General Pathology — MCQs
On this page
Which of the following conditions classically shows a rosette-shaped arrangement of cells?
Which of the following is a proapoptotic marker?
A 45-year-old male presents with weight loss, steatorrhea, and malabsorption. A CT scan of the abdomen reveals a questionable mass in the head of the pancreas. A biopsy specimen microscopically reveals chronic inflammation and atrophy of the pancreatic acini with marked fibrosis. No malignancy is identified. What is the most common cause of this patient's condition in adults?
What is the most reliable investigation for amyloid disease?
Down syndrome is due to which chromosomal abnormality?
Fat necrosis is classically seen in which organ?
Red infarction is typically seen in which organ?
Zellballen pattern on histopathology is observed in which of the following tumors?
Ruffled membrane is characteristically seen in which of the following cells?
Sago spleen is a feature of which of the following conditions?
General Pathology Indian Medical PG Practice Questions and MCQs
Question 831: Which of the following conditions classically shows a rosette-shaped arrangement of cells?
- A. Thecoma of ovary
- B. Ependymoma (Correct Answer)
- C. Neurofibroma
- D. Lymphoma
Explanation: **Explanation:** The correct answer is **Ependymoma**. In pathology, a "rosette" refers to a circular or flower-like arrangement of cells. Ependymomas are neuroepithelial tumors that classically exhibit two types of rosette formations [1]: 1. **Perivascular Pseudorosettes:** Tumor cells are arranged around a central blood vessel, separated by a fibrillary zone (cytoplasmic processes) [1]. This is a hallmark feature found in almost all ependymomas. 2. **True Ependymal Rosettes (True Rosettes):** Tumor cells surround a central lumen (resembling a small duct), mimicking the structure of the central canal of the spinal cord [1]. **Analysis of Incorrect Options:** * **A. Thecoma of ovary:** These are sex cord-stromal tumors composed of spindle-shaped cells with lipid-laden cytoplasm. They typically show a diffuse or fascicular growth pattern, not rosettes. * **C. Neurofibroma:** These are peripheral nerve sheath tumors characterized by a "shredded carrot" appearance due to wavy collagen bundles and spindle cells in a myxoid background. * **D. Lymphoma:** Malignant lymphomas generally present as a diffuse sheet of discohesive, monomorphic round cells. They do not form organized architectural patterns like rosettes. **High-Yield Clinical Pearls for NEET-PG:** * **Homer Wright Rosettes:** Cells surround a central fibrillary core (no lumen/vessel). Seen in **Neuroblastoma**, Medulloblastoma, and Retinoblastoma. * **Flexner-Wintersteiner Rosettes:** Cells surround a central lumen. Highly specific for **Retinoblastoma**. * **Call-Exner Bodies:** Small follicles filled with eosinophilic material, seen in **Granulosa Cell Tumors** (often confused with rosettes). * **Ependymoma Location:** Most common in the fourth ventricle in children and the spinal cord in adults [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1312-1313.
Question 832: Which of the following is a proapoptotic marker?
- A. BCL-X
- B. BAX (Correct Answer)
- C. BCL-2
- D. Mcl-1
Explanation: **Explanation:** Apoptosis (programmed cell death) is tightly regulated by the **BCL-2 family of proteins**, which act as a molecular switch at the mitochondrial membrane [3]. These proteins are divided into two functional groups: anti-apoptotic and pro-apoptotic [1]. **Why BAX is correct:** **BAX** (along with **BAK**) is a quintessential **pro-apoptotic** effector protein [1]. When activated by cellular stress or DNA damage, BAX and BAK undergo conformational changes and oligomerize to form pores in the outer mitochondrial membrane [3]. This process, known as Mitochondrial Outer Membrane Permeabilization (MOMP), allows the release of **Cytochrome c** into the cytosol, which activates the caspase cascade leading to cell death [3]. **Why the other options are incorrect:** * **BCL-2, BCL-X, and Mcl-1** are all **anti-apoptotic** (pro-survival) proteins [1]. They reside in the mitochondrial membrane and cytoplasm, where they bind to and inhibit pro-apoptotic sensors [4]. They prevent the leakage of Cytochrome c, thereby keeping the cell alive [1]. Overexpression of these proteins (especially BCL-2) is a hallmark of many cancers, such as Follicular Lymphoma [2]. **High-Yield NEET-PG Pearls:** * **The "Sensors":** BH3-only proteins (e.g., **BAD, BIM, BID, PUMA, NOXA**) act as sensors of cell stress and initiate the pathway by neutralizing anti-apoptotic proteins. * **The "Executioners":** BAX and BAK are the "gatekeepers" of mitochondrial permeability [5]. * **Mnemonic:** Remember **"BAX/BAK = Back to the grave"** (Pro-apoptotic) and **"BCL-2 = Be Clean and Live"** (Anti-apoptotic). * **Clinical Link:** The $t(14;18)$ translocation leads to BCL-2 overexpression, preventing apoptosis in B-cells [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 64-65. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 65-67. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 80-81.
