Endocrine Pathology — MCQs

Endocrine Pathology Indian Medical PG Practice Questions and MCQs

Question 141: Which of the following is NOT a true statement about pheochromocytoma?

A. 90% are malignant (Correct Answer)
B. 95% occur in the abdomen
C. They secrete catecholamines
D. They arise from sympathetic ganglia

Explanation: ### Explanation **Pheochromocytoma** is a tumor of the chromaffin cells, most commonly arising from the adrenal medulla. The correct answer is **A** because it contradicts the famous **"Rule of 10s"** associated with this condition. #### 1. Why Option A is the Correct Answer (The False Statement) In pheochromocytoma, **10% are malignant**, not 90%. Malignancy is not determined by histological appearance but strictly by the presence of **metastases** to non-chromaffin sites (e.g., bone, liver, lymph nodes) [2]. Approximately 90% of cases are benign. #### 2. Why the Other Options are Incorrect (True Statements) * **Option B:** Roughly **95% occur in the abdomen**, with the vast majority (approx. 85-90%) located in the adrenal medulla and the remainder in extra-adrenal sites like the Organ of Zuckerkandl. * **Option C:** These tumors **secrete catecholamines** (primarily norepinephrine and epinephrine), leading to the classic clinical triad of episodic headache, sweating, and tachycardia [1]. * **Option D:** Extra-adrenal pheochromocytomas (paragangliomas) **arise from sympathetic ganglia** [3]. While the adrenal medulla is the primary site, the sympathetic chain is a common origin for extra-adrenal variants. #### 3. NEET-PG High-Yield Pearls: The "Rule of 10s" To excel in NEET-PG, remember that Pheochromocytoma is the "10% Tumor": * **10%** are Malignant. * **10%** are Bilateral (higher in familial cases). * **10%** are Extra-adrenal (Paragangliomas). * **10%** occur in Children. * **10%** are NOT associated with hypertension. * **25%** are now known to be familial (associated with **MEN 2A/2B, VHL, NF-1, and SDH mutations**) [1]. **Diagnostic Tip:** The most sensitive screening test is **plasma free metanephrines**, while the most specific is **24-hour urinary catecholamines and metanephrines**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1137-1139. [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. Head and Neck, pp. 748-749.

Question 142: In Hashimoto's disease, serum antibodies are mainly against which of the following?

A. Thyroid follicles
B. Thyroxine
C. Thyroglobulins (Correct Answer)
D. Iodine

Explanation: **Explanation:** Hashimoto’s Thyroiditis (Chronic Lymphocytic Thyroiditis) is an autoimmune disorder characterized by the gradual destruction of the thyroid gland by the immune system [1]. The pathogenesis involves a breakdown in self-tolerance to thyroid autoantigens [1]. **Why Thyroglobulins is correct:** In Hashimoto’s disease, the immune system produces specific autoantibodies against components of the thyroid gland. The two most significant antibodies are: 1. **Anti-Thyroglobulin (anti-Tg) antibodies:** These target thyroglobulin, the precursor protein for thyroid hormones stored in the colloid. 2. **Anti-Thyroid Peroxidase (anti-TPO) antibodies:** Formerly known as anti-microsomal antibodies, these target the enzyme responsible for iodine organification. Among the given options, **Thyroglobulins (Option C)** is the primary biochemical target. **Analysis of Incorrect Options:** * **A. Thyroid follicles:** While the follicles are destroyed during the disease process (via CD8+ T-cell mediated cytotoxicity and cytokines), the antibodies are directed against specific molecular antigens (Tg and TPO) within the follicles, not the "follicle" as a generic unit [1]. * **B. Thyroxine (T4):** Antibodies against the thyroid hormones themselves (T3/T4) are extremely rare and are not the diagnostic hallmark of Hashimoto’s. * **C. Iodine:** Iodine is an inorganic element required for hormone synthesis; the body does not produce antibodies against iodine. **High-Yield Clinical Pearls for NEET-PG:** * **Most Sensitive Marker:** Anti-TPO antibodies are more sensitive (present in >90% of cases) than anti-Tg. * **Histopathology:** Characterized by intense **lymphocytic infiltrate** with **germinal centers** and the presence of **Hürthle cells** (metaplastic eosinophilic follicular cells) [1]. * **Genetic Association:** Linked with **HLA-DR3** and **HLA-DR5**. * **Risk:** Patients have an increased risk of developing **B-cell Non-Hodgkin Lymphoma** (specifically MALToma) of the thyroid [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1089-1093.

