Vascular Pathology — MCQs
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Kaposi's sarcoma is a tumor of which system?
A 55-year-old woman presents with several weeks of fever, abdominal pain, weight loss, and fatigue. Three days prior to assessment, she developed a left foot drop. Her blood pressure is 160/90 mm Hg and pulse is 80/min. Physical examination confirms left peroneal nerve damage and a bilateral sensory neuropathy in both legs. There are no skin rashes. Laboratory evaluation reveals an ESR of 105 mm/h, WBC of 14,000/mL, and negative serologic tests for antineutrophil cytoplasmic antibody (ANCA) and ANA. The eosinophil count is normal, and urinalysis is negative for casts, protein, and red cells. A clinical diagnosis of polyarteritis nodosa is made. Which of the following is the most likely mechanism for renal injury in this condition?
von Willebrand factor (vWF) is used as a marker for which of the following conditions?
A 12-year-old boy develops cardiac symptoms attributed to rheumatic fever following a streptococcal throat infection. Years later, at age 34, he is admitted with pulmonary edema. Examination reveals a diastolic murmur at the apex, and mitral stenosis is diagnosed. Before surgical evaluation, which of the following findings can be attributed to mitral stenosis?
What is true about the basic structure of an atherosclerotic plaque?
Which of the following conditions does NOT present with granulomatous vasculitis?
ANCA is found in all except?
Endarteritis obliterans is seen in which of the following conditions?
Which of the following is an example of small vessel vasculitis?
Hypersensitivity angiitis is typically seen in which of the following conditions?
Vascular Pathology Indian Medical PG Practice Questions and MCQs
Question 1: Kaposi's sarcoma is a tumor of which system?
- A. Blood vessels (Correct Answer)
- B. Reticuloendothelial system
- C. Striated muscles
- D. Smooth muscles
Explanation: **Explanation:** **Kaposi’s Sarcoma (KS)** is a low-grade vascular neoplasm caused by **Human Herpesvirus-8 (HHV-8)** [3], [4], also known as Kaposi Sarcoma-associated Herpesvirus (KSHV). 1. **Why Blood Vessels is correct:** KS is a tumor of **endothelial cell origin** [1]. The neoplastic cells (spindle cells) express markers characteristic of both vascular and lymphatic endothelial cells [2] (e.g., CD31, CD34, and podoplanin). Histologically, it is characterized by the proliferation of spindle-shaped cells and the formation of slit-like vascular spaces filled with red blood cells [1]. 2. **Why other options are incorrect:** * **Reticuloendothelial system:** While KS is common in immunocompromised patients (like those with HIV/AIDS), it originates from the endothelium of the vasculature, not from the phagocytic cells (macrophages/monocytes) of the reticuloendothelial system. * **Striated/Smooth muscles:** Tumors of muscle origin are called Rhabdomyosarcomas (striated) or Leiomyosarcomas (smooth). While KS contains spindle cells that may mimic muscle fibers, they lack myogenic markers like desmin or actin. **High-Yield Clinical Pearls for NEET-PG:** * **Four Clinical Variants:** Classic (European), Endemic (African), Iatrogenic (Transplant-associated), and AIDS-associated (Epidemic) [3]. * **Histology Hallmark:** "Slit-like spaces" containing extravasated RBCs and **Hyaline droplets** (representing degenerated RBCs) [1]. * **Diagnostic Marker:** Nuclear staining for **HHV-8 (LANA-1)** is the most specific diagnostic test. * **Association:** It is the most common neoplasm associated with AIDS [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 526-527. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 527-528. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 261-262. [4] 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. 219-220.
Question 2: A 55-year-old woman presents with several weeks of fever, abdominal pain, weight loss, and fatigue. Three days prior to assessment, she developed a left foot drop. Her blood pressure is 160/90 mm Hg and pulse is 80/min. Physical examination confirms left peroneal nerve damage and a bilateral sensory neuropathy in both legs. There are no skin rashes. Laboratory evaluation reveals an ESR of 105 mm/h, WBC of 14,000/mL, and negative serologic tests for antineutrophil cytoplasmic antibody (ANCA) and ANA. The eosinophil count is normal, and urinalysis is negative for casts, protein, and red cells. A clinical diagnosis of polyarteritis nodosa is made. Which of the following is the most likely mechanism for renal injury in this condition?
