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16 Cards in this Set
- Front
- Back
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What is the normal production rate of lactate?
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1 mmol/kg/hour
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What is the energy yield of anaerobic metabolism of glucose vs aerobic metabolism?
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47kcal vs 673kcal
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What is an abnormal resting blood lactate level?
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>2mmol/L
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What are the principle etiologies of lactic acidosis? (3)
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1. oxygen deprivation associated with shock
2. endotoxemia - inhibits pyruvate dehydrogenase 3. thiamine deficiency - cofactor for pyruvate dehydrogenase 4. alkalosis - increases activity of pH-dependent enzymes in the glycolytic pathway |
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Is anion gap a useful screening test for possible lactic acidosis?
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NO
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What is the principal fear in acidosis?
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Risk of impaired myocardial contractility. But this is mitigated by ability of acidosis to stimulate catecholamine release and produce vasodilatation. Also, acidosis may have a protective role in the setting of clinical shock.
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How do you calculate the bicarbonate deficit?
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HCO3 deficit (mEq) - 0.6 x wt(Kg) x (desired HCO3 - measured HCO3)
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Why is alkali therapy not particularly effective for acidosis?
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Bicarbonate is not an effective buffer in the usual pH range of extracellular fluid. Its PK (dissociation constant) is 6.1.
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What are some adverse effects of alkali therapy?
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1. generates CO2 and raises the PCO2 - creates an acid load that must be excreted by lungs and reduces the buffering capacity of sodium bicarbonate
2. can produce hyperlacatemia - increasing function of enzymes in glycolysis |
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What are the two ketones generated with reduced nutrient intake?
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acetoacetate and beta-hydroxybutyrate
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Which ketoacid is detected by the nitroprusside reaction and what is the threshold for detection?
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acetoacetate
3mEq/L |
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Why might the anion gap be normal in DKA?
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renal excretion of ketones are accompanied by an increase in chloride reabsorption
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What is the mgmt of DKA?
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1. insulin - 0.1U/kg IV push, then 0.1U/kg/hr. decrease dose rate 50% when serum HCO3 rises above 16mEq/L
2. Fluid replacement - NS at 1L/hr for first two hours, then 0.5NS at 250-500cc/hr, when BG falls to 250mg/dL, can dextrose and drop rate to 100-250cc/hr 3. Potassium replacement - serum potassium falls dramatically during insulin therapy. 4. Phosphate - after four hours of therapy, if less than 1mg/dL replace with 7.7mg/kg over 4 hours. |
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How should DKA be monitored during therapy?
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anion gap excess/bicarb deficit ratio - should start at 1.0 and resolve toward 0
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What are the mechanisms involved with alcoholic ketoacidosis?
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1. reduced nutrient intake enhances ketone production
2. hepatic oxidation of ethanol generates NADH and enhances beta-hydroxybutyrate formation 3. dehydration impairs ketone excretion in the urine |
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How is alcoholic ketoacidosis managed?
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Infusion of dextrose-containing saline solutions.
Glucose retards hepatic ketone production, and volume promotes renal clearance of ketones. Replace electrolytes as needed. |
