Endocrinology Practice Questions

Q: Excess of calcium intake leads to?

Milk alkali syndrome. ***Milk alkali syndrome*** - **Milk-alkali syndrome** is caused by excessive intake of calcium (especially in the form of calcium carbonate) and absorbable alkali, leading to **hypercalcemia**, metabolic alkalosis, and acute kidney injury. - The combination of abnormally high calcium intake, often from supplements, and the use of antacids or milk, drives this condition. *Cardiomyopathy* - **Cardiomyopathy** refers to diseases of the heart muscle that make it harder for the heart to pump blood, and it is not directly caused by excess calcium intake. - While severe hypercalcemia can affect cardiac function, it typically causes arrhythmias or altered contractility, not a primary **cardiomyopathy**. *Osteomalacia* - **Osteomalacia** is a softening of the bones, typically due to **vitamin D deficiency** or impaired metabolism, leading to inadequate mineralization of new bone matrix. - This condition is caused by insufficient calcium and phosphate for normal bone formation, not by an **excess of calcium intake**. *Osteoporosis* - **Osteoporosis** is a disease where bones become weak and brittle due to **loss of bone mass** and microarchitectural deterioration. [1] - Chronic excess calcium intake does not cause osteoporosis; in fact, adequate calcium intake is crucial for **bone health** and preventing osteoporosis. [1]

Q: An endocrinologist decided to give a 7 year old boy testosterone therapy and continued it till puberty. This therapy is likely to:

Reduce adult stature. Reduce adult stature - Early administration of testosterone, especially before puberty and continued through it, can lead to **premature epiphyseal plate fusion**. - This premature fusion limits the long bones from growing to their full potential, resulting in **shorter adult height**. *Increase adult stature* - While testosterone promotes initial growth spurts, prolonged exposure, particularly too early, leads to accelerated **bone maturation** and closure of growth plates. - This ultimately curtails the total growth period, preventing maximum height attainment. *Cause hypertrophy of penis* - Testosterone therapy in a 7-year-old boy would induce **precocious puberty**, leading to the development of secondary sexual characteristics, including penile enlargement. [1] - However, this is largely considered a side effect of early testosterone exposure and not its primary or most concerning impact on future growth. *Have no effect on adult stature* - Testosterone has a significant impact on bone growth and development, particularly by affecting the **epiphyseal growth plates**. - Therefore, administering testosterone during childhood inevitably influences the final adult stature, either by increasing or decreasing it depending on the timing and duration.

Q: The primary pharmacological intervention to retard avascular necrosis progression is?

Bisphosphonates (Alendronate). ***Bisphosphonates (Alendronate)*** - **Bisphosphonates** inhibit osteoclast-mediated bone resorption and reduce bone cell death, showing promise in preventing progression of early-stage **avascular necrosis**. [1] - Alendronate specifically has been studied for its **bone-preserving effects** in AVN by maintaining bone architecture and potentially slowing femoral head collapse. *Corticosteroid therapy* - **Corticosteroids** are a major **risk factor** for developing avascular necrosis, not a treatment for it. - They cause AVN through mechanisms including **fat embolism**, increased **intraosseous pressure**, and direct **osteocyte toxicity**. *High-dose calcium supplementation* - **Calcium supplementation** supports general bone health but does not address the underlying **vascular disruption** in AVN. - No evidence exists that calcium alone can retard **AVN progression**, which involves interruption of blood supply leading to bone death. *Vitamin D supplementation alone* - **Vitamin D** is essential for calcium absorption and bone mineralization but does not target **AVN pathophysiology**. - Like calcium, it does not address the primary mechanism of **blood supply disruption** that characterizes avascular necrosis.

