Calculate the anion gap for a patient with Na+ 135, K+ 4.5, HCO3- 12, Cl- 99.
What is an anion gap of 24?
What hormone deficiency is pathophysiologic for DKA?
What is insulin?
What history is commonly involved as a precipitant for DKA?
What are infection and lack of insulin?
Order the steps of management for DKA: potassium replacement, IV fluids, insulin gtt.
What are IV fluids -> potassium replacement -> insulin gtt?
What electrolyte abnormality is most associated with ventricular arrhythmias in DKA?
Calculate the expected PCO₂ using Winter's formula for a patient with HCO₃⁻ of 12.
What is 24.0-28.0?
Why does ketosis occur in DKA?
What is energy production via fatty acid metabolism due to inability to use glucose?
What three laboratory findings are pathognomonic for DKA?
What are hyperglycemia, ketonemia, and metabolic acidosis?
What differentiates the two bags used in two bag protocol for DKA management?
What is dextrose in one of the two bags?
Which medication class is associated with increased risk of euglycemic DKA?
What are SGLT2 inhibitors?
ABG demonstrates pH 7.35, PCO₂ 35, HCO₃⁻ 18, Na 138, Cl 100. What acid-base disturbance is present?
What is HAGMA metabolic acidosis with appropriately compensated respiratory alkalosis?
A patient presents with laboratory evidence of ketosis. How do you differentiate starvation ketosis from diabetic ketoacidosis?
What is glucose elevation and level of acidosis?
Name the ideal testing method (blood or urine) and ketone for DKA. Explain why.
What is serum beta hydroxybutyrate (BOHB builds up in the blood first; acetoacetate lags behind BOHB)?
What parameters indicate resolution of DKA?
What is closure of anion gap, pH >7.3, HCO3- >15-18?
What is the underlying etiology of cerebral edema, a complication of DKA?
What are rapid osmotic shifts during correction?
Calculate the delta-delta ratio: AG = 24, HCO₃⁻ = 10. Interpret the disorder.
What is a delta-delta of 1.0? What is a pure HAGMA?
Describe serum potassium vs. total body potassium findings in DKA.
What is increased shifting of potassium extracellularly (into bloodstream) due to acidosis and insulin deficiency, and total body loss due to vomiting and hyperosmolarity-associated urination?
What elements determine the severity of DKA and ultimately disposition?
What are blood pH/bicarbonate and AMS?
When should IV insulin be transitioned to subcutaneous insulin?
What are after the AG closes, stable BGs after overlap of basal insulin for 2-4 hours, and when patient is tolerating PO?
Why might some patients in DKA have leukocytosis without any concomitant infection?
What are increased stress hormones and dehydration raising cell counts?
A patient has Na 128 and glucose 750 mg/dL. Calculate the corrected sodium.
What is a corrected sodium of 144?
Why is measured sodium falsely low in states of hyperglycemia?
What is dilutional hyponatremia secondary to osmolar shifts from hyperglycemia?
Other than severity of elevation of blood glucose, what is another diagnostic difference between DKA and HHS?
What is effective osmolality (elevated but <320 mOsm/kg; HHS presents with >320 mOsm/kg)?
Explain why bicarbonate supplementation is generally not recommended in DKA.
What are increased acidosis, hypokalemia, and delayed ketone clearance?
How does renal failure impact the presentation of DKA?
What are volume overload instead of dehydration, severe hyperkalemia, and delayed clearance of insulin?