Endocrinology Practice Questions

Q: What is the most common cause of a hypersecreting pituitary tumor?

Pituitary adenoma. **Explanation:** **1. Why Pituitary Adenoma is Correct:** Pituitary adenomas are benign neoplasms of the anterior pituitary gland and represent the most common cause of pituitary hormone hypersecretion [1]. These tumors are classified based on size (microadenomas 10mm) and hormone production [1]. The most common hyperfunctioning adenoma is a **Prolactinoma** [3], followed by Growth Hormone-secreting adenomas (causing Acromegaly) [2] and ACTH-secreting adenomas (causing Cushing’s Disease) [4]. **2. Why the Other Options are Incorrect:** * **B. Pituitary Carcinoma:** These are extremely rare. The diagnosis of a pituitary carcinoma requires the presence of systemic or cerebrospinal metastases, not just local invasion. * **C. Autoimmune disease:** Conditions like Lymphocytic Hypophysitis typically lead to **hypopituitarism** (hormone deficiency) due to the destruction of pituitary tissue, rather than hypersecretion. * **D. Transection of the pituitary stalk:** This results in the "Stalk Effect." While it causes a mild rise in Prolactin (due to loss of inhibitory dopamine from the hypothalamus), it causes a **deficiency** of all other anterior pituitary hormones and leads to Diabetes Insipidus (loss of ADH) [3]. It is not a cause of a hypersecreting tumor. **High-Yield Clinical Pearls for NEET-PG:** * **Most common secretory adenoma:** Prolactinoma [3]. * **Most common symptom of any macroadenoma:** Bitemporal hemianopia (due to compression of the optic chiasm) [1]. * **MEN 1 Syndrome:** Remember the "3 Ps"—Pituitary, Parathyroid, and Pancreatic tumors. * **Treatment of choice:** Transsphenoidal surgery is the gold standard for most [2], **except Prolactinomas**, where medical management with Dopamine agonists (Cabergoline/Bromocriptine) is the first-line treatment.

Q: What is the treatment for hyperprolactinemia?

Bromocriptine. The primary treatment for hyperprolactinemia is medical management using **Dopamine Agonists**. Prolactin secretion is under tonic inhibition by dopamine (the prolactin-inhibiting factor) produced in the hypothalamus [2]. **Bromocriptine** is a dopamine receptor agonist that mimics this inhibitory effect, effectively reducing prolactin levels and shrinking prolactin-secreting pituitary adenomas (prolactinomas) [1]. **Analysis of Options:** * **Bromocriptine (Correct):** It is a classic D2 receptor agonist. While **Cabergoline** is now the preferred first-line agent due to higher efficacy and fewer side effects, Bromocriptine remains a standard correct answer in exams and is preferred during pregnancy [1]. * **Estrogen (Incorrect):** Estrogens actually stimulate the lactotrophs in the pituitary and can increase prolactin levels. * **GnRH Analogue (Incorrect):** These are used to suppress the pituitary-gonadal axis in conditions like endometriosis or prostate cancer, but they do not treat hyperprolactinemia. In fact, hyperprolactinemia itself causes low GnRH [3]. * **Cimetidine (Incorrect):** This H2-receptor antagonist is a known **cause** of drug-induced hyperprolactinemia, not a treatment. **NEET-PG High-Yield Pearls:** 1. **Drug of Choice:** Cabergoline is superior to Bromocriptine (longer half-life, twice-weekly dosing). 2. **Hook Effect:** In very high prolactin levels, lab assays may show falsely low results; serial dilution is required for diagnosis. 3. **Indications for Surgery:** Transsphenoidal surgery is reserved for patients who are refractory to or intolerant of dopamine agonists, or those with rapidly progressive visual field defects [1]. 4. **Common Causes:** Always rule out pregnancy, hypothyroidism (high TRH stimulates prolactin), and drugs (antipsychotics, metoclopramide, verapamil) before diagnosing a prolactinoma [2].

Q: A 21-year-old lady presented with a history of tiredness, weight gain, depression, and excessive somnolence. What will NOT be seen in this patient?