- A. nephrotic syndrome
- B. diffuse glomerulonephritis
- C. granuloma formation
- D. necrotizing vasculitis of vessels (Correct Answer)
Explanation: **Explanation:** **Polyarteritis Nodosa (PAN)** is a systemic necrotizing vasculitis that typically affects small-to-medium-sized muscular arteries. The hallmark of PAN is that it **spares the smallest vessels** (capillaries, venules, and arterioles). 1. **Why Option D is Correct:** In PAN, renal involvement is common and is the leading cause of death. However, because PAN does not affect capillaries, it **does not cause glomerulonephritis**. Instead, the renal injury results from **necrotizing vasculitis of the renal arteries** (interlobar and arcuate arteries). This leads to vessel narrowing, thrombosis, and ischemia [1]. The "string of pearls" appearance on angiography is due to microaneurysms forming at sites of transmural necrosis [1]. 2. **Why Other Options are Incorrect:** * **Options A & B:** Nephrotic syndrome and diffuse glomerulonephritis involve the glomerular capillaries. Since PAN spares capillaries, these are not features of the disease. If glomerulonephritis were present, the diagnosis would shift toward Microscopic Polyangiitis (MPA). * **Option C:** Granuloma formation is a characteristic of Granulomatosis with Polyangiitis (Wegener's) or Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss), not PAN [3]. **NEET-PG High-Yield Pearls:** * **ANCA Status:** PAN is characteristically **ANCA-negative** [2]. * **Associations:** Strongly associated with **Hepatitis B surface antigen (HBsAg)** in ~30% of cases [2]. * **Clinical Sign:** "Mononeuritis multiplex" (e.g., foot drop) is a classic presentation. * **Pathology:** Shows **fibrinoid necrosis**; lesions of different stages (acute and healing) coexist in the same vessel [1]. * **Key Exclusion:** PAN **never** involves the pulmonary arteries (unlike other vasculitides). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 517-518. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 687-688. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520.
Question 3: von Willebrand factor (vWF) is used as a marker for which of the following conditions?
- A. Angiosarcoma (Correct Answer)
- B. Polycythemia vera
- C. Leukemia
- D. Option not recalled
Explanation: **Explanation:** **1. Why Angiosarcoma is correct:** von Willebrand factor (vWF), also known as **Factor VIII-related antigen**, is synthesized by endothelial cells and megakaryocytes. In pathology, it serves as a specific **immunohistochemical (IHC) marker** for tumors of vascular endothelial origin. **Angiosarcoma** is a highly malignant neoplasm of endothelial cells; therefore, its cells express vWF, helping pathologists confirm the vascular nature of the tumor, especially in poorly differentiated cases where vessel formation is not obvious [1]. **2. Why other options are incorrect:** * **Polycythemia Vera:** This is a myeloproliferative neoplasm characterized by the overproduction of red blood cells due to a mutation in the *JAK2* gene. It is diagnosed via hemoglobin levels, bone marrow biopsy, and genetic testing, not endothelial markers. * **Leukemia:** These are malignancies of hematopoietic stem cells (white blood cells). They express markers like CD34, CD33, or TdT, depending on the lineage, but do not express vWF as they are not derived from endothelial cells. **3. High-Yield Clinical Pearls for NEET-PG:** * **Other Endothelial Markers:** Besides vWF, other highly specific markers for vascular tumors (like Angiosarcoma and Kaposi Sarcoma) include **CD31** (most specific) and **CD34** [1]. * **Weibel-Palade Bodies:** These are the storage organelles for vWF found within endothelial cells. On electron microscopy, they are a classic diagnostic feature of vascular tumors. * **Angiosarcoma Associations:** Look for a history of chronic lymphedema (Stewart-Treves Syndrome), prior radiation therapy, or exposure to vinyl chloride/thorotrast (liver angiosarcoma). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 527-528.
