Endocrinology — MCQs
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A 20-year-old male is admitted to the ICU for diabetic ketoacidosis (DKA). His mother reports increased thirst and frequent urination recently. He has no prior diabetes diagnosis and no family history of diabetes. His BMI is 42 kg/m2. Anti-GAD antibodies and anti-islet cell antibodies (ICA) are not detected. Which of the following statements is true regarding this patient?
Malignancy associated hypercalcemia is most commonly due to which of the following mechanisms?
A 30-year-old female presents with a need to progressively buy larger and wider shoes and cannot wear any of her rings because they are too small. A physical examination shows a prominent brow, protruding lower jaw, and spaces between all of her teeth. This woman may have a tumor in which one of the following organs or tissues?
What condition is caused by neurotensinoma?
All of the following are associated with Primary aldosteronism EXCEPT?
What is the most common cause of hyperparathyroidism?
Cushing's disease typically presents with which of the following hormonal changes?
A 50-year-old obese female presents with recurrent candidal urinary infections and excessive thirst. She also reports frequent nighttime urination. What is the initial diagnostic test you would prefer for this patient?
Necrobiosis lipoidica is seen in which condition?
Which of the following is not seen in Secondary Adrenal insufficiency?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 671: A 20-year-old male is admitted to the ICU for diabetic ketoacidosis (DKA). His mother reports increased thirst and frequent urination recently. He has no prior diabetes diagnosis and no family history of diabetes. His BMI is 42 kg/m2. Anti-GAD antibodies and anti-islet cell antibodies (ICA) are not detected. Which of the following statements is true regarding this patient?
- A. Due to the young age of onset, type 1 diabetes is suspected.
- B. Because of the presentation with diabetic ketoacidosis, type 1 diabetes is suspected.
- C. The patient has maturity-onset diabetes of the young.
- D. The patient has type 2 diabetes mellitus. (Correct Answer)
Explanation: ### Explanation The correct answer is **D. The patient has type 2 diabetes mellitus.** This patient presents with **Ketosis-Prone Type 2 Diabetes (KPD)**, also known as "Flatbush Diabetes." While DKA is classically associated with Type 1 Diabetes (T1DM), it is increasingly seen in patients with Type 2 Diabetes (T2DM), particularly those with obesity [1]. **Why Option D is correct:** The diagnosis of T2DM is supported by the patient’s **high BMI (42 kg/m²)** and the **absence of pancreatic autoantibodies** (Anti-GAD and ICA). In KPD, patients present with acute insulin deficiency (leading to DKA), often triggered by glucose toxicity which suppresses beta-cell function [1]. With treatment, they later regain significant beta-cell function and can often be managed with oral hypoglycemic agents rather than lifelong insulin [1]. **Why other options are incorrect:** * **Option A & B:** While young age and DKA are "textbook" features of T1DM [2], the presence of morbid obesity and negative autoantibodies strongly point toward T2DM. DKA is no longer considered pathognomonic for T1DM [1]. * **Option C:** Maturity-Onset Diabetes of the Young (MODY) typically presents in non-obese individuals with a strong autosomal dominant family history [3]. This patient has no family history and a high BMI, making MODY unlikely. ### Clinical Pearls for NEET-PG: * **Antibody Testing:** Negative Anti-GAD, ICA, and IA-2 antibodies in a patient with DKA should raise suspicion for Ketosis-Prone T2DM. * **AB Classification:** KPD is often classified using the "Aβ" system (A: Autoantibodies; β: Beta-cell function). This patient fits the **A-β+** category (Antibody negative, preserved beta-cell function). * **Management:** After resolving the initial DKA with insulin, these patients should be re-evaluated for transition to oral drugs (like Metformin) once glucose toxicity resolves [1].
Question 672: Malignancy associated hypercalcemia is most commonly due to which of the following mechanisms?
