Endocrinology Practice Questions

Q: The most common cause of severe hypercalcemia is

Malignancy. ***Malignancy*** - **Malignancy** is the most frequent cause of **severe hypercalcemia**, often resulting from **parathyroid hormone-related peptide (PTHrP) secretion** (humoral hypercalcemia of malignancy) or **bone metastases** causing osteolysis [1]. - Cancers like **squamous cell carcinoma**, **breast cancer**, **multiple myeloma**, and **renal cell carcinoma** are commonly associated with severe hypercalcemia [1]. *Vitamin D toxicity* - While vitamin D toxicity can cause hypercalcemia, it typically leads to **moderate hypercalcemia** and is less common as a cause of **severe hypercalcemia** compared to malignancy [1]. - It usually occurs due to **excessive intake of vitamin D supplements** or activated vitamin D [1]. *Sarcoidosis* - Sarcoidosis can cause hypercalcemia due to **extrarenal production of 1,25-dihydroxyvitamin D** by activated macrophages [1]. - However, the hypercalcemia in sarcoidosis is usually **mild to moderate** and rarely reaches the severity seen with malignancy [1]. *Chronic renal failure* - **Chronic renal failure** is more commonly associated with **hypocalcemia** due to impaired vitamin D activation and hyperparathyroidism [2], [3]. - While some patients with end-stage renal disease and **adynamic bone disease** or **tertiary hyperparathyroidism** can develop hypercalcemia, it is not the most common cause of *severe* hypercalcemia in the general population.

Q: HAIR-AN syndrome consists of which of the following?

All of the options. ***All of the options*** - HAIR-AN syndrome is an acronym representing the combination of **HyperAndrogenism**, **Insulin Resistance**, and **Acanthosis Nigricans**. - This syndrome is often associated with **severe hyperinsulinemia** and is considered a severe form of polycystic ovarian syndrome (PCOS) [1]. *Acanthosis nigricans* - While **acanthosis nigricans** is a key component of HAIR-AN syndrome, it does not, by itself, define the entire syndrome. - This condition is characterized by **darkening and thickening of the skin**, particularly in body folds, and is a marker of insulin resistance. *Insulin resistance* - **Insulin resistance** is central to HAIR-AN syndrome, driving many of its metabolic and dermatological manifestations. - However, the definition of HAIR-AN syndrome requires the presence of hyperandrogenism and acanthosis nigricans in addition to insulin resistance to be complete. *Hyperandrogenism* - **Hyperandrogenism**, characterized by elevated androgen levels leading to symptoms like hirsutism and acne, is a critical feature of HAIR-AN syndrome [1]. - Similar to the other components, hyperandrogenism alone does not constitute the full syndrome, which necessitates the presence of insulin resistance and acanthosis nigricans.

Q: During the evaluation of secondary amenorrhea in a 24-year-old woman, hyperprolactinemia is diagnosed. Which of the following conditions could cause increased circulating prolactin concentrations and amenorrhea in this patient?

Hypothyroidism. ***Hypothyroidism*** - **Primary hypothyroidism** leads to increased **TRH** (thyrotropin-releasing hormone) from the hypothalamus. TRH stimulates both **TSH** (thyroid-stimulating hormone) and **prolactin** release from the pituitary, causing hyperprolactinemia [1]. - Elevated prolactin then inhibits **GnRH** (gonadotropin-releasing hormone) secretion, leading to reduced LH and FSH, which results in **anovulation** and **amenorrhea**. *Stress* - While acute stress can transiently increase **prolactin levels**, severe and chronic stress typically leads to **hypogonadism** via effects on GnRH, but not usually hyperprolactinemia sufficient to cause prolonged amenorrhea. - Stress-induced amenorrhea is more often related to **functional hypothalamic amenorrhea**, characterized by low or normal prolactin, and is primarily a disorder of GnRH pulse generation. *Eating disorders* - Conditions like **anorexia nervosa** or **bulimia nervosa** can cause amenorrhea due to **low body weight** and nutritional deficiencies, leading to **hypothalamic dysfunction** and low estrogen levels [3]. - These disorders typically result in **hypogonadotropic hypogonadism** (low LH, FSH, and estrogen) rather than **hyperprolactinemia**. *Adrenal disorders* - Adrenal disorders like **Cushing's syndrome** or **adrenal insufficiency** can cause menstrual irregularities and amenorrhea, but they are not typically associated with **hyperprolactinemia** [2]. - **Congenital adrenal hyperplasia (CAH)** can cause androgen excess and menstrual irregularities, but prolactin levels are usually normal.

