Endocrinology Practice Questions

Q: Which of the following tumors can secrete erythropoietin?

All of the above. The correct answer is **D. All of the above**. This question tests the concept of **Paraneoplastic Syndromes**, specifically the ectopic production of **Erythropoietin (EPO)**, which leads to secondary polycythemia (erythrocytosis). [1] **Underlying Medical Concept:** While EPO is physiologically produced by the peritubular interstitial cells of the kidney (and the liver in the fetus), certain tumors can undergo "ectopic" hormone production [2]. When these tumors secrete EPO, it stimulates the bone marrow to increase red blood cell production, resulting in an elevated hematocrit and hemoglobin level. **Analysis of Options:** * **Renal Cell Carcinoma (RCC):** This is the most common tumor associated with ectopic EPO production. It is a classic paraneoplastic manifestation of RCC [1]. * **Hepatoma (Hepatocellular Carcinoma):** The liver retains the genetic machinery for EPO production from fetal life; malignancy can reactivate this pathway [1]. * **Cerebellar Hemangioblastoma:** This is a high-yield association, often seen in **Von Hippel-Lindau (VHL) syndrome**. These vascular tumors are well-known secretors of EPO [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for EPO-secreting tumors (Potentially Really High Hematocrit):** **P**heochromocytoma, **R**enal Cell Carcinoma, **H**epatoma, **H**emangioblastoma (Cerebellar), and **U**terine Fibroids (Leiomyoma) [1]. * **Differential Diagnosis:** To distinguish secondary polycythemia (due to tumors) from **Polycythemia Vera**, check the serum EPO level. In Polycythemia Vera, EPO is **low**; in tumor-induced erythrocytosis, EPO is **high**. * **VHL Syndrome:** Always screen for RCC and Pheochromocytoma if a patient presents with a Cerebellar Hemangioblastoma.

Q: A 22-year-old woman presents with recent onset of hirsutism and voice changes. What is the most appropriate initial investigation?

Blood testosterone levels. **Explanation:** The clinical presentation of **rapid-onset hirsutism** accompanied by **virilization** (voice changes/deepening) in a young woman is highly suggestive of an androgen-secreting tumor (ovarian or adrenal). In such cases, the initial step is to document biochemical hyperandrogenism. **1. Why Blood Testosterone is correct:** Serum **Total Testosterone** is the most appropriate initial screening test to assess the severity of androgen excess [1]. Very high levels (>200 ng/dL) are strongly indicative of an androgen-secreting neoplasm [1]. While DHEAS is also measured to rule out adrenal sources, testosterone remains the primary marker for overall androgen status in the initial workup of virilization. **2. Why other options are incorrect:** * **Urine 17-ketosteroids:** This is an obsolete test. It measures metabolites of weak adrenal androgens but is non-specific and has been replaced by more accurate serum assays like DHEAS and Testosterone. * **Blood FSH and LH levels:** These are useful in diagnosing PCOS (where the LH:FSH ratio may be elevated) or primary ovarian failure [1], but they do not help in the direct evaluation of virilizing symptoms. * **Blood Thyroxine and TSH:** While thyroid dysfunction can cause menstrual irregularities, it does not cause virilization or significant hirsutism. **Clinical Pearls for NEET-PG:** * **Rapid progression + Virilization** (clitoromegaly, deepening of voice, male-pattern baldness) = Suspect **Tumor**. * **Gradual onset + Menstrual irregularity** = Suspect **PCOS**. * If Testosterone is >200 ng/dL, perform a Pelvic USG/CT to look for an **Ovarian tumor** (e.g., Sertoli-Leydig cell tumor) [1]. * If DHEAS is >700 µg/dL, perform an Abdominal CT to look for an **Adrenal tumor** [1].