Tachycardia. **Explanation:** The clinical presentation of tiredness, weight gain, depression, and excessive somnolence in a young female is a classic description of **Hypothyroidism** [1]. **Why Tachycardia is the correct answer:** In hypothyroidism, there is a generalized slowing of metabolic processes and a decrease in sympathetic activity. This leads to **Bradycardia** (a slow heart rate) rather than tachycardia. Tachycardia is a hallmark feature of *Hyperthyroidism*, where increased thyroid hormones upregulate beta-adrenergic receptors in the heart [1]. **Analysis of other options:** * **Hypertension:** While it may seem counterintuitive, hypothyroidism often causes **Diastolic Hypertension**. This occurs due to increased systemic vascular resistance and arterial stiffness, despite the low cardiac output. * **Delayed relaxation of tendon reflexes:** Also known as "Woltman’s sign," this is a classic physical finding in hypothyroidism. The slow relaxation phase (pseudomyotonia) is due to delayed calcium reuptake by the sarcoplasmic reticulum in muscles. * **Anemia:** Hypothyroidism is frequently associated with anemia. It can be normocytic (due to decreased erythropoietin), microcytic (due to associated menorrhagia or iron malabsorption), or macrocytic (due to associated Vitamin B12 deficiency in autoimmune cases like Hashimoto’s). **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause:** Hashimoto’s Thyroiditis (look for anti-TPO antibodies). * **Cardiac findings:** Bradycardia, pericardial effusion (low voltage ECG), and muffled heart sounds. * **Dermatological findings:** Non-pitting edema (Myxedema) and loss of the outer one-third of eyebrows (Queen Anne’s sign). * **Metabolic:** Hypercholesterolemia and hyponatremia are common laboratory findings [2].

Q: Which of the following statements is FALSE regarding Nelson's syndrome?

None of the above. ### Explanation: Nelson’s Syndrome **Concept Overview:** Nelson’s syndrome refers to the development of an aggressive, ACTH-secreting pituitary adenoma following a **bilateral adrenalectomy** (usually performed to treat Cushing’s disease) [1]. The underlying mechanism is the loss of negative feedback inhibition by cortisol on the hypothalamus and pituitary gland. Without cortisol to "brake" the system, pre-existing corticotroph microadenomas undergo rapid expansion and hypersecretion. **Why "None of the above" is correct:** All the options provided (A, B, and C) are classic, defining features of Nelson’s syndrome. Since the question asks for the **FALSE** statement, and all listed statements are true, "None of the above" is the correct choice. * **Pituitary tumor (Option B):** The hallmark of the syndrome is the enlargement of a corticotroph adenoma. These tumors are often locally invasive and can cause mass effect symptoms like bitemporal hemianopia. * **High ACTH levels (Option C):** Due to the lack of glucocorticoid feedback and the presence of a functional adenoma, ACTH levels are extremely elevated [1]. * **Skin pigmentation (Option A):** High levels of ACTH (and its precursor POMC) stimulate melanocortin-1 receptors on melanocytes, leading to progressive, intense hyperpigmentation. **NEET-PG High-Yield Pearls:** * **Trigger:** Occurs only after **bilateral adrenalectomy** [1]. * **Clinical Presentation:** Hyperpigmentation + Visual field defects + Headache. * **Diagnosis:** Rising plasma ACTH levels and MRI evidence of an enlarging pituitary mass. * **Prevention:** Modern management of Cushing’s disease (Pituitary surgery/Radiotherapy) has made Nelson’s syndrome rare. * **Treatment:** Surgical resection of the pituitary tumor or radiotherapy.

Q: Which clinical features are characteristic of congenital adrenal hyperplasia?

All of the above. **Explanation:** Congenital Adrenal Hyperplasia (CAH) is a group of autosomal recessive disorders caused by a deficiency in enzymes required for cortisol synthesis [1]. The clinical presentation depends on the specific enzyme deficiency, most commonly **21-hydroxylase deficiency (90% of cases)**. 1. **Female Pseudohermaphroditism (Option A):** In 21-hydroxylase and 11̢β-hydroxylase deficiencies, the blockage of the cortisol pathway shunts precursors toward androgen production. Excess adrenal androgens in utero lead to virilization of female fetuses (ambiguous genitalia), while internal female organs (ovaries/uterus) remain normal. 2. **Hypertension (Option B):** While 21-hydroxylase deficiency causes hypotension, **11β-hydroxylase** and **17α-hydroxylase** deficiencies lead to the accumulation of mineralocorticoid precursors (like 11-deoxycorticosterone). This causes sodium retention and hypertension. 3. **Electrolyte Imbalance (Option C):** In the "salt-wasting" form of 21-hydroxylase deficiency, the lack of aldosterone leads to hyponatremia, hyperkalemia, and metabolic acidosis. Conversely, in hypertensive forms, hypokalemia may occur. Since CAH encompasses various enzymatic defects that can manifest with any of these features, **"All of the above"** is the correct choice. **High-Yield NEET-PG Pearls:** * **Most Common Cause:** 21-hydroxylase deficiency (Marker: Elevated **17-OH Progesterone**). * **The "Rule of 1s":** If the enzyme starts with **1** (11β, 17α), it causes hypertension. If it ends with **1** (21, 11β), it causes virilization (except 17α, which causes sexual infantilism). * **Treatment:** Glucocorticoids (to suppress ACTH and reduce androgen production) and mineralocorticoids if salt-wasting is present.

