Endocrinology — MCQs

A 40-year-old woman presents with symptoms of light-headedness, sweating, palpitations, and hunger, most pronounced when she misses a meal. Her physical examination, vital signs, and past medical history are unremarkable. During an episode, her blood glucose level was 30 mg/dL, and symptoms resolved with juice. What is the most likely diagnosis?

Q683Medium

Addison disease with hypoparathyroidism and mucocutaneous candidiasis is seen with which condition?

Q684Easy

A 35-year-old female with a history of amenorrhea and galactorrhea, and children aged 5 and 6 years, has elevated prolactin levels on blood examination. What is the most likely finding on CT scan of the head?

Q685Medium

A 36-year-old female presents with symptoms of hyperparathyroidism, a tumor in the pancreas, adrenal cortical hyperplasia, pituitary adenomas, an islet cell tumor, and cutaneous angiofibromas. What is the diagnosis?

Q686Easy

Which drug is used for the management of both Type I and Type II Diabetes Mellitus?

Q687Easy

Which of the following laboratory findings is characteristic of primary hypothyroidism?

Q688Medium

A 35-year-old male presents with symptoms of palpitations, tremors, nervousness, and headache. His father has a history of type 2 DM and his mother has a history of psychiatric illness. He has no chronic medical conditions and takes no medications. He appears anxious, sweaty, and shaky. His fingerstick glucose is 45 mg/dl. The patient is administered a bolus of 50% glucose which rapidly improves his symptoms. CECT abdomen shows a mass. Which of the following is likely to be seen after overnight fasting?

Q689Medium

A patient sustains a transaction of the pituitary stalk following an accident. Which of the following clinical manifestations will NOT occur?

Q690Easy

A patient presented with episodes of flushing and hypotension. His urinary 5HIAA levels were found to be increased. What is the diagnosis?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 681: Increased intracellular insulin is characterized by all of the following EXCEPT:

A. Increased insulin secretion
B. Increased glucagon secretion (Correct Answer)
C. Hypoglycemia
D. Hypokalemia

Explanation: **Explanation:** The physiological effects of insulin are primarily anabolic and occur in response to high blood glucose levels [1], [2]. To understand this question, one must recognize the **reciprocal relationship** between insulin and glucagon [4]. **Why "Increased glucagon secretion" is the correct answer:** Insulin and glucagon act as counter-regulatory hormones [3]. When insulin levels are high (hyperinsulinemia), insulin acts directly on the alpha cells of the pancreas to **inhibit** the secretion of glucagon [1], [4]. Therefore, increased insulin is characterized by *decreased* glucagon secretion, making Option B the false statement. **Analysis of Incorrect Options:** * **A. Increased insulin secretion:** This is a direct cause of increased intracellular insulin signaling. In states like insulinoma or post-prandial surges, high circulating insulin leads to increased cellular uptake [2]. * **C. Hypoglycemia:** Insulin promotes glucose uptake into skeletal muscle and adipose tissue via GLUT-4 translocation and inhibits hepatic gluconeogenesis [1], [5]. An excess of insulin inevitably leads to a drop in blood glucose [2], [4]. * **D. Hypokalemia:** Insulin stimulates the **Na+/K+ ATPase pump**, driving potassium from the extracellular fluid into the intracellular compartment [5]. This is the physiological basis for using insulin-glucose infusions to treat hyperkalemia [5]. **NEET-PG High-Yield Pearls:** * **The "Shift" Rule:** Insulin shifts three things into cells: Glucose, Potassium ($K^+$), and Magnesium ($Mg^{2+}$). * **Paracrine Inhibition:** Within the Islets of Langerhans, insulin (from Beta cells) inhibits glucagon (from Alpha cells), and somatostatin (from Delta cells) inhibits both [4]. * **Clinical Correlation:** In Diabetic Ketoacidosis (DKA) management, always check potassium levels before starting insulin, as insulin will further worsen hypokalemia [5].

Question 682: A 40-year-old woman presents with symptoms of light-headedness, sweating, palpitations, and hunger, most pronounced when she misses a meal. Her physical examination, vital signs, and past medical history are unremarkable. During an episode, her blood glucose level was 30 mg/dL, and symptoms resolved with juice. What is the most likely diagnosis?

