pathology MNI Flashcards
what are the two types of cerebral edema
vasogenic bc of disruption of BBB which will make fluid go to the extracellular space. often bc of trauma or meningitis
cytotoxic bc of cell injury such as ischemia, causing inc in intracellular fluid
presenting sx of ex vacuo hydrocephalus vs NPH
ex vacuo presents like dementia or stroke causing loss of brain volume
NPH- whacky wet wobbly (reason unset but probably bc of high CSF volume at one point causing ventricles to large)
increased intracranial pressure characterised by headache
(positional), diplopia (CN-6 palsy), vomiting, and papilledema potentially leading to
vision loss.
epidemiology?
Pseudotumor Cerebri
( Idiopathic Intracranial Hypertension)
usually seen in obese women of child bearing age
lewy body
parkinsons
cytoplasmic inclusions
what are the presentation of the various types of herniations
subfalacine: crushes the anterior cerebral artery causing lock of sense or motor in the lower limbs.
transtetorial herniation: Ipsy down and out, spy blown pupil, hemiparalysis
tonsils: press of cardiac or breathing centers
Kernohan Phenomenon
continuous displacement from transtetorial herniation causes contralateral down and out blown pupil,
parenchymal braininjury
concussion
Chronic Traumatic Encephalopathy (multiple concussions)
croup and contecroup contusions
diffuse axonal injury(neurons stretch beyond elastic point separating grey and white matter)
protein accumulation is of hyperphosphorylated tau protein only
Chronic Traumatic Encephalopathy
linear flame shaped hemorrhages due to stretching of median and paramedian
pontine arteries. Pontine arteries branch from basilar artery running on anterior surface of pons. caused by?
duret hemmorage
caused by herniations/ inc in ICP
foamy macrophages
found in lipohyalinosis of the lenticulostraie arteries
vascular brain injury
epidermal hemmorage(hit the pterion, middle meningeal artery doesn’t cross culture, biconvex, LOC, then fine, then dead
subdural bc of rupture of the bridging veins. prominent in infants and elders
- Swollen brain with wide
gyri & narrowed sulci - Poor demarcation
between gray & white
matter - Eventually tissue
liquefies leaving a fluid
filled cavit
ischemic infracts
which intraparenchymal hemmorages are bc of HTN
location?
-charciod bouard(lenticulostriae)
-slit hemmorages
-primary intraparenchymal hemorrhage
location: basal ganglia
subarachnoid hemorage
berry aneurysm(non traumatic rupture)
tangled network of arteries and veins with no interposing capillaries
cuases
AV malformation
“tangled worms”
causes non htn hemmorage, in newborns causes high output congestive heart failure because of the shunting
fusiform vs saccular ansursym
fusiform is charcoal bouard
saccular is berry(no muscular or internal elastic leaving just hyalinized intimate and adventitia)
Affects larger non-penetrating vessels
supplying the cortex and is therefore typically superficial/ lobar in location, unlike small
penetrating vessels affected by hypertension which are typically subcortical/deep
non htn
amyloid antipathy
associated with
autosomal dominant polycystic kidney
disease, Ehler-Danlos syndrome and other
congenital diseases which can affect
connective tissue of blood vessels.
berry aneurysm
subarachnoid hemmorage complication and how to prevent if possible
-rebleed
-vasospasm give Nimodipine
-healing process causes fibrosis and can obstruct CSF resorption= hydrocephalus
Lumbar puncture: shows high number
of RBCs or xanthochromia (yellowish
CSF due to release of bilirubin after
RBC lysis
berry
alzheimers lobes affected and common cause of death
frontal, parietal, and temporal lobes affecting spacial awareness, character and memory
pneumonia or infection is common cause of death
alzheimer plaque mutations
ab extracellular plaques are APP gene
the tau just comes in after
tau protein cause what kind of plaques and how are they made
normally binds microtubules but after phosphorylation by AB plaque will be unable to bind causing *neurofibrilary tangles inside cells!! the tangles outside the cell are called neuritic plaques
early onset alz mutations
vs late onset
APP (downs 21)
the gamma secretase gene is coded on chromosome 1 and 14 in the presillin 1 and 2
late onset: Apo E4
Narrowing of gyri and widening of cerebral sulci
alzheimers dizease (opposite of ischemia occlusion)
what are the two types of FTLD
- Pick disease. Tau neurofibrillary tangles with pick bodies also intracellular (just tau intracellular)
- intracellular accumulation of TDP-43 a DNA/RNA binding protein
Death of Striatal
Cholinergic Interneurons & Death of Striatal GABAergic Neurons
huntington
Death of
pigmented dopaminergic neurons in Substantia Nigra
parkinsons
Alpha Synuclein aggregates normal and abnormal
parkinsons
normal:Alpha Synuclein is expressed at presynaptic neurons and binds to
presynaptic secretory vesicles containing dopamine and causes
exocytosis of dopamine into synaptic cleft.
abnormal:aggregates are toxic to
dopaminergic neurons in substantia nigra
and cause neurons to undergo programmed
cell death.
Lewy body dementia
when dementia sx arise within 1 year of motor symptoms
if more than one year called dementia secondary to parkinsons disease
autosomal dominant movement disorder associated with degeneration of the
striatum (Caudate and Putamen) causing
huntington
Huntington disease mutation
AD gain of function of HTT causes trinucleotide repeats of CAG (glutamine) which will impare mitochondrial and the synthesis of proteins like Ach and GABA
characteristic Ubiquitinated-Mutant protein intranuclear fragments
made of?
huntingtons disease
Ubiquitinated-Mutant protein and impaired proteolysis
when staining stain for ubiquity
hallmark of HD
the intraNUCLEAR inclusions of ubiquinated huntingtin
chorea and Athetosis
huntington
als mutations
Chromosome 9 hexanucleotide repeat and Superoxide
dismutase gene
what is spared with ALS
intelect, sphincter control, and eye movement, sensation
degeneration of
corticospinal tract in the lateral portion of the spinal
ALS
its not demyelination but actual nerve degeneration
autoimmune demyelinating disorder characterized by disease
activity separated in time, that produce white matter lesions that are
separated in space
MS
commonly statics with optic neuritis
plaques are often periventricular
MS genetic risk factor and non genetic
Genetic HLA DRB1
smoking and low Vitamin D
inc igG in CSF but not in blood
MS
names of post infection demyelinations
Acute Disseminated Enecephalomyelitits
Acute Necrotizing Hemmoragic Encephalomyelitis
non-immune damage to oligodendrocytes
Central Pontine Myelinolysis/Osmotic Demyelination
typically after sudden
correction of hyponatremia that may result in a rapidly evolving quadriplegia and bulbar
palsy bc of oligodendrocyte contraction and apoptosis
confusion
* Ocular palsies
* Ataxia
if left untreated
Wernicke encephalopathy
if left untreated can cause causes korsacoff syndrome where no new memories can be made and will have confabulations
typical brain tumors in kids vs adults
kids: medulloblastoma, pilocytic astrocytoma, ependemoma
adults: glioblastoma(astrocytoma), oligocondroma, meningioma