Endocrinology — MCQs
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What are the most important features of Cushing's syndrome?
Which of the following is the most likely effect of insulin at the cellular receptor level?
A 45-year-old woman presents with sudden attacks of wheezing, shortness of breath, episodic hot flashes, abdominal cramps, and diarrhea. Physical examination shows facial redness, as well as hepatomegaly and pitting edema of the lower legs. A 24-hour urine specimen reveals elevated levels of 5-hydroxyindoleacetic acid (5-HIAA). A CT scan of the abdomen demonstrates multiple 2- to 3-cm nodules throughout the liver and a 2-cm nodule in the jejunum. An echocardiogram would be most expected to demonstrate which of the following?
Sipple syndrome is also known as:
A 34-year-old man is referred for evaluation of hypertension and persistent hypokalemia in spite of taking oral potassium supplements. His blood pressure is 180/110 mm Hg. Serum sodium is 149 mEq/L; potassium, 3.3 mEq/L; bicarbonate, 29 mEq/L; chloride, 103 mEq/L; and blood urea nitrogen, 23 mg/dL. Computed tomography demonstrates a 3-cm mass in the right adrenal gland. The most likely diagnosis is:
Sheehan's syndrome is related to which of the following conditions?
Hypercalcemia is seen in all conditions except?
Which of the following antibodies is involved in the tissue destructive process associated with hypothyroidism in Hashimoto's and atrophic thyroiditis?
A 40-year-old alcoholic man is being treated for tuberculosis with intermittent compliance. He complains of increasing weakness, fatigue, weight loss, and nausea over the preceding 3 weeks. His blood pressure is 80/50 mm Hg, and there is increased pigmentation over the elbows and in the palmar creases. Cardiac examination is normal. What is the best next step in his evaluation?
Alkaline phosphatase is elevated in all conditions below, except?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 321: What are the most important features of Cushing's syndrome?
- A. Centripetal obesity (Correct Answer)
- B. Hypertension
- C. Menorrhagia
- D. Polyuria
Explanation: **Explanation:** **Cushing’s Syndrome** results from chronic exposure to excessive glucocorticoids. Among its diverse clinical manifestations, **Centripetal Obesity** (Option A) is the most characteristic and common feature (occurring in >90% of patients). [1] * **Why it is correct:** Glucocorticoids promote lipogenesis in the trunk and face while inducing lipolysis in the extremities. This results in the classic redistribution of fat, leading to "Moon facies," "Buffalo hump" (supraclavicular and dorsocervical fat pads), and a high waist-to-hip ratio, while the limbs remain thin due to muscle wasting. [1] **Analysis of Incorrect Options:** * **Hypertension (Option B):** While very common in Cushing’s (due to mineralocorticoid effects and increased vascular reactivity), it is a non-specific finding seen in many endocrine and cardiovascular disorders. Centripetal obesity is more "pathognomonic" for the clinical diagnosis. * **Menorrhagia (Option C):** Incorrect. Hypercortisolism typically causes **Oligomenorrhea or Amenorrhea** in women due to the suppression of the hypothalamic-pituitary-gonadal axis. * **Polyuria (Option D):** While secondary diabetes mellitus can occur (causing polyuria), it is a secondary complication rather than a primary diagnostic feature of the syndrome itself. **Clinical Pearls for NEET-PG:** * **Most sensitive initial tests:** 24-hour urinary free cortisol, Late-night salivary cortisol, or Low-dose dexamethasone suppression test (LDDST). [2] * **Proximal Myopathy:** Weakness in the pelvic and shoulder girdles (difficulty climbing stairs) is a highly specific sign. [1] * **Skin changes:** Look for wide (>1 cm), purple striae and easy bruisability due to collagen breakdown. [1] * **Hypokalemic Metabolic Alkalosis:** Often suggests Ectopic ACTH syndrome (e.g., Small Cell Lung Cancer).
Question 322: Which of the following is the most likely effect of insulin at the cellular receptor level?