- A. Tumor lysis syndrome
- B. Parathyroid hormone-related peptide production (Correct Answer)
- C. Interleukin-7 (IL-7) production
- D. Insulin-like growth factor binding protein (IGF-BP) production
Explanation: **Explanation:** Hypercalcemia of malignancy (HCM) is the most common cause of hypercalcemia in hospitalized patients. It occurs via four distinct mechanisms, but the most frequent is **Humoral Hypercalcemia of Malignancy (HHM)**. **Why Option B is Correct:** Approximately **80% of cases** of HCM are caused by the secretion of **Parathyroid Hormone-related Peptide (PTHrP)** by tumor cells [2]. PTHrP mimics the action of PTH by binding to the PTH-1 receptor in bones (increasing osteoclast activity) and kidneys (increasing calcium reabsorption) [1]. It is most commonly associated with **Squamous cell carcinomas** (lung, head, and neck), renal, and breast cancers [3]. Unlike true hyperparathyroidism, PTH levels in these patients are suppressed [3]. **Why Other Options are Incorrect:** * **Option A (Tumor Lysis Syndrome):** This typically causes **hypocalcemia** (due to phosphate release binding with calcium) and hyperuricemia, not hypercalcemia. * **Option C (IL-7):** While cytokines like IL-1, IL-6, and TNF-alpha (Osteoclast Activating Factors) contribute to local osteolytic hypercalcemia (common in Multiple Myeloma), IL-7 is not a primary mediator of malignancy-associated hypercalcemia. * **Option D (IGF-BP):** These proteins regulate growth factor activity but do not play a direct role in calcium homeostasis or the pathogenesis of HCM. **High-Yield Clinical Pearls for NEET-PG:** 1. **Most common mechanism:** PTHrP production (80%). 2. **Second most common mechanism:** Local osteolytic hypercalcemia (20%), seen in Multiple Myeloma and breast cancer bone metastases. 3. **Rare mechanism:** 1,25-dihydroxyvitamin D production (seen in Lymphomas) [3]. 4. **Laboratory findings in HHM:** High Calcium, Low PTH, Low 1,25-(OH)₂D (usually), and High PTHrP. 5. **Treatment of choice:** Aggressive IV hydration (Normal Saline) followed by IV Bisphosphonates (e.g., Zoledronic acid).
Question 673: A 30-year-old female presents with a need to progressively buy larger and wider shoes and cannot wear any of her rings because they are too small. A physical examination shows a prominent brow, protruding lower jaw, and spaces between all of her teeth. This woman may have a tumor in which one of the following organs or tissues?
- A. Hypothalamus (Correct Answer)
- B. Bone marrow
- C. Adrenal glands
- D. Pancreas
Explanation: ### Explanation **Correct Option: A (Hypothalamus)** The clinical presentation describes classic **Acromegaly**, characterized by acral enlargement (increased shoe/ring size), frontal bossing (prominent brow), macrognathia (protruding jaw), and teeth spacing (diastema). While most cases of acromegaly are caused by a Growth Hormone (GH)-secreting pituitary adenoma [1], the question asks for the source of a tumor that could cause this syndrome. In rare instances, **ectopic secretion of Growth Hormone-Releasing Hormone (GHRH)** can lead to somatotroph hyperplasia and secondary acromegaly [3]. The **hypothalamus** is a primary site for GHRH production [2]. A hypothalamic gangliocytoma or hamartoma secreting GHRH can result in the clinical features described. **Analysis of Incorrect Options:** * **B. Bone marrow:** Bone marrow disorders (like multiple myeloma or leukemias) do not cause soft tissue or bony overgrowth characteristic of GH excess. * **C. Adrenal glands:** Adrenal tumors typically present with Cushing’s syndrome (cortisol), Conn’s syndrome (aldosterone), or virilization (androgens), none of which cause acral enlargement [4]. * **D. Pancreas:** While pancreatic neuroendocrine tumors (NETs) can rarely secrete ectopic GHRH or GH, the hypothalamus is a more direct physiological source of GHRH in the context of neuroendocrine regulation. **NEET-PG High-Yield Pearls:** * **Best Initial Test:** Serum IGF-1 levels (more stable than GH) [1]. * **Gold Standard/Confirmatory Test:** Oral Glucose Tolerance Test (OGTT) with GH measurement; failure to suppress GH <1 ng/mL is diagnostic [1]. * **Most Common Cause:** Pituitary Adenoma (Somatotroph adenoma) [3]. * **Ectopic GHRH Sources:** Hypothalamic tumors, Bronchial carcinoid, and Pancreatic NETs. * **Associated Conditions:** Often associated with MEN-1 syndrome (Pituitary, Parathyroid, Pancreas).