Q: In Swyer's syndrome, which of the following statements is true?

Increased FSH and LH. In Swyer's syndrome, which of the following statements is true? ***Increased FSH and LH*** - In **Swyer's syndrome** (46, XY pure gonadal dysgenesis), the **gonads are streak gonads** which are non-functional and thus do not produce sex hormones [2]. - This lack of negative feedback on the hypothalamus and pituitary gland leads to **elevated levels of FSH and LH** [3], [4]. *Testis is absent* - While functional testes are absent, individuals with Swyer's syndrome typically have **streak gonads**, which are dysgenetic and non-functional remnants of gonadal tissue, not fully absent gonads [2]. - The absence of functional testicular tissue is a key feature but stating "testis is absent" is less precise than describing the dysfunctional nature of the streak gonads. *Functional ovaries are absent* - Swyer's syndrome is characterized by a **46, XY karyotype**, meaning the individual is genetically male but has female external genitalia due to a defect in testicular development [2]. - Therefore, the development of functional ovaries would be genetically impossible, and instead, streak gonads are present. *Normal stature* - Individuals with Swyer's syndrome typically have a **normal female phenotype** and are of **normal stature**. - This differentiates it from other forms of gonadal dysgenesis, such as Turner syndrome (45, XO), which is associated with short stature [1].

Q: All are true about primary hyperparathyroidism except which of the following?

Decreased calcium. ***Decreased calcium*** - Primary hyperparathyroidism is characterized by **excessive parathyroid hormone (PTH)** secretion, which leads to **hypercalcemia (increased calcium levels)**, not decreased calcium [1]. - PTH's main actions are to raise serum calcium by increasing **bone resorption**, **renal calcium reabsorption**, and **calcitriol synthesis** [2]. *Nephrolithiasis* - **Hypercalcemia** from primary hyperparathyroidism leads to increased calcium excretion in the urine, increasing the risk of **calcium oxalate stones** (nephrolithiasis) [3]. *Increased alkaline phosphatase* - PTH stimulates osteoclastic activity, leading to **increased bone turnover** and release of enzymes like **alkaline phosphatase**, particularly in cases with significant bone involvement. - Alkaline phosphatase levels may also be elevated due to **osteitis fibrosa cystica**, a severe form of bone disease associated with primary hyperparathyroidism. *Loss of lamina dura* - Chronic hyperparathyroidism can cause characteristic changes in bone, including the **resorption of the lamina dura** around the teeth, which is visible on dental radiographs. - This is a direct consequence of PTH-mediated **osteoclastic activity** in areas of high bone turnover.

Q: In a patient with primary hypothyroidism, what is the expected hormonal profile?

Low T3, low T4, high TSH. ***Low T3, low T4, high TSH*** - In **primary hypothyroidism**, the thyroid gland itself is dysfunctional, leading to reduced production of **thyroid hormones (T3 and T4)** [1]. - The pituitary gland, sensing low thyroid hormone levels, increases **TSH (thyroid-stimulating hormone)** secretion in an attempt to stimulate the failing thyroid [1]. *Low T3, low T4, low TSH* - This profile typically indicates **secondary (central) hypothyroidism**, where the pituitary gland is not producing enough TSH to stimulate a healthy thyroid [2]. - In primary hypothyroidism, the TSH would be high, not low, due to the lack of negative feedback from low T3 and T4 [4]. *High T3, high T4, high TSH* - This hormonal profile is highly suggestive of **thyroid hormone resistance** or a **TSH-secreting pituitary adenoma**, not primary hypothyroidism [3]. - In primary hypothyroidism, T3 and T4 levels are reduced, not elevated. *Normal T3, normal T4, high TSH* - This profile is characteristic of **subclinical hypothyroidism**, where TSH levels are elevated but the thyroid gland is still able to produce enough T3 and T4 to maintain normal peripheral levels. - In overt primary hypothyroidism, T3 and T4 would be low, not normal.

