Endocrinology — MCQs
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What is the fasting blood sugar level diagnostic of overt diabetes mellitus?
A 63-year-old male presented with chronic watery diarrhea associated with flushing, characterized by sudden onset deep red or violaceous erythema of the upper body, often with pruritus, lacrimation, and facial edema. The flushing was noticed to be precipitated by exercise, alcohol, stress, and cheese intake. He has a history of wheezing and clinical examination revealed pellagra-like skin lesions. Which of the following is NOT a useful step in the management of this clinical condition?
Which one of the following oral hypoglycemic agents is not an insulin secretagogue?
Reduction in the flow of saliva is not generally seen in which of the following conditions?
Consumption of which of the following is not associated with the development of diffuse nontoxic goiter?
What is the dose adjustment required for insulin in a patient who is diagnosed with stage IV chronic kidney disease (CKD)?
A 56-year-old man presents with a change in skin color, fatigue, and abdominal pain. He has also noticed increased urine output and thirst. On examination, his skin appears bronze in color, his liver span is 16 cm, and there is loss of body hair, and testicular atrophy. His ferritin is 600 ng/mL (normal 15-200 ng/mL), aspartate amino transferase (AST) 130 U/L (normal 8-20 U/L), alanine amino transferase (ALT) 150 U/L (normal 8-20 U/L), and total bilirubin 0.5 mg/dL (normal 0.1-1 mg/dL). Coagulation tests and albumin level are normal but the random glucose is elevated at 250 mg/dL. Which of the following is the most likely diagnosis?
Which of the following is NOT a characteristic feature of Metabolic Syndrome (Syndrome X)?
Gynaecomastia is seen in which of the following conditions?
A 30-year-old male with NIDDM has a blood pressure of 150/90 mmHg and persistent albuminuria on urine examination. What is the most appropriate line of treatment?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 911: What is the fasting blood sugar level diagnostic of overt diabetes mellitus?
- A. 106 mg/dL
- B. 116 mg/dL
- C. 126 mg/dL (Correct Answer)
- D. 140 mg/dL
Explanation: The diagnosis of Diabetes Mellitus (DM) is based on specific glycemic thresholds established by the American Diabetes Association (ADA) and WHO [1]. ### **Explanation of the Correct Answer** **Option C (126 mg/dL)** is the correct threshold for diagnosing overt diabetes. Fasting is defined as no caloric intake for at least 8 hours. A **Fasting Plasma Glucose (FPG) ≥ 126 mg/dL (7.0 mmol/L)** on two separate occasions (or once with symptoms) indicates that the pancreas cannot maintain basal glucose homeostasis, confirming the diagnosis of DM [1]. ### **Analysis of Incorrect Options** * **Option A (106 mg/dL) & B (116 mg/dL):** These values fall within the **Prediabetes** range (Impaired Fasting Glucose). Prediabetes is defined as an FPG between **100–125 mg/dL** [1]. While these levels indicate increased cardiovascular risk, they do not meet the criteria for overt diabetes. * **Option D (140 mg/dL):** While this value is diagnostic of diabetes (as it is >126 mg/dL), it is not the *minimum* diagnostic threshold. Note that 140 mg/dL is the cutoff for the 2-hour value in an Oral Glucose Tolerance Test (OGTT) to define **Impaired Glucose Tolerance (140–199 mg/dL)**. ### **NEET-PG High-Yield Pearls** To diagnose Diabetes Mellitus, any **one** of the following criteria must be met: 1. **HbA1c:** ≥ 6.5% 2. **Fasting Plasma Glucose (FPG):** ≥ 126 mg/dL [1] 3. **2-hour Post-Prandial (75g OGTT):** ≥ 200 mg/dL 4. **Random Plasma Glucose:** ≥ 200 mg/dL **PLUS** classic symptoms (polyuria, polydipsia, weight loss) [1]. * **Note:** In the absence of unequivocal hyperglycemia, results should be confirmed by repeat testing. * **Screening:** In asymptomatic adults, screening should begin at age 35 (revised from 45).