Question 674: What condition is caused by neurotensinoma?
- A. Cyanosis
- B. Hypertension
- C. Hyperkalemia
- D. None of the above (Correct Answer)
Explanation: A **neurotensinoma** is an extremely rare functional pancreatic neuroendocrine tumor (pNET) that secretes excessive amounts of the peptide **neurotensin**. While neurotensin has several physiological effects, most neurotensinomas are clinically "silent" because the peptide does not produce a distinct, consistent clinical syndrome in humans. [1] **Why "None of the above" is correct:** The primary clinical features associated with neurotensinoma (when present) are **weight loss, diarrhea, and skin flushing**. None of the symptoms listed in the options (cyanosis, hypertension, or hyperkalemia) are characteristic of this tumor. **Analysis of Incorrect Options:** * **A. Cyanosis:** Neurotensinomas may cause flushing (redness), but they do not cause cyanosis (bluish discoloration), which is typically related to deoxygenated hemoglobin or shunting. * **B. Hypertension:** Neurotensin actually acts as a **vasodilator**; therefore, it is more likely to cause hypotension (low blood pressure) rather than hypertension. * **C. Hyperkalemia:** There is no established link between neurotensin and elevated potassium levels. In fact, some pNETs (like VIPomas) are famously associated with *hypokalemia*. **NEET-PG High-Yield Pearls:** * **Diagnosis:** Elevated plasma neurotensin levels (often >250 pmol/L). * **Location:** Most neurotensinomas are found in the **head of the pancreas** and are often large and metastatic at the time of diagnosis. [1] * **Association:** They can occur sporadically or as part of **MEN-1 syndrome**. * **Differential:** If a question mentions "Watery Diarrhea, Hypokalemia, and Achlorhydria (WDHA)," think **VIPoma** (Verner-Morrison Syndrome), not neurotensinoma.
Question 675: All of the following are associated with Primary aldosteronism EXCEPT?
- A. Hypokalaemia
- B. Postural hypotension (Correct Answer)
- C. Hypernatremia
- D. Metabolic alkalosis
Explanation: In **Primary Aldosteronism (Conn’s Syndrome)**, there is autonomous overproduction of aldosterone from the adrenal cortex (usually due to an adrenal adenoma or bilateral hyperplasia) [1]. ### **Why Postural Hypotension is the Correct Answer** Primary aldosteronism is characterized by **volume expansion** and **hypertension** due to excessive sodium and water reabsorption in the distal renal tubules [1]. Because the patient is in a state of chronic volume overload, they do not experience postural hypotension (a drop in blood pressure upon standing). In fact, patients with primary aldosteronism often have resistant hypertension and a suppressed renin-angiotensin system. Postural hypotension is more characteristic of **Addison’s disease** (adrenal insufficiency), where there is a deficiency of mineralocorticoids [1]. ### **Analysis of Incorrect Options** * **A. Hypokalaemia:** Aldosterone promotes potassium excretion in the cortical collecting duct [2]. While not present in all patients, hypokalemia is a classic hallmark of the disease [1]. * **C. Hypernatremia:** Aldosterone increases sodium reabsorption [2]. While the "aldosterone escape" mechanism prevents massive edema [1], serum sodium levels tend to be at the high-normal or slightly elevated range [1]. * **D. Metabolic alkalosis:** To maintain electroneutrality during sodium reabsorption, the kidneys excrete hydrogen ions ($H^+$) alongside potassium, leading to systemic alkalosis [2]. ### **NEET-PG High-Yield Pearls** * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A **PAC:PRA ratio > 20-30** is highly suggestive. * **Confirmatory Test:** Saline infusion test or Oral salt loading test (failure to suppress aldosterone). * **Aldosterone Escape:** This phenomenon explains why patients with Conn's syndrome rarely have clinical edema despite sodium retention, due to increased ANP (Atrial Natriuretic Peptide) levels [1]. * **Treatment:** Spironolactone (medical) or Unilateral Adrenalectomy (surgical for adenoma).
