Endocrine Pathology — MCQs
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In phaeochromocytoma, what substance is found in increased amounts in the urine?
Which of the following neoplasms is primary in the adrenal medulla?
A 65-year-old woman with a history of multinodular goiter complains of increasing nervousness, insomnia, and heart palpitations. She has lost 9 kg (20 lb) over the past 6 months. Physical examination reveals a diffusely enlarged thyroid. There is no evidence of exophthalmos. Laboratory studies show elevated serum levels of T3 and T4. Serologic tests for antithyroid antibodies are negative. Which of the following is an important complication of this patient's endocrinopathy?
The definite diagnosis of malignancy in pheochromocytoma is based on what?
Which of the following organs are not affected in autoimmune polyglandular syndrome type 2?
Which of the following is true regarding medullary carcinoma of the thyroid?
Which of the following is used for measurement in diabetes mellitus?
What is the distinguishing feature of multiple endocrine neoplasia 2B (MEN 2B) from multiple endocrine neoplasia 2A (MEN 2A)?
What is the characteristic histological feature of de Quervain's thyroiditis?
Metastasis in the thyroid gland most commonly originates from which primary carcinoma?
Endocrine Pathology Indian Medical PG Practice Questions and MCQs
Question 31: In phaeochromocytoma, what substance is found in increased amounts in the urine?
- A. Vanillylmandelic acid (VMA) (Correct Answer)
- B. 5-Hydroxyindoleacetic acid (HIAA)
- C. Both VMA and HIAA
- D. Neither VMA nor HIAA
Explanation: ### Explanation **1. Why Vanillylmandelic acid (VMA) is correct:** Pheochromocytoma is a catecholamine-secreting tumor derived from the chromaffin cells of the adrenal medulla [1]. These tumors overproduce epinephrine and norepinephrine. In the body, catecholamines are metabolized by two primary enzymes: **Monoamine oxidase (MAO)** and **Catechol-O-methyltransferase (COMT)**. The end-stage metabolic byproduct of both epinephrine and norepinephrine is **Vanillylmandelic acid (VMA)**. Consequently, elevated urinary levels of VMA (and metanephrines) serve as critical diagnostic markers for this condition [1]. **2. Why the other options are incorrect:** * **5-Hydroxyindoleacetic acid (HIAA):** This is the primary metabolite of **serotonin**. Elevated urinary 5-HIAA is the hallmark diagnostic marker for **Carcinoid Syndrome**, not pheochromocytoma. * **Options C and D:** These are incorrect because VMA and HIAA represent distinct metabolic pathways (catecholamine vs. serotonin metabolism) associated with different neuroendocrine tumors. **3. NEET-PG High-Yield Clinical Pearls:** * **Rule of 10s:** Pheochromocytoma is 10% bilateral, 10% malignant, 10% pediatric, 10% extra-adrenal (Paraganglioma), and 10% familial. * **Best Screening Test:** 24-hour urinary fractionated **metanephrines** (more sensitive than VMA). * **Histology:** Characterized by **Zellballen patterns** (nests of cells surrounded by a vascular stroma) [1]. * **Associated Syndromes:** MEN 2A, MEN 2B, von Hippel-Lindau (VHL), and Neurofibromatosis type 1 (NF1). * **Clinical Triad:** Episodic headache, sweating (diaphoresis), and tachycardia/palpitations in a hypertensive patient [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 419-420. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1138-1139.
Question 32: Which of the following neoplasms is primary in the adrenal medulla?
- A. Pheochromocytoma (Correct Answer)
- B. Eosinophilic adenoma
- C. Arrhenoblastoma
- D. None of the above
Explanation: ### Explanation **Correct Option: A. Pheochromocytoma** Pheochromocytoma is a catecholamine-secreting tumor derived from the **chromaffin cells** of the adrenal medulla [2]. These cells originate from the **neural crest** and are responsible for synthesizing epinephrine and norepinephrine. It is the most common primary tumor of the adrenal medulla in adults. **Incorrect Options:** * **B. Eosinophilic adenoma:** This is a historical term for a growth-hormone-secreting tumor of the **anterior pituitary gland** (Acidophil adenoma), typically associated with gigantism or acromegaly. It is not related to the adrenal gland. * **C. Arrhenoblastoma:** Also known as a Sertoli-Leydig cell tumor, this is a primary **ovarian tumor** that produces androgens, leading to virilization in females. It does not arise from the adrenal medulla. **High-Yield Clinical Pearls for NEET-PG:** * **The Rule of 10s:** Pheochromocytoma is famously known as the 10% tumor: 10% are bilateral, 10% are extra-adrenal (Paragangliomas), 10% are malignant, and 10% occur in children. (Note: Recent genetics suggest up to 25-35% may be familial [1]). * **Clinical Triad:** Episodic headache, sweating (diaphoresis), and tachycardia/palpitations in a patient with hypertension [4]. * **Diagnosis:** Best initial screening test is **Urinary/Plasma Metanephrines**. * **Histology:** Characterized by **Zellballen patterns** (nests of cells surrounded by a vascular stroma) [3]. Cells stain positive for **Chromogranin** and **Synaptophysin**. * **Genetic Associations:** Often associated with **MEN 2A and 2B**, Von Hippel-Lindau (VHL) syndrome, and Neurofibromatosis type 1 (NF1) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1137. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 419-420. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1137-1138. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1138-1139.
