Pathophysiology of Diabetes Flashcards

Which autoantibody is most specific for type 1 diabetes and is present in approximately 70-80% of newly diagnosed patients?

Answer: Glutamic acid decarboxylase antibody (GADA)

GADA (anti-GAD65) is the most commonly detected and most specific autoantibody in type 1 diabetes, present in 70-80% of new-onset patients.

In type 2 diabetes, which physiological defect is considered the PRIMARY initiating mechanism in the majority of patients?

Answer: Peripheral insulin resistance with compensatory hyperinsulinemia

Type 2 diabetes is initiated by peripheral insulin resistance (primarily in muscle, liver, and adipose tissue) with compensatory beta-cell hyperinsulinemia that eventually fails.

The incretin effect refers to which physiological phenomenon?

Answer: Enhanced insulin secretion in response to oral glucose compared to IV glucose due to gut hormones

The incretin effect is the amplification of postprandial insulin secretion triggered by gut hormones (GLP-1, GIP) released after oral glucose ingestion, beyond what IV glucose alone would stimulate.

Which statement about gestational diabetes mellitus (GDM) pathophysiology is correct?

Answer: GDM results from placental hormones increasing insulin resistance, unmasking inadequate beta-cell reserve

Placental hormones (hPL, progesterone, cortisol) progressively increase insulin resistance during pregnancy, and women with insufficient beta-cell reserve cannot compensate, resulting in GDM.

Diabetic ketoacidosis (DKA) occurs primarily because of which underlying pathophysiological mechanism?

Answer: Absolute or near-absolute insulin deficiency combined with counter-regulatory hormone excess driving unregulated lipolysis and ketogenesis

DKA is caused by absolute or severe insulin deficiency plus glucagon/cortisol/catecholamine excess, which drives unregulated lipolysis, fatty acid release, and hepatic ketogenesis.

Which mechanism explains how chronic hyperglycemia causes microvascular complications such as diabetic retinopathy?

Answer: Advanced glycation end-products (AGEs), polyol pathway activation, and oxidative stress damage endothelial cells

Chronic hyperglycemia activates multiple pathways -- AGE formation, polyol accumulation, PKC activation, oxidative stress -- that damage vascular endothelial cells and basement membranes, leading to microvascular complications.