Vascular Pathology — MCQs

Vascular Pathology Indian Medical PG Practice Questions and MCQs

Question 141: Which diagnostic technique is confirmatory for Lymphangiosarcoma?

A. Lymphangiography
B. Ultrasonography
C. Skin biopsy (Correct Answer)
D. Lymphoscintigraphy

Explanation: **Explanation:** **Lymphangiosarcoma** is a rare, highly aggressive malignant tumor of the vascular endothelium, most commonly occurring as a complication of chronic lymphedema (classically post-mastectomy, known as **Stewart-Treves Syndrome**). **1. Why Skin Biopsy is Correct:** The definitive diagnosis of any malignancy, including lymphangiosarcoma, relies on **histopathological examination** [1]. A skin biopsy allows for the visualization of characteristic features such as irregular, anastomosing vascular channels lined by atypical, pleomorphic endothelial cells showing hyperchromasia and frequent mitoses [2]. Immunohistochemistry (IHC) markers like **CD31** and **Podoplanin (D2-40)** are often used on the biopsy specimen to confirm the lymphatic origin of the tumor [2]. **2. Why Other Options are Incorrect:** * **Lymphangiography:** This is a radiographic study of the lymphatic vessels using contrast. While it can show structural abnormalities or blockages in the lymphatic system, it cannot differentiate between benign changes and malignant cells. * **Ultrasonography:** This is a non-invasive imaging tool used to assess soft tissue masses or fluid collections. It can suggest the presence of a lesion but lacks the cellular resolution required for a definitive cancer diagnosis. * **Lymphoscintigraphy:** This is a nuclear medicine study used to evaluate the functional flow of lymph. It is the gold standard for diagnosing lymphedema but cannot confirm a diagnosis of sarcoma. **High-Yield Clinical Pearls for NEET-PG:** * **Stewart-Treves Syndrome:** Lymphangiosarcoma arising in a limb with chronic lymphedema (usually 10+ years) following radical mastectomy and axillary lymph node dissection. * **Clinical Presentation:** Presents as persistent purple-red nodules or bruising-like patches on a chronically swollen limb [2]. * **Key IHC Marker:** **CD31** is the most sensitive and specific marker for endothelial differentiation [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 340-341. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 527-528.

Question 142: Stasis as a cause of thrombosis is important in which of the following?

A. Sickle cell Anemia
B. Venous circulation
C. Polycythemia
D. All of the above (Correct Answer)

Explanation: **Explanation:** The formation of a thrombus is governed by **Virchow’s Triad**, which consists of endothelial injury, stasis (or turbulence) of blood flow, and hypercoagulability [1]. Stasis is a major contributor to thrombosis because it prevents the dilution of activated clotting factors by fresh blood flow and retards the inflow of clotting factor inhibitors [1]. * **Venous Circulation (Option B):** This is the most classic example of stasis-induced thrombosis. Unlike the high-pressure arterial system, the venous system is a low-pressure circuit where blood flow is naturally slower [1]. Immobilization or heart failure further promotes stasis, leading to Deep Vein Thrombosis (DVT) [1]. * **Sickle Cell Anemia (Option A):** In this condition, deoxygenated hemoglobin (HbS) polymerizes, causing red blood cells to become sickle-shaped. these rigid cells increase blood viscosity and adhere to the endothelium, causing "microvascular stasis" (vaso-occlusion), which triggers thrombosis. * **Polycythemia (Option C):** An absolute increase in red blood cell mass significantly increases **blood viscosity**. According to Poiseuille’s Law, increased viscosity leads to decreased flow velocity (stasis), thereby increasing the risk of both arterial and venous thrombosis [2]. **Clinical Pearls for NEET-PG:** * **Virchow’s Triad:** Endothelial injury is the most important factor for arterial thrombosis, while **stasis** is the most important factor for venous thrombosis [1]. * **Lines of Zahn:** These are laminations found in thrombi formed in flowing blood (heart/arteries), helping to distinguish a pre-mortem thrombus from a post-mortem "currant jelly" clot. * **Hyperviscosity Syndromes:** Conditions like Polycythemia Vera, Multiple Myeloma (paraproteinemia), and Leukemia (leukostasis) all promote thrombosis via stasis [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 132-134. [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. 141-142.

