Vascular Pathology — MCQs

Vascular Pathology Indian Medical PG Practice Questions and MCQs

Question 201: What is the most widely accepted theory regarding the cause of atherosclerosis?

A. Lipid infiltration of the intima
B. Lipid infiltration of the intima (Correct Answer)
C. Smoking
D. Hyperlipidemia

Explanation: ### Explanation The pathogenesis of atherosclerosis is best explained by the **Response to Injury Hypothesis**, which posits that the process begins with chronic endothelial injury [1]. This injury leads to increased vascular permeability, allowing for the **lipid infiltration of the intima** [1]. **Why the correct answer is right:** According to the current consensus, once the endothelium is damaged, low-density lipoproteins (LDL) enter the subendothelial space (intima) [1]. Here, they undergo oxidation. These oxidized LDLs are chemotactic for monocytes, which transform into macrophages, ingest the lipids, and become **foam cells** [2]. This accumulation of lipid within the intima is the hallmark of the "fatty streak," the earliest visible lesion of atherosclerosis [2]. **Analysis of incorrect options:** * **Smoking (Option C):** While smoking is a major **risk factor** that causes endothelial dysfunction, it is an external trigger rather than the underlying pathological mechanism itself [1]. * **Hyperlipidemia (Option D):** Similar to smoking, hyperlipidemia is a **predisposing factor**. While high serum cholesterol provides the "raw material" for plaque formation, the actual disease process is the infiltration of those lipids into the vessel wall [1]. * *(Note: Option A and B are identical in the prompt; both refer to the primary pathological mechanism).* **NEET-PG High-Yield Pearls:** * **Earliest Lesion:** Fatty streaks (can be seen in the aortas of children <10 years) [2]. * **Most Common Site:** Lower abdominal aorta > Coronary arteries > Popliteal arteries > Internal carotid arteries. * **Key Cell Type:** The **Smooth Muscle Cell (SMC)** migration from the media to the intima is responsible for converting a fatty streak into a mature fibrofatty plaque [2]. * **Major Complication:** Plaque rupture leading to thrombosis and infarction (MI or Stroke). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 500-505. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 268-270.

Question 202: Onion skin thickening of the arteriolar wall is seen in which of the following conditions?

A. Atherosclerosis
B. Median calcific sclerosis
C. Hyaline arteriolosclerosis
D. Lyme arthritis (Correct Answer)

Explanation: **Explanation:** The characteristic **"onion-skin" thickening** of arteriolar walls is a hallmark of **Hyperplastic Arteriolosclerosis** [1]. While classically associated with malignant hypertension, it is also a pathognomonic histopathological feature of **Lyme arthritis** (caused by *Borrelia burgdorferi*). In Lyme disease, this appearance results from the concentric proliferation of smooth muscle cells and laminated basement membrane thickening, often accompanied by a perivascular lymphocytic infiltrate [2]. **Analysis of Options:** * **A. Atherosclerosis:** Characterized by the formation of intimal "atheromas" (fibrofatty plaques) in large and medium-sized arteries, not concentric arteriolar thickening [2]. * **B. Monckeberg Medial Calcific Sclerosis:** Involves dystrophic calcification of the media of medium-sized muscular arteries. It does not narrow the lumen and lacks the "onion-skin" layers. * **C. Hyaline Arteriolosclerosis:** Seen in chronic hypertension and diabetes mellitus. It shows homogenous, pink, acidophilic thickening of the wall due to plasma protein leakage, leading to luminal narrowing, but lacks the laminated "onion-skin" appearance [2]. **High-Yield Pearls for NEET-PG:** * **Hyperplastic Arteriolosclerosis ("Onion-skinning"):** Seen in Malignant Hypertension (BP >200/120 mmHg), Scleroderma renal crisis, and Lyme arthritis [1]. * **Lyme Disease Triad:** Erythema chronicum migrans (bull’s eye rash), bilateral facial nerve palsy, and arthritis with onion-skin vascular changes. * **Fibrinoid Necrosis:** Often accompanies hyperplastic changes in malignant hypertension, particularly in the kidney (necrotizing arteriolitis) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 943-945. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 498-499.

Question 203: What is the most common association with atherosclerosis?

A. Less physical activity
B. Diabetes Mellitus
C. Increased uptake of unsaturated fatty acids
D. Cigarette smoking (Correct Answer)

Explanation: **Explanation:** Atherosclerosis is a chronic inflammatory response of the arterial wall to endothelial injury. Risk factors are categorized into **Constitutional** (non-modifiable) and **Acquired** (modifiable). [1] **Why Cigarette Smoking is the Correct Answer:** Among the modifiable risk factors, **cigarette smoking** is considered the most potent and clinically significant association for the development and progression of atherosclerosis. It induces endothelial dysfunction through oxidative stress, increases platelet aggregation, elevates LDL levels, and decreases HDL. [1] In the context of NEET-PG, smoking is frequently cited as the strongest independent risk factor for ischemic heart disease and peripheral vascular disease. **Analysis of Incorrect Options:** * **A. Less physical activity:** While a sedentary lifestyle is a recognized risk factor, it is considered a "secondary" or "lesser" risk factor compared to the "Major" factors like smoking, hypertension, and hyperlipidemia. * **B. Diabetes Mellitus:** DM is a major risk factor and significantly accelerates atherosclerosis (often leading to "Mönckeberg-like" calcification and peripheral gangrene). [1] However, statistically, smoking remains the more prevalent and direct trigger for the initial endothelial insult in the general population. * **C. Increased uptake of unsaturated fatty acids:** This is actually a **protective factor**. Diets high in polyunsaturated fats (like Omega-3) help lower serum cholesterol levels, whereas *saturated* or *trans-fats* are associated with increased risk. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Most common site for atherosclerosis:** Abdominal aorta > Coronary arteries > Popliteal arteries > Internal Carotid. * **Earliest lesion:** Fatty streaks (can be seen in children <10 years). * **Key Pathogenetic Step:** Oxidation of LDL (Ox-LDL) which is then engulfed by macrophages to form **Foam Cells**. [1] * **The "Big Four" Modifiable Factors:** Hyperlipidemia, Hypertension, Cigarette Smoking, and Diabetes Mellitus. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 498-504.