Q: All are true about primary aldosteronism except:

Hyperkalemia.. **Explanation:** **Primary Aldosteronism (Conn’s Syndrome)** is characterized by the autonomous overproduction of aldosterone from the adrenal cortex, independent of the renin-angiotensin system. **Why "Hyperkalemia" is the correct (false) statement:** Aldosterone acts on the principal cells of the renal collecting ducts to reabsorb sodium and **excrete potassium and hydrogen ions** [1]. Consequently, the hallmark of primary aldosteronism is **Hypokalemia**, not hyperkalemia [3]. It is important to note that many patients may actually be normokalemic, but they never present with hyperkalemia unless there is concurrent renal failure. **Analysis of other options:** * **Option A:** Primary aldosteronism is indeed the **most common cause of secondary hypertension**, accounting for approximately 5–10% of all hypertensive patients. * **Option C:** Aldosterone causes **sodium retention** by upregulating ENaC channels. While this leads to volume expansion and hypertension, clinical edema is rarely seen due to the "Aldosterone Escape" phenomenon (atrial natriuretic peptide-mediated diuresis) [2]. * **Option D:** The **ARR (Aldosterone-to-Renin Ratio)** is the gold-standard screening test. In primary disease, aldosterone is high while renin is suppressed (due to feedback inhibition), leading to a high ratio (typically >20-30). **NEET-PG High-Yield Pearls:** * **Most common cause:** Adrenal Adenoma (Conn’s Syndrome) > Bilateral Adrenal Hyperplasia. * **Acid-Base Status:** Metabolic alkalosis (due to H+ excretion) [3]. * **Confirmatory Test:** Saline infusion test (failure to suppress aldosterone) or Oral salt loading. * **Treatment:** Spironolactone/Eplerenone (Medical) or Unilateral Adrenalectomy (Surgical).

Q: A 15-year-old girl has been losing weight and exercising vigorously. She feels overweight and wants to lose more weight. On examination, she is thin with muscle wasting. Which of the following physical signs is also suggestive of the diagnosis?

Salivary gland enlargement. **Explanation:** The clinical presentation of a 15-year-old girl with weight loss, vigorous exercise, and a distorted body image (feeling overweight despite being thin) is highly suggestive of **Anorexia Nervosa**. [1] **Why Salivary Gland Enlargement is Correct:** In patients with eating disorders, particularly those who engage in self-induced vomiting (purging subtype), **bilateral painless enlargement of the parotid glands (Sialadenosis)** is a classic physical sign. This occurs due to hypertrophy of the acinar cells, likely triggered by repeated stimulation of the autonomic nervous system during vomiting or nutritional deficiencies. **Analysis of Incorrect Options:** * **B. Coarse body hair:** Patients with anorexia nervosa typically develop **Lanugo hair**—fine, downy, soft hair on the back and arms—as a physiological response to conserve body heat in the absence of insulating fat. Coarse hair is more characteristic of hypothyroidism or PCOS. * **C. Diarrhea:** Anorexia is associated with slowed gastrointestinal motility and decreased intake, leading to **constipation**, not diarrhea. [2] * **D. Tachycardia:** Malnutrition and starvation lead to a hypometabolic state and increased vagal tone, resulting in **bradycardia** and hypotension. [2] Tachycardia would be an unusual finding unless the patient is severely dehydrated or in heart failure. **NEET-PG High-Yield Pearls:** * **Russell’s Sign:** Calluses or scars on the knuckles from self-induced vomiting. * **Electrolyte Abnormalities:** Hypokalemic hypochloremic metabolic alkalosis (due to vomiting). * **Endocrine Profile:** Low FSH, LH, and Estrogen (leading to amenorrhea); "Sick Euthyroid" syndrome (low T3); and elevated Cortisol levels. * **Most common cause of death:** Cardiac arrhythmias (due to electrolyte imbalance) or suicide.

Q: Which of the following is NOT a component of Werner's syndrome?

