Education Pathophysiology and Treatment Flashcards
7 cards from real Diabetes practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 7 Education Pathophysiology and Treatment flashcards as text
In type 2 diabetes, which cellular mechanism primarily causes insulin resistance in skeletal muscle?
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.
A patient with type 1 diabetes presents with blood glucose of 42 mg/dL and is unconscious. Which treatment is most appropriate?
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.
Which incretin hormone primarily stimulates glucose-dependent insulin secretion and suppresses glucagon in type 2 diabetes management?
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.
The Somogyi effect (rebound hyperglycemia) is best described as:
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.
Which pathophysiologic process explains why patients with diabetic ketoacidosis (DKA) develop hyperkalemia despite total body potassium depletion?
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.
A diabetes educator explains that SGLT-2 inhibitors lower blood glucose primarily by:
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.
Lipotoxicity in type 2 diabetes refers to:
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.