Toxic/Metabolic/Nutritional Disease Flashcards Preview

Neuro II > Toxic/Metabolic/Nutritional Disease > Flashcards

Flashcards in Toxic/Metabolic/Nutritional Disease Deck (28)
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1
Q

What is the acute cerebral effect of excessive alcohol?

A

Cerebral edema

2
Q

What are the chronic cerebral effects of excessive alcohol? (many of them)

A

Meningeal fibrosis, cortex white matter volume loss, neuronal loss and dendritic reduction

3
Q

What are the chronic cerebellar vermis effects of excessive alcohol?

A

Folia crests most affected. Granule cell neuronal loss > Purkinje cell neuronal loss.

4
Q

Which toxin plays the biggest role in hepatic encephalopathy?

A

Ammonia

5
Q

In hepatic encephalopathy, grey matter astrocytes transform into which type of astrocytes and what is the effect of this?

A

“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.

6
Q

What is Wilson’s disease and what age-group does it affect?

A

Hepatic failure - disorder of copper metabolism. Young children.

7
Q

What is the inheritance pattern of Wilson’s disease? Which chromosome?

A

Autosomal recessive. Chromosome 13.

8
Q

What physical exam finding is more predominant than neurologic signs in Wilson’s disease?

A

Jaundice

9
Q

Wilson’s disease is fatal without treatment. What is the treatment?

A

Chelating agents?

10
Q

Wilson’s disease causes copper accumulation in the liver. What condition will this then lead to?

A

Hepatic encephalopathy

11
Q

What is Wernicke’s encephalopathy?

A

Thiamine (VitB1) deficiency

12
Q

What does the typical triad of Wernicke’s encephalopathy consist of? (in terms of symptoms and physical exam findings)

A

Ataxia, nystagmus, and confusion

13
Q

Alcoholics are very prone to deficiency of what vitamin?

A

Thiamine (Vitamin B1)

14
Q

Why can sudden glucose intake precipitate the problem of thiamine deficiency?

A

Thiamine is used as a cofactor in glucose metabolism

15
Q

What are the common anatomical brain sites affected by Wernicke’s encephalopathy (thiamine deficiency)?

A

Mammillary bodies > walls of 3rd ventricle > periaqueductal tissue > inferior colliculi > floor of 4th ventricle > thalamus

16
Q

What are the acute neuropathological findings of Wernicke’s encephalopathy?

A

Macro/micropetechial hemorrhages with capillary dilation, demyelination, microglial and macrophage influx, and fibrous gliosis

17
Q

What are the late neuropathological findings of Wernicke’s encephalopathy?

A

Neuronal loss, hemosiderin, mammillary body atrophy

18
Q

What is the treatment for Wernicke’s encephalopathy?

A

Administration of thiamine!

19
Q

Cobalamin (VitB12) is found in what foods?

A

Meat and dairy

20
Q

In the stomach, VitB12 is bound to what?

A

Intrinsic factor

21
Q

Cobalamin deficiency often causes what type of anemia?

A

Megaloblastic anemia

22
Q

Does cobalamin deficiency affect the brain or spinal cord?

A

Cord. Co[balamin]rd.

23
Q

Does spinal cord disease from cobalamin deficiency involve the motor or sensory tract?

A

Both!

24
Q

What are the initial symptoms of cobalamin deficiency?

A

Slight ataxia, numbness, tingling in lower extremities which develops into spastic weakness or even complete paraplegia.

25
Q

What is the initial path lesion in cobalamin deficiency?

A

Spongy vacuolization of cord white matter.

26
Q

What are later path lesions in cobalamin deficiency?

A

Demyelination, macrophage influx, and axonal degeneration.

27
Q

What is the cause of Central Pontine Myelinolysis (CPM)?

A

The rapid correction of hyponatremia (iatrogenic)

28
Q

CPM causes focal demyelinating lesions in which anatomical region of the CNS?

A

Pons