Question 4: A 12-year-old boy develops cardiac symptoms attributed to rheumatic fever following a streptococcal throat infection. Years later, at age 34, he is admitted with pulmonary edema. Examination reveals a diastolic murmur at the apex, and mitral stenosis is diagnosed. Before surgical evaluation, which of the following findings can be attributed to mitral stenosis?
- A. Large left ventricle
- B. Indentation of the middle third of the esophagus by an enlarged left atrium (Correct Answer)
- C. Notching of the ribs
- D. Bounding, full pulse
Explanation: ### Explanation **Correct Answer: B. Indentation of the middle third of the esophagus by an enlarged left atrium** **Mechanism:** In mitral stenosis (MS), the narrowed valve orifice obstructs blood flow from the left atrium (LA) to the left ventricle (LV). This leads to a chronic pressure and volume overload in the **left atrium**, resulting in significant **LA enlargement (dilatation)** [1]. Anatomically, the left atrium lies directly anterior to the esophagus. On a lateral chest X-ray or barium swallow study, an enlarged LA characteristically displaces and indents the middle third of the esophagus posteriorly. This is a classic radiological sign of MS. **Analysis of Incorrect Options:** * **A. Large left ventricle:** In pure mitral stenosis, the LV is "protected" from volume overload. Because less blood passes through the stenotic valve, the LV is typically **normal or small** in size. LV enlargement would suggest mitral regurgitation or aortic valve disease. * **C. Notching of the ribs:** This is a classic sign of **Coarctation of the Aorta**, caused by the development of collateral circulation through the intercostal arteries. * **D. Bounding, full pulse:** Also known as a "water-hammer" pulse, this is characteristic of **Aortic Regurgitation** [2]. In MS, the pulse is typically low-volume (pulsus parvus) due to reduced stroke volume. **NEET-PG High-Yield Pearls:** * **Most common cause of MS:** Rheumatic Heart Disease (99% of cases). * **Earliest sign of LA enlargement on CXR:** Straightening of the left cardiac border. * **Advanced CXR signs:** "Double atrial shadow" (right border) and elevation of the left mainstem bronchus (widening of the carinal angle). * **Ortner’s Syndrome:** Hoarseness of voice due to compression of the left recurrent laryngeal nerve by a massively enlarged LA. * **Auscultation:** Loud S1, Opening Snap (OS), and a mid-diastolic rumbling murmur. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 293-294. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 292-293.
Question 5: What is true about the basic structure of an atherosclerotic plaque?
- A. The plaque is formed by a fibrous cap.
- B. The plaque is formed by the tunica media of the vessel.
- C. The plaque is formed by a fibrous cap. (Correct Answer)
- D. The necrotic core contains collagen, elastin, and proteoglycans.
Explanation: **Explanation:** Atherosclerosis is a chronic inflammatory response of the arterial wall to endothelial injury. An atherosclerotic plaque (atheroma) is an intimal-based lesion composed of two main components: a superficial **fibrous cap** and a deep **necrotic core** [1]. 1. **Why Option C is Correct:** The **fibrous cap** is the defining structural feature that covers the lesion. It is composed of smooth muscle cells (SMCs), macrophages, foam cells, lymphocytes, and a dense extracellular matrix (collagen and elastin) [2]. It separates the highly thrombogenic necrotic core from the circulating blood. 2. **Why Option B is Incorrect:** Atherosclerosis is primarily a disease of the **tunica intima** [2]. While smooth muscle cells migrate from the media into the intima to form the plaque, the structural lesion itself is located within the intimal layer. 3. **Why Option D is Incorrect:** The **necrotic core** (the "gruel") contains lipid (mainly cholesterol and cholesterol esters), debris from dead cells, foam cells, and fibrin [1]. Collagen, elastin, and proteoglycans are structural components found in the **fibrous cap**, not the necrotic core [2]. **High-Yield NEET-PG Pearls:** * **Vulnerable vs. Stable Plaque:** A "vulnerable" plaque (prone to rupture) has a **thin fibrous cap**, a large lipid core, and increased inflammation. A "stable" plaque has a **thick, densely collagenous cap** [1]. * **Earliest Lesion:** The "fatty streak" is the precursor to atherosclerosis, seen even in infants [2]. * **Most Common Site:** Abdominal aorta > Coronary arteries > Popliteal arteries > Internal carotid arteries > Circle of Willis. * **Key Growth Factor:** PDGF (Platelet-Derived Growth Factor) released by activated platelets and macrophages stimulates SMC migration and proliferation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 499-507. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 268-270.
