Endocrinology — MCQs

A 32-year-old male with suspected neurofibromatosis presented with a blood pressure of 178/110 mm Hg, palpitations, and excessive sweating. Today, his blood pressure is 130/80 mm Hg. Physical examination reveals multiple tumors of the oral mucosa and skin. Laboratory investigations reveal: Serum K+: 3.8 mEq/L, Serum Ca2+: 9.4 mg/dL. Genetic studies in this patient will most likely show which of the following?

Q68Medium

Which of the following conditions can cause hypercalcemia?

Q69Medium

A 35-year-old woman complains of attacks of breathlessness, cyanosis, and flushing. Apart from occasional diarrhea, she has no abdominal symptoms. Abdominal examination reveals an enlarged, nodular liver. If laparotomy is performed, what finding would be expected?

Q70Hard

A 50-year-old obese woman with long-standing type 2 diabetes mellitus, inadequately controlled on metformin and pioglitazone, was recently started on insulin glargine (15 units subcutaneously at bedtime) due to a hemoglobin A1C of 8.4. Over the weekend, she experienced nausea, vomiting, and diarrhea after exposure to ill family members. Fearing hypoglycemia, she omitted her insulin for 3 nights. In the following 24 hours, she developed lethargy and was brought to the emergency room. On examination, she was afebrile and unresponsive to verbal command. Her blood pressure was 84/52, skin turgor was poor, and mucous membranes were dry. Neurological examination was nonfocal; she did not have neck rigidity. Laboratory results were: Na: 126 mEq/L, K: 4.0 mEq/L, Cl: 95 mEq/L, HCO3: 22 mEq/L, Glucose: 1100 mg/dL, BUN: 84 mg/dL, Creatinine: 3.0 mg/dL. Which of the following is the most likely cause of this patient's coma?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 61: Type I diabetes mellitus is associated with which of the following?

A. Insulin resistance
B. Defect in mitochondrial DNA
C. Islet cell autoantibodies (Correct Answer)
D. Beta cell dysfunction

Explanation: ### Explanation **Correct Answer: C. Islet cell autoantibodies** **Medical Concept:** Type 1 Diabetes Mellitus (T1DM) is primarily an **autoimmune disease** characterized by the T-cell-mediated destruction of pancreatic beta cells [1]. The presence of **islet cell autoantibodies** (e.g., GAD65, IA-2, Zinc transporter 8, and Insulin autoantibodies) serves as a hallmark marker of this autoimmune process [2]. These antibodies are often present years before clinical symptoms appear and are used to differentiate T1DM from Type 2 DM or Monogenic diabetes. **Analysis of Incorrect Options:** * **A. Insulin resistance:** This is the primary pathophysiological feature of **Type 2 Diabetes Mellitus (T2DM)** and metabolic syndrome. In T1DM, the problem is an absolute deficiency of insulin, not resistance to its action. * **B. Defect in mitochondrial DNA:** This is associated with **Maternally Inherited Diabetes and Deafness (MIDD)**. It follows a non-Mendelian inheritance pattern and is not the mechanism for classic T1DM. * **C. Beta cell dysfunction:** While beta cells are destroyed in T1DM, "dysfunction" (impaired secretion despite cells being present) is more characteristic of the early stages of **T2DM** or **MODY** [3]. In T1DM, there is beta-cell **destruction** leading to absolute deficiency. **High-Yield Clinical Pearls for NEET-PG:** * **HLA Association:** T1DM is strongly linked to **HLA-DR3 and HLA-DR4** [2]. * **Most Common Antibody:** **GAD65 (Glutamic Acid Decarboxylase)** antibodies are the most persistent and commonly tested. * **Honey Moon Phase:** A transient period after diagnosis where the remaining beta cells function temporarily before total exhaustion. * **Histology:** The classic finding in T1DM is **Insulitis** (lymphocytic infiltration of the islets).

Question 62: A male patient presents with headache, profuse sweating, palpitations, and a blood pressure of 160/110 mmHg. Which drug would be most useful in this situation?