Adrenal. Werner’s syndrome, also known as **Multiple Endocrine Neoplasia Type 1 (MEN1)**, is an autosomal dominant disorder caused by a mutation in the *MEN1* gene (encoding the protein menin). [1] It is classically characterized by the **"3 Ps"**: **P**arathyroid, **P**ancreas, and **P**ituitary. * **Why Adrenal is the correct answer:** While adrenal cortical lesions (like adenomas or hyperplasia) can occasionally occur in MEN1 patients, they are **not** considered a primary or defining component of the syndrome. In the context of MEN syndromes, the **Adrenal Medulla** (Pheochromocytoma) is a hallmark of **MEN 2A and 2B**, not MEN 1. * **Why other options are incorrect:** * **Parathyroid (Option C):** This is the most common feature (95% of cases). It typically presents as multiglandular hyperplasia leading to primary hyperparathyroidism. * **Pancreas (Option D):** Enteropancreatic neuroendocrine tumors (NETs) occur in about 40-70% of patients. Gastrinomas (leading to Zollinger-Ellison Syndrome) and Insulinomas are the most frequent. * **Pituitary (Option A):** Anterior pituitary adenomas occur in about 30-40% of cases, with Prolactinomas being the most common subtype. **High-Yield Clinical Pearls for NEET-PG:** 1. **Inheritance:** Autosomal Dominant; Gene located on **Chromosome 11q13**. 2. **Most common initial presentation:** Hypercalcemia due to Hyperparathyroidism. 3. **MEN 2A (Sipple Syndrome):** Medullary Thyroid Carcinoma (MTC), Pheochromocytoma, Parathyroid hyperplasia. 4. **MEN 2B (Williams-Pollock Syndrome):** MTC, Pheochromocytoma, Mucosal neuromas, and Marfanoid habitus. 5. **Memory Aid:** Remember the "3 Ps" for MEN 1 and "MPH" (Medullary, Pheo, Hyperparathyroid) for MEN 2A.

Q: All are TRUE about the management of Humoral hypercalcemia of malignancy (HHM), EXCEPT:

Steroids are not useful. Humoral Hypercalcemia of Malignancy (HHM) is primarily mediated by the secretion of **Parathyroid Hormone-related Protein (PTHrP)** from solid tumors (e.g., squamous cell carcinoma of the lung, renal cell carcinoma) [2]. PTHrP stimulates osteoclastic bone resorption and renal calcium reabsorption. **Why Option D is the Correct Answer (The "Except"):** Steroids (Glucocorticoids) are generally **not useful** in HHM because PTHrP-mediated hypercalcemia does not involve increased Vitamin D production. However, steroids are highly effective in hypercalcemia caused by **lymphomas, sarcoidosis, or Vitamin D toxicity**, where they inhibit the 1-alpha-hydroxylase enzyme. In the context of HHM, saying they are "not useful" is a clinical fact, making it the correct "Except" choice. **Analysis of Other Options:** * **Option A (Oral Phosphorus):** While not first-line for severe cases, oral phosphorus can be used initially in mild hypercalcemia to inhibit bone resorption and promote calcium deposition in bone, provided renal function is adequate. * **Option B (Saline Rehydration):** This is the **initial step** in management. Isotonic saline (0.9% NaCl) restores extracellular fluid volume and promotes urinary calcium excretion (calciuresis). * **Option C (Bisphosphonates):** IV Bisphosphonates (e.g., **Zoledronic acid**, Pamidronate) are the **most effective** long-term treatment for HHM as they potentally inhibit osteoclast activity [1]. **High-Yield NEET-PG Pearls:** * **Most common cause of HHM:** PTHrP secretion (80% of cases). * **Drug of choice for acute management:** Aggressive IV Saline rehydration. * **Most potent Bisphosphonate:** Zoledronic acid. * **Calcitonin:** Used for rapid, short-term reduction of calcium (works within hours) but develops tachyphylaxis (stops working) after 48 hours. * **Denosumab:** A monoclonal antibody against RANKL used in bisphosphonate-refractory hypercalcemia.