Q: Asymptomatic hypercalcemia in a 30-year-old young male is due to:

Primary hyperparathyroidism. ***Primary hyperparathyroidism*** - This is the most common cause of **asymptomatic hypercalcemia**, particularly in younger individuals [2] and when unrelated to malignancy [1]. - It involves excessive secretion of **parathyroid hormone (PTH)**, leading to increased calcium reabsorption from bones, kidneys, and gut [3]. *Occult primary malignancy* - While malignancy can cause hypercalcemia, it typically presents with **symptomatic hypercalcemia** and other signs of systemic illness [1]. - In a 30-year-old, a widespread occult malignancy causing asymptomatic hypercalcemia is less probable than primary hyperparathyroidism [2]. *Familial hypocalciuric hypercalcemia* - This is a rare genetic disorder characterized by **elevated serum calcium** and **low urinary calcium excretion** due to a defective calcium-sensing receptor [1]. - It is typically benign and does not require treatment for hypercalcemia, but it's important to differentiate from primary hyperparathyroidism [1]. *Hypernephroma* - **Renal cell carcinoma (hypernephroma)** can cause hypercalcemia, often via parathyroid hormone-related peptide (PTHrP) secretion [1]. - However, similar to other malignancies, it's more likely to be symptomatic and is less common than primary hyperparathyroidism as an etiology for asymptomatic hypercalcemia in a young adult [2].

Q: A 50-year-old man with advanced tuberculosis and signs of severe acute adrenal insufficiency should be treated immediately with a combination of:

Cortisol and fludrocortisone. ***Cortisol and fludrocortisone*** - **Cortisol** (a **glucocorticoid**) is essential to replace the deficient hormone in acute adrenal insufficiency, addressing symptoms like **hypotension** and **hypoglycemia** [1], [2]. - **Fludrocortisone** (a **mineralocorticoid**) is also critical as patients with primary adrenal insufficiency (such as that caused by advanced tuberculosis) have deficient **aldosterone** production, requiring mineralocorticoid replacement [1]. *Aldosterone and fludrocortisone* - **Aldosterone** is the natural mineralocorticoid, but it's not administered directly as a drug in this context; instead, **fludrocortisone** is used for its mineralocorticoid effects. - While fludrocortisone is appropriate, aldosterone alone would not address the critical glucocorticoid deficiency seen in acute adrenal crisis [1]. *Triamcinolone and dexamethasone* - Both **triamcinolone** and **dexamethasone** are potent **glucocorticoids** but lack significant mineralocorticoid activity. - In acute adrenal insufficiency, both glucocorticoid and mineralocorticoid replacement are crucial, making this combination insufficient [1]. *Dexamethasone and metyrapone* - **Dexamethasone** is a potent **glucocorticoid** but, like **triamcinolone**, lacks sufficient mineralocorticoid activity for complete replacement [1]. - **Metyrapone** is an adrenal enzyme inhibitor used to reduce cortisol production, making it contraindicated in adrenal insufficiency, where cortisol levels are already dangerously low.

Q: An obese female patient presented with hypertension, chronic headache, and normal pituitary function. The most likely diagnosis is

Empty Sella Syndrome. Empty Sella Syndrome - This condition involves herniation of the arachnoid and CSF into the sella turcica, compressing the **pituitary gland**. While the pituitary gland is compressed, its function is often preserved, hence **normal pituitary function**. - Often associated with **obesity**, **hypertension**, and **headaches** (including chronic headaches) due to increased intracranial pressure. *Cushing's disease* - Characterized by **pituitary adenoma** secreting excess **ACTH**, leading to **hypercortisolism**. [1], [2] - Symptoms include central obesity, hypertension, and headaches, but would present with **abnormal pituitary function** (elevated ACTH and cortisol). [1] *Prolactinoma* - A **pituitary tumor** that secretes excessive **prolactin**, causing symptoms like galactorrhea, amenorrhea (in women), and hypogonadism. - While it can cause headaches, it typically leads to **abnormal pituitary function** with elevated prolactin levels, which is not mentioned here. *Hypothyroidism* - A condition caused by **underproduction of thyroid hormones**, leading to symptoms like weight gain, fatigue, cold intolerance, and bradycardia. - While it can be associated with weight gain and some headaches, it does not typically cause **hypertension** as a primary symptom related to the thyroid, and would present with **abnormal thyroid function tests**, not normal pituitary function.