A. Nifedipine
B. Labetalol
C. Prazosin
D. Phenoxybenzamine (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Phenoxybenzamine** The clinical triad of **headache, profuse sweating, and palpitations** in the presence of hypertension is highly suggestive of **Pheochromocytoma** (a catecholamine-secreting tumor of the adrenal medulla). In Pheochromocytoma, there is an excess of circulating catecholamines (epinephrine and norepinephrine) stimulating both alpha and beta-adrenergic receptors. **Phenoxybenzamine** is the drug of choice because it is a **non-selective, irreversible alpha-blocker**. It provides a stable, long-acting blockade that prevents the severe hypertensive crises caused by alpha-1 mediated vasoconstriction. **Why other options are incorrect:** * **Nifedipine (A):** While Calcium Channel Blockers can be used as add-on therapy, they are not the primary choice for initial stabilization in suspected pheochromocytoma. * **Labetalol (B):** This is a combined alpha and beta-blocker, but its **beta-blocking effect outweighs its alpha-blocking effect** (ratio of 1:7). Using it as monotherapy can lead to "unopposed alpha stimulation," causing a paradoxical and life-threatening rise in blood pressure. * **Prazosin (C):** This is a selective, reversible alpha-1 blocker. While sometimes used, its short half-life and risk of first-dose hypotension make it less ideal than phenoxybenzamine for preoperative preparation. **High-Yield Clinical Pearls for NEET-PG:** 1. **Rule of 10s:** 10% are bilateral, 10% are extra-adrenal (Paragangliomas), 10% are malignant, and 10% occur in children. 2. **Sequence of Blockade:** Always start **Alpha-blockade first**, followed by Beta-blockade (usually 2-3 days later) to control tachycardia. Reversing this order can cause a hypertensive crisis. 3. **Pre-operative Goal:** Phenoxybenzamine is typically started 7–14 days before surgery to allow for intravascular volume expansion. 4. **Diagnosis:** The most sensitive initial test is plasma free metanephrines; the most specific is 24-hour urinary catecholamines/metanephrines.

Question 63: On thyroid function tests, the TSH value is raised and the T4 value is decreased. What is the referred diagnosis?

A. Hyperthyroidism
B. Primary hypothyroidism (Correct Answer)
C. Secondary hypothyroidism
D. Subclinical hypothyroidism

Explanation: The diagnosis of thyroid disorders relies on the feedback loop between the anterior pituitary (TSH) and the thyroid gland (T4/T3) [1]. **1. Why Primary Hypothyroidism is correct:** In **Primary Hypothyroidism**, the pathology lies within the thyroid gland itself (e.g., Hashimoto’s thyroiditis) [1], [2]. The gland fails to produce sufficient Thyroxine (T4). Due to the loss of negative feedback, the pituitary gland compensates by increasing the secretion of **Thyroid Stimulating Hormone (TSH)**. Therefore, the classic biochemical profile is a **High TSH and Low T4** [1]. **2. Analysis of Incorrect Options:** * **Hyperthyroidism:** Characterized by an overactive gland, resulting in **High T4** and a suppressed (**Low**) **TSH** [1]. * **Secondary Hypothyroidism:** The pathology is in the pituitary or hypothalamus. Since the pituitary cannot produce TSH, both **TSH and T4 are Low** [2]. * **Subclinical Hypothyroidism:** This is an early stage of thyroid failure where the **TSH is High**, but the thyroid gland still manages to maintain a **Normal T4** level. The patient is often asymptomatic. **Clinical Pearls for NEET-PG:** * **Best Screening Test:** Serum TSH is the most sensitive initial test for thyroid dysfunction. * **Hashimoto’s Thyroiditis:** The most common cause of primary hypothyroidism in iodine-sufficient regions; associated with **Anti-TPO antibodies**. * **Wolff-Chaikoff Effect:** Hypothyroidism induced by excessive iodine ingestion. * **Myxedema Coma:** The most severe expression of hypothyroidism, characterized by altered mental status and hypothermia.

Question 64: Which of the following is NOT a feature of de Quervain's disease?