- A. Stimulating tyrosine kinase (Correct Answer)
- B. Binding to ion channels
- C. Binding to intracellular erb A receptors
- D. Stimulating guanylate cyclase
Explanation: ### Explanation **1. Why Option A is Correct:** The insulin receptor is a **transmembrane glycoprotein** belonging to the receptor tyrosine kinase (RTK) family [1]. It consists of two extracellular alpha subunits (binding site) and two transmembrane beta subunits. When insulin binds to the alpha subunits, it triggers **autophosphorylation** of the beta subunits [2]. This activates the intrinsic **tyrosine kinase** enzyme, which then phosphorylates Insulin Receptor Substrates (IRS-1 to 4) [1]. This cascade ultimately leads to the translocation of GLUT-4 transporters to the cell membrane, facilitating glucose uptake [2]. **2. Why Other Options are Incorrect:** * **Option B (Ion Channels):** This mechanism is characteristic of neurotransmitters (e.g., Acetylcholine at nicotinic receptors) or GABA, not metabolic hormones like insulin. * **Option C (Intracellular erb A receptors):** The *erb A* family refers to **Thyroid Hormone receptors**. These are nuclear receptors that act as transcription factors. Insulin, being a peptide hormone, cannot cross the lipid bilayer and must act on surface receptors. * **Option D (Guanylate Cyclase):** This is the mechanism for **Atrial Natriuretic Peptide (ANP)** and Nitric Oxide (NO), which increase cGMP levels. Insulin does not utilize the cGMP pathway. **3. Clinical Pearls for NEET-PG:** * **Receptor Type:** Insulin uses a **Catalytic Receptor** (Enzyme-linked) [4]. * **Downstream Pathways:** * *PI3K Pathway:* Responsible for most metabolic effects (glucose transport, glycogen synthesis) [2]. * *MAP Kinase Pathway:* Responsible for growth and gene expression [3]. * **Receptor Downregulation:** Chronic hyperinsulinemia (as seen in Type 2 Diabetes/Obesity) leads to a decrease in the number of surface receptors, contributing to **insulin resistance**. * **GLUT-4:** The only insulin-dependent glucose transporter, found primarily in **skeletal muscle and adipose tissue**.
Question 323: A 45-year-old woman presents with sudden attacks of wheezing, shortness of breath, episodic hot flashes, abdominal cramps, and diarrhea. Physical examination shows facial redness, as well as hepatomegaly and pitting edema of the lower legs. A 24-hour urine specimen reveals elevated levels of 5-hydroxyindoleacetic acid (5-HIAA). A CT scan of the abdomen demonstrates multiple 2- to 3-cm nodules throughout the liver and a 2-cm nodule in the jejunum. An echocardiogram would be most expected to demonstrate which of the following?
- A. Aortic stenosis
- B. Bacterial endocarditis
- C. Mitral valve prolapse
- D. Pulmonic stenosis (Correct Answer)
Explanation: The clinical presentation of episodic flushing, wheezing, diarrhea, and abdominal cramps, combined with elevated urinary **5-HIAA** and a jejunal mass with liver metastases, is diagnostic of **Carcinoid Syndrome** [1]. **1. Why Pulmonic Stenosis is Correct:** Carcinoid syndrome occurs when neuroendocrine tumors (usually from the midgut) metastasize to the liver, allowing vasoactive substances like **serotonin** to bypass hepatic metabolism and reach the systemic circulation [1]. These substances cause fibrous plaque-like endocardial thickening. * **Right-sided involvement:** The lungs contain monoamine oxidase (MAO), which degrades serotonin. Therefore, the right heart (tricuspid and pulmonic valves) is exposed to high serotonin levels, leading to **pulmonic stenosis** and **tricuspid regurgitation**. * The patient’s pitting edema and hepatomegaly further suggest right-sided heart failure (Carcinoid Heart Disease). **2. Why Incorrect Options are Wrong:** * **Aortic Stenosis & Mitral Valve Prolapse:** Left-sided valves are typically spared because serotonin is inactivated in the lungs. Left-sided lesions only occur if there is a right-to-left shunt (e.g., PFO) or a primary bronchial carcinoid. * **Bacterial Endocarditis:** This presents with fever, new murmurs, and embolic phenomena (Janeway lesions, Osler nodes), not the classic triad of flushing, diarrhea, and wheezing. **3. NEET-PG High-Yield Pearls:** * **Primary Site:** Most common site for carcinoid tumors is the **ileum/appendix**, but the syndrome only occurs after **liver metastasis** [1]. * **Diagnosis:** Best initial screening test is **24-hour urinary 5-HIAA**. * **Localization:** **Somatostatin receptor scintigraphy** (OctreoScan) is highly sensitive. * **Treatment:** **Octreotide** (somatostatin analog) is used to manage symptoms and "carcinoid crisis." * **Pellagra Connection:** Chronic serotonin production consumes dietary tryptophan, potentially leading to **Niacin (B3) deficiency** (Dermatitis, Diarrhea, Dementia).