Question 143: In a patient with risk factors including smoking, hypertension, diabetes mellitus, and a serum cholesterol level of 280 mg/dl, in which of the following locations would you least expect to find significant atherosclerotic lesions?

A. Left main coronary artery
B. Aortic bifurcation
C. Circle of Willis
D. Pulmonary artery trunk (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Pulmonary artery trunk.** Atherosclerosis is a disease of high-pressure systemic arteries. The fundamental requirement for the development of an atheroma is **hemodynamic stress** (high pressure) and endothelial injury [1]. Under normal physiological conditions, the pulmonary circulation is a **low-pressure system** (mean pressure ~15 mmHg). Therefore, despite the presence of systemic risk factors like hypercholesterolemia and diabetes, the pulmonary artery is protected from atherosclerosis. *Note:* Significant pulmonary atherosclerosis only occurs in the setting of **Pulmonary Hypertension**, where pressures become high enough to damage the arterial intima. **Analysis of Incorrect Options:** * **A. Left main coronary artery:** Coronary arteries are among the most common sites for atherosclerosis due to high pressure and turbulent flow. * **B. Aortic bifurcation:** This is the **most common site** for atherosclerosis [2]. The bifurcation creates significant turbulence, which promotes endothelial dysfunction and plaque formation. * **C. Circle of Willis:** Major cerebral arteries are frequently involved, leading to ischemic strokes or berry aneurysms [2]. **NEET-PG High-Yield Pearls:** 1. **Order of frequency of involvement:** Abdominal aorta (most common) > Coronary arteries > Popliteal arteries > Internal carotid arteries > Circle of Willis. [2] 2. **Vessels spared:** Atherosclerosis typically spares the upper extremity arteries, mesenteric arteries (except at their ostia), and the pulmonary trunk (unless hypertensive). 3. **Key Risk Factor:** Hypercholesterolemia (specifically high LDL) is the most significant independent risk factor for initiating the "Response to Injury" hypothesis of atherosclerosis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 500-503. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 271-272.

Question 144: Hypersensitivity vasculitis most commonly involves which of the following structures?

A. Arterioles
B. Post-capillary venules (Correct Answer)
C. Capillaries
D. Medium sized arteries

Explanation: **Explanation:** **Hypersensitivity Vasculitis** (also known as Leukocytoclastic Vasculitis or Cutaneous Small Vessel Vasculitis) [3] is a Type III hypersensitivity reaction characterized by the deposition of immune complexes in vessel walls [2]. **1. Why Post-capillary Venules are the Correct Answer:** The primary site of involvement in hypersensitivity vasculitis is the **post-capillary venules** [1]. This occurs because these vessels have relatively low flow rates and high permeability, making them the ideal site for the deposition of circulating antigen-antibody complexes. Once deposited, these complexes activate the complement system, leading to the recruitment of neutrophils [2]. The subsequent release of lysosomal enzymes causes fibrinoid necrosis and the characteristic "nuclear dust" (leukocytoclasis) seen on histology [1], [3]. **2. Analysis of Incorrect Options:** * **Arterioles & Capillaries:** While these small vessels can occasionally be involved in systemic vasculitides (like microscopic polyangiitis), they are not the *most common* or primary site for hypersensitivity vasculitis [1]. * **Medium-sized Arteries:** These are the hallmark of diseases like Polyarteritis Nodosa (PAN) and Kawasaki disease. Hypersensitivity vasculitis is strictly a "small vessel vasculitis" [3]. **3. NEET-PG High-Yield Pearls:** * **Clinical Presentation:** Typically presents as **palpable purpura** [3], most commonly on the lower extremities. * **Histopathology:** Look for **fibrinoid necrosis** and **leukocytoclasis** (fragmented neutrophil nuclei) [1], [3]. * **Common Triggers:** Often induced by drugs (penicillin, sulfonamides) [3] or infections (streptococcal). * **Key Distinction:** Unlike Wegener’s or Churg-Strauss, hypersensitivity vasculitis is usually **ANCA-negative**. **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] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 278-279. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 279-280.

Question 145: What is also known as "Pulseless disease"?