Question 33: A 65-year-old woman with a history of multinodular goiter complains of increasing nervousness, insomnia, and heart palpitations. She has lost 9 kg (20 lb) over the past 6 months. Physical examination reveals a diffusely enlarged thyroid. There is no evidence of exophthalmos. Laboratory studies show elevated serum levels of T3 and T4. Serologic tests for antithyroid antibodies are negative. Which of the following is an important complication of this patient's endocrinopathy?
- A. Autoimmune hepatitis
- B. Cardiac arrhythmia (Correct Answer)
- C. Follicular carcinoma of the thyroid
- D. Medullary carcinoma of the thyroid
Explanation: ### Explanation **Diagnosis: Toxic Multinodular Goiter (Plummer Syndrome)** The patient presents with hyperthyroidism (nervousness, weight loss, elevated T3/T4) and a history of multinodular goiter. The absence of exophthalmos (ophthalmopathy) and negative antithyroid antibodies rule out Graves' disease [1]. This clinical picture describes **Toxic Multinodular Goiter**, where nodules become autonomous and hyperfunction independent of TSH. **1. Why Cardiac Arrhythmia is Correct:** Excess thyroid hormones (T3/T4) increase the number and sensitivity of **beta-adrenergic receptors** in the myocardium [1]. This leads to a hypermetabolic state characterized by tachycardia and increased cardiac output. In elderly patients, the most significant and common complication of thyrotoxicosis is **Atrial Fibrillation** and other supraventricular arrhythmias, which can lead to high-output heart failure. **2. Why the Other Options are Incorrect:** * **A. Autoimmune hepatitis:** While associated with Graves' disease (due to shared autoimmune predisposition), it is not a complication of toxic multinodular goiter, which is a structural/functional disorder rather than an autoimmune one. * **C. Follicular carcinoma:** While multinodular goiters are common, they do not typically "transform" into follicular carcinoma. The risk of malignancy in a long-standing multinodular goiter is generally low (approx. 5%) [3]. * **D. Medullary carcinoma:** This arises from parafollicular C-cells and is often associated with MEN 2 syndromes. It is unrelated to hyperthyroidism or multinodular goiter. **Clinical Pearls for NEET-PG:** * **Jod-Basedow Phenomenon:** Hyperthyroidism induced by iodine administration (e.g., contrast dye) in a patient with underlying multinodular goiter. * **Graves vs. Plummer:** Graves has diffuse uptake on scan and extrathyroidal manifestations (pretibial myxedema, exophthalmos) [2]; Plummer shows "patchy" or focal uptake in autonomous nodules. * **Elderly Presentation:** In older patients, hyperthyroidism may present only as "Apathetic Hyperthyroidism" (depression, weight loss, and atrial fibrillation). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1086-1087. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1087-1088. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1093-1094.
Question 34: The definite diagnosis of malignancy in pheochromocytoma is based on what?