Question 324: Sipple syndrome is also known as:
- A. Multiple Endocrine Neoplasia Type 1 (MEN 1)
- B. Multiple Endocrine Neoplasia Type 2A (MEN 2A) (Correct Answer)
- C. Multiple Endocrine Neoplasia Type 2B (MEN 2B)
- D. None of the Above
Explanation: **Explanation:** **Sipple Syndrome** is the eponymous name for **Multiple Endocrine Neoplasia Type 2A (MEN 2A)**. It is an autosomal dominant disorder characterized by a triad of tumors: 1. **Medullary Thyroid Carcinoma (MTC):** Occurs in >90% of cases; often the first manifestation [1]. 2. **Pheochromocytoma:** Usually bilateral and occurs in approximately 50% of patients. 3. **Parathyroid Hyperplasia/Adenoma:** Occurs in 20–30% of patients, leading to hypercalcemia. The underlying genetic defect in MEN 2A is a germline mutation in the **RET proto-oncogene** on chromosome 10 [1]. **Analysis of Incorrect Options:** * **MEN 1 (Wermer Syndrome):** Characterized by the "3 Ps"—Pituitary adenoma, Parathyroid hyperplasia, and Pancreatic neuroendocrine tumors (e.g., Gastrinoma, Insulinoma). It is caused by mutations in the *MEN1* gene (Menin protein) [1]. * **MEN 2B (Wagenmann-Froboese Syndrome):** While it also involves MTC and Pheochromocytoma, it is distinguished from MEN 2A by the presence of **mucosal neuromas**, **Marfanoid habitus**, and intestinal ganglioneuromatosis. Parathyroid involvement is notably absent in MEN 2B. **NEET-PG High-Yield Pearls:** * **Screening:** For patients with a known RET mutation, prophylactic thyroidectomy is recommended (often before age 5 in MEN 2A) [1]. * **Sequence of Surgery:** If a patient has both MTC and Pheochromocytoma, the **Pheochromocytoma must be operated on first** to prevent a hypertensive crisis during thyroid surgery. * **Mnemonic:** Remember MEN 2A as **"MPH"** (Medullary, Pheo, Parathyroid).
Question 325: A 34-year-old man is referred for evaluation of hypertension and persistent hypokalemia in spite of taking oral potassium supplements. His blood pressure is 180/110 mm Hg. Serum sodium is 149 mEq/L; potassium, 3.3 mEq/L; bicarbonate, 29 mEq/L; chloride, 103 mEq/L; and blood urea nitrogen, 23 mg/dL. Computed tomography demonstrates a 3-cm mass in the right adrenal gland. The most likely diagnosis is:
- A. Conn syndrome (Correct Answer)
- B. Addison disease
- C. Cushing syndrome
- D. Sipple syndrome
Explanation: This patient presents with the classic triad of **Primary Hyperaldosteronism (Conn Syndrome)**: hypertension, hypokalemia, and metabolic alkalosis. [1] ### **Why Conn Syndrome is Correct** Conn syndrome is caused by an aldosterone-secreting adrenal adenoma. Excess aldosterone acts on the renal distal convoluted tubule and collecting duct to [2]: 1. **Reabsorb Sodium:** Leading to hypernatremia (149 mEq/L) and hypertension due to volume expansion. 2. **Excrete Potassium:** Leading to persistent hypokalemia (3.3 mEq/L) despite supplementation [2]. 3. **Excrete Hydrogen ions:** Leading to metabolic alkalosis (elevated bicarbonate of 29 mEq/L) [2]. The presence of a **unilateral 3-cm adrenal mass** on CT in the setting of these biochemical abnormalities is diagnostic of an aldosterone-producing adenoma [1]. ### **Why Other Options are Incorrect** * **Addison Disease:** This is primary adrenal insufficiency. It presents with **hypotension, hyperkalemia, and hyponatremia**—the exact opposite of this patient’s profile. * **Cushing Syndrome:** While it can cause hypertension and hypokalemia (due to mineralocorticoid cross-reactivity of cortisol), it typically presents with cushingoid features (buffalo hump, striae, central obesity) and hyperglycemia, which are not mentioned here. * **Sipple Syndrome (MEN 2A):** Characterized by Medullary Thyroid Carcinoma, Pheochromocytoma, and Parathyroid Hyperplasia. While Pheochromocytoma causes hypertension, it does not typically cause persistent hypokalemia or hypernatremia. [1] ### **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 (failure to suppress aldosterone) or Oral Salt Loading test. * **Management:** Surgical resection for unilateral adenoma (Conn’s); medical management with **Spironolactone or Eplerenone** for bilateral adrenal hyperplasia. [1] * **Aldosterone Escape:** Patients with Conn syndrome do not have significant edema due to "atrial natriuretic peptide (ANP) mediated diuresis," which limits volume overload. [3]
Question 326: Sheehan's syndrome is related to which of the following conditions?
