Exhibits
Which other labs would be helpful for the treatment of diabetic ketoacidosis (DKA)? Select all that apply.
White blood cell differential
Hemoglobin A1C
Serum electrolytes
Urine culture
Anion gap
Urine ketones
Correct Answer : C,E,F
A. White blood cell differential. Although infection is a common precipitating factor for DKA, an elevated WBC count is common in DKA due to stress, dehydration, and inflammation rather than infection itself. While a WBC differential may be done if infection is suspected, it is not a primary test for DKA management.
B. Hemoglobin A1C. Hemoglobin A1C (HbA1c) reflects long-term glucose control (past 2-3 months) but does not provide immediate information about the current metabolic status or severity of DKA. While it may be useful in assessing overall diabetes management, it is not essential for acute DKA treatment.
C. Serum electrolytes. Patients with DKA experience significant electrolyte imbalances, particularly potassium depletion due to osmotic diuresis and insulin deficiency. Monitoring serum sodium, potassium, and bicarbonate is crucial for guiding fluid and electrolyte replacement therapy. Potassium levels may appear normal or high initially due to acidosis but typically drop with insulin administration.
D. Urine culture. A urine culture is only indicated if a urinary tract infection (UTI) is suspected as a trigger for DKA. However, routine urine culture is not required in every case of DKA unless there are symptoms of infection such as fever, dysuria, or pyuria.
E. Anion gap. DKA is a form of high anion gap metabolic acidosis, caused by the accumulation of ketones. The anion gap (AG) is calculated as (Na⁺ - [Cl⁻ + HCO₃⁻]), with a value >12 mEq/L indicating metabolic acidosis. Monitoring the anion gap helps assess the severity of acidosis and guide treatment progress, as a decreasing anion gap suggests resolution of ketosis.
F. Urine ketones. Urine ketone testing helps confirm the presence of ketoacidosis, particularly in the initial stages of DKA diagnosis. While serum beta-hydroxybutyrate is a more accurate indicator of ketone levels, urine ketones remain useful for initial screening and monitoring treatment response as they decrease with appropriate management.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
A. Creatine kinase-MB (CK-MB). CK-MB is a cardiac enzyme that rises 3-6 hours after myocardial injury and was previously used to diagnose myocardial infarction (MI). However, it is less specific than troponin and can be elevated in skeletal muscle damage, making troponin the preferred biomarker for cardiac injury.
B. Serum glutamic pyruvic transaminase (SGPT). SGPT (also known as alanine aminotransferase [ALT]) is a liver enzyme and is not a primary marker for cardiac injury. While cardiac arrest and hypoxia can lead to liver damage, monitoring cardiac-specific markers is the priority in this scenario.
C. Lactate dehydrogenase (LDH). LDH is a nonspecific marker of tissue damage that can be elevated in cardiac, hepatic, renal, or other organ injuries. It is not cardiac-specific and is no longer used as a primary diagnostic tool for MI.
D. Cardiac troponin. Troponin (T and I) is the most specific and sensitive biomarker for myocardial injury. The presence of ST elevation in multiple leads suggests acute myocardial infarction (MI) as the cause of cardiac arrest. Troponin levels begin to rise within 2-3 hours, peak at 12-24 hours, and remain elevated for 7-10 days, making them the most important laboratory value to monitor for ongoing cardiac damage.
Correct Answer is {"dropdown-group-1":"B","dropdown-group-2":"D"}
Explanation
- Compensated respiratory acidosis occurs when the lungs retain CO₂, causing acidosis, but the kidneys compensate by increasing bicarbonate (HCO₃⁻) levels. In this case, the pH is low, and the PaCO₂ is within normal limits, which does not indicate a respiratory issue or compensation. Compensation would require an elevated HCO₃⁻, which is not provided in the lab results.
- Compensated metabolic acidosis would require a low pH with a decreased PaCO₂, as the respiratory system compensates by increasing ventilation (hyperventilation) to "blow off" CO₂. Since the PaCO₂ in this case is within normal limits, no significant respiratory compensation has occurred yet, making this uncompensated metabolic acidosis instead.
- Uncompensated respiratory acidosis would present with a low pH and an elevated PaCO₂ (>45 mmHg) due to inadequate ventilation and CO₂ retention. Since the PaCO₂ here is 37 mmHg (within normal range), respiratory acidosis is unlikely. The metabolic component, rather than a respiratory problem, is driving the acidosis.
- Uncompensated metabolic acidosis is characterized by a low pH (7.23) and a normal PaCO₂ (37 mmHg), indicating a primary metabolic problem without sufficient respiratory compensation. In diabetic ketoacidosis (DKA), the lack of insulin results in fat breakdown and ketone production, leading to a drop in pH and metabolic acidosis. This client likely has DKA due to their history of type 1 diabetes and the lack of insulin administration.
- Kussmaul respirations are a compensatory response to metabolic acidosis, seen in conditions like DKA. However, they do not cause acidosis; instead, they are the body's attempt to correct it by exhaling CO₂. Since the ABG shows normal PaCO₂, there is no strong evidence of hyperventilation, suggesting compensation has not yet occurred.
- Starvation can lead to ketoacidosis due to prolonged fasting and fat metabolism, producing ketones. However, in type 1 diabetes, the primary issue is no insulin production, not caloric deprivation. The severity of metabolic acidosis in this client is more likely due to insulin deficiency rather than starvation.
- Tissue hypoxia leads to lactic acidosis, which results from anaerobic metabolism. This can be seen in conditions like sepsis or shock. However, in this case, the client has type 1 diabetes, and the more likely cause of acidosis is ketoacidosis due to insulin deficiency rather than hypoxia.
- A lack of insulin in type 1 diabetes prevents glucose uptake, forcing the body to break down fat, leading to ketone formation and metabolic acidosis. This matches the clinical scenario of a patient with a history of type 1 diabetes, hyperglycemia >500 mg/dL, and metabolic acidosis.
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