Question 143: Which cell type is most commonly involved in non-functioning pituitary adenoma?

A. Gonadotropin producing cell (Correct Answer)
B. Prolactin producing cell
C. GH producing cell
D. TSH producing cell

Explanation: Pituitary adenomas are classified based on their hormone production and clinical presentation. **Non-functioning pituitary adenomas (NFPAs)** are those that do not result in a clinical syndrome of hormone excess [1]. **Why Gonadotroph cells are correct:** The vast majority (approximately 80-90%) of non-functioning pituitary adenomas are derived from **gonadotroph cells**. While these cells possess the machinery to produce LH and FSH (or their subunits like alpha-subunit), they do so inefficiently and in small quantities that usually do not cause a recognizable clinical syndrome. Therefore, they typically present only when they become large enough to cause mass effects [1] (e.g., bitemporal hemianopia or headache). **Analysis of Incorrect Options:** * **Prolactin producing cells:** These are the most common type of **functioning** pituitary adenoma (Prolactinomas) [1]. They present early with galactorrhea and amenorrhea. * **GH producing cells:** These are the second most common functioning adenomas, leading to Gigantism (in children) or Acromegaly (in adults). * **TSH producing cells:** These are the rarest form of pituitary adenomas (Thyrotroph adenomas) and typically present with secondary hyperthyroidism. **High-Yield Pearls for NEET-PG:** 1. **Most common pituitary adenoma overall:** Prolactinoma [1]. 2. **Most common cell type in NFPAs:** Gonadotroph cells (stain positive for SF-1 transcription factor). 3. **Mass Effect:** NFPAs often present as "Macroadenomas" (>1cm) because they lack early hormonal symptoms [1]. 4. **Stalk Effect:** Large NFPAs can compress the pituitary stalk, blocking dopamine (the prolactin-inhibitor), leading to mild elevations in prolactin (pseudoprolactinoma). 5. **Null Cell Adenomas:** A small subset of NFPAs that show no hormone or transcription factor expression on immunohistochemistry. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1079-1081.

Question 144: Which of the following is a variant of papillary carcinoma of the thyroid?

A. Medullary
B. Warthin
C. Columnar cell (Correct Answer)
D. Insular

Explanation: **Explanation:** Papillary Thyroid Carcinoma (PTC) is the most common thyroid malignancy and is characterized by distinct nuclear features (Orphan Annie eye nuclei, nuclear grooves, and pseudoinclusions) [1,3]. It has several histological variants that differ in prognosis and morphology [1]. **Why Columnar Cell is Correct:** The **Columnar cell variant** is a rare but aggressive subtype of PTC. Histologically, it shows tall, columnar cells with stratified nuclei, often mimicking endometrial adenocarcinoma or colonic epithelium. Unlike the classic variant, it frequently lacks typical papillary nuclear features and carries a poorer prognosis due to a higher risk of extrathyroidal extension. **Analysis of Incorrect Options:** * **Medullary (A):** This is a distinct type of thyroid cancer arising from the **parafollicular C-cells** (neuroendocrine origin), not a variant of PTC [2]. It is associated with MEN 2A and 2B syndromes and secretes calcitonin [4]. * **Warthin (B):** While there is a **"Warthin-like variant"** of PTC (which features papillary stalks infiltrated by lymphocytes, resembling a Warthin tumor of the salivary gland), "Warthin" alone refers to a benign salivary gland tumor (adenolymphoma). * **Insular (D):** This is a pattern seen in **Poorly Differentiated Thyroid Carcinoma (PDTC)**. It sits prognostically between well-differentiated (Papillary/Follicular) and undifferentiated (Anaplastic) carcinomas. **High-Yield NEET-PG Pearls:** * **Most common variant of PTC:** Follicular variant [1]. * **Most aggressive variants:** Tall cell, Columnar cell, and Hobnail variants. * **Psammoma bodies:** Present in ~50% of PTC cases; they represent infarcted papillae. * **Genetic markers:** *BRAF* mutations (V600E) are highly specific for PTC, especially the tall cell variant [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1099-1100. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 428-429. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 429-430. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1102-1103.