Question 833: A 45-year-old male presents with weight loss, steatorrhea, and malabsorption. A CT scan of the abdomen reveals a questionable mass in the head of the pancreas. A biopsy specimen microscopically reveals chronic inflammation and atrophy of the pancreatic acini with marked fibrosis. No malignancy is identified. What is the most common cause of this patient's condition in adults?
- A. Abdominal trauma
- B. Chronic alcoholism (Correct Answer)
- C. Gallstones
- D. Hyperlipidemia
Explanation: The clinical presentation of weight loss, steatorrhea (due to exocrine insufficiency), and malabsorption, combined with biopsy findings of **acinar atrophy and marked fibrosis**, is diagnostic of **Chronic Pancreatitis** [1]. **1. Why Chronic Alcoholism is Correct:** In adults, **chronic alcoholism** is the most common cause of chronic pancreatitis (accounting for 60-70% of cases). Alcohol induces the secretion of protein-rich pancreatic fluid, which forms "protein plugs" in the small ducts [2]. these plugs calcify (forming stones) and lead to ductal obstruction, subsequent inflammation, and the replacement of functional parenchyma with dense fibrous tissue [1]. **2. Why Incorrect Options are Wrong:** * **Gallstones:** While gallstones are the most common cause of **acute** pancreatitis, they rarely lead to chronic pancreatitis unless there is recurrent, long-term obstruction. * **Abdominal Trauma:** This is a common cause of acute pancreatitis in children (e.g., bicycle handlebar injuries) or can lead to pancreatic pseudocysts, but it is not a primary driver of chronic fibrotic changes in adults. * **Hyperlipidemia:** Specifically hypertriglyceridemia (Type I, IV, or V), is a known trigger for **acute** pancreatitis episodes but is a much less frequent cause of chronic disease compared to alcohol. **3. High-Yield Pearls for NEET-PG:** * **Classic Triad:** Pancreatic calcifications (visible on X-ray/CT), steatorrhea, and diabetes mellitus [2]. * **Morphology:** The hallmark is irreversible fibrosis. Unlike acute pancreatitis, the inflammation is often patchy and lacks the massive necrosis seen in acute flares [1]. * **Genetic Link:** Mutations in the **PRSS1** (Trypsinogen) or **SPINK1** (Trypsin inhibitor) genes are high-yield causes of hereditary chronic pancreatitis [3]. * **TIGAR-O:** A useful mnemonic for etiologies (Toxic-metabolic, Idiopathic, Genetic, Autoimmune, Recurrent severe acute pancreatitis, Obstructive). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, pp. 893-895. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 407-408. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, pp. 891-892.
Question 834: What is the most reliable investigation for amyloid disease?
- A. Immunoglobulin assay
- B. Ultrasound
- C. Rectal biopsy (Correct Answer)
- D. Urine examination
Explanation: **Explanation:** Amyloidosis is a systemic disorder characterized by the extracellular deposition of misfolded proteins in various tissues [1]. The diagnosis relies on demonstrating these deposits in tissue samples [1]. **Why Rectal Biopsy is Correct:** Rectal biopsy is considered the most reliable and traditional screening investigation for systemic amyloidosis, with a diagnostic yield of approximately **75-85%**. The rectum is highly vascular and easily accessible; amyloid deposits are typically found in the submucosal blood vessels. While **Abdominal Fat Pad Aspiration** is now often the preferred initial screening test due to its non-invasive nature, rectal biopsy remains a gold-standard "reliable" tissue-based investigation in clinical examinations. **Why Other Options are Incorrect:** * **Immunoglobulin Assay:** While this can help identify a plasma cell dyscrasia (like in AL amyloidosis) [1], it does not confirm the presence of amyloid deposits in tissues. * **Ultrasound:** This is an imaging modality that may show organomegaly (e.g., hepatomegaly) or thickened cardiac walls [2], but it lacks the specificity to differentiate amyloid from other infiltrative diseases. * **Urine Examination:** This may detect Bence-Jones proteins or proteinuria (nephrotic syndrome) [2], which are suggestive of underlying causes or complications, but it cannot definitively diagnose amyloidosis. **NEET-PG High-Yield Pearls:** * **Gold Standard Stain:** Congo Red stain, which shows **Apple-green birefringence** under polarized light [1]. * **Most Sensitive Site:** Abdominal fat pad aspiration (80% sensitivity) is the least invasive; Rectal biopsy is the most reliable traditional site. * **Biopsy Site for Specific Organs:** If systemic screening is negative but clinical suspicion is high, biopsy the involved organ (e.g., Kidney or Heart). * **Secondary Amyloidosis (AA):** Most common cause in India is still Tuberculosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 264-269. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 135-140.