Q: All of the following are true about Hashimoto thyroiditis EXCEPT:

EEG is normal. This question refers to **Hashimoto’s Encephalopathy (HE)**, also known as **Steroid-Responsive Encephalopathy associated with Autoimmune Thyroiditis (SREAT)**. This is a rare neuroendocrine syndrome characterized by high titers of anti-thyroid antibodies (Anti-TPO or Anti-Tg) and neuropsychiatric symptoms, occurring independently of the patient's actual thyroid functional status (patients can be euthyroid). **Why Option D is the correct answer:** In Hashimoto’s Encephalopathy, the **EEG is characteristically abnormal** in approximately 90-95% of cases. The most common finding is non-specific **generalized slowing** (delta or theta waves), though periodic sharp wave complexes or triphasic waves may also be seen. Therefore, the statement that the EEG is normal is false. **Analysis of incorrect options:** * **A & B (Myoclonus and Seizures):** These are classic clinical manifestations of HE. Patients often present with a "stroke-like" relapsing-remitting course or a diffuse progressive course involving tremors, myoclonus, and generalized tonic-clonic seizures. * **C (Steroid responsive):** This is the hallmark of the condition. Most patients show dramatic clinical improvement within 24–72 hours of starting high-dose intravenous corticosteroids (e.g., Methylprednisolone). **NEET-PG High-Yield Pearls:** * **Antibody Marker:** Anti-TPO (Thyroid Peroxidase) antibodies are almost always elevated. * **Thyroid Status:** Most patients are clinically euthyroid or only mildly hypothyroid at presentation. * **CSF Findings:** Often shows elevated protein levels with normal cell counts (albuminocytologic dissociation). * **Imaging:** Brain MRI is frequently normal or shows non-specific white matter changes, making EEG a more sensitive (though non-specific) diagnostic tool.

Q: Metyrapone inhibits which of the following enzymes?

11-β-hydroxylase. **Explanation:** **1. Mechanism of Action (Why A is correct):** Metyrapone is a potent inhibitor of the enzyme **11-β-hydroxylase** (*CYP11B1*). This enzyme is responsible for the final step of cortisol synthesis: converting 11-deoxycortisol into cortisol [1]. By blocking this enzyme, metyrapone causes a decrease in plasma cortisol levels. This reduction triggers a compensatory increase in ACTH secretion (via the negative feedback loop), which in turn leads to an accumulation of the precursor **11-deoxycortisol**. **2. Analysis of Incorrect Options:** * **Option B (21-β-hydroxylase):** This enzyme converts Progesterone to 11-deoxycorticosterone (DOC) [3]. Deficiency of this enzyme is the most common cause of Congenital Adrenal Hyperplasia (CAH), but it is not the target of Metyrapone [3]. * **Option C & D:** Since Metyrapone is highly selective for 11-β-hydroxylase, these options are incorrect. **3. Clinical Pearls for NEET-PG:** * **Metyrapone Stimulation Test:** Used to assess the integrity of the Hypothalamic-Pituitary-Adrenal (HPA) axis [2]. In a normal response, blocking cortisol should lead to a rise in ACTH and 11-deoxycortisol. A failure of 11-deoxycortisol to rise suggests pituitary or hypothalamic insufficiency. * **Therapeutic Use:** It is used for the medical management of **Cushing’s Syndrome** (especially when surgery is contraindicated) to control hypercortisolism. * **Side Effects:** Because it blocks the final step of cortisol but not the androgen pathway, it can cause **hirsutism** (due to androgen excess) and **hypertension** (due to the mineralocorticoid effects of accumulated 11-deoxycortisol). * **Pregnancy:** Metyrapone is the drug of choice for treating Cushing’s syndrome in pregnancy.

Q: Lab investigations of a patient show low T4 and elevated TSH. Which of the following is the most likely diagnosis?