Question 145: All of the following are histological features of papillary carcinoma of the thyroid, except:

A. Complex branching papillae with fibrovascular core
B. Orphan Annie eye nuclei and intranuclear grooves
C. Psammoma bodies
D. Amyloid deposits (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Amyloid deposits**, as these are the hallmark histological feature of **Medullary Carcinoma of the Thyroid (MTC)**, not Papillary Carcinoma. In MTC, the amyloid is derived from the deposition of altered **calcitonin** molecules secreted by neoplastic parafollicular C-cells. **Analysis of Options:** * **A. Complex branching papillae:** Papillary Thyroid Carcinoma (PTC) is characterized by a papillary architecture consisting of stalks of fibrovascular cores covered by a single or multiple layers of cuboidal to columnar epithelial cells [1]. * **B. Orphan Annie eye nuclei and intranuclear grooves:** These are the "nuclear signatures" of PTC [1], [2]. **Orphan Annie eye nuclei** refer to large, overlapping nuclei with finely dispersed chromatin (optically clear appearance) [1]. **Intranuclear grooves** and **pseudoinclusions** (cytoplasmic invaginations) are also critical diagnostic criteria [1]. * **C. Psammoma bodies:** These are concentric calcified lamellated structures found in approximately 40-50% of PTC cases. They represent the end stage of necrotic individual papillae. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common:** PTC is the most common thyroid malignancy (85% of cases) and has an excellent prognosis [2]. * **Risk Factor:** Prior exposure to **ionizing radiation** is the strongest risk factor. * **Genetics:** Associated with **BRAF mutations** (most common) and **RET/PTC rearrangements** [3]. * **Spread:** PTC characteristically spreads via the **lymphatics** (cervical lymphadenopathy), whereas Follicular Carcinoma spreads hematogenously [2]. * **Diagnosis:** Nuclear features are diagnostic even in the absence of papillae (e.g., Follicular variant of PTC) [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1099. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 429-430. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1099-1100.

Question 146: Which of the following endocrine glands is NOT involved in Multiple Endocrine Neoplasia Type I (MEN-1)?

A. Pituitary
B. Pancreas
C. Parathyroid
D. Thyroid (Correct Answer)

Explanation: Multiple Endocrine Neoplasia Type 1 (MEN-1), also known as **Wermer Syndrome**, is an autosomal dominant disorder caused by a mutation in the *MEN1* tumor suppressor gene (encoding the protein Menin) [1]. **Why Thyroid is the correct answer:** While thyroid abnormalities (like adenomas or goiter) can occasionally coexist in patients with MEN-1, the **Thyroid gland is not part of the classic diagnostic triad**. Medullary Thyroid Carcinoma (MTC) is a hallmark of MEN-2A and MEN-2B, but not MEN-1 [1]. **Analysis of Incorrect Options:** The classic MEN-1 syndrome is characterized by the **"3 Ps"**: * **Parathyroid (Option C):** This is the most common manifestation (95% of cases). It typically presents as multiglandular parathyroid hyperplasia leading to primary hyperparathyroidism [1]. * **Pancreas (Option B):** Pancreatic neuroendocrine tumors (PanNETs) are the leading cause of morbidity/mortality [1]. Common types include Gastrinomas (Zollinger-Ellison Syndrome) and Insulinomas. * **Pituitary (Option A):** Anterior pituitary adenomas occur in about 25% of patients [1], with **Prolactinoma** being the most frequent subtype. **High-Yield Clinical Pearls for NEET-PG:** * **Gene Locus:** Chromosome **11q13** [1]. * **Most common initial presentation:** Hypercalcemia (due to Parathyroid hyperplasia). * **Other associated tumors:** Adrenal cortical tumors, carcinoid tumors (thymic, bronchial, GI), and cutaneous lesions (angiofibromas, lipomas). * **Rule of 3s:** Remember **P**arathyroid, **P**ancreas, and **P**ituitary to distinguish MEN-1 from MEN-2 (which involves Medullary Thyroid Cancer and Pheochromocytoma) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1079, 1104-1105, 1125, 1139-1140.

Question 147: Which of the following statements is TRUE regarding papillary carcinoma of the thyroid?

A. Cells exhibit intranuclear vacuolation.
B. Amyloid deposition is observed.
C. The tumor is encapsulated. (Correct Answer)
D. It comprises 10-15% of all thyroid cancers.