A. Microscopic polyarteritis
B. Giant cell arteritis
C. Takayasu's arteritis (Correct Answer)
D. Polyarteritis nodosa

Explanation: **Explanation:** **Takayasu’s Arteritis (Correct Answer):** Takayasu’s arteritis is a chronic, granulomatous large-vessel vasculitis that primarily involves the **aorta and its major branches** [2]. The inflammation leads to transmural scarring, intimal thickening, and severe narrowing (stenosis) of the arterial lumina. When the subclavian arteries are involved, it results in markedly diminished or absent peripheral pulses in the upper extremities, earning it the classic moniker **"Pulseless Disease."** It typically affects young females (under age 40) and often presents with a significant blood pressure discrepancy between the arms [1]. **Why the other options are incorrect:** * **Microscopic Polyangiitis (MPA):** A small-vessel vasculitis associated with p-ANCA. It primarily affects capillaries, venules, and arterioles (e.g., necrotizing glomerulonephritis), not the large arteries responsible for peripheral pulses. * **Giant Cell Arteritis (GCA):** While also a large-vessel granulomatous vasculitis, it most commonly involves the **extracranial branches of the carotid artery** (e.g., temporal artery). While it is related to Takayasu’s, it occurs in patients >50 years and rarely causes the generalized "pulseless" phenomenon of the upper limbs [1], [2]. * **Polyarteritis Nodosa (PAN):** A medium-vessel vasculitis characterized by necrotizing inflammation and "string of pearls" aneurysms. It typically affects renal and visceral arteries but spares the lungs and does not cause large-vessel occlusion. **High-Yield NEET-PG Pearls:** * **Demographics:** "Young Asian Female" is the classic patient profile. * **Histopathology:** Granulomatous inflammation of the media with elastic lamina fragmentation. * **Diagnosis:** Elevated ESR and angiography (showing "tapering" or "tree-barking" of the aorta). * **Clinical Sign:** Bruits over the carotid or subclavian arteries and coldness/claudication of extremities. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 516-517. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 688-689.

Question 146: In which of the following conditions is c-ANCA typically seen?

A. Wegener's granulomatosis (Correct Answer)
B. Polyarteritis nodosa
C. Churg-Strauss syndrome
D. Bechet's syndrome

Explanation: **Explanation:** **Wegener’s Granulomatosis (Granulomatosis with Polyangiitis - GPA)** is the classic condition associated with **c-ANCA** (cytoplasmic Antineutrophil Cytoplasmic Antibody) [1]. The target antigen for c-ANCA is **Proteinase-3 (PR3)** [1]. GPA is characterized by a triad of necrotizing granulomas in the respiratory tract, necrotizing vasculitis of small-to-medium vessels, and focal necrotizing glomerulonephritis (often crescentic) [1]. **Analysis of Incorrect Options:** * **Polyarteritis Nodosa (PAN):** This is a medium-vessel vasculitis typically associated with **Hepatitis B** infection. Crucially, PAN is **ANCA-negative**. It involves transmural inflammation with fibrinoid necrosis but spares the pulmonary arteries. * **Churg-Strauss Syndrome (Eosinophilic Granulomatosis with Polyangiitis - EGPA):** This condition is primarily associated with **p-ANCA** (perinuclear ANCA), which targets **Myeloperoxidase (MPO)**. It is characterized by asthma, peripheral eosinophilia, and extravascular granulomas. * **Behcet’s Syndrome:** This is a multi-system inflammatory disorder presenting with the triad of oral ulcers, genital ulcers, and uveitis. It is associated with the **HLA-B51** allele and is not linked to ANCA. **High-Yield Pearls for NEET-PG:** * **c-ANCA (PR3-ANCA):** Highly specific for Wegener’s Granulomatosis (GPA) [1]. * **p-ANCA (MPO-ANCA):** Seen in Microscopic Polyangiitis (MPA), Churg-Strauss (EGPA), and Primary Sclerosing Cholangitis (PSC). * **Pauci-immune Glomerulonephritis:** A hallmark of ANCA-associated vasculitides (GPA, MPA, EGPA), meaning there is little to no antibody deposition on immunofluorescence [2][3]. * **Wegener's Triad:** Upper Respiratory Tract + Lower Respiratory Tract + Kidneys [1]. **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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-519.