- A. Presence of metastasis (Correct Answer)
- B. Cellular pleomorphism
- C. Nuclear pleomorphism
- D. Mitotic figures
Explanation: **Explanation:** The diagnosis of malignancy in pheochromocytoma is unique because it cannot be determined by the histological appearance of the primary tumor alone [1]. **1. Why "Presence of Metastasis" is correct:** Pheochromocytoma is often referred to as the "10% tumor." Unlike most other neoplasms, there are no reliable microscopic features (like atypia or mitoses) that definitively predict clinical behavior [1]. Therefore, the **only absolute criterion** for malignancy is the presence of **metastatic spread** to non-chromaffin sites where paraganglionic tissue is not normally found, such as the liver, lungs, bone, or regional lymph nodes. **2. Why other options are incorrect:** * **Cellular and Nuclear Pleomorphism:** These features are common in many endocrine tumors (often called "endocrine atypia") and can be seen in perfectly benign pheochromocytomas. They do not correlate with biological aggressiveness. * **Mitotic Figures:** While an increased mitotic rate may be suggestive of a more aggressive tumor, it is not diagnostic of malignancy in this specific context. Even tumors with low mitotic activity can metastasize. **3. High-Yield Clinical Pearls for NEET-PG:** * **The Rule of 10s:** 10% are malignant, 10% are bilateral, 10% are extra-adrenal (paragangliomas), and 10% occur in children. (Note: Modern genetics suggest up to 25-30% may be familial). * **Zellballen Pattern:** The classic histological arrangement where tumor cells are grouped in small nests surrounded by a vascular stroma. * **PASS Score:** The *Pheochromocytoma of the Adrenal Gland Scaled Score* is used to estimate malignant potential, but metastasis remains the "gold standard" for diagnosis. * **Genetics:** Mutations in the **SDHB** gene are the strongest predictors of metastatic potential. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 419-420.
Question 35: Which of the following organs are not affected in autoimmune polyglandular syndrome type 2?
- A. Parathyroid
- B. Thyroid
- C. Adrenal (Correct Answer)
- D. Pancreas
Explanation: ### Explanation **Autoimmune Polyglandular Syndrome Type 2 (APS-2)**, also known as **Schmidt Syndrome**, is a polygenic autoimmune disorder characterized by a specific triad of endocrine failures. **Why "Adrenal" is the correct answer (in the context of "not affected"):** There appears to be a common point of confusion in the question's framing. In APS-2, the **Adrenal gland is almost always affected** (Addison’s disease is a mandatory component). However, if the question asks which organ is **NOT** affected in APS-2 compared to APS-1, the answer is the **Parathyroid**. Hypoparathyroidism is a hallmark of **APS-1** but is characteristically **absent in APS-2** [3], [4]. *Note: If the provided key marks "Adrenal" as the correct answer for "not affected," it is likely a typographical error in the source material, as Addison's disease is the cornerstone of APS-2.* **Analysis of Options:** * **Adrenal (Option C):** Involved in 100% of APS-2 cases as autoimmune adrenalitis (Addison’s disease). * **Thyroid (Option B):** Frequently involved as Hashimoto’s thyroiditis or Graves' disease (Schmidt Syndrome = Addison’s + Thyroid disease) [2], [5]. * **Pancreas (Option D):** Involved as Type 1 Diabetes Mellitus (Carpenter’s Syndrome = Addison’s + Thyroid disease + T1DM) [1]. * **Parathyroid (Option A):** This is the organ **not** typically affected in APS-2. It is instead the classic feature of APS-1 (along with Mucocutaneous Candidiasis) [3]. **High-Yield Clinical Pearls for NEET-PG:** 1. **APS-1 (APECE D):** Mutation in **AIRE gene** (Chr 21). Triad: Chronic Mucocutaneous Candidiasis, Hypoparathyroidism, and Addison’s disease. 2. **APS-2 (Schmidt Syndrome):** Associated with **HLA-DR3/DR4**. More common in adults. 3. **The Triad of APS-2:** Addison’s disease + Autoimmune Thyroid disease + Type 1 Diabetes Mellitus. 4. **Order of occurrence:** T1DM often presents first, followed by Addison’s and then Thyroid dysfunction. **References:** [1] Kumar v, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 219-220. [2] Kumar v, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1089-1090. [3] Kumar v, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1107-1108. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 432-433. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 426-427.
Question 36: Which of the following is true regarding medullary carcinoma of the thyroid?
- A. Arises from parafollicular cells
- B. Amyloid in stroma
- C. Secretes calcitonin
- D. All of the above (Correct Answer)
Explanation: **Medullary Thyroid Carcinoma (MTC)** is a neuroendocrine neoplasm that accounts for approximately 5% of thyroid cancers. It is a high-yield topic for NEET-PG due to its unique origin and histopathological features. ### **Explanation of Options:** * **A. Arises from parafollicular cells:** Unlike papillary and follicular carcinomas which arise from follicular cells, MTC originates from **Parafollicular C-cells** (derived from the neural crest) [2]. These cells are responsible for the secretion of calcitonin [2]. * **B. Amyloid in stroma:** A hallmark histological feature of MTC is the presence of **acellular amyloid deposits** in the stroma [2]. This amyloid is formed by the deposition of pro-calcitonin molecules and stains positive with **Congo Red** (showing apple-green birefringence under polarized light). * **C. Secretes calcitonin:** Since it arises from C-cells, MTC is functionally active and secretes high levels of **Calcitonin** [1],[2]. This serves as a highly specific tumor marker for diagnosis and monitoring postoperative recurrence [1]. ### **High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** Approximately 25% of cases are familial, associated with **MEN 2A and 2B** syndromes [1]. All familial cases involve a mutation in the **RET proto-oncogene**. * **Histology:** Shows a "polygonal to spindle-shaped" cell pattern [2]. On electron microscopy, characteristic **membrane-bound neurosecretory granules** are seen. * **Staining:** Positive for Calcitonin, Chromogranin A, and Synaptophysin. * **Clinical Presentation:** Patients may present with diarrhea due to the secretion of VIP (Vasoactive Intestinal Peptide) or serotonin [1],[2]. * **Prophylaxis:** In MEN 2 carriers, prophylactic thyroidectomy is often recommended early in life. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1102-1103. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 428-431.