Explanation: ### Explanation: Papillary Thyroid Carcinoma (PTC) **Correct Option: C (The tumor is encapsulated)** While most Papillary Thyroid Carcinomas (PTC) are non-encapsulated and infiltrative, a specific variant known as the **Encapsulated Variant of PTC** exists [1], [3]. In the context of this specific question and standard pathology textbooks, PTC can present as a well-circumscribed, encapsulated lesion [3]. *Note: Recent classifications now categorize non-invasive encapsulated follicular-patterned lesions as NIFTP to reflect their indolent nature.* **Analysis of Incorrect Options:** * **A. Cells exhibit intranuclear vacuolation:** This is a distractor. PTC is characterized by **intranuclear inclusions** (pseudo-inclusions) and **intranuclear grooves**, but "vacuolation" is not a standard pathological term used to describe the diagnostic nuclear features (Orphan Annie eye nuclei) [3]. * **B. Amyloid deposition is observed:** This is a classic feature of **Medullary Thyroid Carcinoma (MTC)**, derived from parafollicular C-cells, where calcitonin converts into amyloid. PTC is characterized by **Psammoma bodies** (concentric calcifications), not amyloid. * **D. It comprises 10-15% of all thyroid cancers:** This is incorrect. PTC is the **most common** thyroid malignancy, accounting for **>85%** of cases [2]. The 10-15% range is more characteristic of Follicular Carcinoma [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Nuclear Features (Diagnostic Gold Standard):** Orphan Annie eye nuclei (ground-glass chromatin), nuclear grooves, and intranuclear pseudo-inclusions [3]. * **Psammoma Bodies:** Present in ~50% of cases; highly suggestive of PTC. * **Risk Factor:** Prior exposure to **ionizing radiation** is the most significant risk factor. * **Genetics:** Associated with **BRAF mutations** (most common) and **RET/PTC rearrangements** [1]. * **Spread:** Primarily via **lymphatics** to cervical lymph nodes (unlike Follicular, which spreads hematogenously) [2]. * **Prognosis:** Excellent, with a 10-year survival rate >95% [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1099-1100. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 429-430. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1099.

Question 148: All of the following are associated with Multiple Endocrine Neoplasia type 2 (MEN-2) except?

A. Pheochromocytoma
B. Islet cell hyperplasia (Correct Answer)
C. Medullary carcinoma of the thyroid
D. Parathyroid adenoma

Explanation: **Explanation:** The Multiple Endocrine Neoplasia (MEN) syndromes are autosomal dominant disorders characterized by tumors arising in multiple endocrine organs. This question tests the ability to distinguish between **MEN-1 (Wermer Syndrome)** and **MEN-2 (Sipple Syndrome)** [1]. **Why Islet Cell Hyperplasia is the correct answer:** Islet cell hyperplasia (or tumors like Gastrinomas and Insulinomas) is a classic component of **MEN-1**, not MEN-2 [2]. The "3 Ps" of MEN-1 are **P**arathyroid hyperplasia/adenoma, **P**ituitary adenoma, and **P**ancreatic islet cell tumors. Therefore, it is the "except" in this list. **Analysis of incorrect options (Components of MEN-2):** * **Medullary Thyroid Carcinoma (MTC):** This is the most consistent feature of MEN-2 (seen in nearly 100% of cases) [3]. It arises from C-cell hyperplasia. * **Pheochromocytoma:** Occurs in approximately 50% of patients with MEN-2A and MEN-2B [1]. They are often bilateral and multifocal. * **Parathyroid Adenoma/Hyperplasia:** This is seen in **MEN-2A** (20-30% of cases) [1] but is notably **absent in MEN-2B**. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Mutation:** MEN-1 is caused by mutations in the *MEN1* gene (Menin protein). MEN-2 (both 2A and 2B) is caused by gain-of-function mutations in the **RET proto-oncogene** [1]. * **MEN-2B Distinction:** Patients with MEN-2B present with MTC and Pheochromocytoma (like 2A) but also exhibit **Mucosal neuromas** and a **Marfanoid habitus** [1], while lacking parathyroid involvement. * **Prophylactic Surgery:** Due to the high penetrance of MTC, prophylactic thyroidectomy is often indicated in children carrying the *RET* mutation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1137. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1125. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1102-1103.

Question 149: Subcutaneous and visceral lipomas are associated with which type of multiple endocrine neoplasia (MEN) syndrome?

