A Diabetic Who Does Not Check His Sugar

Correct answer: C. ASA III

• A. ASA I is a healthy patient with no systemic disease and no smoking or significant alcohol use.
• B. ASA IV is severe systemic disease that is a CONSTANT THREAT TO LIFE — recent myocardial infarction or stroke within three months, unstable angina, an ejection fraction under 40%, or end-stage renal disease on dialysis.
• C. CORRECT. ASA III is severe systemic disease that is not incapacitating — and that is exactly what UNCONTROLLED or unmonitored diabetes represents. He does not know his glucose, he is inconsistent with his medication, and he has symptoms of hyperglycaemia. Contrast this with a patient whose type 2 diabetes is well controlled on stable medication with a documented HbA1c: that patient is ASA II.
• D. ASA II is mild systemic disease that is WELL CONTROLLED — controlled hypertension, controlled diabetes, controlled asthma, pregnancy, obesity with BMI 30–40, or being a current smoker.

Note: The single word that shifts a chronic disease from ASA II to ASA III is CONTROLLED versus UNCONTROLLED. It applies identically to diabetes, hypertension, asthma and epilepsy.

Correct answer: B. The proportion of haemoglobin that has become glycated, reflecting average glucose over 2–3 months

• A. Urinary glucose (glycosuria) appears once the renal threshold of about 180 mg/dL is exceeded. It is a crude and outdated screen.
• B. CORRECT. HbA1c is GLYCATED HAEMOGLOBIN — glucose binds non-enzymatically and irreversibly to haemoglobin in proportion to how much glucose the red cell has been exposed to. Because red cells live about 120 days, the result reflects average glycaemia over roughly the preceding 8–12 weeks and cannot be manipulated by fasting on the morning of the test. Targets: under 5.7% normal, 5.7–6.4% prediabetes, 6.5% or above diabetic, and under 7% is the usual treatment goal.
• C. Beta-cell reserve is assessed with C-peptide, which is co-secreted with endogenous insulin and distinguishes endogenous from injected insulin.
• D. That is a capillary or venous glucose measurement — a single point in time, which is precisely the limitation HbA1c overcomes.

Note: HbA1c is unreliable where red cell lifespan is abnormal — haemolytic anaemia, recent transfusion, chronic kidney disease, pregnancy and some haemoglobinopathies all distort it.

Correct answer: B. Lipids (fatty acids)

• A. Carbon dioxide is a metabolic end product, not a substrate for synthesis.
• B. CORRECT. Without adequate insulin, cells cannot take up glucose, so the body switches to LIPOLYSIS. Free fatty acids are released from adipose tissue, travel to the liver and undergo beta-oxidation to acetyl-CoA. When acetyl-CoA production overwhelms the capacity of the citric acid cycle, the excess is diverted into KETOGENESIS, producing acetoacetate, beta-hydroxybutyrate and acetone. Acetone is volatile and exhaled — hence the characteristic fruity or acetone breath odour.
• C. Some amino acids are ketogenic (leucine, lysine), but they are a minor contributor. The dominant substrate is fatty acid.
• D. Glucose is what the cells cannot access. Its metabolism yields pyruvate and then acetyl-CoA, but ketogenesis in diabetes is driven by fat, not carbohydrate.

Note: This is why diabetic KETOACIDOSIS is a complication of HYPERglycaemia, not hypoglycaemia — and it is the trap this recall item was built around.

Correct answer: D. Insulin resistance

• A. This DOES occur. Confusion, slurred speech, aggression, drowsiness and eventually seizure and coma are the NEUROGLYCOPENIC symptoms, arising as the brain is starved of its obligate fuel.
• B. This DOES occur, as part of the same adrenergic surge.
• C. This DOES occur. Sweating, tremor, palpitations, hunger and anxiety are the ADRENERGIC warning symptoms, driven by the catecholamine counter-regulatory response.
• D. CORRECT — this is the exception. INSULIN RESISTANCE is the defining pathophysiology of type 2 diabetes: the tissues fail to respond to insulin that is present, often in excess. Type 1 diabetes is an autoimmune destruction of the beta cells producing an absolute insulin DEFICIENCY, and hypoglycaemia in type 1 results from too much exogenous insulin relative to food and activity.

Note: In the chair: if the patient is CONSCIOUS and can swallow, give 15 g of oral carbohydrate and recheck in 15 minutes. If UNCONSCIOUS, give nothing by mouth — intramuscular glucagon 1 mg or intravenous dextrose, and activate EMS. Never assume an unwell diabetic is hyperglycaemic; hypoglycaemia kills far faster.