Adrenal Disorders in Pregnancy — MCQs

10 questions

A hypertensive patient wants to conceive. Which of the following medications needs to be stopped before pregnancy?

A 3 week neonate with ambiguous genitalia presented with Na+ 127 meq/L, K+ 7.2 meq/L with BP 52/24 mm Hg and was managed with IV fluids. What is the next step of management?

A pregnant woman comes to OPD for regular ANC checkup. She gives history of previous child diagnosed with congenital adrenal hyperplasia. What drug is given in this pregnancy to prevent development of CAH in this child?

Best way to localize extra-adrenal pheochromocytoma:

Which of the following is the principal steroid secreted by the fetal adrenal cortex?

Which of the following is a component of the classic triad used for clinical diagnosis of pheochromocytoma?

Which test is essential in a patient with suspected Cushing's syndrome for diagnosis confirmation?

Which one of the following drugs is used for fetal therapy in congenital adrenal hyperplasia?

All are true about hormone functions except:

Q10

Which of the following statements about placental hormones is true?

Adrenal Disorders in Pregnancy Indian Medical PG Practice Questions and MCQs

Question 1: A hypertensive patient wants to conceive. Which of the following medications needs to be stopped before pregnancy?

A. ACE inhibitors (Correct Answer)
B. Alpha Methyl dopa
C. Calcium Channel Blockers
D. Labetalol
E. Hydralazine

Explanation: ***ACE inhibitors*** - **ACE inhibitors** are **teratogenic** and can cause **fetal kidney damage**, **oligohydramnios**, and **fetal death** if used during pregnancy. - They should be discontinued before conception or immediately upon pregnancy confirmation, and an alternative safe antihypertensive should be initiated. *Alpha Methyl dopa* - **Alpha-methyldopa** is considered one of the **first-line agents** for managing **hypertension in pregnancy** due to its established safety profile. - It reduces peripheral resistance without significantly affecting renal or uteroplacental blood flow. *Calcium Channel Blockers* - **Calcium channel blockers (CCBs)** like nifedipine and amlodipine are **generally considered safe** for use during pregnancy, especially dihydropyridines. - They are often used as **second-line treatments** for managing hypertension in pregnant women. *Labetalol* - **Labetalol** is a **beta-blocker** that is widely used and considered **safe** for treating **hypertension in pregnancy**. - It effectively lowers blood pressure without significant adverse effects on the fetus. *Hydralazine* - **Hydralazine** is a direct vasodilator that is **safe** for use in pregnancy and is commonly used for **acute management** of severe hypertension in pregnant women. - It has a long history of safe use during pregnancy without teratogenic effects.

Question 2: A 3 week neonate with ambiguous genitalia presented with Na+ 127 meq/L, K+ 7.2 meq/L with BP 52/24 mm Hg and was managed with IV fluids. What is the next step of management?

A. Hydrocortisone administration (Correct Answer)
B. Calcium gluconate
C. Broad spectrum antibiotics
D. Spironolactone

Explanation: ***Hydrocortisone administration*** - The combination of **ambiguous genitalia**, low **sodium**, high **potassium**, and **hypotension** in a neonate strongly suggests **congenital adrenal hyperplasia (CAH)** due to 21-hydroxylase deficiency, leading to salt-wasting adrenal crisis. - **Hydrocortisone** is crucial for replacing deficient **cortisol** and addressing the underlying adrenal insufficiency, which is the definitive treatment for this endocrine emergency. - Cortisol replacement helps restore hemodynamic stability and, along with fluid resuscitation, addresses the electrolyte imbalance. *Calcium gluconate* - While **hyperkalemia** is present at 7.2 meq/L, which is severe and potentially life-threatening, **calcium gluconate** provides only **cardiac membrane stabilization** without treating the underlying cause. - In clinical practice, calcium gluconate may be given for immediate cardiac protection in severe hyperkalemia, but the **definitive management** of CAH-related adrenal crisis requires **hormonal replacement**. - The question asks for the next step after IV fluids are initiated, and hydrocortisone addresses the root cause of the metabolic derangements. *Broad spectrum antibiotics* - There is no clinical indication in the stem to suggest a bacterial infection that would warrant **broad-spectrum antibiotics**. - Although critically ill neonates may sometimes receive empiric antibiotics, the presentation clearly points to an **endocrine emergency** rather than sepsis. *Spironolactone* - **Spironolactone** is an **aldosterone antagonist** and a **potassium-sparing diuretic**. - Administering it would worsen the already existing **hyperkalemia** and **hyponatremia**, making it absolutely contraindicated in this clinical scenario.