Question 835: Down syndrome is due to which chromosomal abnormality?
- A. Trisomy 21
- B. Translocation involving chromosome 21
- C. Translocation involving chromosome 22
- D. All of the above (Correct Answer)
Explanation: **Explanation:** Down Syndrome (Trisomy 21) is the most common chromosomal disorder and a frequent topic in NEET-PG [1]. While it is synonymous with an extra copy of chromosome 21, the genetic mechanisms leading to this state vary: 1. **Trisomy 21 (95% of cases):** The most common cause is **meiotic non-disjunction**, where chromosomes fail to separate during gametogenesis (usually maternal meiosis I) [2]. This results in a karyotype of **47, XX/XY, +21** [1]. 2. **Robertsonian Translocation (approx. 4%):** This occurs when the long arm of chromosome 21 attaches to another acrocentric chromosome (usually **14 or 22**). Although the total chromosome count remains 46, there is effectively a triple dose of chromosome 21 genetic material [1]. * *Note:* While translocation involving chromosome 14 is most common, translocation involving **chromosome 22** is also a documented cause of Down syndrome. 3. **Mosaicism (approx. 1%):** Caused by mitotic non-disjunction during early embryonic development, leading to two cell line (one normal, one trisomic) [1]. **Why "All of the above" is correct:** The question asks for chromosomal abnormalities that cause Down syndrome. Since Trisomy 21 (Option A), Translocation involving 21 (Option B), and Translocation involving 22 (Option C) are all recognized genetic etiologies, Option D is the most comprehensive answer. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factor:** Increased maternal age (>35 years) is the strongest risk factor for non-disjunction [2]. * **Screening:** First-trimester screening shows **increased nuchal translucency**, **decreased PAPP-A**, and **increased β-hCG**. * **Quadruple Test:** Decreased AFP, decreased Estriol, increased hCG, and increased Inhibin-A. * **Clinical Associations:** Endocardial cushion defects (ASD/VSD), early-onset Alzheimer’s, and increased risk of ALL/AML (M7 subtype). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-172. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 40-41.
Question 836: Fat necrosis is classically seen in which organ?
- A. Heart
- B. Brain
- C. Lungs
- D. Breast (Correct Answer)
Explanation: **Explanation:** **Fat necrosis** is a specialized form of cell death occurring in adipose tissue [1]. It is not a specific pattern of necrosis (like coagulative or liquefactive) but rather a descriptive clinical term [1]. It occurs when activated lipases release fatty acids from triglycerides, which then combine with calcium to form chalky white deposits—a process known as **saponification** [1]. **Why Breast is Correct:** The **Breast** is a classic site for fat necrosis because it contains a high proportion of adipose tissue. It typically occurs following **trauma** or surgery. Clinically, it is highly significant for NEET-PG because it presents as a painless, hard mass that can mimic breast carcinoma both clinically and radiologically. **Why Other Options are Incorrect:** * **Heart:** Ischemia in the myocardium leads to **Coagulative Necrosis**, characterized by the preservation of cell outlines and protein denaturation. * **Brain:** Ischemia or infection in the CNS leads to **Liquefactive Necrosis** due to the high lipid content and lack of a supportive connective tissue framework, resulting in a liquid viscous mass. * **Lungs:** Typically associated with **Caseous Necrosis** (in Tuberculosis), which has a "cheese-like" friable appearance [1], or coagulative necrosis in pulmonary infarction. **High-Yield Clinical Pearls for NEET-PG:** * **Two Main Types:** Fat necrosis is seen in **Traumatic** (e.g., Breast) and **Enzymatic** (e.g., Acute Pancreatitis) settings. * **Acute Pancreatitis:** This is the most common cause of enzymatic fat necrosis, where pancreatic lipases escape into the omentum and peritoneal cavity [1]. * **Microscopic Appearance:** Characterized by "shadowy outlines" of necrotic adipocytes with basophilic calcium deposits and surrounding inflammation [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 55.
