Diabetes Pathophysiology Flashcards
7 cards from real BC ADM practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 7 Diabetes Pathophysiology flashcards as text
Which mechanism best explains the progressive beta-cell decline seen in type 2 diabetes over time?
Answer: Glucotoxicity and lipotoxicity causing oxidative stress and apoptosis
Chronic hyperglycemia (glucotoxicity) and elevated free fatty acids (lipotoxicity) generate reactive oxygen species that drive beta-cell apoptosis and functional decline.
In type 1 diabetes, which HLA haplotypes confer the highest genetic risk?
Answer: HLA-DR3/DR4 and DQ2/DQ8 alleles
HLA-DR3/DR4 and DQ2/DQ8 haplotypes account for the majority of genetic susceptibility to type 1 diabetes by influencing autoreactive T-cell responses.
What is the primary defect in maturity-onset diabetes of the young type 2 (MODY2)?
Answer: Loss-of-function mutations in the glucokinase gene
MODY2 results from heterozygous glucokinase mutations that raise the glucose threshold for insulin secretion, causing mild stable fasting hyperglycemia.
How does insulin resistance in skeletal muscle contribute to postprandial hyperglycemia?
Answer: Impaired GLUT4 translocation reduces glucose uptake in the largest glucose-disposal organ
Skeletal muscle accounts for ~80% of postprandial glucose disposal; defective insulin-stimulated GLUT4 translocation here is a major driver of postprandial hyperglycemia.
Which phenomenon describes the worsening of fasting hyperglycemia due to early-morning rises in cortisol and growth hormone?
Answer: Dawn phenomenon
The dawn phenomenon is caused by pre-dawn surges in cortisol and growth hormone that increase hepatic glucose output and reduce peripheral insulin sensitivity.
In the pathogenesis of diabetic ketoacidosis, which hormonal ratio is most critical?
Answer: Low insulin-to-glucagon ratio
An absolute or relative insulin deficiency combined with glucagon excess (low insulin-to-glucagon ratio) drives unchecked lipolysis, ketogenesis, and hepatic glucose output in DKA.
Which cellular process links chronic hyperglycemia to the development of diabetic nephropathy via the polyol pathway?
Answer: Excess glucose is converted to sorbitol by aldose reductase, depleting NADPH and glutathione
Aldose reductase converts excess glucose to sorbitol, consuming NADPH and depleting glutathione, which increases oxidative stress and contributes to nephropathy.