–>brain pushes itself out through calvarium
upward transtentorial
tumor from posterior fossa –>cerebellum and/or brainstem pushed upward
foramen magnum/tonsillar herniation
cerebellar tonsils pushed through foramen magnum–>collapse vessls–>medulla infarct
duret hemmorhage
brain pushed downt hrough transtentorium but blood vessels attache dto bone and held in place
pons and messencephalon slow ttrip south
hemmorhage into them
cerebellar gangliocytoma
cowden’s syndrome
cerebellar hemangioblastoma
von-hippel-lindau syndrome
schwannoma of CN VIII
NF2
glioblastome multiforme is a
astrocytic tumor
pilocytic astrocytoma WHO grade
1
ganglioglioma
neurons mixed with real glioma
anablastic cells
wild and crazy
primitive cells
so undifferentiated; barely any cytoplasm; stay alive but not differentiating in anyway
medulloepithelioma
rare birdl on the edge of reality
craniopharyngiom
from epithelial rests embryologically and border the sella turcica
germ cell tumors
same as tumors you find in ovaries and testes but are in the brain
non-menigothelial tumors of the meninges
benign mesenchymal
malignant mesenchymal
primary melanocytic lesions
hemopoietic neoplasms
hemangioblastoma
tumor of cerebellum; tiny blood vessels+ big foam cells in between
chordoma
cells derived from primative notochord; can occur in the sacrum –> vertebral bodies –> clivus of skull
chodroma
benign cartilagnious tumor
chondrosarcoma
malignant cartilagnious tumor
hypothalamic neuronal hamartoma
bits of tissue mixed together
nasal glial heterotopia
something totally normal that isnt in a place it should be
grade III astrocytoma
anaplastic astrocytoma
no tumor boundaries, naked nuclei, necrosis
grade IV- glioblastoma multiforme
death sentence
oligodendroglioma WHO grade
II
f
oligodendroglioma path
fried egg
translocation oligodendroglioma
1p:19q
ganglioma
WHO grade I
ganglioma cells
big, funny looking occasionally binucleate neuronal forms in the tumor
ependymoma
nuclear-free zone
glio-vascular rosettes
“pseudo-rosette”-glio vascular rosette
primitive neuroectodermal tumors
small blue cells
WHO grade IV
blastomas
small cells tightly packed together with very little cytoplasm
rosettes- w. or w/o central lumens
schwanoma histo
verocay bodies- lines of nuclei then fibers crossing nuclei-free zone
most common intracranial tumor
meningoma
histology of meningioma
cellular whorls
psmomma bodies
nuclear pseudinclusions
cortical location
alzheimers disease
picks disease/frontotemporal dementia
diffuse lewy body disease
corticobasal degen
caudate
huntingtons
midbrain
parkinson’s disease
multiple system atrophy (shy drager)
progressive supranuclear palsy
spinocerebellar
spinocerebellar ataxia
fredreich’s ataxia
motor system
ALS
spinomuscular atrophy
tau 17q211
not found in alz
problem with drugs that target y-secretase
if you block y-secretase, you may also interfere with notch protein–>problems with CNS differentiation–>lethal KO
if you immunize against the AB peptide
if people develop autoimmune encephalitis–>disaster
linked to chromosome 17
FTD and Parkinsons (FTDP-17)
taupathy
corticobasal degeneration
PSP
Path of CBD
heavy aggregation in cortical gray and white matter (threadlike processes)
pathology in cerebrum
PSP
basal ganglia, diencephalon, brain stemp
striatonigral degeneration
synucleopathy, but no lewy bodies
olivopontocerebellar atrophy
profound pathoogy as pons melts away; cerebellum atrophies, superior olivary nucleus shrinks
shy drager syndrome
familial autonomic failure–>postural hypotension
parkinsonian-dementia in guam
high content of aluminum in brains
TDP43
bind and escort DNA and RNA into ER
mutations–>death of motor neurons–>muscles die
ALS issue with
supernucleotide dismutase
fredreich’s ataxia
repeats GAA
auto recessive
clumsiness, nystagmus, hyporefelxia, pos babinksi
onset in children
cardiac fibrosis–>cardiomyopathy
cells that are most suceptible to ischemia
hippocampal cells in CA1
purkinje cells in cerebellum
how long until red neuron develops
6-8 hours
24-36 hrs
neutrophils at boundary
36-73 hrs
macrophages replace neutrophils
7-9 days
astrocytes begin to become reactive and progress towards full glial scar
watershed/boundary zone infarction
blood pressure drops to level where proximal part of territory is perfused, but distal is not
venous infarcts are
hemorrhagic
telangiectasias
tiny blood vessels that are dilated more than they should be
cavernous hemangiomas
hemangiomas made of veins; hemorrhages and seizures are possible
AVM
tangle of vessels in brain or on its surface that bypassnormal brain tissue and directly divert blood frm the arteries to the veins
congophillic angiopathy
amyloid precursor preotin
looks like subdural hematoma, but neurosurgeon knows it is not
microscopic CJD
sponge background
red reactive astrocytes
dont see a single neuron
startle myoclonic
CJD
JC virus causes
PML
herpes tends to infect
temporal lobe
herpes encephalitis has infiltration of
almost only macrophages & lymphocytes
lymphocytic perivascular cuffing
think virus, esp in patients with latered mental state
cowdry type A
herpes virus
HIV encephalitis
giant celsl
CNS lymphoma
primitive, enlarged b cells–>look like plasma cells
PML gross
parietal occipital lobe melting- white matter
toxo
small hemmorhagic, necrotic lesions
toxoplasma pseudocyst: organism has replicated and filled cell
found in normal people; but held in check by immune system
if brain abscess…
body walls it off with collagen
other MS like diseases
Charcot
Schlider’s-fastttt
Balo’s concentric-altering patterns of myelin and then no myelin
Acute hemorrhagic encephalomyelitis/Weston Hurst Disease
diffuse hemorrhages as signature