- A. Panhypopituitarism (Correct Answer)
- B. Hypothyroidism
- C. Hypogonadism
- D. Hyperparathyroidism
Explanation: **Explanation:** **Sheehan’s Syndrome** is a classic cause of **Panhypopituitarism**. It occurs due to ischemic necrosis of the anterior pituitary gland following severe postpartum hemorrhage (PPH) and hypotension [1]. During pregnancy, the pituitary gland enlarges (hypertrophies) to meet increased hormonal demands, making it highly susceptible to ischemia if blood pressure drops significantly during delivery. **Why Option A is correct:** Panhypopituitarism refers to the deficiency of all or most anterior pituitary hormones (GH, LH, FSH, TSH, and ACTH). In Sheehan’s syndrome, the ischemic insult typically affects the entire anterior lobe, leading to a global loss of function [1]. The earliest clinical sign is often the failure to lactate (due to Prolactin deficiency) and failure to resume menses (due to Gonadotropin deficiency). **Why other options are incorrect:** * **B & C (Hypothyroidism/Hypogonadism):** While these conditions occur as *part* of Sheehan’s syndrome (secondary to TSH and LH/FSH deficiency), they are incomplete descriptions [2]. "Panhypopituitarism" is the more comprehensive and accurate clinical diagnosis. * **D (Hyperparathyroidism):** This involves the parathyroid glands, which are independent of the pituitary-hypothalamic axis and are not affected by Sheehan’s syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Pathophysiology:** Ischemic necrosis of the enlarged pituitary gland. * **Clinical Presentation:** Failure of lactation (earliest sign), secondary amenorrhea, loss of pubic/axillary hair, and features of secondary adrenal insufficiency. * **Diagnosis:** Low levels of target organ hormones (T4, Cortisol, Estrogen) with inappropriately low/normal trophic hormones (TSH, ACTH, FSH/LH) [2]. * **MRI Finding:** In the chronic stage, MRI reveals an **"Empty Sella."** * **Posterior Pituitary:** Usually spared because it has a direct arterial blood supply, unlike the anterior lobe which relies on the low-pressure portal venous system.
Question 327: Hypercalcemia is seen in all conditions except?
