Endocrine Pathology — MCQs
On this page
Subperiosteal resorption and increased thickness of the skull is seen in which condition?
Follicular carcinoma of the thyroid is mostly due to a mutation of which gene?
A 50-year-old man has had a nonhealing ulcer on the bottom of his foot for 2 months. On examination, the 2-cm ulcer overlies the right first metatarsal head. There is reduced sensation to pinprick in his feet, and his visual acuity is reduced bilaterally. His serum creatinine is 2.9 mg/dL. Which of the following laboratory test findings is he most likely to have?
Zellballen pattern is found in the histology of which of the following conditions?
Amyloid stroma is seen in which type of thyroid carcinoma?
A patient undergoes total thyroidectomy for a mass lesion of the thyroid. During the surgery, the surgeon notes that the parathyroid glands appeared enlarged. The thyroid lesion shows neuroendocrine-type cells and amyloid deposition. This patient's thyroid and parathyroid lesions may be related to which of the following oncogenes?
All of the following are helpful for the diagnosis of medullary carcinoma of the thyroid except?
Treatment with the antihypertensive drug spironolactone leads to the formation of spironolactone bodies in which part of the adrenal gland?
Askanazy cells are microscopic findings in which of the following conditions?
Serum calcitonin is a tumor marker for which of the following thyroid pathologies?
Endocrine Pathology Indian Medical PG Practice Questions and MCQs
Question 91: Subperiosteal resorption and increased thickness of the skull is seen in which condition?
- A. Rickets
- B. Osteomalacia
- C. Hyperparathyroidism (Correct Answer)
- D. Thalassemia
Explanation: ### Explanation **Correct Answer: C. Hyperparathyroidism** The hallmark of **Hyperparathyroidism (HPT)**, particularly the primary and secondary forms, is increased osteoclastic activity due to elevated Parathyroid Hormone (PTH). PTH stimulates osteoblasts to release RANK-L, which activates osteoclasts to resorb bone [1]. * **Subperiosteal resorption:** This is the most specific radiographic sign of HPT [1]. It occurs most commonly on the radial aspect of the middle phalanges of the 2nd and 3rd fingers [1]. * **Skull Involvement:** In the skull, this resorption creates a mottled, granular appearance known as the **"Salt and Pepper" skull**. While there is resorption, there is also compensatory reactive bone formation, which can lead to an overall **increase in the thickness** of the calvarium. --- ### Why the other options are incorrect: * **A & B. Rickets and Osteomalacia:** These conditions are characterized by a failure of **osteoid mineralization** (due to Vitamin D deficiency) [3]. While they can show "Looser’s zones" (pseudofractures), they do not typically present with subperiosteal resorption or increased skull thickness. * **D. Thalassemia:** While Thalassemia causes skull changes due to extramedullary hematopoiesis (widening of the diploic space), it classically presents with a **"Crew-cut" or "Hair-on-end"** appearance on X-ray, not subperiosteal resorption. --- ### NEET-PG High-Yield Pearls: 1. **Osteitis Fibrosa Cystica (von Recklinghausen disease of bone):** The advanced stage of bone disease in HPT characterized by bone pain, cysts, and fractures [2]. 2. **Brown Tumors:** These are non-neoplastic collections of osteoclasts, reactive giant cells, and hemorrhagic debris (hemosiderin gives the brown color) seen in HPT [2]. 3. **Rugger-Jersey Spine:** A classic radiological sign of secondary hyperparathyroidism (renal osteodystrophy) showing bands of increased bone density at the vertebral endplates [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1194. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1105-1106. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 668-669.
Question 92: Follicular carcinoma of the thyroid is mostly due to a mutation of which gene?