A. Excess growth hormone
B. Cushing disease
C. Thyrotoxicosis
D. Tumor of the pancreatic beta-cells (Correct Answer)

Explanation: **Explanation:** The clinical presentation describes a classic case of **Whipple’s Triad**, which is the diagnostic cornerstone for an **Insulinoma** (a tumor of the pancreatic beta-cells). [1] **1. Why the Correct Answer is Right:** The patient exhibits symptoms of hypoglycemia (neuroglycopenic: light-headedness; autonomic: sweating, palpitations, hunger) specifically during fasting states. The diagnosis is confirmed by Whipple’s Triad: * Symptoms of hypoglycemia. * Low plasma glucose (30 mg/dL) at the time of symptoms. [2] * Relief of symptoms following the administration of glucose (juice). Insulinomas are the most common islet cell tumors of the pancreas. They autonomously secrete insulin regardless of blood glucose levels, leading to profound fasting hypoglycemia. [1] **2. Why the Incorrect Options are Wrong:** * **Excess Growth Hormone (Acromegaly):** Growth hormone is a counter-regulatory hormone that antagonizes insulin. Excess GH typically leads to secondary diabetes mellitus or impaired glucose tolerance, not hypoglycemia. * **Cushing Disease:** Excess cortisol (another counter-regulatory hormone) promotes gluconeogenesis and insulin resistance, leading to hyperglycemia. * **Thyrotoxicosis:** While it causes palpitations and sweating, it typically presents with weight loss despite increased appetite and heat intolerance. It does not cause fasting hypoglycemia; in fact, it may slightly elevate blood glucose due to increased glycogenolysis. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** The gold standard for insulinoma is the **72-hour fasting test**, showing high insulin and **C-peptide** levels despite hypoglycemia. [1] * **Localization:** Endoscopic Ultrasound (EUS) is highly sensitive for locating these small tumors. * **Rule of 10s:** 10% are malignant, 10% are multiple, and 10% are associated with **MEN-1 syndrome**. * **Factitious Disorder:** High insulin with *low* C-peptide suggests exogenous insulin injection. High insulin and high C-peptide with a positive screen for sulfonylureas suggests oral hypoglycemic abuse. [1]

Question 683: Addison disease with hypoparathyroidism and mucocutaneous candidiasis is seen with which condition?

A. Isolated autoimmune adrenalitis
B. Triple A syndrome
C. Autoimmune polyglandular syndrome 2
D. Autoimmune polyglandular syndrome 1 (Correct Answer)

Explanation: **Explanation:** The clinical triad of **Chronic Mucocutaneous Candidiasis (CMC)**, **Hypoparathyroidism**, and **Addison’s Disease** is the hallmark of **Autoimmune Polyglandular Syndrome Type 1 (APS-1)**, also known as **APECED** (Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy) [1]. 1. **Why APS-1 is correct:** It is an autosomal recessive disorder caused by a mutation in the **AIRE (Autoimmune Regulator) gene** on chromosome 21 [1]. This gene is crucial for promoting self-tolerance in the thymus. The components typically appear in a specific chronological order: Candidiasis (infancy), followed by Hypoparathyroidism (childhood), and finally Addison’s disease (adolescence). Diagnosis requires at least two of these three primary features [1]. 2. **Why other options are incorrect:** * **Isolated autoimmune adrenalitis:** This refers to Addison’s disease occurring alone without other endocrinopathies or candidiasis. * **Triple A Syndrome (Allgrove Syndrome):** Characterized by **A**chalasia cardia, **A**lacrimia, and **A**drenal insufficiency (ACTH resistance). It does not involve hypoparathyroidism or candidiasis. * **APS-2 (Schmidt Syndrome):** This is more common than APS-1 and is characterized by Addison’s disease plus autoimmune thyroid disease and/or Type 1 Diabetes Mellitus. It notably **lacks** hypoparathyroidism and candidiasis [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** APS-1 is Autosomal Recessive; APS-2 is Polygenic (linked to HLA-DR3/DR4) [1]. * **Order of Appearance:** In APS-1, Mucocutaneous Candidiasis is usually the first manifestation. * **Ectodermal Dystrophy:** Look for enamel hypoplasia, vitiligo, and nail dystrophy in APS-1 cases. * **Mnemonic:** APS-1 = **C**andidiasis, **A**ddison’s, **H**ypoparathyroidism (**CAH**).