Question 6: Which of the following conditions does NOT present with granulomatous vasculitis?
- A. Polyarteritis nodosa
- B. Wegener's granulomatosis
- C. Churg-Strauss syndrome
- D. Microscopic polyangiitis (Correct Answer)
Explanation: ### Explanation The key to answering this question lies in distinguishing between **necrotizing vasculitis with granulomas** and **necrotizing vasculitis without granulomas**. **Why Microscopic Polyangiitis (MPA) is the correct answer:** Microscopic polyangiitis is a systemic necrotizing vasculitis that affects small vessels (capillaries, venules, and arterioles). While it shares many clinical features with Wegener’s granulomatosis (GPA), it is histologically characterized by **pauci-immune necrotizing vasculitis without any evidence of granulomatous inflammation** [1]. This absence of granulomas is the primary pathological feature that differentiates MPA from GPA [1]. **Analysis of Incorrect Options:** * **Polyarteritis nodosa (PAN):** Classically described as a necrotizing inflammation of medium-sized arteries [3]. While it does not typically show "classic" giant cell granulomas, it is often grouped with conditions that can show complex inflammatory infiltrates; however, in the context of this specific comparison, MPA is the most definitive "non-granulomatous" small-vessel vasculitis. (Note: PAN is also uniquely associated with Hepatitis B). * **Wegener’s granulomatosis (GPA):** Characterized by a "triad" of acute necrotizing granulomas of the respiratory tract, necrotizing vasculitis, and renal disease (crescentic glomerulonephritis) [2]. Granulomas are a hallmark [2]. * **Churg-Strauss syndrome (EGPA):** Characterized by eosinophil-rich granulomatous inflammation involving the respiratory tract and necrotizing vasculitis of small to medium vessels, typically associated with asthma [2]. **High-Yield Clinical Pearls for NEET-PG:** * **ANCA Status:** MPA and GPA are both ANCA-associated. MPA is typically **p-ANCA (anti-MPO)** positive, whereas GPA is typically **c-ANCA (anti-PR3)** positive [2]. * **The "No" Rule for MPA:** No granulomas, no upper respiratory involvement (usually), and no asthma. * **Vessel Size:** Both MPA and GPA affect small vessels, while PAN affects medium-sized vessels and **spares the capillaries** (hence, no pulmonary involvement in PAN) [1], [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-519. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 517-518.
Question 7: ANCA is found in all except?
