Review Practice Exercise 1

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Practice Exercise 1

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Question 1:

Which placental hormone is primarily responsible for increasing maternal insulin resistance during the second and third trimesters of pregnancy, contributing to the development of Gestational Diabetes Mellitus?

A. Estrogen B. Prolactin C. Human Placental Lactogen (hPL) D. Relaxin

Answer and Explanation

Choice A:

Estrogen increases during pregnancy but does not significantly contribute to insulin resistance. Its primary roles include uterine growth and vascularization, not glucose metabolism. While it modulates insulin sensitivity indirectly, it lacks the potent anti-insulin effects of hPL.

Choice B:

Prolactin is secreted by the anterior pituitary and supports lactogenesis. It has minor effects on glucose metabolism, but it does not induce the level of insulin resistance required to cause gestational diabetes. Its concentration does not correlate with the timing of GDM onset.

Choice C:

Human placental lactogen (hPL) is secreted by the syncytiotrophoblast and rises progressively during pregnancy. It directly induces insulin resistance by antagonizing insulin receptors and promoting lipolysis, ensuring glucose availability for the fetus. Its peak action coincides with the onset of gestational diabetes, making it the primary hormone responsible.

Choice D:

Relaxin is involved in cervical ripening and pelvic ligament relaxation. It has no role in glucose regulation or insulin resistance. Its secretion pattern and physiological effects are unrelated to the metabolic changes seen in gestational diabetes.

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Question 2:

When discussing the pathophysiology of GDM, the nurse explains that the pancreas's inability to produce sufficient insulin to overcome increased insulin resistance is due to:

A. Hypertrophy of beta cells. B. Impaired alpha-cell function. C. Pancreatic beta-cell dysfunction. D. Excessive glucagon secretion.

Answer and Explanation

Choice A:

Hypertrophy of beta cells would imply increased insulin production. In GDM, the issue is not cell enlargement but functional impairment. Beta cells may appear morphologically normal or even hypertrophic, but their secretory capacity is inadequate.

Choice B:

Alpha-cell function relates to glucagon secretion, not insulin production. Alpha-cell impairment would affect counter-regulatory responses to hypoglycemia, not the hyperglycemia seen in GDM. The question focuses on insulin insufficiency, making alpha-cell dysfunction irrelevant.

Choice C:

Pancreatic beta-cell dysfunction is the primary defect in GDM. Beta cells fail to augment insulin secretion in response to rising insulin resistance. This dysfunction is due to genetic predisposition, chronic inflammation, and lipotoxicity. The question stem directly refers to the pancreas's inability to produce sufficient insulin, confirming beta-cell failure.

Choice D:

Excessive glucagon secretion contributes to hyperglycemia but is not the primary defect in GDM. Glucagon increases hepatic glucose output, but the central issue is insulin resistance and inadequate beta-cell compensation. Glucagon excess is secondary and not causative.

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Question 3:

What is the role of human placental lactogen in GDM pathophysiology?

A. Increases insulin production B. Enhances lipolysis and insulin resistance C. Decreases maternal glucose levels D. Promotes fetal hypoglycemia

Answer and Explanation

Choice A:

Human placental lactogen does not increase insulin production. It impairs insulin action, requiring the pancreas to compensate. The hormone’s role is antagonistic to insulin, not stimulatory. Beta-cell compensation is a separate physiological response, not driven by hPL.

Choice B:

Human placental lactogen enhances lipolysis and induces insulin resistance by antagonizing insulin receptors. This shifts maternal metabolism toward fat utilization while sparing glucose for fetal use. Its action is central to the pathophysiology of GDM, where insulin resistance exceeds pancreatic compensatory capacity.

Choice C:

Human placental lactogen increases maternal glucose levels by reducing insulin sensitivity. It promotes glucose availability for the fetus, not reduction. Its metabolic effects oppose insulin, leading to elevated maternal glucose if insulin secretion is insufficient.

Choice D:

Human placental lactogen does not promote fetal hypoglycemia. It ensures fetal glucose supply by increasing maternal glucose levels. Fetal hypoglycemia may occur postpartum due to persistent fetal hyperinsulinemia, but this is unrelated to hPL’s direct action.

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Question 4:

When discussing the pathophysiology of Gestational Diabetes Mellitus, which of the following statements are accurate regarding the role of pregnancy hormones? Select all that apply

A. Progesterone increases insulin sensitivity. B. Cortisol exhibits anti-insulin effects. C. Human placental lactogen (hPL) increases maternal insulin resistance. D. Estrogen directly stimulates insulin production. E. These hormones ensure continuous glucose supply to the fetus.

Answer and Explanation

Choice A:

Progesterone does not increase insulin sensitivity. It contributes to insulin resistance by interfering with insulin receptor signaling. Its role is synergistic with other placental hormones in reducing maternal glucose uptake.

Choice B:

Cortisol exhibits anti-insulin effects by promoting gluconeogenesis and impairing peripheral glucose uptake. It increases maternal blood glucose levels, contributing to insulin resistance during pregnancy. Its concentration rises progressively, peaking in the third trimester.

Choice C:

Human placental lactogen increases maternal insulin resistance by antagonizing insulin receptors and stimulating lipolysis. This spares glucose for fetal use and shifts maternal metabolism toward fat utilization. It is the most potent diabetogenic hormone in pregnancy.

Choice D:

Estrogen does not directly stimulate insulin production. It modulates vascular tone and supports uterine growth, but its influence on glucose metabolism is indirect. It may affect insulin sensitivity but does not enhance beta-cell secretion.

Choice E:

These hormones ensure continuous glucose supply to the fetus by impairing maternal insulin action. This metabolic shift prioritizes fetal growth and development. Glucose crosses the placenta via facilitated diffusion, driven by maternal hyperglycemia.

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Question 5:

Which of the following are key pathophysiological differences between preexisting diabetes mellitus and gestational diabetes mellitus in pregnancy? Select all that apply

A. Preexisting diabetes involves chronic hyperglycemia predating conception. B. Gestational diabetes typically resolves postpartum. C. Preexisting type 1 diabetes is characterized by insulin resistance only. D. Gestational diabetes arises from de novo insulin resistance in the second trimester. E. Preexisting diabetes carries no risk of congenital anomalies.

Answer and Explanation

Choice A:

Preexisting diabetes involves chronic hyperglycemia that begins before conception. This includes both type 1 and type 2 diabetes. The presence of elevated glucose during embryogenesis increases risk of congenital malformations, especially cardiac and neural tube defects.

Choice B:

Gestational diabetes typically resolves postpartum because the diabetogenic placental hormones (human placental lactogen, cortisol, progesterone) decline after delivery. Insulin resistance diminishes, and glucose tolerance often normalizes unless underlying type 2 diabetes is unmasked.

Choice C:

Preexisting type 1 diabetes is not characterized by insulin resistance only. It is defined by absolute insulin deficiency due to autoimmune beta-cell destruction. Insulin resistance may occur later due to exogenous insulin use or obesity, but it is not the primary defect.

Choice D:

Gestational diabetes arises from de novo insulin resistance in the second trimester due to rising levels of human placental lactogen, cortisol, and progesterone. This resistance peaks between 24 and 28 weeks, impairing maternal glucose uptake and increasing fetal glucose exposure.

Choice E:

Preexisting diabetes carries a significant risk of congenital anomalies if glycemic control is poor during the first trimester. Hyperglycemia during organogenesis increases risk of cardiac defects, neural tube defects, and caudal regression syndrome. Tight glucose control before conception reduces this risk.

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Practice Exercise 1

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