Q: Which is the most common cranial nerve involved in pituitary apoplexy?

Oculomotor nerve. ***Oculomotor nerve*** - The **oculomotor nerve (III)** runs along the cavernous sinus, in close proximity to the pituitary gland, making it highly vulnerable to compression or damage from an expanding pituitary tumor or hemorrhage. - Involvement typically presents with **ptosis**, **diplopia**, and a **dilated pupil**, which are common symptoms in pituitary apoplexy [1]. *Optic nerve* - While the **optic nerves (II)** can be affected in pituitary apoplexy due to superior extension of the mass, leading to visual field defects, it is less commonly involved than the oculomotor nerve. - Visual symptoms often present as **bitemporal hemianopsia** if the optic chiasm is compressed. *Facial nerve* - The **facial nerve (VII)** is located far from the pituitary gland and cavernous sinus, making its involvement in pituitary apoplexy extremely rare. - Damage to the facial nerve would typically result in **facial weakness** or **paralysis**, which is not a hallmark symptom of pituitary apoplexy. *Abducens nerve* - The **abducens nerve (VI)** traverses the cavernous sinus, but it is less frequently affected than the oculomotor nerve in pituitary apoplexy. - Involvement would cause **lateral gaze palsy** (inability to abduct the eye).

Question 1

The most common cause of severe hypercalcemia is

Accepted Answer

Malignancy

Answer

Vitamin D toxicity

Answer

Sarcoidosis

Answer

Chronic renal failure

Question 2

HAIR-AN syndrome consists of which of the following?

Accepted Answer

All of the options

Answer

Acanthosis nigricans

Answer

Insulin resistance

Answer

Hyperandrogenism

Question 3

During the evaluation of secondary amenorrhea in a 24-year-old woman, hyperprolactinemia is diagnosed. Which of the following conditions could cause increased circulating prolactin concentrations and amenorrhea in this patient?

Accepted Answer

Hypothyroidism

Answer

Stress

Answer

Eating disorders

Answer

Adrenal disorders

Question 4

In Swyer's syndrome, which of the following statements is true?

Accepted Answer

Increased FSH and LH

Answer

Testis is absent

Answer

Normal stature

Answer

Functional ovaries are absent

Question 5

All are true about primary hyperparathyroidism except which of the following?

Accepted Answer

Decreased calcium

Answer

Nephrolithiasis

Answer

Loss of lamina dura

Answer

Increased alkaline phosphatase

Question 6

In a patient with primary hypothyroidism, what is the expected hormonal profile?

Accepted Answer

Low T3, low T4, high TSH

Answer

High T3, high T4, high TSH

Answer

Low T3, low T4, low TSH

Answer

Normal T3, normal T4, high TSH

Question 7

Asymptomatic hypercalcemia in a 30-year-old young male is due to:

Accepted Answer

Primary hyperparathyroidism

Answer

Hypernephroma

Answer

Occult primary malignancy

Answer

Familial hypocalciuric hypercalcemia

Question 8

A 50-year-old man with advanced tuberculosis and signs of severe acute adrenal insufficiency should be treated immediately with a combination of:

Accepted Answer

Cortisol and fludrocortisone

Answer

Triamcinolone and dexamethasone

Answer

Dexamethasone and metyrapone

Answer

Aldosterone and fludrocortisone

Question 9

An obese female patient presented with hypertension, chronic headache, and normal pituitary function. The most likely diagnosis is

Accepted Answer

Empty Sella Syndrome

Answer

Cushing's disease

Answer

prolactinoma

Answer

Hypothyroidism

Question 10

Which is the most common cranial nerve involved in pituitary apoplexy?

Accepted Answer

Oculomotor nerve

Answer

Facial nerve

Answer

Optic nerve

Answer

Abducens nerve

Endocrinology — MCQs

Endocrinology — MCQs

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