Toxic/metab/nutirtional diseases Flashcards
(47 cards)
acute alcohol intoxication in large quantity cause death by
finding in brain
central cardiorespiratory paralysis
massive cerebral edema, flattening of gyri, obliteration of sulci
chronically effect of alcohol on cerebral hemispheres
hemispheres shrink via diffuse loss of white matter (atrophy) and meningeal fibrosis
some neurons lost from frontal cortex with cell body shrink, retract dendrites, incr lipofuscin
chronically effect of alcohol on cerebellum
degeneration of superior vermis
folial crests are more affected than deeper structures (and lose purkinje, granule) with incr astrocytes
clinical presentation of alcoholic cerebellar degeneration
1) truncal instab
2) leg ataxia
3) wide based gait
how does cirrhotic liver affect brain
liver can’t process toxins –> heepatic encephalopathy likely due to ammonia
change proportion of excit/inhib NT or make false NT
hepatic cirrhosis characterized by what symptoms
1) confusion, forgetfulness
2) asterixis
3) stupor, coma
define hepatic encpehalopahty and mechanism of ammonia intox
fulminant liver failure due to high ICP from high blood ammonia from GI hemorrhage and severe cirrhosis (above 200)
ammonia from protein catabolism and urease-containing bacteria
ammonia not convert to urea (portal HTN) –> ammonia enter BBB and taken up by astrocytes
astrocyte’s glutamine synthetase for detox overwhelmed
histology of astrocytes in hepatic encephalopathy
alzheimer type 2 cells
astrocytes with
1) swollen nuclei
2) little cytoplasm
in deep cortex, globus pallidus, dentate nucelus of cerebellum
wernicke’s encephalopathy and korsakoff psychosis due to
assoc with
histo changes
thiamine b1 deficiency
assoc with
1) chronic etoh
2) poor food intake
3) absorb problem (G tube and hyperemesis )
4) malutilization and incr excretion
edema, necrosis, demyelination, neuron loss, gliosis
wernicke’s encephalopathy and korsakoff psychosis precipitated by
sudden glucose intake without thiamine
B1 needed for transketolase fxn and cofactor for glucose metab
triad of wernicke’s encephalopathy
1) ataxia
2) nystagmus
3) confusion
reversible if treat with thiamine
korsakoff syndrome
1) memory loss
2) confabulation = create false memories to fill gaps
irreversible
what structure involved in wernicke’s and korsakoff
mamillary bodies but also
1) wall of 3rd ventricle
2) periaquductal
3) inferior colliculi and thalamus
4) floor of 4th ventricle
acute stage of wernicke’s and korsakoff histologically
macro and microscopic petechial hemorrhage
prominant and dilated capillaries
imaging of wernicke’s and korsakoff
disrupt BBB from cytotoxic edema causing astrocyte swelling –> gives off NO –> change glutamate –> more free radicals
subacute vs acute wernicke’s and korsakoff
subacute
1) myelin lost
2) microglia and macrophage influx
3) fibrous gliosis
chronic
1) loss neurons
2) hemosiderin
3) mamillary atrophy
treatment of wernicke’s and korsakoff
IV thiamine
describe central pontine myelinolysis
symm demyelination affects pons usu from rapid correction of hyponatremia
symptoms of central pontine myelinolysis
triangular regions of demyelination with spared axons and neurons
quadriparesis
pseudobulbar palsy
pseudocoma
sites of vulnerability in central pontine myelinolysis
ventral pons
extrapontine sites
treatment of central pontine myelinolysis
slow treatment of hyponatremia
colbalamin deficiency
occurs due to
importance of colbalimin
decr intake (strict vegan or GI cancer), pernicious anemia (most common) and immune mediated atrophic gastritis
cobalimin impt for methionine synthase for myelination
colbalamin deficiency can cause
megaloblastic anemia
colbalamin deficiency
early signs
later sign
paresthesias and ataxia (loss of DC/ML from swelling of myelin) and lower limb paresthesia
spastic paraparesia
ataxia
lower limb/trunk sensory defect
treatable dementia from patchy white matter dmg, psychoses
incontinence
orthostatic hypotension