Question 684: A 35-year-old female with a history of amenorrhea and galactorrhea, and children aged 5 and 6 years, has elevated prolactin levels on blood examination. What is the most likely finding on CT scan of the head?

A. Pituitary adenoma (Correct Answer)
B. Craniopharyngioma
C. Sheehan's syndrome
D. Pinealoma

Explanation: ### Explanation **Correct Answer: A. Pituitary Adenoma** The clinical presentation of **amenorrhea** (absence of menstruation) and **galactorrhea** (inappropriate milk production) in a non-pregnant female is the classic "Amenorrhea-Galactorrhea Syndrome." This is most commonly caused by a **Prolactinoma**, a functional pituitary adenoma [1]. **Pathophysiology:** Elevated prolactin levels (hyperprolactinemia) inhibit the pulsatile release of GnRH from the hypothalamus. This leads to decreased FSH and LH, resulting in secondary amenorrhea and infertility [1]. Simultaneously, prolactin directly stimulates mammary tissue to produce milk. In a 35-year-old female, a prolactin-secreting pituitary adenoma is the most frequent pathological cause of these symptoms. **Analysis of Incorrect Options:** * **B. Craniopharyngioma:** These are suprasellar tumors derived from Rathke’s pouch. While they can cause hyperprolactinemia via "stalk effect" (compression of the pituitary stalk preventing dopamine from reaching the pituitary), they typically present with visual field defects (bitemporal hemianopia) and growth retardation in children, rather than isolated galactorrhea in adults [1]. * **C. Sheehan's Syndrome:** This refers to postpartum pituitary necrosis due to severe obstetric hemorrhage. It results in **panhypopituitarism** (deficiency of all hormones), leading to a *failure* to lactate and permanent amenorrhea, rather than excessive milk production. * **D. Pinealoma:** These tumors of the pineal gland typically present with Parinaud syndrome (upward gaze palsy) and precocious puberty (in children) due to HCG production, not isolated hyperprolactinemia. **High-Yield Clinical Pearls for NEET-PG:** * **Drug-induced hyperprolactinemia:** Always rule out dopamine antagonists (e.g., Metoclopramide, Haloperidol, Risperidone) before diagnosing an adenoma [1]. * **Microadenoma vs. Macroadenoma:** Microadenomas are <10 mm; Macroadenomas are >10 mm [1]. * **Treatment of Choice:** Medical management with **Dopamine agonists** (Cabergoline > Bromocriptine) is the first-line treatment for prolactinomas, unlike most other pituitary tumors which require surgery [1].

Question 685: A 36-year-old female presents with symptoms of hyperparathyroidism, a tumor in the pancreas, adrenal cortical hyperplasia, pituitary adenomas, an islet cell tumor, and cutaneous angiofibromas. What is the diagnosis?

A. Multiple Endocrine Neoplasia type 1 (MEN 1) (Correct Answer)
B. Multiple Endocrine Neoplasia type 2A (MEN 2A)
C. Multiple Endocrine Neoplasia type 2B (MEN 2B)
D. Multiple Endocrine Neoplasia type 2C (MEN 2C)

Explanation: The patient presents with the classic triad of **MEN 1 (Wermer Syndrome)**, often remembered by the **"3 Ps"**: **P**arathyroid hyperplasia (leading to hyperparathyroidism), **P**ancreatic islet cell tumors (e.g., gastrinomas, insulinomas), and **P**ituitary adenomas (most commonly prolactinomas) [1]. The presence of **cutaneous angiofibromas**, collagenomas, and lipomas are recognized dermatological manifestations specific to MEN 1. While adrenal cortical hyperplasia can occur in MEN 1, it is less common than the primary triad but helps differentiate it from other syndromes. The condition is caused by a mutation in the **MEN1 gene** on chromosome **11q13**, which encodes the protein **menin**. **Why other options are incorrect:** * **MEN 2A (Sipple Syndrome):** Characterized by Medullary Thyroid Carcinoma (MTC), Pheochromocytoma, and Parathyroid hyperplasia. It lacks pituitary and pancreatic involvement. * **MEN 2B:** Characterized by MTC, Pheochromocytoma, and distinct physical features like **Mucosal neuromas** and a **Marfanoid habitus**. It does not involve the parathyroid or pancreas. * **MEN 2C:** This is an obsolete term sometimes previously used to describe familial medullary thyroid carcinoma without other endocrine features; it is not a standard diagnosis in modern classification. **NEET-PG High-Yield Pearls:** * **Most common initial presentation of MEN 1:** Primary Hyperparathyroidism (seen in >90% of patients by age 40). * **Most common pancreatic tumor in MEN 1:** Gastrinoma (Zollinger-Ellison Syndrome). * **Inheritance:** All MEN syndromes are **Autosomal Dominant** [1]. * **MEN 2 Association:** Both 2A and 2B are associated with mutations in the **RET proto-oncogene**.