- A. Wegener's granulomatosis
- B. Churg-Strauss syndrome
- C. Microscopic Polyangiitis
- D. Bacterial Vasculitis (Correct Answer)
Explanation: **Explanation:** **ANCA (Anti-Neutrophil Cytoplasmic Antibodies)** are autoantibodies directed against enzymes found in the primary granules of neutrophils and lysosomes of monocytes. They are the hallmark of **ANCA-associated vasculitides (AAV)**, which are characterized by "pauci-immune" (minimal immune complex deposition) inflammation of small vessels [2] [4]. 1. **Why Bacterial Vasculitis is the correct answer:** Bacterial vasculitis is caused by direct microbial invasion of the vessel wall (e.g., *Neisseria meningitidis* or septic emboli) [1]. It is an **infectious pathology**, not an autoimmune one. Therefore, it does not involve the production of ANCA. 2. **Analysis of Incorrect Options:** * **Wegener’s Granulomatosis (Granulomatosis with Polyangiitis - GPA):** Strongly associated with **c-ANCA** (PR3-ANCA) in >90% of active cases [3]. It typically involves the triad of upper/lower respiratory tract and kidneys. * **Churg-Strauss Syndrome (Eosinophilic Granulomatosis with Polyangiitis - EGPA):** Associated with **p-ANCA** (MPO-ANCA) in about 40-50% of cases. It is characterized by asthma, eosinophilia, and granulomas. * **Microscopic Polyangiitis (MPA):** Strongly associated with **p-ANCA** (MPO-ANCA) in ~70-80% of cases. Unlike GPA, it lacks granulomatous inflammation [4]. **NEET-PG High-Yield Pearls:** * **c-ANCA (Cytoplasmic):** Target antigen is **Proteinase-3 (PR3)**. Most specific for GPA [3]. * **p-ANCA (Perinuclear):** Target antigen is **Myeloperoxidase (MPO)**. Seen in MPA, EGPA, and Primary Sclerosing Cholangitis. * **Pauci-immune Glomerulonephritis:** If a biopsy shows crescentic GN with no Ig/Complement deposits, always check ANCA levels [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 513-514. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 514-515. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-519.
Question 8: Endarteritis obliterans is seen in which of the following conditions?
- A. Marfan's syndrome
- B. Turner's syndrome
- C. Neurosyphilis (Correct Answer)
- D. Ankylosing spondylitis
Explanation: **Explanation:** **Endarteritis obliterans** is a hallmark pathological feature of **Tertiary Syphilis**, including Neurosyphilis and Cardiovascular syphilis [1]. It is characterized by the concentric proliferation of the tunica intima and fibrosis of the adventitia in small arteries (vasa vasorum) [1]. This leads to luminal narrowing and eventual occlusion, resulting in ischemic necrosis of the tissues supplied by these vessels. In neurosyphilis, this process affects the small meningovascular arteries, leading to strokes and parenchymal damage [1]. **Analysis of Options:** * **Neurosyphilis (Correct):** Syphilis is the classic cause of endarteritis obliterans. In the aorta, it involves the vasa vasorum, leading to "tree-barking" of the intima and aortic aneurysms [1]. In the CNS, it causes meningovascular syphilis [1]. * **Marfan’s Syndrome:** This is a connective tissue disorder characterized by **Cystic Medial Necrosis** (fragmentation of elastic fibers) of the aorta, leading to aortic dissection, not endarteritis. * **Turner’s Syndrome:** This is associated with **Coarctation of the aorta** (pre-ductal) and bicuspid aortic valves, but not obliterative endarteritis. * **Ankylosing Spondylitis:** While it can cause aortitis and aortic regurgitation, the primary pathology is inflammation of the aortic root and valve rings, distinct from the specific obliterative small-vessel changes seen in syphilis. **High-Yield Clinical Pearls for NEET-PG:** * **Heubner’s Arteritis:** A specific form of endarteritis obliterans involving the small/medium arteries of the brain in neurosyphilis. * **Tree-bark appearance:** Gross appearance of the syphilitic aorta due to intimal scarring following vasa vasorum occlusion [1]. * **Other associations:** Endarteritis obliterans can also be seen in the base of chronic peptic ulcers and in the blood vessels of the placenta (Hofbauer cells). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 386-389.
Question 9: Which of the following is an example of small vessel vasculitis?