Hashimoto's disease. ### Explanation **Core Concept: Primary Hypothyroidism** The laboratory profile of **low T4 (thyroxine)** and **elevated TSH (Thyroid Stimulating Hormone)** is the hallmark of **Primary Hypothyroidism** [1]. In this condition, the thyroid gland itself is failing to produce hormones. Due to the loss of negative feedback on the pituitary gland, TSH secretion increases significantly to compensate [1]. **Why Hashimoto’s Disease is Correct:** Hashimoto’s thyroiditis is the most common cause of primary hypothyroidism in iodine-sufficient regions [1]. It is an autoimmune destruction of the thyroid gland. Because the pathology resides in the gland, T4 is low and TSH is high. **Analysis of Incorrect Options:** * **Graves’ Disease:** This is a cause of *hyperthyroidism*. It presents with **high T4** and **suppressed (low) TSH** due to thyroid-stimulating antibodies [1]. * **Pituitary Failure (Secondary Hypothyroidism):** If the pituitary fails, it cannot produce TSH. Therefore, the labs would show **low T4** and **low or inappropriately normal TSH** [1]. * **Hypothalamic Failure (Tertiary Hypothyroidism):** Similar to pituitary failure, a lack of TRH leads to **low T4** and **low TSH** [1]. **NEET-PG High-Yield Pearls:** * **Most sensitive initial test** for thyroid function: **Serum TSH**. * **Subclinical Hypothyroidism:** Elevated TSH with **normal** Free T4 levels [1]. * **Antibody Marker:** Anti-TPO (Thyroid Peroxidase) antibodies are positive in >90% of Hashimoto’s cases. * **Histology Hint:** Look for **Hurthle cells** (Askanazy cells) and lymphocytic infiltration with germinal centers on biopsy.

Question 1

Which of the following tumors can secrete erythropoietin?

Accepted Answer

All of the above

Answer

Cerebellar hemangioblastoma

Answer

Hepatoma

Answer

Renal cell carcinoma

Question 2

A 22-year-old woman presents with recent onset of hirsutism and voice changes. What is the most appropriate initial investigation?

Accepted Answer

Blood testosterone levels

Answer

Urine 17-ketosteroids

Answer

Blood FSH and LH levels

Answer

Blood thyroxine and TSH levels

Question 3

All are true about primary aldosteronism except:

Accepted Answer

Hyperkalemia.

Answer

It is one of the most common causes of secondary hypertension.

Answer

Sodium retention.

Answer

Ratio of plasma aldosterone to plasma renin activity (PA/PRA) is a useful screening test.

Question 4

A 15-year-old girl has been losing weight and exercising vigorously. She feels overweight and wants to lose more weight. On examination, she is thin with muscle wasting. Which of the following physical signs is also suggestive of the diagnosis?

Accepted Answer

Salivary gland enlargement

Answer

Coarse body hair

Answer

Diarrhea

Answer

Tachycardia

Question 5

Which of the following is NOT a component of Werner's syndrome?

Accepted Answer

Adrenal

Answer

Pituitary

Answer

Parathyroid

Answer

Pancreas

Question 6

All are TRUE about the management of Humoral hypercalcemia of malignancy (HHM), EXCEPT:

Accepted Answer

Steroids are not useful

Answer

Oral phosphorus initially

Answer

Saline rehydration is used

Answer

Bisphosphonates are very effective

Question 7

All of the following are true about Hashimoto thyroiditis EXCEPT:

Accepted Answer

EEG is normal

Answer

Myoclonus

Answer

Seizures

Answer

Steroid responsive encephalopathy

Question 8

Metyrapone inhibits which of the following enzymes?

Accepted Answer

11-β-hydroxylase

Answer

21-β-hydroxylase

Answer

Both

Answer

None

Question 9

Lab investigations of a patient show low T4 and elevated TSH. Which of the following is the most likely diagnosis?

Accepted Answer

Hashimoto's disease

Answer

Graves' disease

Answer

Pituitary failure

Answer

Hypothalamic failure

Question 10

A patient has a pituitary tumor, specifically a prolactinoma, that encircles the carotid artery. What is the best line of management?

Accepted Answer

Transsphenoidal surgical resection

Answer

Observation

Answer

Radiotherapy

Answer

Medical management with dopamine agonists

Endocrinology — MCQs

Endocrinology — MCQs

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