- A. HRAS
- B. KRAS
- C. NRAS (Correct Answer)
- D. NTRK1
Explanation: **Explanation:** Follicular Carcinoma of the Thyroid (FTC) is characterized by specific genetic alterations that drive follicular cell proliferation [1]. The most common mutations involve the **RAS oncogene family**, specifically point mutations in **NRAS**. 1. **Why NRAS is correct:** Mutations in the RAS family (NRAS, HRAS, and KRAS) are found in approximately 40-50% of Follicular Carcinomas [1]. Among these, **NRAS** is the most frequently mutated isoform. These mutations activate the MAPK and PI3K/AKT signaling pathways, promoting uncontrolled cellular growth [1]. Another significant genetic hallmark of FTC is the **PAX8-PPARG** fusion gene (t(2;3)(q13;p25)), seen in about 30-35% of cases. 2. **Why other options are incorrect:** * **HRAS & KRAS:** While these are part of the RAS family and can be mutated in FTC, they occur much less frequently than NRAS. * **NTRK1:** Rearrangements involving *NTRK1* are typically associated with **Papillary Thyroid Carcinoma (PTC)**, not Follicular Carcinoma [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Follicular Carcinoma:** Spreads primarily via **hematogenous route** (to lungs and bone). Lymphatic spread is rare (unlike PTC). * **Diagnosis:** Cannot be made by FNAC. Histological evidence of **capsular or vascular invasion** is mandatory to distinguish FTC from Follicular Adenoma [2]. * **Iodine Deficiency:** FTC is more common in areas with dietary iodine deficiency [1]. * **Hürthle Cell Carcinoma:** A variant of FTC characterized by abundant granular eosinophilic cytoplasm (due to mitochondria) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1097-1098. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1096-1097.
Question 93: A 50-year-old man has had a nonhealing ulcer on the bottom of his foot for 2 months. On examination, the 2-cm ulcer overlies the right first metatarsal head. There is reduced sensation to pinprick in his feet, and his visual acuity is reduced bilaterally. His serum creatinine is 2.9 mg/dL. Which of the following laboratory test findings is he most likely to have?
- A. Glucosuria (Correct Answer)
- B. Hypoalbuminemia
- C. Hypokalemia
- D. Leukopenia
Explanation: **Explanation:** The clinical presentation describes a classic triad of **diabetic complications**: peripheral neuropathy (non-healing foot ulcer and reduced sensation), retinopathy (reduced visual acuity), and nephropathy (elevated serum creatinine of 2.9 mg/dL). These findings collectively point to a long-standing diagnosis of **Diabetes Mellitus (DM)** [1]. **Why Glucosuria is the correct answer:** In Diabetes Mellitus, insulin deficiency or resistance leads to persistent hyperglycemia [2]. When blood glucose levels exceed the renal threshold (approximately **180 mg/dL**), the proximal convoluted tubules can no longer reabsorb the excess glucose, leading to its excretion in the urine (**Glucosuria**). This is the hallmark laboratory finding in uncontrolled DM [1]. **Analysis of Incorrect Options:** * **B. Hypoalbuminemia:** While diabetic nephropathy eventually leads to proteinuria (microalbuminuria progressing to nephrotic-range proteinuria), hypoalbuminemia typically occurs in the late stages of nephrotic syndrome. Glucosuria is a more direct and common finding associated with the primary disease process. * **C. Hypokalemia:** Patients with diabetic ketoacidosis or renal failure (suggested by high creatinine) are more prone to **hyperkalemia** due to insulin deficiency or decreased potassium excretion, rather than hypokalemia. * **D. Leukopenia:** Diabetes is associated with impaired leukocyte *function* (chemotaxis and phagocytosis), which increases infection risk, but it does not typically cause a decrease in the absolute white blood cell count (leukopenia). **NEET-PG High-Yield Pearls:** * **Diabetic Nephropathy:** The earliest clinical sign is **microalbuminuria** (30-300 mg/day). The characteristic histopathological finding is **Kimmelstiel-Wilson (KW) nodules** (nodular glomerulosclerosis). * **Sorbitol Pathway:** Peripheral neuropathy and cataracts in DM are caused by the accumulation of sorbitol via the polyol pathway (Aldose reductase enzyme). * **Foot Ulcers:** These are multifactorial, resulting from a combination of **ischemia** (microangiopathy) and **neuropathy** (loss of protective sensation). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 434-435. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1116-1117.