A. Autoimmune in etiology (Correct Answer)
B. Increased ESR
C. Tends to regress spontaneously
D. Painful and associated with enlargement of the thyroid

Explanation: **Explanation:** **De Quervain’s Thyroiditis** (also known as Subacute Granulomatous Thyroiditis) is a self-limiting inflammatory condition of the thyroid, typically following a viral upper respiratory tract infection. **1. Why Option A is the Correct Answer:** Unlike Hashimoto’s or Graves’ disease, de Quervain’s is **not autoimmune** in etiology. It is believed to be **post-viral** in origin (associated with Coxsackievirus, Mumps, or Adenovirus). While it is associated with the HLA-B35 haplotype, it does not involve chronic autoimmune destruction; rather, it is a transient inflammatory response. Low-titre thyroid autoantibodies appear transiently in the serum, but high-titre autoantibodies suggest a different underlying autoimmune pathology [1]. **2. Analysis of Other Options:** * **Option B (Increased ESR):** This is a hallmark of the disease. A characteristically high ESR (often >50–100 mm/hr) and elevated C-reactive protein (CRP) are diagnostic clues used to differentiate it from other forms of thyrotoxicosis [1]. * **Option C (Regresses spontaneously):** The disease is typically self-limiting [1]. It follows a triphasic course: an initial thyrotoxic phase (due to leakage of preformed hormones), followed by a transient hypothyroid phase, and finally a return to euthyroidism within 2–6 months. * **Option D (Painful enlargement):** This is the most common clinical presentation. Patients present with a **tender, painful goiter** where pain often radiates to the jaw or ears, accompanied by systemic symptoms like fever and malaise [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Radioactive Iodine Uptake (RAIU):** Characteristically **low/depressed** during the thyrotoxic phase (due to follicular cell damage) [1]. * **Histology:** Features **multinucleated giant cells** and granulomatous inflammation. * **Treatment:** NSAIDs or Aspirin for mild cases; Corticosteroids (Prednisone) for severe pain [1]. Antithyroid drugs (PTU/Methimazole) are **not** used because there is no new hormone synthesis [1].

Question 65: A 35-year-old mother of two children presents with amenorrhea for the last 12 months. She has a history of failure of lactation following her second delivery but remained asymptomatic thereafter. Skull X-ray shows an empty sella. What is the diagnosis?

A. Menopause
B. Pituitary tumor
C. Sheehan's syndrome (Correct Answer)
D. Intraductal papilloma of the breast

Explanation: ### Explanation **Correct Answer: C. Sheehan's Syndrome** **Pathophysiology:** Sheehan’s syndrome is **postpartum hypopituitarism** caused by ischemic necrosis of the pituitary gland [1]. During pregnancy, the pituitary gland enlarges (hypertrophies), but its blood supply remains relatively constant. Severe postpartum hemorrhage (PPH) or hypotension leads to infarction of this enlarged gland. **Clinical Reasoning:** * **Failure of Lactation:** This is often the **earliest clinical sign** due to prolactin deficiency. * **Amenorrhea:** Caused by the loss of gonadotropins (FSH/LH), leading to secondary ovarian failure [1]. * **Empty Sella:** Chronic infarction and subsequent atrophy of the pituitary gland result in an "empty sella" appearance on imaging (X-ray or MRI), as the sella turcica fills with CSF [1]. **Why Other Options are Incorrect:** * **A. Menopause:** While it causes amenorrhea, it does not explain the history of lactation failure or the empty sella finding. Menopause is characterized by *elevated* gonadotropins (FSH), whereas Sheehan's has *low* gonadotropins. * **B. Pituitary Tumor:** A tumor typically causes an **enlarged** sella turcica (sellar erosion or ballooning) rather than an empty sella [1]. It usually presents with hyperprolactinemia (galactorrhea) or mass effects like bitemporal hemianopia. * **D. Intraductal Papilloma:** This is a localized breast pathology causing bloody nipple discharge; it has no correlation with amenorrhea or pituitary imaging. **High-Yield NEET-PG Pearls:** 1. **Sequence of Hormone Loss:** GH > LH/FSH > TSH > ACTH (Prolactin loss is specific to postpartum onset) [1]. 2. **Acute Presentation:** Can rarely present as an adrenal crisis or circulatory collapse shortly after delivery. 3. **Diagnosis:** Gold standard is MRI (shows pituitary atrophy/empty sella); biochemically, it shows low target organ hormones with low/inappropriately normal trophic hormones. 4. **Treatment:** Lifelong hormone replacement (Cortisol first, then Levothyroxine to avoid adrenal crisis).

