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2 Cards in this Set
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Wernickes encephalopathy
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Wernicke-Korsakoff syndrome is the best known neurologic complication of thiamine (vitamin B1) deficiency.
chronic alcoholism Thiamine is a cofactor for several key enzymes important in energy metabolism deficiency initiates neuronal injury by inhibiting metabolism in brain regions Pathology — Acute WE lesions are characterized by vascular congestion, microglial proliferation, and petechial hemorrhages. In chronic cases, there is demyelination, gliosis, and loss of neuropil with relative preservation of neurons. Classic signs — The classic triad of Wernicke's encephalopathy (WE) includes: Encephalopathy Oculomotor dysfunction Gait ataxia Tx: thiamine IV administration |
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SIADH
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excessive release of antidiuretic hormone (ADH or vasopressin) from the posterior pituitary gland or another source. The result is hyponatremia and sometimes fluid overload. It is usually found in patients diagnosed with small-cell carcinoma of the lung, pneumonia, brain tumors, head trauma, strokes, meningitis, and encephalitis.
ADH acts in the distal portion of the renal tubule (Distal Convoluted Tubule) as well as on the collecting duct and causes the retention of water, but not solute. Hence, ADH activity effectively dilutes the blood (decreasing the concentrations of solutes such as sodium). Management of SIADH includes: Treating underlying causes when possible. Long-term fluid restriction of 1,200–1,800 mL/day[2] to increase serum sodium. Intravenous saline - For very symptomatic patients (severe confusion, convulsions, or coma) hypertonic saline (3-5%) 200-300 ml IV in 3-4 h should be given |