- A. Takayasu arteritis
- B. Kawasaki disease
- C. Polyarteritis nodosa (PAN)
- D. Churg-Strauss syndrome (Correct Answer)
Explanation: Vasculitides are classified based on the size of the predominant vessel involved [4]. **Churg-Strauss Syndrome** (now known as Eosinophilic Granulomatosis with Polyangiitis or EGPA) is the correct answer because it is a **small vessel vasculitis** [5]. It typically affects capillaries, venules, and arterioles and is characterized by the triad of asthma, peripheral eosinophilia, and necrotizing vasculitis with extravascular granulomas. It is frequently associated with **p-ANCA (anti-MPO)**. **Analysis of Incorrect Options:** * **Takayasu Arteritis (Option A):** This is a **large vessel vasculitis**. It primarily affects the aorta and its major branches. It is often called "Pulseless disease" and typically affects young Asian females. * **Kawasaki Disease (Option B):** This is a **medium vessel vasculitis**. It is a leading cause of acquired heart disease in children, characterized by "strawberry tongue," desquamating rash, and a high risk of coronary artery aneurysms. * **Polyarteritis Nodosa (Option C):** This is a classic **medium vessel vasculitis** [3]. It involves necrotizing inflammation of medium-sized muscular arteries. Notably, PAN is **not** associated with ANCA but is strongly linked to **Hepatitis B** infection. **High-Yield Clinical Pearls for NEET-PG:** * **Small Vessel Vasculitis Classification:** Divided into **ANCA-associated** (GPA/Wegener’s, MPA, and EGPA/Churg-Strauss) and **Immune Complex-mediated** (Henoch-Schönlein Purpura, Cryoglobulinemic vasculitis) [1], [4]. * **EGPA Hallmark:** Look for a history of refractory asthma or allergic rhinitis in the clinical vignette. * **Vessel Size Rule:** If the question mentions "palpable purpura," think small vessel; if it mentions "claudication" or "absent pulses," think large vessel [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 279-280. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 278-279. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 514-515. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 536-537.
Question 10: Hypersensitivity angiitis is typically seen in which of the following conditions?
- A. Systemic lupus erythematosus
- B. Polyarteritis nodosa
- C. Henoch-Schonlein purpura (Correct Answer)
- D. Buerger's disease
Explanation: **Explanation:** **Hypersensitivity Angiitis** (also known as Leukocytoclastic Vasculitis) is a form of small-vessel vasculitis characterized by the inflammation of arterioles, capillaries, and venules [1]. The hallmark histological finding is the fragmentation of neutrophil nuclei (**leukocytoclasis**) within the vessel walls [1], [4]. **Why Henoch-Schönlein Purpura (HSP) is correct:** HSP is the classic example of hypersensitivity angiitis. It is an IgA-mediated systemic small-vessel vasculitis that typically follows an upper respiratory tract infection. It presents with the clinical triad of **palpable purpura** (usually on lower extremities), arthralgia, and abdominal pain. The underlying mechanism is a Type III hypersensitivity reaction where IgA immune complexes deposit in vessel walls, triggering a leukocytoclastic response [2], [5]. **Analysis of Incorrect Options:** * **Polyarteritis Nodosa (PAN):** This is a **medium-vessel** vasculitis [3]. It is characterized by necrotizing inflammation and "string of pearls" appearance on imaging. It characteristically spares the lungs and is not classified as hypersensitivity angiitis. * **Systemic Lupus Erythematosus (SLE):** While SLE can cause various types of vasculitis due to immune complex deposition, it is a multisystem autoimmune disease [5]. HSP is a more specific and primary representative of the hypersensitivity angiitis category in standardized exams. * **Buerger’s Disease (Thromboangiitis Obliterans):** This is a segmental, thrombosing inflammation of medium and small-sized **arteries** (not just microvessels), strongly associated with heavy tobacco use. It does not show the classic leukocytoclastic features of hypersensitivity angiitis. **High-Yield Pearls for NEET-PG:** * **Microscopic Polyangiitis (MPA)** is another major cause of hypersensitivity angiitis but is differentiated from HSP by the presence of **p-ANCA** and lack of IgA deposits [4]. * **HSP Key Association:** It is the most common vasculitis in children. * **Renal involvement:** In HSP, renal biopsy shows IgA nephropathy (Berger’s disease-like features). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 278-280. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 278-279. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-519. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 514-515.
Practice by Chapter
Atherosclerosis
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Hypertensive Vascular Disease
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Aneurysms and Dissection
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Vasculitis
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Venous Disease and Thrombosis
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Vascular Tumors
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Varicose Veins and Lymphatics
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Pathology of Vascular Interventions
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Vascular Diseases in Specific Organs
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Congenital Vascular Anomalies
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