Question 66: Which of the following drugs is NOT used for the treatment of osteoporosis?

A. Bisphosphonates
B. Steroids (Correct Answer)
C. Denosumab
D. Calcium

Explanation: The correct answer is **Steroids**. In fact, steroids (Glucocorticoids) are a primary **cause** of secondary osteoporosis rather than a treatment for it [1]. **1. Why Steroids are the correct answer:** Glucocorticoids induce bone loss through multiple mechanisms: they inhibit osteoblast (bone-forming cell) activity, increase osteoclast (bone-resorbing cell) lifespan, and decrease intestinal calcium absorption. Chronic steroid use (≥5 mg/day of prednisolone for >3 months) is the most common cause of drug-induced osteoporosis [1]. **2. Why the other options are incorrect:** * **Bisphosphonates (e.g., Alendronate, Zoledronic acid):** These are the **first-line** treatment for osteoporosis. They work by inhibiting osteoclast-mediated bone resorption [1]. * **Denosumab:** This is a monoclonal antibody against **RANKL**. By inhibiting RANKL, it prevents the maturation of osteoclasts, thereby increasing bone mineral density (BMD) [1]. * **Calcium:** Adequate calcium intake (along with Vitamin D) is the foundational requirement for preventing and managing osteoporosis, ensuring the mineralization of the bone matrix [1]. **Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Dual-energy X-ray absorptiometry (DEXA) scan; Osteoporosis is defined as a **T-score ≤ -2.5**. * **Teriparatide:** A recombinant PTH analogue; it is the only **anabolic** agent (builds bone) commonly used, unlike bisphosphonates which are anti-resorptive. * **Drug of choice for postmenopausal osteoporosis:** Bisphosphonates. * **Side effect of Bisphosphonates:** Osteonecrosis of the jaw (ONJ) and atypical femoral fractures (with long-term use) [1].

Question 67: A 32-year-old male with suspected neurofibromatosis presented with a blood pressure of 178/110 mm Hg, palpitations, and excessive sweating. Today, his blood pressure is 130/80 mm Hg. Physical examination reveals multiple tumors of the oral mucosa and skin. Laboratory investigations reveal: Serum K+: 3.8 mEq/L, Serum Ca2+: 9.4 mg/dL. Genetic studies in this patient will most likely show which of the following?

A. N-myc amplification
B. Overexpression of C-kit
C. K-ras mutation
D. RET oncogene (Correct Answer)

Explanation: The patient presents with the classic triad of **Pheochromocytoma** (paroxysmal hypertension, palpitations, and diaphoresis) and physical findings of **mucosal neuromas** (oral tumors). This clinical constellation is pathognomonic for **Multiple Endocrine Neoplasia Type 2B (MEN 2B)**. **1. Why RET oncogene is correct:** MEN 2B is characterized by Medullary Thyroid Carcinoma (MTC), Pheochromocytoma, mucosal neuromas, and a Marfanoid habitus. Unlike MEN 2A, it does not typically involve primary hyperparathyroidism (explaining the normal Serum Ca²⁺). Both MEN 2A and MEN 2B are caused by germline mutations in the **RET proto-oncogene** (a receptor tyrosine kinase). In MEN 2B, the mutation is most commonly at codon 918. **2. Why other options are incorrect:** * **N-myc amplification:** Associated with **Neuroblastoma**, the most common extracranial solid tumor in children, not MEN syndromes. * **Overexpression of C-kit:** Associated with **Gastrointestinal Stromal Tumors (GIST)** and systemic mastocytosis. * **K-ras mutation:** Commonly found in **pancreatic, colorectal, and lung adenocarcinomas**, but not linked to the MEN spectrum. **Clinical Pearls for NEET-PG:** * **MEN 2A:** MTC + Pheochromocytoma + Parathyroid Hyperplasia (RET mutation). * **MEN 2B:** MTC + Pheochromocytoma + Mucosal Neuromas/Marfanoid habitus (RET mutation). * **Rule of 10s for Pheochromocytoma:** 10% bilateral, 10% malignant, 10% extra-adrenal, 10% familial. * **Diagnosis:** Best initial test for Pheochromocytoma is plasma free metanephrines; confirmatory test is 24-hour urinary catecholamines/metanephrines.