- A. Milk alkali syndrome
- B. Hyperparathyroidism
- C. Vitamin A deficiency (Correct Answer)
- D. Vitamin D intoxication
Explanation: **Explanation:** The correct answer is **Vitamin A deficiency**. Hypercalcemia is a common metabolic abnormality characterized by elevated serum calcium levels. To answer this question, one must distinguish between conditions that increase calcium levels and those that do not. **1. Why Vitamin A deficiency is the correct answer:** Vitamin A deficiency does not cause hypercalcemia. In fact, it is **Vitamin A toxicity (Hypervitaminosis A)** that is associated with hypercalcemia [2]. Excessive Vitamin A stimulates osteoclast activity, leading to increased bone resorption and the release of calcium into the bloodstream. Therefore, deficiency has no such effect. **2. Analysis of incorrect options:** * **Milk-alkali syndrome:** This is caused by the excessive ingestion of calcium and absorbable antacids (like calcium carbonate). It leads to the triad of hypercalcemia, metabolic alkalosis, and renal insufficiency [1]. * **Hyperparathyroidism:** This is the most common cause of hypercalcemia in outpatient settings. Increased Parathyroid Hormone (PTH) enhances bone resorption, renal calcium reabsorption, and intestinal calcium absorption (via Vitamin D) [1], [3]. * **Vitamin D intoxication:** Excessive Vitamin D increases intestinal absorption of calcium and phosphorus, as well as bone resorption, leading to significant hypercalcemia [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Hypercalcemia:** "Stones (renal), Bones (aches), Groans (abdominal pain), and Psychic Overtones (confusion/depression)." * **Most common cause overall:** Primary Hyperparathyroidism [1]. * **Most common cause in hospitalized patients:** Malignancy (often via PTHrP) [1]. * **ECG finding:** Shortened QT interval is a classic sign of hypercalcemia. * **Thiazide diuretics** can also cause hypercalcemia by increasing renal calcium reabsorption [1], whereas **Loop diuretics** (Furosemide) are used to treat it ("Loops Lose Calcium").
Question 328: Which of the following antibodies is involved in the tissue destructive process associated with hypothyroidism in Hashimoto's and atrophic thyroiditis?
- A. Thyroperoxidase antibody (Correct Answer)
- B. Thyroglobulin antibody
- C. TSH receptor antibody
- D. Thyroid stimulating antibody
Explanation: **Explanation:** **1. Why Thyroperoxidase (TPO) antibody is correct:** Hashimoto's thyroiditis and atrophic thyroiditis are characterized by autoimmune-mediated destruction of the thyroid parenchyma. **Anti-TPO antibodies** are present in >95% of patients with Hashimoto’s. While T-cell mediated cytotoxicity (CD8+ cells) is the primary driver of cell death, Anti-TPO antibodies are directly involved in the destructive process by fixing complement and mediating **Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)**. They serve as the most sensitive immunological marker for autoimmune thyroiditis and correlate closely with the degree of thyroid inflammation. **2. Why the other options are incorrect:** * **Thyroglobulin (Tg) antibody:** While often present in Hashimoto’s (60-80%), these antibodies are less sensitive and less specific than Anti-TPO. They are generally considered secondary markers and are not the primary drivers of tissue destruction. * **TSH receptor antibody (TRAb):** This is a broad category. Specifically, **TSH-receptor blocking antibodies** can cause hypothyroidism (atrophic thyroiditis) by preventing TSH from binding [1], but they cause atrophy rather than the classic inflammatory destruction associated with TPO antibodies. * **Thyroid stimulating antibody (TSI):** These are a subtype of TRAb that mimic TSH to cause hyperthyroidism in **Graves' disease** [1]. They do not cause tissue destruction or hypothyroidism. **Clinical Pearls for NEET-PG:** * **Most sensitive marker** for Hashimoto’s: Anti-TPO antibody. * **Histology of Hashimoto’s:** Lymphocytic infiltrate with germinal centers and **Hurthle cells** (Askanazy cells/oxyphilic cells). * **Risk factor:** Hashimoto’s increases the risk of **Thyroid B-cell Lymphoma** (Non-Hodgkin’s). * **Atrophic Thyroiditis:** Represents the end-stage of thyroid autoimmune destruction where the goiter is absent, often associated with TSH-receptor blocking antibodies. [1]
Question 329: A 40-year-old alcoholic man is being treated for tuberculosis with intermittent compliance. He complains of increasing weakness, fatigue, weight loss, and nausea over the preceding 3 weeks. His blood pressure is 80/50 mm Hg, and there is increased pigmentation over the elbows and in the palmar creases. Cardiac examination is normal. What is the best next step in his evaluation?