Question 147: Hyaline arteriosclerosis is seen in which condition?

A. Benign hypertension (Correct Answer)
B. Malignant hypertension
C. Renal artery stenosis
D. Ischemic cardiomyopathy

Explanation: **Explanation:** **Hyaline arteriosclerosis** is a characteristic vascular lesion primarily associated with **benign hypertension** and diabetes mellitus [1], [3]. 1. **Why Benign Hypertension is Correct:** In benign hypertension, chronic hemodynamic stress causes plasma proteins to leak across the injured endothelium into the vessel wall (**extravasation**). This is followed by increased synthesis of smooth muscle cell matrix [3]. Microscopically, this appears as **homogeneous, pink, hyaline thickening** of the arteriolar walls with luminal narrowing [1]. This process leads to downstream ischemia, classically seen as *benign nephrosclerosis* in the kidneys [2]. 2. **Why Other Options are Incorrect:** * **Malignant Hypertension:** This is associated with **Hyperplastic arteriosclerosis**, characterized by "onion-skin" concentric laminations of smooth muscle cells and basement membrane, often accompanied by **fibrinoid necrosis** (necrotizing arteriolitis) [3], [4]. * **Renal Artery Stenosis:** This is a pre-renal cause of hypertension usually caused by atherosclerosis or fibromuscular dysplasia, rather than a systemic small-vessel change like hyaline arteriosclerosis. * **Ischemic Cardiomyopathy:** This is a consequence of atherosclerosis in large/medium-sized coronary arteries, not a primary pathology of the arterioles. **High-Yield Clinical Pearls for NEET-PG:** * **Hyaline vs. Hyperplastic:** Remember "Benign = Pink/Hyaline" and "Malignant = Onion-skin/Hyperplastic." * **Diabetes Connection:** Hyaline arteriosclerosis is more severe in diabetic patients, even without hypertension, due to non-enzymatic glycosylation of proteins [3]. * **Organ Impact:** It is the hallmark of **Benign Nephrosclerosis**, leading to granular, shrunken kidneys [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 943-945. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 541-542. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 498-499. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 945.

Question 148: Glomus cells are found in which of the following conditions?

A. Carotid body tumor (Correct Answer)
B. Thyroid carcinoma
C. Liver carcinoma
D. Glomous tumor

Explanation: **Explanation:** The correct answer is **A. Carotid body tumor**. **Understanding the Concept:** The **Carotid Body Tumor** (also known as a Chemodectoma or Paraganglioma) arises from the extra-adrenal neuroendocrine cells located at the bifurcation of the common carotid artery [1]. These tumors are histologically characterized by clusters of **Glomus cells** (Type I chief cells), which contain neurosecretory granules [1]. These clusters are separated by a vascular stroma and are classically described as **"Zellballen"** (cell balls) patterns. **Why other options are incorrect:** * **B & C (Thyroid/Liver Carcinoma):** These are epithelial malignancies [3]. Thyroid carcinomas (like Papillary or Follicular) and Liver carcinomas (HCC) have distinct cellular origins (follicular cells and hepatocytes, respectively) and do not contain glomus cells [2]. * **D (Glomus Tumor):** This is a common distractor. A **Glomus Tumor** (Glomangioma) arises from the **glomus body** (a specialized arteriovenous anastomosis involved in thermoregulation), typically found under the fingernails. While the names are similar, the cells in a Glomus Tumor are modified smooth muscle cells, whereas the cells in a Carotid Body Tumor are neuroendocrine paraganglionic cells. **High-Yield Clinical Pearls for NEET-PG:** * **Zellballen Pattern:** The pathognomonic histological arrangement seen in Paragangliomas/Carotid body tumors. * **Lyre Sign:** On angiography, the splaying of the internal and external carotid arteries by the tumor mass. * **Fontaine’s Sign:** The tumor is vertically fixed but horizontally mobile (due to its attachment to the carotid bifurcation). * **Stains:** Glomus cells (Type I) are positive for **Chromogranin** and **Synaptophysin**, while the surrounding Sustentacular cells (Type II) are positive for **S-100**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 748-749. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 430-431. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 428-429.