Question 912: A 63-year-old male presented with chronic watery diarrhea associated with flushing, characterized by sudden onset deep red or violaceous erythema of the upper body, often with pruritus, lacrimation, and facial edema. The flushing was noticed to be precipitated by exercise, alcohol, stress, and cheese intake. He has a history of wheezing and clinical examination revealed pellagra-like skin lesions. Which of the following is NOT a useful step in the management of this clinical condition?
- A. Lanreotide can be used to control the symptoms.
- B. Hepatic chemoembolization using doxorubicin is effective.
- C. Interferon Alpha can be effective in controlling the symptoms.
- D. Rapamycin is useful to control symptoms. (Correct Answer)
Explanation: ### **Explanation** The clinical presentation of chronic watery diarrhea, violaceous flushing (precipitated by alcohol/cheese), wheezing, and pellagra-like skin lesions (due to niacin deficiency caused by tryptophan depletion) is diagnostic of **Carcinoid Syndrome**. This syndrome typically occurs when a neuroendocrine tumor (NET) has metastasized to the liver, allowing vasoactive substances like serotonin to bypass hepatic metabolism [1]. **Why Option D is the Correct Answer (Incorrect Management Step):** **Rapamycin (Sirolimus)** is an mTOR inhibitor primarily used as an immunosuppressant. While **Everolimus** (a rapamycin analog) is approved for treating the *progression* of advanced neuroendocrine tumors, it is not used for the acute or symptomatic control of carcinoid syndrome symptoms (flushing and diarrhea). Therefore, Rapamycin is not a standard step in symptom management. **Analysis of Other Options:** * **Option A (Lanreotide):** Somatostatin analogs (Octreotide/Lanreotide) are the first-line treatment for symptomatic control as they inhibit the release of serotonin and other peptides. * **Option B (Hepatic Chemoembolization):** Since symptoms usually arise from hepatic metastases, debulking the tumor via chemoembolization (using agents like Doxorubicin) reduces the hormone load and effectively palliates symptoms. * **Option C (Interferon Alpha):** This can be used as an add-on therapy to somatostatin analogs to control symptoms and potentially stabilize tumor growth. ### **High-Yield Clinical Pearls for NEET-PG** * **Diagnosis:** The best initial screening test is **24-hour urinary 5-HIAA** (5-hydroxyindoleacetic acid) levels. * **Localization:** **68Ga-DOTATATE PET/CT** is the most sensitive imaging modality for neuroendocrine tumors. * **Cardiac Involvement:** Look for **Hedinger Syndrome** (fibrosis of the right-sided heart valves, specifically tricuspid regurgitation and pulmonary stenosis). * **Pellagra Connection:** Serotonin is synthesized from **Tryptophan** [2]. Excessive production in carcinoid syndrome shunts tryptophan away from Niacin (Vitamin B3) synthesis, leading to pellagra (Dermatitis, Diarrhea, Dementia) [2].
Question 913: Which one of the following oral hypoglycemic agents is not an insulin secretagogue?
- A. Gliclazide
- B. Glimiperide
- C. Repaglinide
- D. Rosiglitazone (Correct Answer)
Explanation: **Explanation:** The core concept tested here is the classification of oral hypoglycemic agents (OHAs) based on their mechanism of action. **Insulin secretagogues** are drugs that stimulate the pancreas to release insulin, whereas **insulin sensitizers** improve the body's response to existing insulin. **Why Rosiglitazone is the Correct Answer:** Rosiglitazone belongs to the **Thiazolidinedione (TZD)** class. Its primary mechanism is as a selective agonist for the nuclear receptor **PPAR-γ** (Peroxisome Proliferator-Activated Receptor gamma) [3]. It works as an **insulin sensitizer**, primarily increasing glucose uptake in peripheral tissues (adipose and muscle) and decreasing hepatic glucose production [3]. It does **not** stimulate the pancreatic beta cells to secrete insulin. **Why the other options are incorrect:** * **Gliclazide & Glimepiride (Options A & B):** These are **Sulfonylureas** (Second and Third generation, respectively). They are classic secretagogues that work by closing ATP-sensitive K+ channels in the pancreatic beta-cell membrane, leading to depolarization and subsequent insulin release [1]. * **Repaglinide (Option C):** This belongs to the **Meglitinide** class. Like sulfonylureas, meglitinides are short-acting secretagogues that stimulate insulin release by binding to a distinct site on the same K+ channel complex. **High-Yield Clinical Pearls for NEET-PG:** * **TZD Side Effects:** Weight gain, peripheral edema, and increased risk of heart failure (due to fluid retention) and bone fractures [1]. * **Hypoglycemia Risk:** Secretagogues (Sulfonylureas/Meglitinides) carry a high risk of hypoglycemia [1], whereas sensitizers (Metformin/TZDs) generally do not cause hypoglycemia when used as monotherapy. * **Metformin:** The first-line drug for Type 2 DM; it is an insulin sensitizer (AMPK activator), not a secretagogue [2].