Question 94: Zellballen pattern is found in the histology of which of the following conditions?
- A. Neuroblastoma
- B. Paraganglioma (Correct Answer)
- C. Ewing's Sarcoma
- D. Renal Cell Carcinoma (RCC)
Explanation: **Explanation:** The **Zellballen pattern** (German for "cell balls") is the characteristic histological hallmark of tumors derived from the **extra-adrenal paraganglia (Paraganglioma)** and the **adrenal medulla (Pheochromocytoma)** [1]. **1. Why Paraganglioma is Correct:** Paragangliomas are neuroendocrine tumors. Their histology features nests or clusters of round-to-oval **chief cells** (containing catecholamines) surrounded by a delicate vascular stroma and a peripheral layer of spindle-shaped **sustentacular cells** [1]. This nested architectural arrangement is termed the "Zellballen" pattern. **2. Analysis of Incorrect Options:** * **Neuroblastoma:** Characterized by **Homer-Wright rosettes**, where tumor cells surround a central fibrillar area (pseudorosettes), rather than organized nests [1]. * **Ewing’s Sarcoma:** Shows a monotonous sheet of small, round blue cells with scant cytoplasm. It may occasionally show **Homer-Wright rosettes**, but not a Zellballen pattern. * **Renal Cell Carcinoma (RCC):** The most common subtype (Clear Cell RCC) shows a **nested or alveolar pattern** of cells with clear cytoplasm and distinct cell membranes, but it lacks the specific neuroendocrine sustentacular framework of Zellballen [3]. **3. High-Yield Clinical Pearls for NEET-PG:** * **IHC Markers:** Chief cells are positive for **Chromogranin** and **Synaptophysin**, while sustentacular cells are positive for **S-100**. * **Rule of 10s:** Historically associated with Pheochromocytoma (10% bilateral, 10% malignant, 10% extra-adrenal). * **Genetic Associations:** Often linked to mutations in the **SDH (Succinate Dehydrogenase)** gene family, VHL, and RET proto-oncogene [3, 4]. **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. Head and Neck, pp. 748-749. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1137.
Question 95: Amyloid stroma is seen in which type of thyroid carcinoma?
- A. Papillary carcinoma
- B. Medullary carcinoma (Correct Answer)
- C. Anaplastic carcinoma
- D. Follicular carcinoma
Explanation: **Explanation:** **Medullary Thyroid Carcinoma (MTC)** is the correct answer because it originates from the **Parafollicular C-cells**, which are neuroendocrine cells [1] responsible for secreting **Calcitonin**. In MTC, excessive calcitonin molecules undergo misfolding and aggregate to form insoluble fibrils. These fibrils deposit within the tumor stroma as **amyloid** [2]. On histopathology, this is visualized as acellular, eosinophilic material [2] that shows characteristic **apple-green birefringence** under polarized light when stained with **Congo Red**. **Analysis of Incorrect Options:** * **Papillary Carcinoma:** The most common thyroid cancer; it is characterized by nuclear features (Orphan Annie eyes, pseudoinclusions) and **Psammoma bodies** (laminated calcifications), not amyloid. * **Follicular Carcinoma:** Characterized by capsular or vascular invasion [2]. It produces thyroglobulin, which does not form amyloid. * **Anaplastic Carcinoma:** An extremely aggressive, undifferentiated tumor. It presents with pleomorphic giant cells or spindle cells [2] but lacks a specific amyloid stroma. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Association:** Approximately 25% of MTC cases are familial, associated with **RET proto-oncogene** mutations (MEN 2A and 2B syndromes) [1]. * **Tumor Marker:** Serum **Calcitonin** is used for both diagnosis and monitoring recurrence [1]. * **IHC Marker:** Positive for **Carcinoembryonic Antigen (CEA)** [1] and Chromogranin. * **Prophylaxis:** In patients with known RET mutations, prophylactic thyroidectomy is often indicated. **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 96: A patient undergoes total thyroidectomy for a mass lesion of the thyroid. During the surgery, the surgeon notes that the parathyroid glands appeared enlarged. The thyroid lesion shows neuroendocrine-type cells and amyloid deposition. This patient's thyroid and parathyroid lesions may be related to which of the following oncogenes?