Q: In hypoparathyroidism:

Plasma calcium is low and inorganic phosphorous high. ***Plasma calcium is low and inorganic phosphorous high*** - **Hypoparathyroidism** is characterized by insufficient parathyroid hormone (PTH) production, leading to decreased bone resorption and reduced renal reabsorption of calcium [1]. This results in **hypocalcemia** (low plasma calcium) [1]. - PTH also promotes renal excretion of phosphate [2]. With insufficient PTH, renal phosphate excretion is impaired, leading to **hyperphosphatemia** (high inorganic phosphorus) [1]. *Plasma calcium is high and inorganic phosphorous low* - This profile is characteristic of **primary hyperparathyroidism**, where excessive PTH causes increased bone resorption and renal calcium reabsorption (high calcium), and increased renal phosphate excretion (low phosphorus). - It directly contradicts the defining features of hypoparathyroidism [1]. *Plasma calcium and inorganic phosphorous are low* - While plasma calcium is low in hypoparathyroidism, plasma inorganic phosphorus is characteristically high, not low [1]. - A combination of low calcium and low phosphorus can be seen in conditions like **vitamin D deficiency** (osteomalacia), but not directly in pure hypoparathyroidism [1]. *Plasma calcium and inorganic phosphorous are high* - This combination of high calcium and high phosphorus is uncommon and not typically seen in either hypoparathyroidism or hyperparathyroidism. - It could potentially indicate conditions like **milk-alkali syndrome** or **vitamin D intoxication**, but not hypoparathyroidism, which is defined by low calcium [1].

Q: Congenital adrenal hyperplasia is the most common cause of

Female pseudohermaphroditism (androgenized female 46XX). ***Female pseudohermaphroditism (androgenized female 46XX)*** - Congenital adrenal hyperplasia (CAH), particularly **21-hydroxylase deficiency**, leads to overproduction of **adrenal androgens**. [3] - In a 46,XX fetus, this excess androgen exposure results in masculinization of external genitalia, while internal female organs (uterus, ovaries) are present, defining **female pseudohermaphroditism**. [3] *True hermaphroditism* - Characterized by the presence of both **ovarian and testicular tissue** in the same individual. [2] - This condition is rare and not directly caused by the hormonal imbalances seen in CAH. *Male pseudohermaphroditism (underandrogenized male 46XY)* - Occurs in individuals with a **46,XY karyotype** who have testes but whose external genitalia are ambiguous or female due to **insufficient androgen production or action**. - Conditions like **androgen insensitivity syndrome** or defects in testosterone synthesis cause this, not CAH. [3] *Turner's syndrome* - A chromosomal disorder with a **45,XO karyotype**, primarily affecting females. [1] - It is characterized by features such as **short stature**, gonadal dysgenesis (streak gonads), and various congenital anomalies, and it is not a form of pseudohermaphroditism related to adrenal function. [1]

Q: Which of the following is caused by congenital 17 hydroxylase deficiency:

Hypertension. ***Hypertension*** - **Congenital 17-hydroxylase deficiency** leads to impaired synthesis of **cortisol** and **sex steroids**, resulting in an accumulation of **mineralocorticoid precursors (corticosterone and deoxycorticosterone)** [1]. - Increased levels of these mineralocorticoids cause **sodium and water retention**, leading to **hypertension** and **hypokalemia**. *Virilism* - **17-hydroxylase deficiency** impairs **androgen synthesis**, preventing the development of male secondary sexual characteristics [2]. - Individuals with this deficiency often present with **female external genitalia** regardless of their genetic sex, or **under-virilization** in genetic males, not virilism [2]. *Hyperkalemia* - The excess mineralocorticoids (deoxycorticosterone) in **17-hydroxylase deficiency** promote **sodium reabsorption** and **potassium excretion** in the kidneys [1]. - This leads to **hypokalemia**, which is the opposite of hyperkalemia. *Hermaphroditism* - **17-hydroxylase deficiency** affects the development of gonads and internal reproductive organs depending on genetic sex. - Genetic males (**XY**) with this deficiency typically develop **female external genitalia** (pseudohermaphroditism or 46, XY DSD), while genetic females (**XX**) typically present as normal females but with **primary amenorrhea** [2]. This genetic condition does not result in true hermaphroditism (presence of both ovarian and testicular tissue) [2].