A. MEN 1 (Correct Answer)
B. MEN 2A
C. MEN 2B
D. MEN 2C

Explanation: **Explanation:** **MEN 1 (Wermer Syndrome)** is characterized by the "3 Ps": **P**arathyroid hyperplasia, **P**ancreatic islet cell tumors, and **P**ituitary adenomas [1]. However, for NEET-PG, it is crucial to recognize the **non-endocrine manifestations** of MEN 1. These include cutaneous lesions such as **lipomas** (both subcutaneous and visceral), angiofibromas, and collagenomas. The presence of multiple lipomas in a patient with endocrine dysfunction is a strong clinical marker for the MEN1 gene mutation (located on chromosome 11q13) [2]. **Analysis of Incorrect Options:** * **MEN 2A (Sipple Syndrome):** Characterized by Medullary Thyroid Carcinoma (MTC), Pheochromocytoma, and Parathyroid hyperplasia [3]. It is not associated with lipomas. * **MEN 2B:** Characterized by MTC, Pheochromocytoma, and a distinct phenotype including **Mucosal Neuromas** (on the tongue/lips) and a **Marfanoid habitus** [3]. While it involves skin/nerve findings, lipomas are not a feature. * **MEN 2C:** This is an outdated term sometimes used for familial Medullary Thyroid Carcinoma (FMTC) without other endocrine features. It does not involve lipomas. **High-Yield Clinical Pearls for NEET-PG:** * **MEN 1 Gene:** Encodes the protein **Menin**, a tumor suppressor [1]. * **Most common initial presentation of MEN 1:** Primary Hyperparathyroidism (Hypercalcemia) [2]. * **Most common Pancreatic tumor in MEN 1:** Gastrinoma (Zollinger-Ellison Syndrome) [1]. * **MEN 2 Gene:** Associated with the **RET proto-oncogene** (tyrosine kinase receptor) [3]. * **Prophylactic Thyroidectomy:** Indicated in MEN 2A and 2B due to the 100% penetrance of Medullary Thyroid Carcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1139-1140. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1104-1105. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1137.

Question 150: A 55-year-old man, who is on dialysis due to end-stage renal disease, complains of pain in his jaw and left arm for 6 months. An X-ray of the left arm reveals multiple, small bone cysts and pathologic fractures. What is the appropriate diagnosis for this patient's bone lesions?

A. Chronic osteomyelitis
B. Marble bone disease
C. Osteitis fibrosa cystica (Correct Answer)
D. Osteoid osteoma

Explanation: ### Explanation **Correct Answer: C. Osteitis fibrosa cystica** **Mechanism:** The patient has **End-Stage Renal Disease (ESRD)**, which leads to **Secondary Hyperparathyroidism**. In ESRD, phosphate retention and decreased Vitamin D activation ($1,25-(OH)_2D_3$) cause hypocalcemia, which chronically stimulates the Parathyroid glands to secrete **Parathyroid Hormone (PTH)** [3]. High PTH levels increase osteoclast activity, leading to subperiosteal bone resorption and the replacement of marrow with fibrous tissue [1]. This process results in the formation of cystic lesions and "Brown tumors" (masses of fibrous tissue and hemorrhage) [1]. This constellation of skeletal changes is known as **Osteitis fibrosa cystica** (also called von Recklinghausen’s disease of bone) [1]. **Why Incorrect Options are Wrong:** * **A. Chronic osteomyelitis:** This is a persistent bone infection characterized by a *sequestrum* (dead bone) and *involucrum* (new bone formation). It typically presents with fever, sinus tracts, and localized swelling rather than generalized cystic changes related to renal failure. * **B. Marble bone disease (Osteopetrosis):** This is a genetic disorder of defective osteoclast function resulting in abnormally dense, "stone-like" bones. It presents with increased bone density on X-ray, not cystic radiolucencies. * **C. Osteoid osteoma:** A benign bone-forming tumor characterized by a small radiolucent *nidus* (usually <2cm) surrounded by reactive sclerosis, typically causing nocturnal pain relieved by aspirin. It does not present with multiple cysts or a history of renal failure. **NEET-PG High-Yield Pearls:** * **Radiological Hallmark:** Subperiosteal resorption of the radial aspect of the middle phalanges is the most sensitive sign of hyperparathyroidism. * **Brown Tumors:** These are not true neoplasms; they are collections of osteoclasts, reactive giant cells, and hemorrhagic debris (hemosiderin gives the "brown" color) [1]. * **Renal Osteodystrophy:** A broader term encompassing osteitis fibrosa cystica, osteomalacia, and osteoporosis associated with chronic kidney disease [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1105-1106. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 668-669. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1106-1107.

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Pituitary Gland Disorders

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Thyroid Gland Diseases

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Parathyroid Gland Pathology

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Adrenal Medullary Disorders

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Pancreatic Endocrine Disorders

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Diffuse Neuroendocrine System

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