Question 686: Which drug is used for the management of both Type I and Type II Diabetes Mellitus?

A. Glipizide
B. Tolbutamide
C. Metformin
D. Insulin (Correct Answer)

Explanation: **Explanation:** **Insulin** is the correct answer because it is the only pharmacological agent essential for Type 1 Diabetes Mellitus (T1DM) and frequently required for Type 2 Diabetes Mellitus (T2DM). [1] * **Type 1 DM:** Characterized by absolute insulin deficiency due to autoimmune destruction of pancreatic beta cells. Exogenous insulin is life-saving and mandatory for survival. [1] * **Type 2 DM:** Characterized by insulin resistance and progressive beta-cell exhaustion. While initial management involves lifestyle changes and oral hypoglycemics, many patients eventually require insulin for glycemic control (secondary failure) or during acute stress, surgery, or pregnancy. [1] **Analysis of Incorrect Options:** * **Glipizide & Tolbutamide (Sulfonylureas):** These drugs act by stimulating insulin secretion from functional pancreatic beta cells (via the SUR1 receptor). Since T1DM patients have no functional beta cells, these drugs are ineffective and contraindicated. * **Metformin (Biguanide):** Its primary mechanism is the inhibition of hepatic gluconeogenesis and improvement of peripheral insulin sensitivity [1]. It requires endogenous insulin to be effective; therefore, it is not a standard treatment for T1DM (where insulin is absent), though it is sometimes used as an adjunct in obese T1DM patients. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Pramlintide:** An amylin analogue that can also be used in both T1DM and T2DM (as an adjunct to insulin). * **Insulin Requirement:** In T1DM, the typical daily dose is **0.5–1.0 U/kg/day**. * **Honeymoon Phase:** A transient period in early T1DM where exogenous insulin requirements decrease significantly due to temporary recovery of remaining beta cells. * **Drug of Choice:** Insulin is the drug of choice for DM during **pregnancy** and for patients with **end-stage renal or hepatic failure**. [1]

Question 687: Which of the following laboratory findings is characteristic of primary hypothyroidism?

A. Decreased T3, decreased T4, increased TSH (Correct Answer)
B. Decreased T3, increased T4, decreased TSH
C. Normal T3, normal T4, increased TSH
D. Decreased T3, decreased T4, normal TSH

Explanation: ### Explanation **Correct Answer: A. Decreased T3, decreased T4, increased TSH** **Understanding the Concept:** Primary hypothyroidism occurs due to a failure of the thyroid gland itself (most commonly Hashimoto’s thyroiditis). When the thyroid gland cannot produce sufficient thyroid hormones (**T4 and T3**), the negative feedback loop to the pituitary gland is lost [1]. In response, the anterior pituitary increases the secretion of **Thyroid Stimulating Hormone (TSH)** to "force" the thyroid to work [2]. Therefore, the hallmark of primary hypothyroidism is a **high TSH** accompanied by **low free T4** [1]. **Analysis of Incorrect Options:** * **Option B (Decreased T3, increased T4, decreased TSH):** This pattern is physiologically inconsistent. High T4 would typically suppress TSH, not occur alongside a low TSH unless there is an exogenous source, but T3 would not be low. * **Option C (Normal T3, normal T4, increased TSH):** This is the characteristic profile of **Subclinical Hypothyroidism**. The pituitary is sensing a mild deficiency and compensating by raising TSH to keep T4/T3 within the normal range. * **Option D (Decreased T3, decreased T4, normal/low TSH):** This indicates **Secondary (Central) Hypothyroidism**, where the pathology lies in the pituitary or hypothalamus. The thyroid is capable of working, but the "stimulus" (TSH) is missing. **NEET-PG High-Yield Pearls:** 1. **TSH is the most sensitive screening test** for thyroid dysfunction. 2. **T4 vs. T3:** T4 is the primary secretory product of the thyroid; T3 is often the last to fall in hypothyroidism because peripheral conversion of T4 to T3 is maintained. 3. **Hashimoto’s Thyroiditis:** The most common cause of primary hypothyroidism in iodine-sufficient areas; associated with **Anti-TPO antibodies**. 4. **Wolff-Chaikoff Effect:** Hypothyroidism induced by a large load of iodine (e.g., amiodarone).