Question 837: Red infarction is typically seen in which organ?
- A. Kidney
- B. Brain
- C. Small intestine (Correct Answer)
- D. Heart
Explanation: **Explanation:** Infarction is classified into two types based on the amount of hemorrhage: **Red (Hemorrhagic)** and **White (Anemic)** [2]. **Why Small Intestine is Correct:** Red infarcts occur in tissues with a **dual blood supply**, loose textures, or where blood can collect in the infarcted zone [2]. The small intestine is a classic example because it has extensive collateral circulation (mesenteric arcades) [1]. When an arterial occlusion occurs, blood from collateral vessels seeps into the necrotic area. Additionally, red infarcts are characteristic of **venous occlusions** (e.g., mesenteric venous thrombosis) and **reperfusion injury**, both of which are common in the bowel [2]. **Analysis of Incorrect Options:** * **Kidney (A) & Heart (D):** These are solid organs with **end-arterial circulation**. When an artery is blocked, there is no secondary supply to bleed into the necrotic zone, resulting in a **White (Anemic) Infarct** [2]. * **Brain (B):** While the brain can undergo "hemorrhagic transformation," it typically undergoes **Liquefactive Necrosis**. In the context of primary arterial occlusion, it is generally considered a pale infarct unless reperfused. **High-Yield NEET-PG Pearls:** * **Mnemonic for Red Infarcts (S-L-O-B):** **S**pongiose tissue (Lung), **L**oose tissue (Testis/Ovary), **O**cclusion (Venous), **B**lood (Dual supply/Small Intestine/Liver). * **White Infarcts** occur in solid organs with a single blood supply: **Heart, Spleen, and Kidney** [2]. * **Morphology:** Red infarcts remain red/firm, while white infarcts are wedge-shaped with the apex pointing toward the occlusion [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 785-786. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 140.
Question 838: Zellballen pattern on histopathology is observed in which of the following tumors?
- A. Gastrointestinal stromal tumor (GIST)
- B. Astrocytoma
- C. Carotid body tumor (Correct Answer)
- D. Retinoblastoma
Explanation: **Explanation:** The **Zellballen pattern** is the characteristic histopathological hallmark of **Paragangliomas**, including the **Carotid body tumor** and Pheochromocytoma [1]. **Why the correct answer is right:** Paragangliomas are neuroendocrine tumors derived from extra-adrenal chromaffin cells [3]. On microscopy, the tumor cells (chief cells) are arranged in well-defined, nested, or organoid clusters called **"Zellballen"** (German for "cell balls") [1]. These nests are surrounded by a delicate vascular stroma and peripheral spindle-shaped **sustentacular cells** [2]. **Analysis of incorrect options:** * **Gastrointestinal stromal tumor (GIST):** Characterized by bundles of **spindle cells** or epithelioid cells. It is defined by the expression of **CD117 (c-KIT)**. * **Astrocytoma:** Typically shows a fibrillary background with pleomorphic astrocytes. High-grade versions (Glioblastoma) show pseudopalisading necrosis and microvascular proliferation. * **Retinoblastoma:** Characterized by small round blue cells forming **Flexner-Wintersteiner rosettes** (true rosettes with a central lumen) or Homer Wright rosettes. **High-Yield Clinical Pearls for NEET-PG:** * **Carotid Body Tumor:** Usually presents as a painless, slow-growing mass in the neck that is mobile laterally but not vertically (Fontaine’s sign) [3]. * **Immunohistochemistry (IHC):** Chief cells are positive for **Synaptophysin** and **Chromogranin**, while sustentacular cells are positive for **S-100**. * **Rule of 10s:** Historically associated with Pheochromocytoma (10% bilateral, 10% malignant, 10% extra-adrenal), though genetic understanding is evolving. * **Salt and Pepper Chromatin:** A common feature of neuroendocrine tumors, including those showing Zellballen patterns. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1137-1138. [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 839: Ruffled membrane is characteristically seen in which of the following cells?