Question 37: Which of the following is used for measurement in diabetes mellitus?
- A. HbA
- B. HbS
- C. HbA2
- D. HbA1c (Correct Answer)
Explanation: **Explanation:** **Correct Answer: D. HbA1c** HbA1c (Glycated Hemoglobin) is the gold standard for monitoring long-term glycemic control in Diabetes Mellitus [1]. It is formed by the **non-enzymatic glycosylation** of the N-terminal valine of the hemoglobin beta chain. Since the average lifespan of a red blood cell is approximately **120 days**, HbA1c levels reflect the average blood glucose concentration over the preceding **2–3 months**. According to ADA criteria, an HbA1c value of **≥ 6.5%** is diagnostic for Diabetes Mellitus [1]. **Analysis of Incorrect Options:** * **A. HbA:** This is normal adult hemoglobin ($̑_2̒_2$), comprising about 95–97% of total hemoglobin in adults. It is not a specific marker for glucose monitoring. * **B. HbS:** This is the abnormal hemoglobin found in **Sickle Cell Anemia**, resulting from a point mutation (glutamic acid replaced by valine at the 6th position of the $̒$-chain). * **C. HbA2:** This is a minor adult hemoglobin ($̑_2̔_2$). Elevated levels (typically >3.5%) are a key diagnostic marker for **Beta-Thalassemia minor**. **High-Yield Clinical Pearls for NEET-PG:** * **Fructosamine Test:** Reflects glycemic control over the past **2–3 weeks** (useful when HbA1c is unreliable, e.g., in hemolytic anemia). * **False Low HbA1c:** Seen in conditions with shortened RBC lifespan (Hemolytic anemia, recent blood loss, or pregnancy). * **False High HbA1c:** Seen in conditions like Iron Deficiency Anemia (due to increased RBC age/structural changes). * **Target HbA1c:** For most non-pregnant adults with diabetes, the goal is **< 7%** to reduce microvascular complications. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1109-1111.
Question 38: What is the distinguishing feature of multiple endocrine neoplasia 2B (MEN 2B) from multiple endocrine neoplasia 2A (MEN 2A)?
- A. Medullary thyroid carcinoma
- B. Pheochromocytoma
- C. Parathyroid hyperplasia
- D. Mucosal and gastrointestinal neuromas (Correct Answer)
Explanation: **Explanation:** The Multiple Endocrine Neoplasia (MEN) syndromes are autosomal dominant conditions caused by germline mutations. Both MEN 2A and MEN 2B are caused by mutations in the **RET proto-oncogene**, but they are distinguished by their specific clinical constellations [1]. **1. Why Option D is correct:** The presence of **mucosal neuromas** (typically on the tongue, lips, and eyelids) and **gastrointestinal ganglioneuromatosis** (leading to megacolon) is the hallmark of **MEN 2B** [1]. Additionally, MEN 2B patients characteristically exhibit a **Marfanoid habitus** (long limbs, joint laxity) [1]. These features are entirely absent in MEN 2A. **2. Why the other options are incorrect:** * **Options A & B (Medullary Thyroid Carcinoma and Pheochromocytoma):** These are common to **both** MEN 2A and MEN 2B [1]. In fact, MTC occurs in nearly 100% of patients in both syndromes, often being more aggressive in MEN 2B. * **Option C (Parathyroid Hyperplasia):** This is a key component of **MEN 2A** (occurring in 20-30% of cases) but is notably **absent** in MEN 2B [1]. **High-Yield Clinical Pearls for NEET-PG:** * **MEN 1 (Wermer Syndrome):** 3 Ps — **P**ituitary, **P**arathyroid, **P**ancreas. * **MEN 2A (Sipple Syndrome):** 2 Ps — **P**heochromocytoma, **P**arathyroid + MTC [1]. * **MEN 2B:** 1 P — **P**heochromocytoma + MTC + Neuromas/Marfanoid habitus [1]. * **Prophylactic Thyroidectomy:** Recommended in both MEN 2A and 2B due to the inevitable risk of MTC; however, it is performed much earlier in MEN 2B (often in infancy) due to higher virulence. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1137.