Question 676: What is the most common cause of hyperparathyroidism?
- A. Di George syndrome
- B. Post-thyroid surgery (Correct Answer)
- C. McCune-Albright syndrome
- D. Parathyroid hypoplasia
Explanation: The question asks for the most common cause of **hypoparathyroidism** (Note: While the prompt mentions hyperparathyroidism, the options and correct answer clearly indicate a discussion on *hypoparathyroidism*). **1. Why "Post-thyroid surgery" is correct:** The most common cause of acquired hypoparathyroidism in adults is **iatrogenic injury** during neck surgery. This typically occurs during total thyroidectomy, parathyroidectomy, or radical neck dissection for head and neck malignancies. The mechanism involves either the accidental removal of the parathyroid glands or, more commonly, the disruption of their delicate blood supply (primarily from the inferior thyroid artery). **2. Why the other options are incorrect:** * **Di George Syndrome (22q11.2 deletion):** This is a congenital cause characterized by the failure of the 3rd and 4th pharyngeal pouches to develop. While it causes parathyroid hypoplasia, it is a rare genetic condition compared to surgical trauma. * **McCune-Albright Syndrome:** This is a triad of polyostotic fibrous dysplasia, café-au-lait spots, and autonomous endocrine hyperfunction (most commonly **precocious puberty**). It is associated with hyperfunction, not hypocalcemia/hypoparathyroidism. * **Parathyroid Hypoplasia:** This refers to the underdevelopment of the glands (as seen in Di George). While it causes hypoparathyroidism, it is significantly less common than postoperative causes. **Clinical Pearls for NEET-PG:** * **Acute Presentation:** Look for signs of hypocalcemia like **Chvostek sign** (facial twitching on tapping the facial nerve) and **Trousseau sign** (carpal spasm induced by BP cuff inflation). * **ECG Finding:** The classic finding in hypocalcemia is **prolonged QT interval** [1]. * **Lab Profile:** Low Serum Calcium, High Serum Phosphate, and Low/Inappropriately Normal PTH [1]. * **Hungry Bone Syndrome:** A transient state of profound hypocalcemia following surgery for hyperparathyroidism due to sudden "shuttling" of calcium into the bones.
Question 677: Cushing's disease typically presents with which of the following hormonal changes?
- A. Increased ACTH and increased cortisol (Correct Answer)
- B. Decreased ACTH and decreased cortisol
- C. Increased ACTH and decreased cortisol
- D. Increased catecholamines
Explanation: **Explanation:** **Cushing’s Disease** specifically refers to hypercortisolism caused by a **pituitary adenoma** (usually a microadenoma) that hypersecretes Adrenocorticotropic Hormone (ACTH) [1]. 1. **Why Option A is correct:** In Cushing’s disease, the primary pathology is in the anterior pituitary [2]. The adenoma secretes excessive **ACTH**, which chronically stimulates the adrenal cortex to produce and release high levels of **cortisol**. Unlike normal physiological states, the pituitary tumor is relatively resistant to the negative feedback inhibition usually exerted by high cortisol levels, leading to a state where both hormones are elevated [1]. 2. **Why other options are incorrect:** * **Option B:** Decreased ACTH and cortisol characterize **Addison’s disease** (primary adrenal insufficiency) or secondary adrenal insufficiency. * **Option C:** Increased ACTH with decreased cortisol is seen in **Primary Adrenal Insufficiency** (Addison’s), where the pituitary tries to compensate for low cortisol by producing more ACTH. * **Option D:** Increased catecholamines are the hallmark of **Pheochromocytoma**, not Cushing’s disease. **High-Yield Clinical Pearls for NEET-PG:** * **Cushing’s Syndrome vs. Disease:** "Syndrome" is the clinical state of excess cortisol (most common cause is exogenous steroids). "Disease" is specifically the pituitary-dependent cause [2]. * **Screening Tests:** Overnight Dexamethasone Suppression Test (ONDST) or 24-hour urinary free cortisol [3]. * **Localization:** High-dose dexamethasone suppression test (8mg) typically suppresses cortisol by >50% in Cushing’s **Disease**, but fails to suppress it in **Ectopic ACTH syndrome** (e.g., Small Cell Lung Cancer). Once presence is confirmed, measurement of plasma ACTH is key for differential diagnosis [1]. * **Gold Standard for Localization:** Inferior Petrosal Sinus Sampling (IPSS).