- A. bcl-2
- B. C-myc
- C. erb-B2
- D. ret (Correct Answer)
Explanation: **Explanation:** The clinical presentation points towards **Multiple Endocrine Neoplasia Type 2A (MEN 2A)**. The thyroid lesion described—featuring neuroendocrine cells and amyloid deposition (derived from calcitonin)—is a classic description of **Medullary Thyroid Carcinoma (MTC)** [3]. The finding of enlarged parathyroid glands indicates **Parathyroid Hyperplasia** [1]. 1. **Why 'ret' is correct:** The **RET proto-oncogene** (located on chromosome 10q11.2) encodes a receptor tyrosine kinase. Germline gain-of-function mutations in *RET* are the genetic hallmark of the MEN 2 syndromes (MEN 2A and 2B) and Familial Medullary Thyroid Carcinoma (FMTC) [1]. In MEN 2A (Sipple Syndrome), patients typically develop MTC (100%), Pheochromocytoma (50%), and Parathyroid Hyperplasia (10-30%) [1]. 2. **Why other options are incorrect:** * **bcl-2:** An anti-apoptotic gene associated with Follicular Lymphoma [t(14;18)]. * **C-myc:** A transcription factor oncogene associated with Burkitt Lymphoma [t(8;14)]. * **erb-B2 (HER2/neu):** A growth factor receptor gene commonly amplified in Breast and Gastric carcinomas. **High-Yield Clinical Pearls for NEET-PG:** * **Amyloid in MTC:** Stains with **Congo Red** (showing apple-green birefringence) and is composed of pro-calcitonin [3]. * **MEN 2A vs. 2B:** Both involve MTC and Pheochromocytoma. However, MEN 2A includes Parathyroid Hyperplasia, while MEN 2B includes Mucosal Neuromas and Marfanoid habitus [1]. * **Prophylactic Thyroidectomy:** In patients with known *RET* mutations, thyroidectomy is often performed early in life because MTC is almost inevitable. * **Screening:** Calcitonin levels are used for both diagnosis and monitoring recurrence of MTC [2]. **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, pp. 1102-1103. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 430-431.
Question 97: All of the following are helpful for the diagnosis of medullary carcinoma of the thyroid except?
- A. Spindle cell stroma with few follicles
- B. Amyloid deposition
- C. Calcitonin in stroma
- D. Histological confirmation of mitochondria is essential for diagnosis (Correct Answer)
Explanation: **Medullary Thyroid Carcinoma (MTC)** is a neuroendocrine tumor derived from the **parafollicular C-cells** of the thyroid [1][2]. 1. **Why Option D is the Correct Answer (The "Except"):** Histological confirmation of mitochondria is **not** a diagnostic requirement for MTC. While MTC cells contain numerous membrane-bound neuroendocrine granules (visible on electron microscopy), mitochondria are a universal organelle found in almost all cells and lack diagnostic specificity. In contrast, tumors like Hürthle cell carcinoma are characterized by an abundance of mitochondria (oncocytic change), but even there, "essential confirmation" is rarely the standard for diagnosis. 2. **Analysis of Other Options:** * **Option A (Spindle cell stroma):** MTC is highly heterogeneous. It can present with various patterns, including nests, trabeculae, or **spindle-shaped cells**. The absence of thyroid follicles is a key feature, as MTC does not arise from follicular epithelium. * **Option B (Amyloid deposition):** This is the **pathognomonic hallmark** of MTC [2]. The amyloid consists of altered **calcitonin** fibrils and stains positive with Congo Red (showing apple-green birefringence). * **Option C (Calcitonin):** Since MTC arises from C-cells, it secretes calcitonin [1]. Immunohistochemistry for calcitonin is the gold standard for confirming the diagnosis. **NEET-PG High-Yield Pearls:** * **Origin:** Parafollicular C-cells (derived from the **neural crest**). * **Genetics:** Associated with **RET proto-oncogene** mutations (MEN 2A and 2B syndromes) [1]. * **Biomarker:** Serum Calcitonin is used for diagnosis and monitoring recurrence; CEA is also often elevated [1]. * **Microscopy:** Look for "salt and pepper" chromatin (typical of neuroendocrine tumors) and stromal amyloid [2]. **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. 430-431.