Question 688: A 35-year-old male presents with symptoms of palpitations, tremors, nervousness, and headache. His father has a history of type 2 DM and his mother has a history of psychiatric illness. He has no chronic medical conditions and takes no medications. He appears anxious, sweaty, and shaky. His fingerstick glucose is 45 mg/dl. The patient is administered a bolus of 50% glucose which rapidly improves his symptoms. CECT abdomen shows a mass. Which of the following is likely to be seen after overnight fasting?

A. Serum insulin, Serum pro-insulin, C-peptide levels: Normal, Normal, Normal
B. Serum insulin, Serum pro-insulin, C-peptide levels: Increased, Increased, Increased (Correct Answer)
C. Serum insulin, Serum pro-insulin, C-peptide levels: Increased, Normal, Decreased
D. Serum insulin, Serum pro-insulin, C-peptide levels: Decreased, Increased, Increased

Explanation: ### **Explanation** The clinical presentation of symptomatic hypoglycemia (palpitations, tremors, sweating) relieved by glucose administration, combined with a CECT finding of an abdominal mass, is classic for an **Insulinoma**—a beta-cell tumor of the pancreas. **1. Why Option B is Correct:** In a patient with an insulinoma, there is autonomous, unregulated secretion of insulin. Because insulin is synthesized as **pro-insulin** and cleaved into equal parts of **insulin** and **C-peptide** before secretion, all three markers will be elevated during a period of hypoglycemia (e.g., after an overnight fast). [1] * **Insulin:** High (autonomous secretion). * **C-peptide:** High (indicates endogenous production). * **Pro-insulin:** High (often >20% of total immunoreactive insulin in tumor cases). **2. Why Other Options are Incorrect:** * **Option A:** Normal levels during hypoglycemia are inappropriate; insulin should be suppressed (typically <3 μU/mL) when blood glucose is <55 mg/dL. * **Option C:** This pattern (High Insulin, Low C-peptide) is characteristic of **Exogenous Insulin Surreptitious Use**. Since synthetic insulin does not contain C-peptide, the high systemic insulin suppresses endogenous production. * **Option D:** This pattern does not correspond to any common clinical entity. Low insulin with high C-peptide is physiologically impossible as they are secreted in a 1:1 molar ratio. [1] **3. Clinical Pearls for NEET-PG:** * **Whipple’s Triad:** 1. Symptoms of hypoglycemia, 2. Low plasma glucose (<55 mg/dL), 3. Relief of symptoms after glucose administration. [2] * **Gold Standard Diagnosis:** 72-hour supervised fast (though many patients trigger symptoms within 12–24 hours). * **Localization:** Most insulinomas are small, solitary, and benign. Endoscopic Ultrasound (EUS) is highly sensitive for localization. * **Factitious Hypoglycemia:** Always check **Sulfonylurea levels** in the urine/blood to rule out oral hypoglycemic abuse, which also presents with high insulin and high C-peptide. [1]

Question 689: A patient sustains a transaction of the pituitary stalk following an accident. Which of the following clinical manifestations will NOT occur?