Question 914: Reduction in the flow of saliva is not generally seen in which of the following conditions?
- A. Elderly diabetics
- B. Patients undergoing radiation therapy
- C. Patients suffering from parkinsonism (Correct Answer)
- D. Patients on phenothiazine drugs
Explanation: In Parkinsonism, patients frequently present with **sialorrhea** (excessive drooling). It is a common misconception that this is due to increased saliva production; in reality, it is caused by **impaired swallowing (dysphagia)** and infrequent spontaneous swallowing due to muscular rigidity and bradykinesia. Therefore, the flow of saliva is not reduced; rather, it pools and escapes the mouth. **Explanation of Options:** * **Elderly Diabetics:** Chronic hyperglycemia leads to autonomic neuropathy affecting the salivary glands and osmotic diuresis, which causes dehydration and subsequent **xerostomia** (dry mouth). * **Radiation Therapy:** Radiation to the head and neck causes direct inflammatory and fibrotic damage to the acinar cells of the salivary glands (especially the parotids), leading to a significant and often permanent reduction in salivary flow. * **Phenothiazine Drugs:** These are typical antipsychotics with significant **anticholinergic properties**. They block muscarinic receptors on salivary glands, leading to decreased secretions and dry mouth. * **Parkinsonism (Correct):** As noted, salivary flow is normal or even slightly decreased physiologically, but the clinical presentation is always one of "apparent" excess due to poor clearance. **NEET-PG High-Yield Pearls:** * **Sialorrhea in Parkinson’s:** Managed with anticholinergics (e.g., Glycopyrrolate) or Botulinum toxin injections into the salivary glands. * **Drug-induced Xerostomia:** Common culprits include Atropine, Tricyclic Antidepressants (TCAs), Antihistamines, and Diuretics. * **Sjögren’s Syndrome:** An autoimmune condition characterized by the triad of xerostomia, keratoconjunctivitis sicca, and often RA. It is a classic cause of reduced salivary flow.
Question 915: Consumption of which of the following is not associated with the development of diffuse nontoxic goiter?
- A. Cauliflower
- B. Cassava root
- C. Brussel sprouts
- D. Eggplant (Correct Answer)
Explanation: The development of a **diffuse nontoxic goiter** (simple goiter) is often linked to the ingestion of **goitrogens**—substances that interfere with thyroid hormone synthesis, leading to a compensatory rise in TSH and subsequent thyroid enlargement [1]. **Why Eggplant is the Correct Answer:** **Eggplant (Option D)** does not contain significant amounts of goitrogenic compounds. It is a member of the Solanaceae family and is not associated with thyroid inhibition or goiter formation. **Why the Other Options are Incorrect:** * **Cauliflower (Option A) and Brussel sprouts (Option C):** These belong to the **Cruciferous (Brassicaceae)** family. They contain **glucosinolates**, which are metabolized into **thiocyanates**. Thiocyanates competitively inhibit the sodium-iodide symporter (NIS), preventing iodine uptake by the thyroid gland [1]. * **Cassava root (Option B):** This is a major source of goitrogens in certain geographical regions. It contains **linamarin**, a cyanogenic glycoside that, when ingested, is converted into thiocyanate. In areas with borderline iodine deficiency, heavy cassava consumption is a leading cause of endemic goiter. **Clinical Pearls for NEET-PG:** * **Mechanism:** Goitrogens primarily act by inhibiting the **iodide trap** (thiocyanates) or inhibiting **thyroid peroxidase (TPO)** (propylthiouracil-like compounds). * **Iodine Interaction:** The goitrogenic effect of cruciferous vegetables and cassava is significantly amplified in the presence of **concomitant iodine deficiency**. * **Other Goitrogens:** Lithium, Amiodarone, and certain flavonoids (found in millet) are also high-yield goitrogenic substances to remember for the exam [1].
