Diabetic Ketoacidosis and HHS Flashcards

A patient with DKA has a serum potassium of 5.8 mEq/L on presentation. When should potassium supplementation be initiated?

Answer: When potassium falls below 5.5 mEq/L

Potassium supplementation should be added to IV fluids when serum K+ falls below 5.5 mEq/L to prevent hypokalemia from insulin-driven cellular uptake.

Which of the following best explains the mechanism of anion gap metabolic acidosis in DKA?

Answer: Accumulation of beta-hydroxybutyrate and acetoacetate

DKA causes anion gap acidosis due to accumulation of ketoacids (beta-hydroxybutyrate and acetoacetate) from unregulated fatty acid oxidation.

A 28-year-old with type 1 DM presents with DKA. Blood glucose is 420 mg/dL and beta-hydroxybutyrate is elevated. After 8 hours of treatment, glucose is 180 mg/dL but pH remains 7.15 and anion gap is still elevated. What is the most appropriate next step?

Answer: Add dextrose to IV fluids and continue insulin

When glucose falls below 200-250 mg/dL before anion gap closes, dextrose should be added to IV fluids to allow continuation of insulin until ketoacidosis resolves.

What is the most common precipitating factor for DKA in patients with established type 1 diabetes?

Answer: Insulin omission

Insulin omission (non-adherence) is the most common precipitating cause of DKA in patients with known type 1 diabetes.

A patient with HHS has a serum osmolality of 345 mOsm/kg and blood glucose of 1100 mg/dL. Which IV fluid is most appropriate for initial resuscitation?

Answer: 0.9% NaCl (isotonic saline)

Isotonic normal saline (0.9% NaCl) is used first in HHS to restore circulating volume before transitioning to hypotonic fluids for free water replacement.

Which laboratory finding would most strongly suggest HHS rather than DKA in a hyperglycemic patient?

Answer: Absence of significant ketonemia with pH > 7.3

The hallmark distinguishing feature of HHS from DKA is the absence of significant ketoacidosis (pH > 7.3, bicarbonate > 18 mEq/L, minimal ketonemia).

A patient recovering from DKA develops worsening headache, confusion, and pupillary changes 6 hours into treatment. What is the most likely diagnosis?

Answer: Cerebral edema

Cerebral edema is a life-threatening complication of DKA treatment, most common in children, caused by rapid fluid shifts and osmotic changes during correction.

A 55-year-old with type 2 DM on an SGLT2 inhibitor presents with fatigue, nausea, and blood glucose of 210 mg/dL. pH is 7.20, bicarbonate 12, and urine ketones are large. What is this presentation called?

Answer: Euglycemic DKA

Euglycemic DKA, associated with SGLT2 inhibitors, presents with ketoacidosis but relatively normal blood glucose due to glycosuria and altered glucagon/insulin ratio.

What is the target rate of serum glucose reduction during the initial phase of DKA treatment?

Answer: 50-75 mg/dL per hour

The recommended rate of glucose reduction in DKA is 50-75 mg/dL per hour to avoid rapid osmotic shifts that could precipitate cerebral edema.

Which of the following is the most appropriate insulin regimen for mild DKA (pH 7.25-7.30, patient alert and tolerating oral intake)?

Answer: Subcutaneous rapid-acting insulin only

Mild DKA in a patient able to eat can be managed with subcutaneous rapid-acting insulin alone rather than IV infusion, per ADA guidelines.

A patient with DKA has a corrected sodium of 148 mEq/L. How is corrected sodium calculated in hyperglycemia?

Answer: Add 1.6 mEq/L for every 100 mg/dL glucose above 100

Corrected sodium is calculated by adding 1.6 mEq/L (or 2.4 mEq/L per some guidelines) for every 100 mg/dL glucose above 100 to account for osmotic dilution.

A patient with DKA has a serum phosphate of 1.1 mg/dL. Which complication is most closely associated with severe hypophosphatemia in DKA?

Answer: Respiratory muscle weakness and hemolytic anemia

Severe hypophosphatemia in DKA can cause respiratory muscle weakness, hemolysis, and rhabdomyolysis, though routine phosphate replacement is not recommended.

When transitioning from IV insulin to subcutaneous insulin at the end of DKA treatment, what is the most important timing consideration?

Answer: Give subcutaneous long-acting insulin 2 hours before stopping IV insulin

Long-acting subcutaneous insulin should be administered at least 2 hours before stopping IV insulin to prevent recurrence of ketoacidosis due to insulin gap.

In DKA, which of the following best explains the Kussmaul breathing pattern seen on examination?

Answer: Respiratory compensation for metabolic acidosis

Kussmaul respirations (deep, labored breathing) represent the respiratory system's attempt to blow off CO2 and compensate for the severe metabolic acidosis of DKA.