Question 3: A pregnant woman comes to OPD for regular ANC checkup. She gives history of previous child diagnosed with congenital adrenal hyperplasia. What drug is given in this pregnancy to prevent development of CAH in this child?

A. Hydrocortisone
B. Betamethasone
C. Dexamethasone (Correct Answer)
D. Prednisolone

Explanation: ***Dexamethasone*** - **Dexamethasone** is given to pregnant women with a previous child affected by CAH to help prevent the development of **congenital adrenal hyperplasia** (specifically **21-hydroxylase deficiency**, the most common form) in the fetus. - Treatment must be started **early in pregnancy (ideally before 9 weeks gestation)** to be effective in preventing virilization in affected female fetuses. - **Dexamethasone** crosses the placenta efficiently and suppresses fetal adrenal androgen production, which can reduce or prevent **virilization** in affected female fetuses. - It is the preferred corticosteroid for prenatal treatment due to its ability to cross the placenta without being inactivated. *Hydrocortisone* - **Hydrocortisone** is a glucocorticoid that is often used to replace cortisol in individuals with CAH after birth, but it is not typically used for prenatal prevention. - Its shorter half-life and higher mineralocorticoid activity make it less suitable for transplacental suppression compared to dexamethasone. - Additionally, it does not cross the placenta as effectively as dexamethasone. *Betamethasone* - **Betamethasone** is primarily used in pregnancy to accelerate fetal lung maturation in cases of anticipated preterm birth. - While it is a long-acting corticosteroid that can cross the placenta, it does not have the specific indication or established efficacy for preventing CAH development prenatally. *Prednisolone* - **Prednisolone** is used for various inflammatory and autoimmune conditions, and while it's a corticosteroid, it is largely **inactivated by placental 11β-hydroxysteroid dehydrogenase type 2** before reaching the fetus. - This placental inactivation (approximately 90% is converted to inactive prednisolone) makes it ineffective for suppressing fetal adrenal androgen production to prevent CAH.

Question 4: Best way to localize extra-adrenal pheochromocytoma:

A. X-ray
B. Clinical examination
C. VMA excretion
D. Nuclear medicine scan (MIBG scan) (Correct Answer)

Explanation: ***Nuclear medicine scan (MIBG scan)*** - **Iodine-131-metaiodobenzylguanidine (MIBG) scan** is the imaging modality of choice for localizing extra-adrenal pheochromocytomas due to its high specificity for **neuroendocrine tumors** like pheochromocytomas and paragangliomas. - MIBG is structurally similar to **norepinephrine** and is actively taken up by adrenergic neurons, allowing visualization of hypersecreting chromaffin cells wherever they are located in the body. *X-ray* - **X-rays** provide limited soft tissue detail and are generally not useful for localizing pheochromocytomas, especially extra-adrenal ones. - They may show calcifications in some tumors but lack the sensitivity and specificity needed for definitive localization. *Clinical examination* - A **clinical examination** can identify signs and symptoms suggestive of pheochromocytoma (e.g., hypertension, palpitations, sweating) but cannot localize the tumor itself. - Localization requires **imaging studies** due to the variable and often deep-seated location of these tumors. *VMA excretion* - **Vanillylmandelic acid (VMA) excretion** is a biochemical test used to diagnose pheochromocytoma by measuring catecholamine metabolites in urine. - While it confirms the presence of a catecholamine-secreting tumor, it provides **no information about the tumor's location**.

Question 5: Which of the following is the principal steroid secreted by the fetal adrenal cortex?