Question 678: A 50-year-old obese female presents with recurrent candidal urinary infections and excessive thirst. She also reports frequent nighttime urination. What is the initial diagnostic test you would prefer for this patient?
- A. HbA1c
- B. Oral glucose tolerance test
- C. Plasma C-peptide level
- D. Random plasma glucose level (Correct Answer)
Explanation: ### Explanation The patient presents with classic symptoms of **Diabetes Mellitus (DM)**: osmotic symptoms (excessive thirst/polydipsia, polyuria/nocturia) and signs of immunosuppression (recurrent candidal infections) [1]. **1. Why Random Plasma Glucose (RPG) is the correct choice:** According to the ADA and WHO diagnostic criteria, in a patient with **unequivocal symptoms of hyperglycemia** (polyuria, polydipsia, weight loss) or a **hyperglycemic crisis**, a **Random Plasma Glucose (RPG) ≥ 200 mg/dL (11.1 mmol/L)** is sufficient to diagnose Diabetes Mellitus [1]. It is the most practical and immediate initial test in a symptomatic patient to confirm the diagnosis without requiring the patient to be in a fasting state. **2. Why other options are incorrect:** * **HbA1c (Option A):** While an HbA1c ≥ 6.5% is diagnostic for DM, it reflects average glycemia over 3 months. In a symptomatic patient, a glucose level provides immediate confirmation of the current metabolic state. * **Oral Glucose Tolerance Test (Option B):** OGTT is highly sensitive but is usually reserved for cases where fasting glucose is borderline (Prediabetes) or for screening Gestational Diabetes. It is cumbersome and unnecessary if the patient is already symptomatic. * **Plasma C-peptide (Option C):** This test is used to differentiate between Type 1 and Type 2 DM by measuring endogenous insulin production. It is not a diagnostic test for the presence of diabetes itself. **Clinical Pearls for NEET-PG:** * **Diagnostic Criteria for DM:** 1. Fasting Plasma Glucose (FPG) ≥ 126 mg/dL. 2. 2-hour post-load glucose (OGTT) ≥ 200 mg/dL. 3. HbA1c ≥ 6.5%. 4. **Symptomatic patient** with RPG ≥ 200 mg/dL [1]. * Recurrent fungal infections (Candidiasis) in an obese middle-aged female should always trigger a workup for Type 2 Diabetes [1]. * For asymptomatic patients, two abnormal test results (from the same sample or two separate samples) are required for diagnosis. In symptomatic patients, one positive RPG is enough.
Question 679: Necrobiosis lipoidica is seen in which condition?