Question 149: Migratory thrombophlebitis is seen in all except?

A. Carcinoma of pancreas
B. Carcinoma of prostate
C. Carcinoma of lung
D. Carcinoma of breast (Correct Answer)

Explanation: **Explanation:** **Migratory Thrombophlebitis (Trousseau Syndrome)** is a paraneoplastic syndrome characterized by recurrent episodes of venous thrombosis that appear in different locations over time (migratory) [1]. It is caused by the release of procoagulants (like mucin and tissue factor) from malignant cells, which trigger the extrinsic coagulation pathway [1]. **Why Carcinoma of Breast is the correct answer:** While breast cancer is associated with a general hypercoagulable state, it is **not** classically associated with Migratory Thrombophlebitis. Trousseau syndrome is most strongly linked to **mucin-secreting adenocarcinomas**, particularly those involving the gastrointestinal and respiratory tracts. **Analysis of Incorrect Options:** * **Carcinoma of Pancreas:** This is the most common association. Pancreatic cancer (especially of the body and tail) frequently secretes procoagulant mucins that lead to systemic activation of the clotting cascade. * **Carcinoma of Lung:** Adenocarcinomas of the lung are well-documented causes of Trousseau syndrome due to their mucin-producing nature. * **Carcinoma of Prostate:** Advanced prostate cancer is a known trigger for migratory thrombophlebitis, often presenting with complex coagulopathies. **NEET-PG High-Yield Pearls:** * **Trousseau Sign of Malignancy:** Do not confuse this with the "Trousseau sign of latent tetany" (carpopedal spasm during BP cuff inflation in hypocalcemia). * **Pathogenesis:** Tumor cells secrete **mucin**, which interacts with L-selectin and P-selectin, leading to the formation of microthrombi. * **Clinical Significance:** The appearance of migratory thrombophlebitis can often precede the clinical diagnosis of an occult visceral malignancy by months or years [1]. * **Most Common Site:** Pancreas (classic association). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 522-523.

Question 150: Histopathological examination of an elderly male patient reveals fragmentation of the elastic lamina, lymphocyte infiltration, and multinucleated giant cells. What is the most likely diagnosis?

A. Giant cell arteritis (Correct Answer)
B. Takayasu arteritis
C. Polyarteritis nodosa
D. Kawasaki disease

Explanation: ### Explanation **Correct Answer: A. Giant Cell Arteritis (GCA)** The histopathological description is classic for **Giant Cell (Temporal) Arteritis**. The key diagnostic features provided are: 1. **Fragmentation of the Internal Elastic Lamina:** This is a hallmark of the disease, caused by T-cell mediated injury [1]. 2. **Granulomatous Inflammation:** Characterized by lymphocyte infiltration and **multinucleated giant cells** (found in ~75% of cases) [1]. 3. **Demographics:** It predominantly affects **elderly patients** (>50 years) [1]. **Why other options are incorrect:** * **B. Takayasu Arteritis:** While histologically identical to GCA (granulomatous inflammation), it typically affects **young females (<40 years)** and involves the aortic arch and its major branches ("Pulseless disease") [1]. * **C. Polyarteritis Nodosa (PAN):** This is a necrotizing vasculitis of medium-sized vessels [3]. Histology shows **fibrinoid necrosis** and a pleomorphic infiltrate (neutrophils/eosinophils), but *not* giant cells [3][4]. It characteristically spares the lungs. * **D. Kawasaki Disease:** This affects **children** and presents with "strawberry tongue" and coronary artery aneurysms. Histology shows transmural inflammation but lacks granulomas or giant cells. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Most commonly involves the **Temporal Artery** [2]. * **Clinical Presentation:** Jaw claudication, scalp tenderness, and unilateral headache [1][2]. * **Complication:** Sudden **blindness** (ophthalmic artery involvement) is a medical emergency [2]. * **Association:** Strongly associated with **Polymyalgia Rheumatica** (proximal muscle pain/stiffness) [1]. * **Diagnosis:** Elevated ESR/CRP; Temporal artery biopsy is the gold standard (requires a long segment due to **"skip lesions"**). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 516-517. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 688-689. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 517-518. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 687-688.

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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