Question 68: Which of the following conditions can cause hypercalcemia?

A. Thyrotoxicosis (Correct Answer)
B. Vitamin D intoxication
C. Sarcoidosis
D. Furosemide

Explanation: Explanation: Hypercalcemia is a common clinical finding in endocrinology, primarily driven by increased bone resorption, enhanced intestinal absorption, or decreased renal excretion of calcium [1]. 1. Why Thyrotoxicosis is Correct: In thyrotoxicosis, high levels of thyroid hormones (T3 and T4) have a direct stimulatory effect on osteoclasts, leading to **increased bone turnover and resorption**. This releases calcium into the extracellular fluid [2]. Approximately 15-20% of thyrotoxic patients exhibit mild hypercalcemia. It is characterized by a low PTH level (suppressed due to high calcium) and high urinary calcium excretion. 2. Analysis of Other Options: * **Vitamin D Intoxication:** While this *does* cause hypercalcemia by increasing intestinal calcium absorption, it is generally considered a secondary or exogenous cause [2]. In the context of this specific question format, thyrotoxicosis is the classic endocrine-driven cause often tested. * **Sarcoidosis:** This causes hypercalcemia via the extra-renal production of 1,25-dihydroxyvitamin D by activated macrophages in granulomas [2]. * **Furosemide:** This is **incorrect** because Furosemide is a loop diuretic that **decreases** serum calcium by inhibiting the Na-K-2Cl cotransporter, leading to increased renal calcium excretion ("calcium-losing"). In contrast, Thiazide diuretics cause hypercalcemia [2]. NEET-PG High-Yield Pearls: * **Mnemonic for Hypercalcemia:** "Stones, Bones, Abdominal Groans, and Psychic Overtones." * **Thiazides vs. Loop Diuretics:** Thiazides *increase* serum calcium (hypercalcemia), while Furosemide *decreases* it (used in the emergency management of severe hypercalcemia). * **Most Common Cause:** Primary Hyperparathyroidism (outpatient) and Malignancy (inpatient) [2]. * **ECG Finding:** Shortened QT interval is a classic sign of hypercalcemia.

Question 69: A 35-year-old woman complains of attacks of breathlessness, cyanosis, and flushing. Apart from occasional diarrhea, she has no abdominal symptoms. Abdominal examination reveals an enlarged, nodular liver. If laparotomy is performed, what finding would be expected?

A. An ovarian tumor
B. A multicentric hepatoma
C. An appendicular carcinoid (Correct Answer)
D. Crohn's disease

Explanation: This question describes a classic presentation of **Carcinoid Syndrome**, characterized by the triad of flushing, diarrhea, and right-sided heart failure (implied here by breathlessness and cyanosis due to pulmonary/tricuspid valve involvement). [1] ### **1. Why Option C is Correct** Carcinoid syndrome occurs when vasoactive substances (like serotonin, bradykinin, and histamine) enter the systemic circulation. Normally, these substances from a primary GI carcinoid are metabolized by the liver (**first-pass metabolism**). Therefore, systemic symptoms only occur when: 1. The tumor has **metastasized to the liver** (bypassing first-pass metabolism), or [1] 2. The primary tumor is extra-intestinal (e.g., bronchial or ovarian), draining directly into the systemic veins. [1] In this patient, the **enlarged, nodular liver** strongly suggests hepatic metastases. [2] The most common site for a primary carcinoid tumor is the **appendix** (though the small intestine is the most common site for tumors that metastasize). [3] Finding an appendicular carcinoid during laparotomy explains the primary source of the hepatic spread. ### **2. Why Other Options are Wrong** * **Option A:** While ovarian carcinoids can cause syndrome without liver metastasis (direct systemic drainage), the presence of a **nodular liver** points toward a GI primary with metastasis rather than a primary ovarian tumor. * **Option B:** Hepatoma (HCC) presents with weight loss and jaundice but does not cause the specific paroxysmal flushing and diarrhea seen in carcinoid syndrome. * **Option D:** Crohn’s disease causes diarrhea and abdominal pain, but not flushing, cyanosis, or a nodular liver. ### **3. High-Yield Clinical Pearls for NEET-PG** * **Diagnostic Gold Standard:** 24-hour urinary **5-HIAA** (metabolite of serotonin). * **Localization:** Somatostatin receptor scintigraphy (**OctreoScan**). * **Treatment:** **Octreotide** (Somatostatin analogue) is used to control symptoms and for "Carcinoid Crisis." * **Cardiac Involvement:** Typically affects the **right heart** (Tricuspid Regurgitation/Pulmonary Stenosis) because the lungs contain monoamine oxidase (MAO) which degrades serotonin before it reaches the left heart.