Question 916: What is the dose adjustment required for insulin in a patient who is diagnosed with stage IV chronic kidney disease (CKD)?
- A. Increased insulin dose
- B. Decreased insulin dose (Correct Answer)
- C. No change in insulin dose
- D. Add DPP-4 inhibitor
Explanation: **Explanation:** The correct answer is **B. Decreased insulin dose**. **1. Why the correct answer is right:** The kidneys play a dual role in insulin metabolism: they are responsible for approximately 30-40% of the metabolic clearance of exogenous insulin and contribute to glucose homeostasis through gluconeogenesis. In Stage IV Chronic Kidney Disease (CKD), the Glomerular Filtration Rate (GFR) is significantly reduced (15-29 mL/min). This leads to: * **Reduced Insulin Clearance:** Insulin circulates for a longer duration, increasing the risk of prolonged hypoglycemia [1]. * **Decreased Renal Gluconeogenesis:** The failing kidney produces less glucose, further lowering the body's overall glucose output. Consequently, to prevent severe hypoglycemia, the total daily dose of insulin must be reduced (typically by 25-50% when GFR <15-30 mL/min). **2. Why the incorrect options are wrong:** * **Option A:** Increasing the dose would exacerbate the risk of life-threatening hypoglycemia due to the impaired clearance mentioned above. * **Option C:** "No change" is dangerous in CKD. As renal function declines, the "Burnt-out Diabetes" phenomenon can occur, where previously required insulin doses become excessive. * **Option D:** While some DPP-4 inhibitors (like Linagliptin) can be used in CKD without adjustment, adding another hypoglycemic agent does not address the primary need to adjust the existing insulin regimen to account for reduced clearance. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of Thumb for Insulin in CKD:** * GFR >50 mL/min: No adjustment. * GFR 10-50 mL/min: Reduce dose by 25%. * GFR <10 mL/min: Reduce dose by 50%. * **Drug of Choice:** Insulin remains the preferred glycemic control agent in advanced CKD, but with cautious downward titration. * **Metformin Contraindication:** Traditionally contraindicated if CrCl <30 mL/min due to the risk of Lactic Acidosis.
Question 917: A 56-year-old man presents with a change in skin color, fatigue, and abdominal pain. He has also noticed increased urine output and thirst. On examination, his skin appears bronze in color, his liver span is 16 cm, and there is loss of body hair, and testicular atrophy. His ferritin is 600 ng/mL (normal 15-200 ng/mL), aspartate amino transferase (AST) 130 U/L (normal 8-20 U/L), alanine amino transferase (ALT) 150 U/L (normal 8-20 U/L), and total bilirubin 0.5 mg/dL (normal 0.1-1 mg/dL). Coagulation tests and albumin level are normal but the random glucose is elevated at 250 mg/dL. Which of the following is the most likely diagnosis?