A. Dehydroepiandrosterone (Correct Answer)
B. Progesterone
C. Corticosterone
D. Cortisol

Explanation: ***Dehydroepiandrosterone*** - The **fetal adrenal cortex**, particularly the **fetal zone**, is highly active in synthesizing **steroid hormones**, with **dehydroepiandrosterone (DHEA)** being its principal secretion. - **DHEA** serves as a crucial precursor for **estrogen synthesis** in the placenta, which is essential for maintaining pregnancy. *Progesterone* - **Progesterone** is primarily synthesized by the **placenta** during pregnancy and by the **corpus luteum** in the early stages; it is not the main steroid secreted by the fetal adrenal cortex. - While progesterone is important for maintaining uterine quiescence, its production by the fetal adrenal gland is minimal compared to its placental synthesis. *Corticosterone* - **Corticosterone** is a glucocorticoid mainly produced by the adult adrenal cortex, and its synthesis in the fetal adrenal gland is less significant compared to DHEA. - In humans, **cortisol** is the primary glucocorticoid, while corticosterone is more prominent in rodents. *Cortisol* - **Cortisol** is the main glucocorticoid produced by the adult adrenal cortex, playing roles in stress response and metabolism, but it is not the principal steroid secreted by the fetal adrenal cortex. - While the fetal adrenal gland does produce some cortisol, its primary function is **DHEA** production for placental estrogen synthesis.

Question 6: Which of the following is a component of the classic triad used for clinical diagnosis of pheochromocytoma?

A. Hyperkalemia
B. Hypertension
C. Headache (Correct Answer)
D. Bradycardia

Explanation: ***Headache*** - **Headache** is a key symptom in the classic triad for pheochromocytoma, caused by the **vasoconstrictive effects** of catecholamine surges. - The other two components of the classic triad are **palpitations** and **sweating**. *Hyperkalemia* - **Hyperkalemia** is not a typical manifestation of pheochromocytoma; rather, these tumors produce **catecholamines** that can lead to hyperglycemia. - Mineralocorticoid excess (e.g., in aldosteronism) is more commonly associated with electrolyte imbalances like hyperkalemia or hypokalemia. *Hypertension* - While **hypertension** is a hallmark feature of pheochromocytoma, it is a general sign rather than one of the specific three components of the classic clinical triad used for initial diagnostic suspicion. - The classic triad focuses on the most prominent and specific symptoms that suggest a **catecholamine-secreting tumor**. *Bradycardia* - **Bradycardia** is contrary to the expected cardiovascular effects of pheochromocytoma, which typically causes **tachycardia** (palpitations) due to excessive catecholamine release. - Catecholamines, such as **epinephrine** and **norepinephrine**, increase heart rate and myocardial contractility.

Question 7: Which test is essential in a patient with suspected Cushing's syndrome for diagnosis confirmation?

A. Serum aldosterone
B. Serum renin
C. Plasma ACTH
D. 24-hour urine cortisol (Correct Answer)

Explanation: ***24-hour urine cortisol*** - This test measures the **total amount of cortisol excreted** in the urine over a 24-hour period, reflecting the average daily cortisol production. [1] - An **elevated 24-hour urine free cortisol** is a primary diagnostic test to confirm hypercortisolism in suspected Cushing's syndrome. [1] *Serum aldosterone* - This test is primarily used in the diagnosis of **hyperaldosteronism**, such as Conn's syndrome, which causes hypertension and hypokalemia. - While related to the adrenal glands, **aldosterone levels are not directly used to diagnose Cushing's syndrome**. *Serum renin* - This test is part of the workup for **hypertension** and is used in conjunction with aldosterone to assess the **renin-angiotensin-aldosterone system**. - It is **not a direct or essential test** for the diagnosis of Cushing's syndrome. *Plasma ACTH* - While **plasma ACTH** is crucial for differentiating between different causes of Cushing's syndrome (e.g., ACTH-dependent vs. ACTH-independent), it is **not the initial diagnostic test to confirm the presence of hypercortisolism**. [2] - **Confirmation of cortisol excess** typically precedes ACTH measurement to determine the etiology. [2]

Question 8: Which one of the following drugs is used for fetal therapy in congenital adrenal hyperplasia?