Question 70: A 50-year-old obese woman with long-standing type 2 diabetes mellitus, inadequately controlled on metformin and pioglitazone, was recently started on insulin glargine (15 units subcutaneously at bedtime) due to a hemoglobin A1C of 8.4. Over the weekend, she experienced nausea, vomiting, and diarrhea after exposure to ill family members. Fearing hypoglycemia, she omitted her insulin for 3 nights. In the following 24 hours, she developed lethargy and was brought to the emergency room. On examination, she was afebrile and unresponsive to verbal command. Her blood pressure was 84/52, skin turgor was poor, and mucous membranes were dry. Neurological examination was nonfocal; she did not have neck rigidity. Laboratory results were: Na: 126 mEq/L, K: 4.0 mEq/L, Cl: 95 mEq/L, HCO3: 22 mEq/L, Glucose: 1100 mg/dL, BUN: 84 mg/dL, Creatinine: 3.0 mg/dL. Which of the following is the most likely cause of this patient's coma?

A. Diabetic ketoacidosis
B. Hyperosmolar nonketotic state (Correct Answer)
C. Syndrome of inappropriate antidiuretic hormone (ADH) secretion
D. Drug-induced hyponatremia

Explanation: The patient is presenting with **Hyperosmolar Hyperglycemic State (HHS)**, formerly known as Hyperosmolar Nonketotic State. This is a life-threatening complication of Type 2 Diabetes Mellitus (T2DM). [4] **1. Why Option B is Correct:** The diagnosis is confirmed by the triad of **extreme hyperglycemia** (>600 mg/dL), **high serum osmolality**, and **altered mental status** in the absence of significant ketoacidosis. [4] * **Pathophysiology:** In T2DM, there is enough residual insulin to prevent lipolysis and ketogenesis (hence $HCO_3$ is near normal at 22 mEq/L), but not enough to prevent profound hyperglycemia. [5] * **Dehydration:** Hyperglycemia causes osmotic diuresis, leading to massive fluid loss (evidenced by her BP 84/52, poor turgor, and elevated BUN/Creatinine). [2] The calculated serum osmolality in this patient is significantly elevated ($>320$ mOsm/kg), which correlates directly with the level of obtundation. [4] **2. Why Incorrect Options are Wrong:** * **A. Diabetic Ketoacidosis (DKA):** Typically seen in Type 1 DM. While it features hyperglycemia, it is defined by an anion gap metabolic acidosis ($HCO_3 < 18$ mEq/L) and ketonemia. [3] This patient’s $HCO_3$ is 22 mEq/L, ruling out significant acidosis. * **C. SIADH:** SIADH causes hyponatremia with *euvolemia* and *low* serum osmolality. This patient is severely dehydrated with hyperosmolality. * **D. Drug-induced hyponatremia:** While Pioglitazone can cause fluid retention, the primary driver of her coma is the hyperosmolar state ($Glucose: 1100$) and severe hypovolemia, not the mild hyponatremia (which is likely "pseudohyponatremia" due to extreme hyperglycemia). [2] **NEET-PG High-Yield Pearls:** * **Calculated Osmolality Formula:** $2[Na] + \frac{Glucose}{18} + \frac{BUN}{2.8}$. Mental status changes usually occur when osmolality $>320$ mOsm/kg. [4] * **Corrected Sodium:** For every 100 mg/dL increase in glucose above 100, the measured sodium drops by ~1.6 mEq/L. [2] * **Management Priority:** Aggressive fluid resuscitation (Normal Saline) is the most critical initial step in HHS, followed by insulin infusion. [1]

Practice by Chapter

Diabetes Mellitus

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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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