- A. White fibrous cartilage
- B. Osteoblast
- C. Osteoclast (Correct Answer)
- D. Elastic cartilage
Explanation: ### Explanation **Correct Answer: C. Osteoclast** **Mechanism and Concept:** The **ruffled membrane** is a specialized, highly folded area of the plasma membrane found in **osteoclasts**. It is located at the site where the cell attaches to the bone surface (Howship’s lacunae). These finger-like projections significantly increase the surface area for the secretion of lysosomal enzymes (like Cathepsin K) and protons ($H^+$ ions via proton pumps). This acidic microenvironment is essential for the resorption of the mineralized bone matrix. The ruffled membrane is functionally surrounded by a "sealing zone" (clear zone) that prevents the leakage of these resorptive enzymes into the surrounding tissue. **Analysis of Incorrect Options:** * **A & D (Cartilage):** White fibrous and elastic cartilage consist of chondrocytes embedded in a matrix. Chondrocytes do not possess ruffled membranes as their primary function is matrix maintenance, not active mineralized tissue resorption. * **B (Osteoblast):** Osteoblasts are bone-forming cells [1]. They are characterized by an abundant rough endoplasmic reticulum (RER) and a prominent Golgi apparatus for protein synthesis (collagen), but they lack the resorptive machinery of the ruffled membrane [1]. **High-Yield Facts for NEET-PG:** * **Origin:** Osteoclasts are derived from the **Monocyte-Macrophage lineage** (Hematopoietic stem cells), unlike osteoblasts which come from mesenchymal stem cells. * **Markers:** Osteoclasts are identified by **TRAP** (Tartrate-Resistant Acid Phosphatase) positivity. * **Regulation:** **RANKL** (produced by osteoblasts) binds to **RANK** receptors on osteoclast precursors to stimulate differentiation. **Osteoprotegerin (OPG)** acts as a decoy receptor to inhibit this process. * **Clinical Correlation:** In **Osteopetrosis** (Marble Bone Disease), there is a functional defect in osteoclasts (often due to carbonic anthedrase II deficiency), leading to the disappearance of the ruffled membrane and failure of bone resorption. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1182-1184.
Question 840: Sago spleen is a feature of which of the following conditions?
- A. Chronic congestion of the spleen
- B. Malaria
- C. Amyloidosis (Correct Answer)
- D. Pneumocystis carinii infection
Explanation: **Explanation:** **Amyloidosis (Correct Answer):** Sago spleen is a classic gross pathological manifestation of **systemic amyloidosis** [1]. In this condition, amyloid fibrils are deposited primarily in the **white pulp** (splenic follicles). On gross examination, these deposits appear as pale, translucent, waxy granules resembling grains of **sago** (a starch derived from palm stems). This pattern is distinct from "Lardaceous spleen," where amyloid is deposited in the **red pulp**, leading to large, map-like waxy areas. **Why other options are incorrect:** * **Chronic Congestion:** Typically seen in portal hypertension (e.g., Cirrhosis), this leads to **congestive splenomegaly**. Microscopically, it is characterized by **Gamna-Gandy bodies** (siderofibrotic nodules containing calcium and hemosiderin), not sago-like granules. * **Malaria:** Chronic malaria results in massive splenomegaly (Ague cake spleen). The spleen appears slate-grey or black due to the accumulation of **hemozoin pigment** (malarial pigment) within the reticuloendothelial cells. * **Pneumocystis carinii:** While it can cause extrapulmonary lesions in immunocompromised patients, it typically presents as foamy, eosinophilic exudates in tissues, not the organized follicular deposition seen in sago spleen. **High-Yield Clinical Pearls for NEET-PG:** * **Sago Spleen:** Amyloid in **White Pulp** (Follicular) [1]. * **Lardaceous Spleen:** Amyloid in **Red Pulp** (Sinusoidal) [1]. * **Stain of Choice:** **Congo Red** (shows Apple-green birefringence under polarized light) [1]. * **Most common protein in Secondary Amyloidosis:** AA (Amyloid Associated) protein, often secondary to chronic infections like TB or Bronchiectasis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 264-269.
Practice by Chapter
Cell Injury and Cell Death
Practice Questions
Adaptations of Cellular Growth
Practice Questions
Accumulations and Deposits
Practice Questions
Acute and Chronic Inflammation
Practice Questions
Tissue Repair and Wound Healing
Practice Questions
Hemodynamic Disorders
Practice Questions
Genetic Disorders
Practice Questions
Environmental Pathology
Practice Questions
Nutritional Diseases
Practice Questions
Molecular Basis of Disease
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free