Practice Test Geeks(BC ADM) Advanced Diabetes Management Certification Practice Test
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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

  1. Which incretin hormone is deficient or has a blunted response in type 2 diabetes and normally stimulates insulin secretion in a glucose-dependent manner?

    Answer: Glucagon-like peptide-1 (GLP-1)

    GLP-1 secretion is reduced and its insulinotropic effect is blunted in type 2 diabetes, while GIP secretion is relatively preserved but its response is also diminished.

  2. In latent autoimmune diabetes in adults (LADA), which antibody is most commonly detected at diagnosis?

    Answer: Glutamic acid decarboxylase antibody (GADA)

    GADA (anti-GAD65) is the most sensitive and specific autoantibody for LADA, distinguishing it from type 2 diabetes in adults who initially appear non-insulin-dependent.

  3. What role does islet amyloid polypeptide (IAPP/amylin) play in the pathophysiology of type 2 diabetes?

    Answer: Aggregated IAPP fibrils are cytotoxic to beta cells and contribute to islet destruction

    IAPP co-secreted with insulin forms toxic oligomeric and fibrillar aggregates within islets that impair beta-cell function and promote apoptosis in type 2 diabetes.

  4. Which mechanism explains why patients with type 2 diabetes have elevated fasting hepatic glucose output despite elevated insulin levels?

    Answer: Selective hepatic insulin resistance impairs suppression of gluconeogenesis while lipogenesis remains intact

    In T2D, selective hepatic insulin resistance dissociates pathways: gluconeogenesis suppression fails (raising fasting glucose) while lipogenic pathways remain insulin-sensitive, worsening dyslipidemia.

  5. Which adipokine is decreased in obesity and type 2 diabetes and normally improves insulin sensitivity?

    Answer: Adiponectin

    Adiponectin activates AMPK in muscle and liver to improve insulin sensitivity; its levels are paradoxically low in obese and type 2 diabetic individuals.

  6. In neonatal diabetes mellitus, which genetic mutation most commonly causes a permanently open KATP channel, preventing insulin secretion?

    Answer: Activating mutations in KCNJ11 (Kir6.2) or ABCC8 (SUR1)

    Gain-of-function mutations in KCNJ11 or ABCC8 keep the KATP channel open regardless of intracellular ATP levels, preventing membrane depolarization and insulin secretion.

  7. Which mechanism best explains how chronic hyperglycemia causes endothelial dysfunction and accelerated atherosclerosis in diabetes?

    Answer: Advanced glycation end-products (AGEs) cross-link proteins and activate RAGE, promoting inflammation and oxidative stress

    AGEs accumulate on long-lived proteins and activate the receptor RAGE, triggering NF-κB–driven inflammatory cascades and oxidative stress that impair endothelial function and accelerate plaque formation.