Q: Which of the following is NOT typically seen in hemochromatosis?

Desferrioxamine is the treatment of choice. Hereditary Hemochromatosis (HH) is an autosomal recessive disorder characterized by excessive intestinal iron absorption, leading to iron deposition in various organs. **Why Option D is the correct answer (False statement):** The treatment of choice for hereditary hemochromatosis is **therapeutic phlebotomy**, not chelation [1]. Phlebotomy is more effective, less toxic, and cheaper for removing iron in HH. **Desferrioxamine** (an iron chelator) is reserved for patients with secondary hemochromatosis (e.g., Thalassemia major) where phlebotomy is contraindicated due to anemia, or in cases of severe iron-overload cardiomyopathy. **Analysis of Incorrect Options:** * **A. Hypogonadism:** This is the most common endocrinopathy in HH. It is usually **hypogonadotropic hypogonadism** caused by iron deposition in the anterior pituitary (gonadotrophs), leading to decreased libido and impotence [2]. * **B. Arthropathy:** Occurs in ~50% of patients. It characteristically involves the **2nd and 3rd metacarpophalangeal (MCP) joints** and is often associated with calcium pyrophosphate deposition (pseudogout). * **C. Bronze Diabetes:** This refers to the classic triad of hyperpigmentation (due to melanin and iron deposition) and diabetes mellitus (due to iron deposition in pancreatic beta cells) [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Gene Mutation:** Most commonly the **HFE gene (C282Y mutation)** on Chromosome 6 [2]. * **Screening:** Best initial test is **Transferrin Saturation** (>45% is suggestive). * **Gold Standard:** Liver biopsy (to assess cirrhosis and calculate the Hepatic Iron Index) [1]. * **MRI:** MRI T2* is the non-invasive method of choice to quantify hepatic and cardiac iron [1]. * **Early Sign:** "Hook-like" osteophytes on X-ray of the MCP joints.

Question 1

What is the most common cause of a hypersecreting pituitary tumor?

Accepted Answer

Pituitary adenoma

Answer

Pituitary carcinoma

Answer

Autoimmune disease of the pituitary

Answer

Transection of the pituitary stalk

Question 2

What is the treatment for hyperprolactinemia?

Accepted Answer

Bromocriptine

Answer

Estrogen

Answer

GnRH analogue

Answer

Cimetidine

Question 3

A 36-year-old female, asymptomatic but with raised 24-hour urinary cortisol levels and raised ACTH, shows suppression in a high-dose dexamethasone suppression test. MRI of the head reveals no enlargement of the pituitary gland. What should be the next step in this case?

Accepted Answer

Inferior petrosal sinus venous sampling

Answer

MRI to assess the adrenals

Answer

CT of the chest

Answer

Corticotropin-releasing hormone (CRH) levels

Question 4

A 35-year-old female with children aged 5 and 6 years presents with amenorrhea and galactorrhea. Blood examination reveals increased prolactin. What is the most likely finding on CT of the head?

Accepted Answer

Pituitary adenoma

Answer

Craniopharyngioma

Answer

Sheehan's syndrome

Answer

Pinealoma

Question 5

Thyrotoxicosis not associated with hyperthyroidism is caused by all EXCEPT?

Accepted Answer

TSH-secreting pituitary adenoma

Answer

Factitious thyrotoxicosis

Answer

Granulomatous thyroiditis

Answer

Struma ovarii

Question 6

A 21-year-old lady presented with a history of tiredness, weight gain, depression, and excessive somnolence. What will NOT be seen in this patient?

Accepted Answer

Tachycardia

Answer

Hypertension

Answer

Delayed relaxation of tendon reflexes

Answer

Anemia

Question 7

Which of the following statements is FALSE regarding Nelson's syndrome?

Accepted Answer

None of the above

Answer

Skin pigmentation

Answer

Pituitary tumor

Answer

High ACTH levels

Question 8

Which clinical features are characteristic of congenital adrenal hyperplasia?

Accepted Answer

All of the above

Answer

Female pseudohermaphroditism

Answer

Hypertension

Answer

Electrolyte imbalance

Question 9

Which of the following conditions is associated with hypocalcemia?

Accepted Answer

Both Medullary carcinoma of the thyroid and Tumor lysis syndrome

Answer

Medullary carcinoma of the thyroid

Answer

Squamous cell carcinoma of the lung

Answer

Tumor lysis syndrome

Question 10

Which of the following is NOT typically seen in hemochromatosis?

Accepted Answer

Desferrioxamine is the treatment of choice

Answer

Hypogonadism

Answer

Arthropathy

Answer

Bronze diabetes

Endocrinology — MCQs

Endocrinology — MCQs

On this page

Practice by Chapter

Want unlimited practice?