Toxic/Metabolic/Nutritional Disease Flashcards
What is the acute cerebral effect of excessive alcohol?
Cerebral edema
What are the chronic cerebral effects of excessive alcohol? (many of them)
Meningeal fibrosis, cortex white matter volume loss, neuronal loss and dendritic reduction
What are the chronic cerebellar vermis effects of excessive alcohol?
Folia crests most affected. Granule cell neuronal loss > Purkinje cell neuronal loss.
Which toxin plays the biggest role in hepatic encephalopathy?
Ammonia
In hepatic encephalopathy, grey matter astrocytes transform into which type of astrocytes and what is the effect of this?
“Alzheimer II” astrocytes - metabolically active astrocytes. This happens especially in the deep cerebral cortex and subcortical structures (globus pallidus especially). Astrocytes become overwhelmed and degenerate leading to encephalopathy.
What is Wilson’s disease and what age-group does it affect?
Hepatic failure - disorder of copper metabolism. Young children.
What is the inheritance pattern of Wilson’s disease? Which chromosome?
Autosomal recessive. Chromosome 13.
What physical exam finding is more predominant than neurologic signs in Wilson’s disease?
Jaundice
Wilson’s disease is fatal without treatment. What is the treatment?
Chelating agents?
Wilson’s disease causes copper accumulation in the liver. What condition will this then lead to?
Hepatic encephalopathy
What is Wernicke’s encephalopathy?
Thiamine (VitB1) deficiency
What does the typical triad of Wernicke’s encephalopathy consist of? (in terms of symptoms and physical exam findings)
Ataxia, nystagmus, and confusion
Alcoholics are very prone to deficiency of what vitamin?
Thiamine (Vitamin B1)
Why can sudden glucose intake precipitate the problem of thiamine deficiency?
Thiamine is used as a cofactor in glucose metabolism
What are the common anatomical brain sites affected by Wernicke’s encephalopathy (thiamine deficiency)?
Mammillary bodies > walls of 3rd ventricle > periaqueductal tissue > inferior colliculi > floor of 4th ventricle > thalamus
What are the acute neuropathological findings of Wernicke’s encephalopathy?
Macro/micropetechial hemorrhages with capillary dilation, demyelination, microglial and macrophage influx, and fibrous gliosis
What are the late neuropathological findings of Wernicke’s encephalopathy?
Neuronal loss, hemosiderin, mammillary body atrophy
What is the treatment for Wernicke’s encephalopathy?
Administration of thiamine!
Cobalamin (VitB12) is found in what foods?
Meat and dairy
In the stomach, VitB12 is bound to what?
Intrinsic factor
Cobalamin deficiency often causes what type of anemia?
Megaloblastic anemia
Does cobalamin deficiency affect the brain or spinal cord?
Cord. Co[balamin]rd.
Does spinal cord disease from cobalamin deficiency involve the motor or sensory tract?
Both!
What are the initial symptoms of cobalamin deficiency?
Slight ataxia, numbness, tingling in lower extremities which develops into spastic weakness or even complete paraplegia.
What is the initial path lesion in cobalamin deficiency?
Spongy vacuolization of cord white matter.
What are later path lesions in cobalamin deficiency?
Demyelination, macrophage influx, and axonal degeneration.
What is the cause of Central Pontine Myelinolysis (CPM)?
The rapid correction of hyponatremia (iatrogenic)
CPM causes focal demyelinating lesions in which anatomical region of the CNS?
Pons
