8 Flashcards
(25 cards)
What is the primary apolipoprotein in LDL particles?
Apolipoprotein B-100 (apoB-100) is embedded in LDL and necessary for receptor-mediated uptake in tissues.
Which lipoprotein is the largest and richest in triglycerides?
Chylomicrons, with over 85% triglyceride content, transport dietary lipids from the intestine.
Describe the significance of very-low-density lipoprotein (VLDL) in lipid metabolism.
VLDL transports endogenous triglycerides from the liver to peripheral tissues and eventually becomes IDL and LDL after triglyceride removal.
How does HDL reduce atherosclerotic risk?
HDL mediates reverse cholesterol transport by carrying cholesterol from peripheral tissues back to the liver for excretion.
What liver function alteration is associated with non-alcoholic fatty liver disease (NAFLD) in metabolic syndrome?
Elevated ALT and AST levels due to hepatocellular lipid accumulation and injury.
List four major types of diabetes mellitus.
Type 1 diabetes mellitus (autoimmune β-cell destruction), Type 2 diabetes mellitus (insulin resistance and relative insulin deficiency), gestational diabetes, and maturity-onset diabetes of the young (MODY).
What is latent autoimmune diabetes of adults (LADA)?
A slowly progressive form of autoimmune diabetes in adults that shares features of both type 1 and type 2 and often initially misdiagnosed as type 2.
Why is measuring glycated hemoglobin (HbA1c) clinically valuable?
HbA1c reflects average blood glucose over the preceding 8–12 weeks, helping assess long-term glycemic control.
Define the normal fasting blood glucose range and the threshold for diagnosing diabetes.
Normal fasting blood glucose is 4–6 mM; a fasting level >11 mM is diagnostic of hyperglycemia and likely diabetes.
How does a glucose tolerance test distinguish between normal and diabetic responses?
In a healthy individual, blood glucose returns to normal (<7.8 mM) within 2 hours post-glucose load, whereas in diabetes, glucose remains elevated (>11 mM).
What metabolic changes occur in diabetic ketoacidosis (DKA)?
Insulin deficiency causes increased lipolysis, elevated free fatty acids, excessive ketone body production, metabolic acidosis, and osmotic diuresis leading to dehydration.
Which ketone bodies rise first in the blood during the onset of DKA?
Beta-hydroxybutyrate (β-HB) and acetoacetate increase initially; acetone is produced in smaller quantities and exhaled.
How does hyperglycemia in DKA contribute to dehydration?
High plasma glucose exceeds renal tubular reabsorption, leading to osmotic diuresis and loss of water (polyuria), causing dehydration.
What is the typical renal threshold for glucose reabsorption in healthy individuals?
Approximately 10 mM (180 mg/dL); above this, glucose spills into urine (glycosuria).
Explain the compensatory hyperinsulinemia seen in early type 2 diabetes.
Insulin resistance in peripheral tissues prompts pancreatic β-cells to increase insulin secretion to maintain normoglycemia initially.
What happens to β-cell function over time in untreated type 2 diabetes?
Chronic hyperstimulation leads to β-cell dysfunction, declining insulin secretion, and worsening hyperglycemia.
Why is fasting insulin elevated before the clinical diagnosis of type 2 diabetes?
The pancreas compensates for insulin resistance by secreting more insulin to maintain normal glucose levels until β-cells begin failing.
How can urinary dipstick testing be used in the initial assessment of suspected diabetes?
Detection of glucose and ketones in urine indicates hyperglycemia and potential ketoacidosis, warranting further blood testing.
Which test provides a “snapshot” of plasma glucose at a single time point, and why is timing important?
Fasting blood glucose; it must be measured after an overnight fast to avoid postprandial variability.
What is the expected 2-hour post-load blood glucose in a normal oral glucose tolerance test?
Less than 7.8 mM (140 mg/dL) at 2 hours; values ≥11.1 mM (200 mg/dL) indicate diabetes.
In type 2 diabetes, which phase of insulin response is often blunted first?
The first-phase insulin response (immediate release of preformed insulin granules) is impaired early, causing postprandial hyperglycemia.
How does increased free fatty acid release in DKA affect hepatic gluconeogenesis?
Free fatty acids provide substrates (glycerol) and upregulate gluconeogenic enzymes, further elevating blood glucose.
Why is monitoring serum potassium critical in DKA management?
Insulin treatment drives potassium into cells, risking hypokalemia; initial hyperkalemia may mask total body potassium depletion.
Which lipid profile change is most characteristic of uncontrolled type 2 diabetes?
Elevated triglycerides (increased VLDL) and low HDL, often with small dense LDL particles.