- A. Diabetes mellitus
- B. Amyloidosis
- C. Wilson's disease
- D. Hemochromatosis (Correct Answer)
Explanation: ### Explanation The clinical presentation of **"Bronze Diabetes"**—characterized by the triad of skin hyperpigmentation, diabetes mellitus, and cirrhosis—is a classic hallmark of **Hereditary Hemochromatosis (HH)** [2]. **1. Why Hemochromatosis is correct:** Hemochromatosis is an autosomal recessive disorder (most commonly a mutation in the **HFE gene**) leading to excessive iron absorption [2]. The excess iron (hemosiderin) deposits in various organs, causing damage: * **Pancreas:** Deposition in islet cells leads to secondary diabetes (polyuria, polydipsia, glucose 250 mg/dL) [2]. * **Liver:** Deposition leads to hepatomegaly (16 cm span) and elevated transaminases (AST/ALT) [1]. * **Skin:** Increased melanin production and iron deposition cause the characteristic "bronze" color [2]. * **Pituitary/Gonads:** Iron deposition in the pituitary leads to hypogonadotropic hypogonadism, explaining the **testicular atrophy** and loss of body hair [2]. * **Laboratory markers:** Elevated **ferritin** (600 ng/mL) is a key indicator of increased iron stores [1]. **2. Why other options are incorrect:** * **Diabetes Mellitus:** While the patient has hyperglycemia, isolated DM does not explain the hepatomegaly, hyperpigmentation, or elevated ferritin. * **Amyloidosis:** Can cause organomegaly, but typically presents with restrictive cardiomyopathy or nephrotic syndrome, not bronze skin or the specific iron profile seen here. * **Wilson's Disease:** Involves **copper** deposition. It typically presents in younger patients with neuropsychiatric symptoms and Kayser-Fleischer rings, rather than bronze skin and diabetes. **3. NEET-PG High-Yield Pearls:** * **Screening Test of Choice:** Transferrin saturation (>45% is highly suggestive). * **Gold Standard Diagnosis:** Liver biopsy with **Perls' Prussian Blue stain** (quantifies hepatic iron index) [1]. * **MRI Finding:** T2* weighted MRI shows low signal intensity in the liver due to iron [1]. * **Treatment:** Therapeutic phlebotomy is the mainstay; Desferrioxamine is used if phlebotomy is contraindicated [1]. * **Most common cause of death:** Hepatocellular Carcinoma (HCC) [2].
Question 918: Which of the following is NOT a characteristic feature of Metabolic Syndrome (Syndrome X)?
- A. Hyperglycemia
- B. Hypoinsulinemia (Correct Answer)
- C. Abdominal obesity
- D. Hypertriglyceridemia
Explanation: **Explanation:** Metabolic Syndrome (also known as Syndrome X or Insulin Resistance Syndrome) is a cluster of metabolic abnormalities that significantly increase the risk of cardiovascular disease and Type 2 Diabetes Mellitus [4]. **Why Hypoinsulinemia is the correct answer:** The core pathophysiology of Metabolic Syndrome is **Insulin Resistance** [2]. In this state, peripheral tissues (muscle, liver, adipose) do not respond effectively to insulin. To compensate, the pancreas secretes *more* insulin to maintain glucose homeostasis, leading to **Hyperinsulinemia**, not hypoinsulinemia. Hypoinsulinemia is typically seen in Type 1 Diabetes or late-stage Type 2 Diabetes due to beta-cell exhaustion [1][2]. **Analysis of Incorrect Options:** * **Hyperglycemia:** Insulin resistance leads to impaired fasting glucose or overt Type 2 Diabetes, making hyperglycemia a defining component [1]. * **Abdominal Obesity:** Central (android) obesity is a key driver of the syndrome [4]. Adipose tissue in the visceral compartment is metabolically active and releases pro-inflammatory cytokines and free fatty acids that worsen insulin resistance [4]. * **Hypertriglyceridemia:** Dyslipidemia in Metabolic Syndrome is characterized by high triglycerides and low HDL levels (the "atherogenic lipid triad"). **NEET-PG High-Yield Pearls:** * **NCEP ATP III Criteria:** Diagnosis requires $\geq$ 3 of the following: 1. **Waist Circumference:** $>102$ cm (M) or $>88$ cm (F). *Note: For South Asians, the cutoff is lower ($>90$ cm M, $>80$ cm F).* 2. **Triglycerides:** $\geq 150$ mg/dL. 3. **HDL Cholesterol:** $<40$ mg/dL (M) or $<50$ mg/dL (F). 4. **Blood Pressure:** $\geq 130/85$ mmHg. 5. **Fasting Glucose:** $\geq 100$ mg/dL. * **Acanthosis Nigricans:** A common clinical sign of underlying insulin resistance. * **First-line Management:** Therapeutic lifestyle changes (weight loss and exercise) [3].