Question 98: Treatment with the antihypertensive drug spironolactone leads to the formation of spironolactone bodies in which part of the adrenal gland?
- A. Adrenal cortex (Correct Answer)
- B. Adrenal medulla
- C. Renal cortex
- D. Renal medulla
Explanation: **Explanation:** **1. Why Adrenal Cortex is Correct:** Spironolactone is a potassium-sparing diuretic and an aldosterone antagonist. When patients are treated with spironolactone, it leads to the formation of **Spironolactone bodies** specifically within the cells of the **Adrenal Cortex** (most commonly in the *Zona Glomerulosa*). [1] These bodies are characteristic **eosinophilic, laminated, round-to-oval cytoplasmic inclusions** (often 2–10 µm in size). They represent whorls of smooth endoplasmic reticulum. Their formation is a result of the drug's interference with steroidogenesis, particularly the inhibition of aldosterone synthesis, leading to a compensatory "overworking" of the smooth endoplasmic reticulum in the cortical cells. **2. Why Incorrect Options are Wrong:** * **Adrenal Medulla:** This part of the gland is derived from the neural crest and secretes catecholamines (epinephrine/norepinephrine). [2] It does not involve steroid hormone synthesis and therefore does not develop spironolactone bodies. * **Renal Cortex & Renal Medulla:** While spironolactone acts on the distal convoluted tubules and collecting ducts in the kidney to exert its diuretic effect [3], the histological hallmark of "spironolactone bodies" is an **anatomical finding in the steroid-producing cells** of the adrenal gland, not the renal parenchyma. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Staining:** Spironolactone bodies are strongly eosinophilic on H&E stain and are **PAS-negative** (unlike some other inclusions). * **Location:** Though primarily in the *Zona Glomerulosa*, they can occasionally be seen in the *Zona Fasciculata*. * **Reversibility:** These bodies disappear once the drug is discontinued. * **Conn’s Syndrome Connection:** In exams, these are often mentioned in the context of patients being treated for primary hyperaldosteronism (Conn’s Syndrome) prior to surgical resection of an adrenal adenoma. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1129-1130. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1125-1126. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 420-421.
Question 99: Askanazy cells are microscopic findings in which of the following conditions?
