Pathophysiology Flashcards

Which of the following best describes the pathophysiology of hyperosmolar hyperglycemic state (HHS)?

Answer: Relative insulin deficiency sufficient to prevent ketosis but insufficient to control glucose

In HHS, residual insulin secretion is enough to suppress hepatic ketogenesis but insufficient to prevent extreme hyperglycemia, resulting in severe hyperosmolality without significant ketoacidosis.

The Somogyi effect refers to morning hyperglycemia caused by:

Answer: Rebound hyperglycemia following nocturnal hypoglycemia

The Somogyi effect describes rebound hyperglycemia occurring after nocturnal hypoglycemia triggers counterregulatory hormone release (glucagon, epinephrine, cortisol) that overshoots glucose correction.

Peripheral insulin resistance in skeletal muscle primarily involves impairment of:

Answer: Insulin receptor tyrosine kinase activity and IRS-1 phosphorylation

Skeletal muscle insulin resistance centers on defective insulin receptor tyrosine kinase activation and downstream IRS-1 phosphorylation, impairing PI3K/Akt signaling and GLUT-4 translocation.

In type 2 diabetes pathogenesis, the role of adipose tissue dysfunction includes:

Answer: Ectopic fat deposition and pro-inflammatory adipokine release

Dysfunctional adipose tissue in type 2 diabetes releases excess free fatty acids, pro-inflammatory cytokines (TNF-α, IL-6), and reduced adiponectin, contributing to systemic insulin resistance and inflammation.

Counterregulatory hormone deficiency in long-standing type 1 diabetes most commonly manifests as:

Answer: Impaired glucagon response to hypoglycemia

After several years of type 1 diabetes, the glucagon counterregulatory response to hypoglycemia becomes severely blunted, contributing to hypoglycemia unawareness and increased severe hypoglycemia risk.

Neonatal diabetes mellitus differs from type 1 diabetes primarily in that it:

Answer: Results from monogenic mutations affecting beta-cell function rather than autoimmunity

Neonatal diabetes is a monogenic disorder caused by mutations in genes such as KCNJ11 or ABCC8 that impair beta-cell ATP-sensitive potassium channels, and is not autoimmune in origin.

The mechanism by which obesity promotes type 2 diabetes risk involves which adipose-related pathway?

Answer: Macrophage infiltration into adipose tissue generating chronic low-grade inflammation

Enlarged adipocytes recruit macrophages that release TNF-α and IL-6, creating chronic low-grade inflammation that impairs insulin signaling in muscle and liver, linking obesity to insulin resistance.