Diabetes Education Certification Education Pathophysiology and Treatment 2 — Questions and Answers
Question 1: In type 2 diabetes, which cellular mechanism primarily causes insulin resistance in skeletal muscle?
- Increased GLUT4 translocation
- Impaired insulin receptor substrate (IRS-1) phosphorylation (Correct answer)
- Excess glucagon secretion
- Reduced hepatic glucose output
Correct answer: Impaired insulin receptor substrate (IRS-1) phosphorylation
Defective IRS-1 phosphorylation downstream of the insulin receptor disrupts the PI3K/Akt signaling cascade needed for GLUT4 translocation and glucose uptake in skeletal muscle.
Question 2: A patient with type 1 diabetes presents with blood glucose of 42 mg/dL and is unconscious. Which treatment is most appropriate?
- 15 g oral glucose gel under the tongue
- 1 mg glucagon intramuscular injection (Correct answer)
- IV infusion of 0.9% normal saline
- Subcutaneous rapid-acting insulin
Correct answer: 1 mg glucagon intramuscular injection
An unconscious hypoglycemic patient cannot safely swallow; 1 mg IM glucagon stimulates hepatic glycogenolysis to raise blood glucose rapidly.
Question 3: Which incretin hormone primarily stimulates glucose-dependent insulin secretion and suppresses glucagon in type 2 diabetes management?
- Amylin
- Glucose-dependent insulinotropic polypeptide (GIP)
- Glucagon-like peptide-1 (GLP-1) (Correct answer)
- Peptide YY
Correct answer: Glucagon-like peptide-1 (GLP-1)
GLP-1, secreted by intestinal L-cells, enhances glucose-dependent insulin release, suppresses glucagon, and slows gastric emptying, making it a key target for GLP-1 receptor agonist therapies.
Question 4: The Somogyi effect (rebound hyperglycemia) is best described as:
- Morning hyperglycemia due to growth hormone and cortisol surge
- Hyperglycemia following nocturnal hypoglycemia triggered by counter-regulatory hormones (Correct answer)
- Post-meal hyperglycemia due to delayed gastric emptying
- Hyperglycemia caused by excessive carbohydrate intake at bedtime
Correct answer: Hyperglycemia following nocturnal hypoglycemia triggered by counter-regulatory hormones
The Somogyi effect occurs when nocturnal hypoglycemia triggers a counter-regulatory hormone surge (epinephrine, glucagon, cortisol) that causes rebound morning hyperglycemia.
Question 5: Which pathophysiologic process explains why patients with diabetic ketoacidosis (DKA) develop hyperkalemia despite total body potassium depletion?
- Renal failure preventing potassium excretion
- Acidosis causing intracellular potassium to shift extracellularly (Correct answer)
- Excessive dietary potassium intake
- Insulin driving potassium into cells
Correct answer: Acidosis causing intracellular potassium to shift extracellularly
In acidosis, hydrogen ions move into cells in exchange for potassium ions moving out, raising serum potassium even when total body stores are depleted.
Question 6: A diabetes educator explains that SGLT-2 inhibitors lower blood glucose primarily by:
- Stimulating pancreatic beta cells to release more insulin
- Blocking renal glucose reabsorption in the proximal tubule (Correct answer)
- Slowing intestinal glucose absorption
- Increasing peripheral insulin sensitivity
Correct answer: Blocking renal glucose reabsorption in the proximal tubule
SGLT-2 inhibitors block the sodium-glucose cotransporter-2 in the proximal renal tubule, causing urinary glucose excretion of approximately 60–80 g/day regardless of insulin levels.
Question 7: Lipotoxicity in type 2 diabetes refers to:
- Fat accumulation in peripheral joints causing pain
- The harmful effect of excess free fatty acids on beta cell function and insulin signaling (Correct answer)
- Hyperlipidemia causing atherosclerosis exclusively
- Lipoatrophy at insulin injection sites
Correct answer: The harmful effect of excess free fatty acids on beta cell function and insulin signaling
Elevated circulating free fatty acids promote beta cell apoptosis, impair insulin signaling via ceramide and diacylglycerol pathways, and contribute to progressive insulin resistance.
In type 2 diabetes, which cellular mechanism primarily causes insulin resistance in skeletal muscle?