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20 Cards in this Set

  • Front
  • Back
primary and secondary pathological causes of metabolic encephalopathy
primary: decreased oxygen/glucosed
secondary: altered electrolytes, increased metabolic byproducts b/c liver/kidney disease
What 3 things are clinically seen/not seen in metabolic encephalopathy?
1. Impaired Renticular Activating system which alters consciousness
2. diffuse and bilateral cortical activity (decreased concentration, slow, delusions/hallucinations, babinkski, myclonic jerks)
3. pupillary light and oculo-vestibular reflexes are intact b/c brainstem is not harmed
What is the primary and secondary etiologies of metabolic encephalopathy?
Primary: hypoxia
Secondary: hypoglycemia, hypernatremia, hypo/hypercalcemia, hypomagnesium, kidney/liver dysfunction
What are the gross and microscopic changes seen in hypoic metabolic encephatlopathy?
Gross: cortical atrophy
Micro: neuronal necrosis in vulnerable aras (hypothalamus, purkinje cells, etc)
What are the microscopic changes seen in B1/Thymine deficiency?
- hemorrhages in thalamus, mamillary, walls of thalamus, perventricular gray, floor of the 4th ventricle
What is the triad seen in WErnicke's Encephalopathy due to B1 deficiency?
1. confusion (walls of 3rd)
2. gait instability (floor of the 4th)
3. ocular defects (CN 3,4,6)
B1/Thiamine deficiency most often seen in?
alcoholics
What is Korsacoff psychosis?
impaired recent memories and polyneuropathy seen after Wernicke's Encephalopathy (sometimes)
What is the pathological cause of B12/Cyanocobalamin deficiency?
- loss of intrinsic factor and inability to absorb B12
What are the 2 pathological symptoms seen with B12 deficiency
- MAcrocytic anemia
- neuro symptoms that involve posterior and lateral columns
What are the first signs and progressive neuro symptoms seen in B12 deficiency?
Primary: decrease vibratory/position sense in extremities, stiffness/babinksi, hyperreflexia
Later: encephalopathy and decrease in vision (lose myelin)
What is the pathological different of toxic disorders vs metabolic/nutrtion?
- bilateral findings that may be assymetric
Describe lead toxicity
- attacks immature endothelial cells
- metabolic encephalopathy
Describe mercury toxicity
- impaires neuronal ribosomes which causes the granular layer of the cerebellum to be lost
Describe MPTP toxicity
- toxic to dopaminergic cells
- parkinson disease
Describe what happens with toxic levels of phenytoin
-impaires cerebellar neurons
- nystagmus and cerebellar dysfunction
Describe what happens in Clostritidum tetani toxcity
- travels up peripheral nerves to anterior horn cells
- blocks inhibitory interneurons causing spasms
Describe what happens in Botulinum toxin
- prevents release of ACh from peripheral nerves
- Descending paralysis
Describe what happens in diptheria
- attacks Schwann cells
- neuropathy of pharynx and can progress to limbs
Describe what happens when consume Jimson Weed
- muscarinic parasympathetic Neumuscular junction block (like atropine)
- mydriatic that does not respond to pilocarpine