- A. Complete blood count with iron and iron-binding capacity
- B. Erythrocyte sedimentation rate (ESR)
- C. Early morning serum cortisol and cosyntropin stimulation test (Correct Answer)
- D. Blood cultures
Explanation: ### **Explanation** The clinical presentation of hypotension (80/50 mm Hg), hyperpigmentation (elbows and palmar creases), and constitutional symptoms (weakness, weight loss, nausea) in a patient with tuberculosis (TB) strongly suggests **Primary Adrenal Insufficiency (Addison’s Disease)** [1]. **1. Why Option C is Correct:** In developing countries like India, **Tuberculosis** is the most common cause of primary adrenal insufficiency [1], [2]. TB causes destruction of the adrenal cortex, leading to a deficiency of both cortisol and aldosterone. * **Hyperpigmentation** occurs because the lack of cortisol feedback leads to increased ACTH secretion; ACTH shares a precursor (POMC) with Melanocyte-Stimulating Hormone (MSH). * **Diagnosis:** The gold standard for diagnosis is the **Cosyntropin (ACTH) stimulation test** [1]. A subnormal rise in serum cortisol after administration of synthetic ACTH confirms adrenal insufficiency. An **early morning serum cortisol** (<3 µg/dL) is also highly suggestive [1]. **2. Why Other Options are Incorrect:** * **Option A & B:** While anemia of chronic disease or an elevated ESR may be present in TB, they are non-specific and do not address the life-threatening hemodynamic instability (hypotension) or the classic signs of adrenal failure. * **Option D:** Blood cultures are used to rule out sepsis. While sepsis can cause hypotension, it does not explain the chronic hyperpigmentation or the specific history of TB. ### **NEET-PG High-Yield Pearls** * **Most common cause of Addison’s Disease:** Worldwide/Developed countries = Autoimmune (Adrenalitis); India/Developing countries = Tuberculosis [1], [2]. * **Electrolyte abnormalities:** Hyponatremia, Hyperkalemia, and Metabolic Acidosis (due to aldosterone deficiency). * **Radiology:** In TB-related Addison’s, CT may show **enlarged, calcified adrenal glands** [1]. In autoimmune cases, glands are usually atrophic. * **Treatment:** Glucocorticoid (Hydrocortisone) and Mineralocorticoid (Fludrocortisone) replacement [1]. In acute crisis, IV fluids and high-dose IV Hydrocortisone are mandatory.
Question 330: Alkaline phosphatase is elevated in all conditions below, except?
- A. Rickets
- B. Osteomalacia
- C. Hypoparathyroidism
- D. Hypophosphatemia (Correct Answer)
Explanation: **Explanation:** Alkaline Phosphatase (ALP) is a marker of **osteoblastic activity**. In bone pathology, ALP levels rise whenever there is increased bone turnover or compensatory mineralization attempts [2]. **Why Hypophosphatemia is the correct answer:** Hypophosphatemia (low serum phosphate) is a biochemical finding, not a bone disease itself. While chronic hypophosphatemia can *lead* to rickets or osteomalacia [1], the state of low phosphate alone does not inherently increase osteoblastic activity. In fact, in the rare genetic condition **Hypophosphatasia**, ALP levels are characteristically **low**, making it a high-yield exception to the rule of elevated ALP in metabolic bone diseases. **Analysis of Incorrect Options:** * **Rickets & Osteomalacia:** These conditions involve defective mineralization of the osteoid (in children and adults, respectively) [1]. To compensate for the weak bone matrix, osteoblasts increase their activity, leading to a significant **elevation in serum ALP** [1]. * **Hypoparathyroidism:** This is a tricky distractor. While ALP is often **normal** in hypoparathyroidism (due to low bone turnover), it is **not typically elevated**. However, in the context of this specific question, Hypophosphatemia is the "more correct" answer as it is often associated with low ALP (Hypophosphatasia), whereas the other conditions are classically associated with high ALP. **NEET-PG High-Yield Pearls:** 1. **Isolated ALP elevation:** Think of Paget’s Disease of bone (highest levels) or early Vitamin D deficiency. 2. **Low ALP levels:** Seen in Hypophosphatasia, Zinc deficiency, Magnesium deficiency, and Vitamin C deficiency (Scurvy). 3. **Normal ALP in Bone Disease:** Typically seen in Multiple Myeloma (unless a fracture is healing) and Osteoporosis.
Practice by Chapter
Diabetes Mellitus
Practice Questions
Thyroid Disorders
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Adrenal Gland Disorders
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Pituitary Disorders
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Calcium and Bone Metabolism
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Reproductive Endocrinology
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Lipid Disorders
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Endocrine Hypertension
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Multiple Endocrine Neoplasia
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Obesity and Metabolic Syndrome
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Neuroendocrine Tumors
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Endocrine Emergencies
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