Q: A five year old boy presents with precocious puberty and a Blood pressure of 130/80 mm Hg. Estimation of which of the following will help in diagnosis

17 hydroxy - progesterone. ***17 hydroxy - progesterone*** - Precocious puberty with hypertension suggests a form of **congenital adrenal hyperplasia (CAH)**, specifically 11β-hydroxylase deficiency or 21-hydroxylase deficiency. - While **17-hydroxyprogesterone** is highly elevated in 21-hydroxylase deficiency, its levels also rise in 11β-hydroxylase deficiency due to the block in cortisol synthesis leading to increased ACTH stimulation. *Cortisol* - **Cortisol** levels are typically low or normal in CAH due to enzyme deficiencies blocking its synthesis, but measuring cortisol directly is not the primary diagnostic test. - The elevated blood pressure is due to accumulation of precursor steroids with mineralocorticoid activity, not directly due to high cortisol. *11-deoxycortisol* - **11-deoxycortisol** (compound S) is a precursor that accumulates specifically in **11β-hydroxylase deficiency**, leading to hypertension and precocious puberty. - While it's a key marker for this specific type of CAH, 17-hydroxyprogesterone is a broader initial screening marker as it is elevated in both 21-hydroxylase and 11β-hydroxylase deficiencies, which are the most common forms leading to these symptoms. *Aldosterone* - **Aldosterone** levels are usually low in both 21-hydroxylase and 11β-hydroxylase deficiencies, often contributing to salt wasting in the salt-wasting form of 21-hydroxylase deficiency. - Although the patient has hypertension, it is caused by the accumulation of other mineralocorticoid-like precursors, not elevated aldosterone.

Q: Association of sexual precocity, multiple cystic bone lesions and endocrinopathies are seen in:

McCune-Albright's syndrome. ***McCune-Albright's syndrome*** - This syndrome is characterized by the classic triad of **precocious puberty**, **polyostotic fibrous dysplasia** (multiple cystic bone lesions), and **café-au-lait spots**. - It is caused by a somatic activating mutation in the **GNAS1 gene**, leading to constitutive activation of G protein-coupled receptors in affected tissues, resulting in hormonal overproduction and dysplastic changes. *Hepatoblastoma* - Hepatoblastoma is a **malignant liver tumor** primarily affecting infants and children. - While it can, in rare cases, produce human chorionic gonadotropin (hCG) causing precocious puberty, it is not typically associated with widespread cystic bone lesions or other endocrinopathies characteristic of McCune-Albright's. *Androblastoma* - An androblastoma (also known as a **Sertoli-Leydig cell tumor**) is a rare **gonadal stromal tumor** that secretes androgens. - It can cause **virilization** and, in prepubertal girls, precocious puberty, but it does not cause multiple cystic bone lesions or other systemic endocrine disorders as seen in McCune-Albright's. *Granulosa cell tumor* - Granulosa cell tumors are **ovarian stromal tumors** that can produce **estrogen**, leading to precocious puberty in young girls. - While they are a cause of precocious puberty, they do not typically present with the extensive cystic bone lesions or the full spectrum of endocrinopathies found in McCune-Albright's syndrome.

Q: All statements are true for osteomalacia except:

Raised serum calcium. ***Raised serum calcium*** - **Osteomalacia** is characterized by defective **bone mineralization**, predominantly due to **vitamin D deficiency** (or abnormal metabolism) or phosphate deficiency [1]. - This typically leads to **hypocalcemia** (low serum calcium), not elevated calcium, as vitamin D is essential for calcium absorption from the gut [1], [3]. *Muscular weakness* - **Proximal muscle weakness**, particularly in the thighs and pelvic girdle, is a common symptom of **osteomalacia** [1]. - This **myopathy** is thought to be directly related to **vitamin D deficiency** and the resulting metabolic disturbances affecting muscle function [1]. *Looser's zone on X-ray* - **Looser's zones**, also known as **pseudofractures**, are characteristic radiological findings in **osteomalacia** [2]. - These are areas of **unmineralized osteoid** that appear as radiolucent bands perpendicular to the bone cortex, often found in the femoral neck, pubic rami, or ribs [2]. *Commoner in females* - **Osteomalacia** is indeed more common in **females**, particularly in those of **childbearing age** or with **multiple pregnancies**, due to increased calcium and vitamin D demands. - **Postmenopausal women** are also at higher risk, often linked to reduced sun exposure, dietary deficiencies, or medication use.

Q: A 35-year-old woman presents with 6-month history of skin rash and fatigue. Physical examination shows pallor and a necrotizing erythematous skin rash of her lower body. Laboratory studies reveal mild anemia and fasting blood glucose of 160 mg/dL. A CT scan of the abdomen demonstrates a 2-cm mass in the pancreas. Which of the following is the most likely diagnosis?