Question 39: What is the characteristic histological feature of de Quervain's thyroiditis?
- A. Mononuclear cell infiltration
- B. Histiocytic reaction
- C. Giant cell infiltration (Correct Answer)
- D. Eosinophilia
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. **Why the correct answer is right:** The hallmark of de Quervain’s thyroiditis is the **granulomatous inflammation**. The process begins with follicular destruction and colloid leakage, which triggers an intense inflammatory response. The characteristic histological finding is the presence of **multinucleated giant cells** (foreign-body type) surrounding fragments of colloid or forming organized granulomas. This "giant cell infiltration" is the most specific diagnostic feature on biopsy. **Analysis of incorrect options:** * **A. Mononuclear cell infiltration:** While lymphocytes and plasma cells are present, this is a non-specific finding seen in almost all inflammatory thyroid conditions (e.g., Hashimoto’s). * **B. Histiocytic reaction:** Although macrophages (histiocytes) are involved in forming the granuloma, the presence of fused histiocytes forming **giant cells** is the defining characteristic for this condition. * **D. Eosinophilia:** Eosinophilic infiltration is not a primary feature of de Quervain’s; it is more commonly associated with drug-induced reactions or specific rare conditions like Riedel’s thyroiditis (occasionally). **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** It is the **most common cause of a painful thyroid gland**. Look for a patient with a tender, enlarged thyroid and a high ESR. * **Etiology:** Often follows a viral prodrome (Coxsackievirus, Mumps, Adenovirus). * **Laboratory:** Characterized by a "triphasic" course (Hyperthyroidism → Hypothyroidism → Euthyroidism). * **Radioiodine Uptake (RAIU):** Classically **decreased** (low uptake) despite symptoms of thyrotoxicosis, due to follicular damage.
Question 40: Metastasis in the thyroid gland most commonly originates from which primary carcinoma?
- A. Testis
- B. Prostate
- C. Breast (Correct Answer)
- D. Lungs
Explanation: **Explanation:** Metastatic involvement of the thyroid gland is relatively uncommon in clinical practice but is frequently identified during autopsies. Among all primary malignancies, **Breast Carcinoma** is the most common source of metastasis to the thyroid gland. **Why Breast Carcinoma is correct:** The thyroid gland is a highly vascular organ, receiving one of the highest rates of blood flow per gram of tissue. Breast cancer, being a common malignancy with a high propensity for hematogenous spread, frequently seeds the thyroid [1]. Large autopsy series consistently rank breast cancer as the leading primary site, followed closely by renal cell carcinoma and lung cancer. **Analysis of Incorrect Options:** * **Testis & Prostate:** While these cancers frequently metastasize to bones and lymph nodes, they rarely involve the thyroid gland. Their patterns of spread do not typically favor the thyroid parenchyma. * **Lungs:** Lung carcinoma is the second or third most common source of thyroid metastasis. While common, it statistically trails behind breast cancer in most comprehensive pathological studies. **High-Yield NEET-PG Pearls:** * **Most common primary site (Autopsy):** Breast Carcinoma [1]. * **Most common primary site (Clinical/Surgical series):** Renal Cell Carcinoma (RCC). This is because RCC metastases are often solitary and present as a cold nodule, leading to surgical resection, whereas breast/lung metastases are often part of widespread terminal disease. * **Diagnostic Clue:** Metastatic lesions usually present as "cold nodules" on radionuclide scans and often mimic primary thyroid anaplastic carcinoma on cytology. * **Immunohistochemistry (IHC):** Metastatic lesions will be **negative for TTF-1 and Thyroglobulin** (unless the primary is lung, where TTF-1 may be positive), helping differentiate them from primary thyroid tumors. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 456-457.
Practice by Chapter
Pituitary Gland Disorders
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Thyroid Gland Diseases
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Parathyroid Gland Pathology
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Adrenal Cortical Disorders
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Adrenal Medullary Disorders
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Pancreatic Endocrine Disorders
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Multiple Endocrine Neoplasia Syndromes
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Diffuse Neuroendocrine System
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Laboratory Diagnosis of Endocrine Diseases
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