Question 919: Gynaecomastia is seen in which of the following conditions?
- A. Klinefelter's syndrome
- B. Lepromatous leprosy
- C. HIV
- D. All of the above (Correct Answer)
Explanation: **Explanation:** Gynecomastia is the benign proliferation of glandular breast tissue in males, primarily caused by an imbalance between estrogen and androgen action [1]. **1. Klinefelter’s Syndrome (47, XXY):** This is the most common congenital cause of primary hypogonadism. The extra X chromosome leads to testicular dysgenesis, resulting in low testosterone levels and elevated gonadotropins (LH/FSH) [2]. High LH stimulates aromatase activity in Leydig cells, increasing the conversion of testosterone to estradiol, thus causing gynecomastia [2]. **2. Lepromatous Leprosy:** Chronic infection with *Mycobacterium leprae* often involves the testes (orchitis). This leads to testicular atrophy and primary hypogonadism, resulting in decreased testosterone production and subsequent gynecomastia. **3. HIV Infection:** Gynecomastia in HIV patients is multifactorial. It can be a result of the disease itself (hypogonadism), lipodystrophy associated with **Highly Active Antiretroviral Therapy (HAART)**—specifically Protease Inhibitors and Efavirenz—or secondary to liver dysfunction (reduced clearance of estrogens). **Clinical Pearls for NEET-PG:** * **Physiological Gynecomastia:** Occurs in three peaks: Neonatal (maternal estrogens), Pubertal (transient imbalance), and Senile (declining testosterone) [1]. * **Drug-induced Gynecomastia (High Yield Mnemonic: DISCO):** **D**igoxin, **I**soniazid, **S**pironolactone (most common drug cause), **C**imetidine, **O**estrogens/Ketoconazole [1]. * **Grading:** The Simon Scale is used to grade the severity of gynecomastia. * **Workup:** Always rule out testicular tumors (e.g., Leydig cell tumor) by checking serum hCG and Alpha-fetoprotein (AFP) if a mass is palpable [1].
Question 920: A 30-year-old male with NIDDM has a blood pressure of 150/90 mmHg and persistent albuminuria on urine examination. What is the most appropriate line of treatment?
- A. No treatment
- B. Regular urine examination and blood sugar monitoring
- C. Administer lisinopril and restrict sodium intake (Correct Answer)
- D. Restrict sodium intake only
Explanation: ### Explanation The patient presents with **Diabetic Nephropathy**, characterized by persistent albuminuria and hypertension (150/90 mmHg). In patients with diabetes and albuminuria, the primary goal is to slow the progression to End-Stage Renal Disease (ESRD). **Why Option C is Correct:** * **ACE Inhibitors (e.g., Lisinopril):** These are the drugs of choice for diabetic patients with albuminuria. They provide a **renoprotective effect** beyond blood pressure control by causing preferential vasodilation of the **efferent arteriole**. This reduces intraglomerular capillary pressure and decreases the leakage of albumin [1]. * **Sodium Restriction:** Reducing salt intake is essential as it enhances the antiproteinuric and antihypertensive effects of ACE inhibitors. **Why Other Options are Incorrect:** * **Option A & B:** These represent a "wait and watch" approach. Diabetic nephropathy is a progressive condition; failing to intervene pharmacologically when albuminuria and hypertension are present leads to rapid decline in GFR [1]. * **Option D:** While sodium restriction is beneficial, it is insufficient as a monotherapy. It does not address the hemodynamic changes in the glomerulus that ACE inhibitors specifically target. **NEET-PG High-Yield Pearls:** 1. **First Sign:** The earliest clinical sign of diabetic nephropathy is **Microalbuminuria** (30–300 mg/day) [4]. 2. **Drug of Choice:** ACE Inhibitors or ARBs are preferred even if the patient is normotensive but has albuminuria [1]. 3. **Pathology:** The hallmark histological finding is **Kimmelstiel-Wilson (KW) nodules** (nodular glomerulosclerosis) [2]. 4. **Target BP:** According to most guidelines (ADA/KDIGO), the target BP for diabetic patients with chronic kidney disease is **<130/80 mmHg** [3].
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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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