A. Hydrocortisone
B. Prednisolone
C. Fludrocortisone
D. Dexamethasone (Correct Answer)

Explanation: ***Dexamethasone*** - Administered to the mother, **dexamethasone** crosses the placenta and suppresses the fetal adrenal gland's excessive androgen production in **congenital adrenal hyperplasia (CAH)**. - This therapy aims to prevent or reduce the **virilization of female fetuses** when CAH is suspected based on genetic screening of the parents. *Hydrocortisone* - **Hydrocortisone** is a glucocorticoid used for replacement therapy in children and adults with CAH, but it is not typically used for prenatal fetal therapy. - Its shorter half-life and mineralocorticoid activity make it less suitable for transplacental suppression compared to dexamethasone. *Prednisolone* - While prednisolone is a glucocorticoid, it is poorly metabolized by the placenta and does not effectively cross into the fetal circulation to reach therapeutic concentrations. - Therefore, it is not an effective drug for directly treating the fetus in utero. *Fludrocortisone* - **Fludrocortisone** is a mineralocorticoid used in CAH to prevent **salt-wasting crises** by promoting sodium retention, but it does not suppress androgen production. - It is part of postnatal treatment for CAH, not a prenatal fetal therapy to prevent virilization.

Question 9: All are true about hormone functions except:

A. Cortisol regulates plasma volume (Correct Answer)
B. Thyroid hormones regulate metabolism
C. ADH regulates blood osmolality
D. Insulin regulates blood glucose

Explanation: ***Cortisol regulates plasma volume*** - While cortisol plays a role in fluid balance by influencing **renal perfusion** and the action of other hormones like ADH, its primary role is not the direct regulation of plasma volume. - **Aldosterone** is the primary hormone directly responsible for regulating plasma volume through its effects on sodium and water reabsorption in the kidneys. *Thyroid hormones regulate metabolism* - **Thyroid hormones** (T3 and T4) are crucial for regulating the body's metabolic rate, influencing factors like energy production, protein synthesis, and cellular oxygen consumption. - They impact the metabolism of **carbohydrates, fats, and proteins**, affecting nearly every cell in the body. *ADH regulates blood osmolality* - **Antidiuretic hormone (ADH)**, also known as vasopressin, primarily regulates blood osmolality by controlling the reabsorption of water in the renal collecting ducts. - It increases the permeability of collecting ducts to water, thus concentrating urine and **reducing plasma osmolality** when it's high. *Insulin regulates blood glucose* - **Insulin** is a key hormone produced by the pancreas that regulates blood glucose levels by facilitating the uptake of glucose into cells for energy or storage. - It plays a crucial role in lowering blood glucose after meals by promoting **glucose utilization** and inhibiting glucose production by the liver.

Question 10: Which of the following statements about placental hormones is true?

A. hCS plays a role in maternal glucose metabolism. (Correct Answer)
B. hCG levels remain consistently high throughout pregnancy.
C. The luteal-placental shift occurs around 10-12 weeks of gestation.
D. Progesterone production requires fetal adrenal precursors.

Explanation: **Correct: *hCS plays a role in maternal glucose metabolism.*** - **Human chorionic somatomammotropin (hCS)**, also known as placental lactogen, has **anti-insulin effects** that reduce maternal glucose utilization. - This action diverts glucose to the fetus, helping to meet the growing **fetal energy demands**. *Incorrect: hCG levels remain consistently high throughout pregnancy.* - **hCG (human chorionic gonadotropin)** levels peak in the first trimester (around 8-10 weeks) and then **decline and plateau** at much lower levels for the remainder of the pregnancy. - Its primary role is to maintain the **corpus luteum** during early pregnancy. *Incorrect: The luteal-placental shift occurs around 10-12 weeks of gestation.* - The **luteal-placental shift**, where the placenta takes over progesterone production from the corpus luteum, occurs around **7-9 weeks of gestation**. - By 10-12 weeks, the placenta is already the primary producer of progesterone. *Incorrect: Progesterone production requires fetal adrenal precursors.* - **Progesterone** is synthesized by the placenta from **maternal cholesterol** without requiring fetal steroid precursors. - **Estrogen**, particularly **estriol**, on the other hand, relies on **fetal adrenal androgens** as precursors.

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