A. Diabetes mellitus (Correct Answer)
B. Diabetes insipidus
C. Hyperprolactinemia
D. Hypothyroidism

Explanation: Pituitary stalk transection (also known as Pituitary Stalk Interruption Syndrome when congenital) disrupts the connection between the hypothalamus and the pituitary gland. This results in the loss of hypothalamic control over the pituitary hormones. **Why Diabetes Mellitus is the Correct Answer:** Diabetes Mellitus (DM) is a disorder of glucose metabolism primarily involving **insulin** (produced by the pancreas). Pituitary stalk injury affects the hypothalamic-pituitary axis, not the endocrine pancreas. Therefore, stalk transection does not cause DM. In fact, due to the loss of Growth Hormone (GH) and Cortisol (which are insulin-antagonists), patients may actually experience increased insulin sensitivity or hypoglycemia [1]. **Analysis of Incorrect Options:** * **Diabetes Insipidus (DI):** The hypothalamus produces Antidiuretic Hormone (ADH), which travels down the stalk to be stored in the posterior pituitary. Transection interrupts this flow, leading to a deficiency of ADH and resulting in central DI [1]. * **Hyperprolactinemia:** Prolactin is the only anterior pituitary hormone under tonic **inhibition** by hypothalamic **Dopamine** (Prolactin-Inhibiting Factor). Stalk transection removes this inhibitory "brake," leading to an isolated rise in Prolactin levels [1]. * **Hypothyroidism:** The pituitary fails to receive Thyroid-Releasing Hormone (TRH) from the hypothalamus, leading to secondary (central) hypothyroidism due to low TSH [1]. **High-Yield Clinical Pearls for NEET-PG:** * **The "Stalk Effect":** Any lesion compressing the pituitary stalk (like a Craniopharyngioma) that causes a mild rise in Prolactin (<200 ng/mL) is termed the "Stalk Effect." * **Panhypopituitarism:** Stalk transection typically leads to a deficiency of all anterior pituitary hormones (GH, LH, FSH, TSH, ACTH) *except* Prolactin, which increases [1]. * **Triphasic Response:** Acute stalk injury often causes a triphasic response in water balance: initial DI, followed by a period of SIADH (due to leaking ADH from dying neurons), and finally permanent DI.

Question 690: A patient presented with episodes of flushing and hypotension. His urinary 5HIAA levels were found to be increased. What is the diagnosis?

A. Pheochromocytoma
B. Carcinoid syndrome (Correct Answer)
C. Addison's disease
D. SIADH

Explanation: ### Explanation **Correct Answer: B. Carcinoid syndrome** **1. Why it is correct:** Carcinoid syndrome is caused by the systemic release of vasoactive substances, primarily **serotonin (5-HT)**, from neuroendocrine tumors (most commonly originating in the ileum and metastasizing to the liver). [1] * **Urinary 5-HIAA (5-Hydroxyindoleacetic acid):** This is the end-metabolite of serotonin. Elevated 24-hour urinary 5-HIAA is the gold-standard biochemical marker for diagnosing carcinoid syndrome. * **Clinical Presentation:** The classic triad includes **flushing**, secretory diarrhea, and wheezing. While serotonin usually causes hypertension, other co-released mediators like bradykinins and histamine can lead to **hypotension** during a "carcinoid crisis." **2. Why the other options are incorrect:** * **A. Pheochromocytoma:** Presents with the "classic triad" of headache, sweating, and palpitations. It is characterized by **hypertension** (not hypotension) and elevated urinary **VMA/metanephrines**, not 5-HIAA. [3] * **C. Addison’s Disease:** While it causes hypotension (due to cortisol/aldosterone deficiency) and skin hyperpigmentation, it does not cause episodic flushing or elevated 5-HIAA. * **D. SIADH:** Characterized by hyponatremia and concentrated urine. It does not present with flushing or 5-HIAA abnormalities. [2] **3. High-Yield Clinical Pearls for NEET-PG:** * **Localization:** Carcinoid tumors of the midgut only cause the syndrome once they **metastasize to the liver**, bypassing the portal metabolism (first-pass effect). [1] * **Cardiac Involvement:** Look for **Right-sided heart failure** (Tricuspid regurgitation and Pulmonary stenosis) due to endocardial fibrosis. Left-sided valves are usually spared as the lungs metabolize serotonin. * **Pellagra Connection:** Excessive serotonin production consumes dietary **Tryptophan**, leading to Niacin (Vitamin B3) deficiency, which can cause Pellagra (Dermatitis, Diarrhea, Dementia). * **Management:** **Octreotide** (somatostatin analog) is the drug of choice to control symptoms.

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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