- A. Dermatomyositis
- B. Lyme disease
- C. Diabetes mellitus (Correct Answer)
- D. Symmonds disease
Explanation: **Explanation:** **Necrobiosis Lipoidica (NL)**, historically known as Necrobiosis Lipoidica Diabeticorum, is a chronic granulomatous skin disorder. While its exact pathogenesis is idiopathic, it is strongly associated with **Diabetes Mellitus (Option C)** [2]. It is estimated that approximately 0.3% of diabetic patients develop NL, and conversely, over 60% of patients with NL have underlying diabetes. The condition is characterized by collagen degeneration (necrobiosis), a granulomatous response, and thickening of blood vessel walls. **Analysis of Options:** * **Dermatomyositis (Option A):** This is an inflammatory myopathy characterized by Gottron papules, Heliotrope rash, and proximal muscle weakness [1], not NL. * **Lyme Disease (Option B):** Caused by *Borrelia burgdorferi*, it typically presents with Erythema Chronicum Migrans (a "bull's eye" rash) [3]. * **Symmonds Disease (Option D):** This refers to panhypopituitarism (often due to pituitary necrosis). It does not have a primary association with necrobiotic skin lesions. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** Classically presents as well-demarcated, yellowish-brown, atrophic plaques with a "glazed" or "porcelain" appearance and prominent **telangiectasia**, usually on the **pretibial area** (shins). * **Correlation with Glycemic Control:** Importantly, the severity or progression of NL does **not** correlate with blood glucose levels or HbA1c control. * **Differential Diagnosis:** Must be distinguished from *Granuloma Annulare*, which also involves collagen necrobiosis but lacks the atrophy and telangiectasia seen in NL. * **Complication:** Though rare, squamous cell carcinoma can develop within chronic NL scars.
Question 680: Which of the following is not seen in Secondary Adrenal insufficiency?
- A. Hyperpigmentation (Correct Answer)
- B. Postural hypotension
- C. Hypoglycemia
- D. Lassitude
Explanation: In **Secondary Adrenal Insufficiency (SAI)**, the pathology lies in the pituitary gland (decreased ACTH) or hypothalamus (decreased CRH), rather than the adrenal cortex itself [2]. ### Why Hyperpigmentation is NOT seen: Hyperpigmentation is a hallmark of **Primary Adrenal Insufficiency (Addison’s Disease)** [1]. In Primary AI, the lack of cortisol feedback causes a massive compensatory increase in **ACTH** and its precursor, **Pro-opiomelanocortin (POMC)**. POMC is cleaved into ACTH and **Melanocyte-Stimulating Hormone (MSH)**; high levels of these hormones stimulate melanocytes, leading to skin and mucosal darkening. In SAI, ACTH levels are low or inappropriately normal, so hyperpigmentation does not occur. ### Analysis of Incorrect Options: * **Postural Hypotension:** While more severe in Primary AI (due to mineralocorticoid deficiency), it can still occur in SAI due to decreased vascular tone and reduced cardiac output resulting from cortisol deficiency. * **Hypoglycemia:** Cortisol is a counter-regulatory hormone that promotes gluconeogenesis. Its absence in SAI leads to impaired glucose production, especially during fasting or stress. * **Lassitude:** General fatigue, weakness, and lethargy are universal symptoms of glucocorticoid deficiency regardless of the site of the lesion [4]. ### NEET-PG High-Yield Pearls: 1. **Mineralocorticoids:** In SAI, the Renin-Angiotensin-Aldosterone System (RAAS) remains intact. Therefore, **hyperkalemia is absent** in SAI (a common "except" question) [2]. 2. **Aldosterone:** Is preserved in SAI but lost in Primary AI. 3. **Most Common Cause:** The most common cause of SAI is the **abrupt withdrawal of long-term exogenous steroid therapy**. 4. **Cosyntropin Test:** Used to differentiate; in SAI, the adrenals may be "atrophied" and fail to respond to an acute ACTH bolus [3].
Practice by Chapter
Diabetes Mellitus
Practice Questions
Thyroid Disorders
Practice Questions
Adrenal Gland Disorders
Practice Questions
Pituitary Disorders
Practice Questions
Calcium and Bone Metabolism
Practice Questions
Reproductive Endocrinology
Practice Questions
Lipid Disorders
Practice Questions
Endocrine Hypertension
Practice Questions
Multiple Endocrine Neoplasia
Practice Questions
Obesity and Metabolic Syndrome
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Neuroendocrine Tumors
Practice Questions
Endocrine Emergencies
Practice Questions
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