Metabolic and Toxic diseases Flashcards
regions of the brain that are vulnerable to hypoxic and ischemic states
CA1 region of hippocampus
pyramidal neurons in the cerebral neocortex
purkinje cells in the cerebellum
basal ganglia
regions of the brain that are vulnerable to hypoglycemic injury
CA1 region of hippocampus
pyramidal neruons in the cerebral neocortex
basal ganglia
NOT purkinje cells
Thiamine deficiency. What does it cause?
aka B1 deficiency
causes Wernicke encephalopathy and beriberi
Wernicke encephalopathy: signs and symptoms. cause. prognosis
usually due to chronic alcoholism may be associated with GI disorders gaze palsies nystagmus ataxia apathy acute confusion usually reversible
Wernicke encephalopathy: brain changes
petechial hemorrhage of mammillary bodies
prominent capillaries with endothelial hyperplasia, surrounding edema, and reactive astrocytosis with relative neuronal preservation.
Korsakoff syndrome symptoms
psychoss with retrograde and anterograde amnesia amd confabulation caused by prolonged thiamine deficiency
korsakoff syndrome changes
atrophy with brown discoloration. histologically, they are gliotic, slightly songiotic with mild loss of neurons, and hemosiderin laden macrophages. usually involves medial dorsal thalamic nuclei
Wilson’s disease: pathophysiology, signs and symptoms
autosomal recelssive disorder characterized with toxic levels of copper in many tissues, esp. the liver, brain, and eye. leads to low serum ceruloplasmin. may cause behavioral changes, frank psychosis, or Parkinsonism
locations of attack for wilson’s disease
PUTAMEN and caudate nuclei. many also have kaiser- fleischer rings in the eyes if CNS is involved (kayser-fleisher rings: green brown deposits of copper in the corneal limbus)
pathologic characteristics of hepatic encephalopathy
alzheimer type II astrocytosis in gray matter, esp. of the globus pallidus, caudate, and dentate nucleus.
alzheimer type II astrocytes: enlarged vesicular nuclei with marginated chromatin and scanty cytoplasm (tiny nucleolus dot with clearing around it. relatively specific for hyperammonemia
Kernicterus: who, etiology, pathogenesis
often in newborn premies with maternal fetal incompatibilities that led to hemolysis. hemolysis releases more bilirubin than the premie liver can handle. lots of indirect/unconjugated bilirubin in blood: neuronal death. may also cause cardiac less common now due to decr. in hemolytic jaundice of the newborn.
pathology of kernicterus
yellow discoloration of many nuclei, esp. around the 4th ventricle
Reye syndrome
acute non-inflammatory encephalopathy associated with fatty degenration of the liver. viral illness plus aspirin in kids may precipitate episodes. see cerebral swelling and ischemic changes
carbon monoxide poisoning
right after exposure (first few hours), brain is swollen and cherry red. 24-48 hrs later petechial hemorrhages in white matter and pallidum. sometimes pallidal necrosis.
Lead poisoning
rare but possible
see capillary damage with hemorrhage and necrosis.
edema with uncal or tonsillar herniation is possible. due to direct effects of lead on endothelial cells.
chronic ethanol abuse pathologies
- atrophy of the anterior-superior cerebellar vermis–> truncal ataxia
- fetal necous system: micrencephaly, neuroglial heterotropia, hydrocephalus, and hypolasia of cerntrum semiovale and cerebellum.
cyanide and sulphide toxicities
lead to death from cardiac failure and brain damage. immediate death when medulla is hyperpolarized. central necrosis if survived.
amphetmine and cociane pathology in the brain
amphetamines: hemorrhage (necrotizing vasculitis)
cocaine: edemam hemorrhage from HTN, and vasculitis
methotrexate path
necrotizing leukoencephalopathy is a potiential side
isoniazid pathology
usually axonal degeneration in PNS