- A. De Quervain's thyroiditis
- B. Riedel's thyroiditis
- C. Hashimoto's thyroiditis (Correct Answer)
- D. None of the above
Explanation: **Explanation:** **Askanazy cells** (also known as Hürthle cells or oxyphil cells) are the hallmark microscopic finding in **Hashimoto’s thyroiditis**. These are transformed follicular epithelial cells that have become enlarged and polygonal due to an abundance of granular, eosinophilic cytoplasm [1]. This characteristic appearance is caused by a massive accumulation of dysfunctional mitochondria, representing a metaplastic response to chronic inflammation and injury. **Analysis of Options:** * **Option C (Correct):** In Hashimoto’s thyroiditis, the thyroid parenchyma shows a dense lymphocytic infiltrate with germinal center formation [1]. The remaining follicles are lined by these eosinophilic Askanazy cells [1]. * **Option A (Incorrect):** **De Quervain’s (Subacute Granulomatous) thyroiditis** is characterized by granulomatous inflammation, multinucleated giant cells, and microabscesses, typically following a viral infection. * **Option B (Incorrect):** **Riedel’s thyroiditis** is characterized by dense, "woody" fibrous tissue replacing the thyroid parenchyma, often extending into adjacent neck structures (IgG4-related disease). **High-Yield Clinical Pearls for NEET-PG:** * **Hürthle Cell Neoplasms:** While Askanazy cells are common in Hashimoto’s, a predominant mass of these cells can indicate a Hürthle cell adenoma or carcinoma. * **Antibodies:** Hashimoto’s is most strongly associated with **Anti-TPO** (Antithyroid peroxidase) and **Anti-Tg** (Antithyroglobulin) antibodies. * **Risk of Malignancy:** Patients with Hashimoto’s have an increased risk of developing **B-cell Non-Hodgkin Lymphoma** (specifically MALToma) and Papillary Thyroid Carcinoma [2]. * **HLA Association:** Strongly linked with **HLA-DR3** and **HLA-DR5**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1089-1091. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 235-236.
Question 100: Serum calcitonin is a tumor marker for which of the following thyroid pathologies?
- A. Anaplastic carcinoma
- B. Papillary carcinoma
- C. Medullary carcinoma (Correct Answer)
- D. Follicular carcinoma
Explanation: ### Explanation **Correct Answer: C. Medullary Carcinoma** **1. Why Medullary Carcinoma is correct:** Medullary Thyroid Carcinoma (MTC) originates from the **Parafollicular C-cells** of the thyroid [2]. These cells are neuroendocrine in origin and their primary physiological function is the secretion of **Calcitonin** [3]. In MTC, serum calcitonin levels are significantly elevated, making it a highly specific and sensitive tumor marker for diagnosis, monitoring treatment response, and detecting recurrence [1]. **2. Why the other options are incorrect:** * **Papillary (B) and Follicular (D) Carcinomas:** These are "Differentiated Thyroid Cancers" (DTC) arising from the thyroid follicular cells [3]. Their primary tumor marker is **Thyroglobulin**, not calcitonin. * **Anaplastic Carcinoma (A):** This is an undifferentiated, highly aggressive tumor. While it arises from follicular cells, it is so poorly differentiated that it usually does not produce thyroglobulin or calcitonin. **3. NEET-PG High-Yield Pearls:** * **Origin:** C-cells are derived from the **Ultimobranchial body** (Neural crest cells). * **Histology:** Look for polygonal cells in a "nest-like" pattern with **Amyloid stroma** (formed by altered calcitonin pro-peptides) [1]. Amyloid stains positive with **Congo Red** (Apple-green birefringence). * **Genetics:** Approximately 25% of cases are familial, associated with **MEN 2A and 2B** syndromes involving **RET proto-oncogene** mutations [1]. * **Prophylaxis:** In patients with known RET mutations, prophylactic thyroidectomy is often indicated. * **CEA:** Carcinoembryonic Antigen (CEA) is also often elevated in MTC and used as a secondary marker [1]. **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. 424-426. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 428-429.
Practice by Chapter
Pituitary Gland Disorders
Practice Questions
Thyroid Gland Diseases
Practice Questions
Parathyroid Gland Pathology
Practice Questions
Adrenal Cortical Disorders
Practice Questions
Adrenal Medullary Disorders
Practice Questions
Pancreatic Endocrine Disorders
Practice Questions
Multiple Endocrine Neoplasia Syndromes
Practice Questions
Diffuse Neuroendocrine System
Practice Questions
Pineal Gland Pathology
Practice Questions
Laboratory Diagnosis of Endocrine Diseases
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free