Glucagonoma. ***Glucagonoma*** - The necrotizing erythematous skin rash (necrolytic migratory erythema), mild anemia, hyperglycemia (fasting blood glucose 160 mg/dL), and a pancreatic mass are classic features of a **glucagonoma**. [1] - **Glucagon** excess leads to skin rash, glucose intolerance due to its counter-regulatory effects on insulin, and often anemia. [1] *Insulinoma* - An insulinoma typically presents with symptoms of **hypoglycemia** (e.g., sweating, palpitations, confusion), especially in the fasting state. [2] - While it involves a pancreatic mass, the patient's hyperglycemia and specific skin rash are inconsistent with insulinoma. [2] *Gastrinoma* - Gastrinomas cause **Zollinger-Ellison syndrome**, characterized by severe peptic ulcer disease, abdominal pain, and diarrhea due to excessive **gastrin** production. [1] - The patient's symptoms, particularly the skin rash and hyperglycemia, are not typical of a gastrinoma. *Carcinoid tumor* - Carcinoid tumors can arise in various locations, including the pancreas, but typically produce **serotonin** and other vasoactive substances. [1] - Symptoms usually include **flushing**, diarrhea, and bronchospasm (carcinoid syndrome), which are absent in this patient's presentation. [1]

Question 1

Excess of calcium intake leads to?

Accepted Answer

Milk alkali syndrome

Answer

Cardiomyopathy

Answer

Osteomalacia

Answer

Osteoporosis

Question 2

An endocrinologist decided to give a 7 year old boy testosterone therapy and continued it till puberty. This therapy is likely to:

Accepted Answer

Reduce adult stature

Answer

Increase adult stature

Answer

Cause hypertrophy of penis

Answer

Have no effect on adult stature

Question 3

The primary pharmacological intervention to retard avascular necrosis progression is?

Accepted Answer

Bisphosphonates (Alendronate)

Answer

High-dose calcium supplementation

Answer

Vitamin D supplementation alone

Answer

Corticosteroid therapy

Question 4

In hypoparathyroidism:

Accepted Answer

Plasma calcium is low and inorganic phosphorous high

Answer

Plasma calcium is high and inorganic phosphorous low

Answer

Plasma calcium and inorganic phosphorous are low

Answer

Plasma calcium and inorganic phosphorous are high

Question 5

Congenital adrenal hyperplasia is the most common cause of

Accepted Answer

Female pseudohermaphroditism (androgenized female 46XX)

Answer

True hermaphroditism

Answer

Male pseudohermaphroditism (underandrogenized male 46XY)

Answer

Turner's syndrome

Question 6

Which of the following is caused by congenital 17 hydroxylase deficiency:

Accepted Answer

Hypertension

Answer

Virilism

Answer

Hyperkalemia

Answer

Hermaphroditism

Question 7

A five year old boy presents with precocious puberty and a Blood pressure of 130/80 mm Hg. Estimation of which of the following will help in diagnosis

Accepted Answer

17 hydroxy - progesterone

Answer

Cortisol

Answer

11-deoxycortisol

Answer

Aldosterone

Question 8

Association of sexual precocity, multiple cystic bone lesions and endocrinopathies are seen in:

Accepted Answer

McCune-Albright's syndrome

Answer

Hepatoblastoma

Answer

Androblastoma

Answer

Granulosa cell tumor

Question 9

All statements are true for osteomalacia except:

Accepted Answer

Raised serum calcium

Answer

Muscular weakness

Answer

Loosers zone on X-ray

Answer

Commoner in females

Question 10

A 35-year-old woman presents with 6-month history of skin rash and fatigue. Physical examination shows pallor and a necrotizing erythematous skin rash of her lower body. Laboratory studies reveal mild anemia and fasting blood glucose of 160 mg/dL. A CT scan of the abdomen demonstrates a 2-cm mass in the pancreas. Which of the following is the most likely diagnosis?

Accepted Answer

Glucagonoma

Answer

Insulinoma

Answer

Gastrinoma

Answer

Carcinoid tumor

Endocrinology — MCQs

Endocrinology — MCQs

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