Question 204: An atheromatous plaque does not contain which of the following?

A. Platelets
B. Neutrophils (Correct Answer)
C. Smooth muscle fibres
D. Monocytes

Explanation: **Explanation:** The correct answer is **Neutrophils**. Atherosclerosis is fundamentally a **chronic inflammatory process** of the arterial wall [1] [2]. While various inflammatory cells are involved, neutrophils are characteristically absent from the stable atheromatous plaque. **1. Why Neutrophils are the correct answer:** Neutrophils are the hallmark of *acute* inflammation [2]. An atheromatous plaque is a chronic lesion. The cellular infiltrate in atherosclerosis primarily consists of macrophages (derived from monocytes), T-lymphocytes, and smooth muscle cells [1]. Neutrophils do not play a structural or primary inflammatory role in the plaque's composition, though they may be seen briefly during acute complications like plaque rupture or secondary infection. **2. Analysis of Incorrect Options:** * **Monocytes:** These are crucial to plaque formation. They enter the subendothelial space, differentiate into **macrophages**, and engulf oxidized LDL to become **foam cells**, which form the "fatty streak" [1]. * **Smooth Muscle Fibers:** These migrate from the media to the intima in response to growth factors (like PDGF). They synthesize collagen and extracellular matrix to form the **fibrous cap** that stabilizes the plaque. * **Platelets:** These adhere to areas of endothelial dysfunction or microscopic denudation. They release growth factors that drive smooth muscle proliferation and are a major component if the plaque becomes complicated by thrombosis. **High-Yield NEET-PG Pearls:** * **Earliest lesion:** The "Fatty Streak" (seen even in children). * **Key Cell Type:** The **Macrophage/Foam cell** is the dominant inflammatory cell [1]. * **Vulnerability:** A "thin-cap" fibroatheroma with a large lipid core and many macrophages is most prone to rupture. * **Location:** Most common site is the **Abdominal Aorta**, followed by Coronary arteries, Popliteal arteries, and Internal Carotids. **References:** [1] 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. 200-202. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 104-105.

Question 205: What is the most common source of systemic emboli?

A. Varicose veins
B. Mural thrombi (Correct Answer)
C. Cardiac thrombi
D. Pulmonary embolism

Explanation: **Explanation:** The correct answer is **Mural thrombi**. Systemic arterial emboli refer to emboli that travel through the arterial circulation. Approximately **80%** of these emboli arise from intracardiac mural thrombi [1]. * **Why Mural Thrombi is correct:** Mural thrombi are thrombi that adhere to the wall of a heart chamber or the aorta. The majority (about 80%) originate from the left ventricular wall (following a myocardial infarction) or the left atrial appendage (secondary to atrial fibrillation) [1], [2]. Because these thrombi are located in the left side of the heart, they enter the systemic arterial circulation upon detachment, leading to infarctions in organs like the brain, lower extremities, or kidneys [1], [2]. * **Why Option A (Varicose veins) is incorrect:** Thrombi in varicose veins or deep veins of the legs typically lead to **Pulmonary Embolism (PE)**, not systemic embolism, as they travel through the venous system to the right side of the heart and into the pulmonary arteries. * **Why Option C (Cardiac thrombi) is incorrect:** While mural thrombi are a *type* of cardiac thrombi, "Mural thrombi" is the more specific and standard pathological term used in textbooks (like Robbins Pathology) to describe the source of systemic emboli. * **Why Option D (Pulmonary embolism) is incorrect:** Pulmonary embolism is a *consequence* of venous thromboembolism, not a source of systemic arterial emboli. **High-Yield NEET-PG Pearls:** * **Most common site of lodgment:** Lower extremities (75%) and the brain (10%) [1], [2]. * **Paradoxical Embolism:** A rare scenario where a venous embolus enters the systemic circulation via a right-to-left shunt (e.g., Patent Foramen Ovale). * **Fat Embolism Triad:** Hypoxemia, neurological symptoms, and petechial rash (usually 1-3 days after a long bone fracture). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 136-137. [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. 145-146.

Question 206: Buerger disease affects which layers of the artery?

A. Tunica intima
B. All of the above (Correct Answer)
C. Tunica media
D. Tunica adventitia

Explanation: **Explanation:** **Buerger disease**, also known as **Thromboangiitis Obliterans (TAO)**, is a non-atherosclerotic, segmental, inflammatory disease that primarily affects small and medium-sized arteries and veins of the extremities [1]. The correct answer is **"All of the above"** because Buerger disease is characterized by **panangiitis**. Unlike atherosclerosis, which primarily involves the tunica intima, or Monckeberg medial sclerosis, which affects the tunica media, Buerger disease involves an intense inflammatory process that spans the **entire thickness of the vessel wall** (Tunica intima, media, and adventitia). * **Tunica Intima:** The disease starts with an inflammatory thrombus that contains microabscesses (Neutrophils surrounded by granulomatous inflammation). * **Tunica Media & Adventitia:** The inflammation extends through these layers, often leading to secondary fibrosis that can encase the adjacent nerve and vein (forming a neurovascular bundle "block") [1]. **Why other options are incorrect:** While the disease does affect the intima, media, and adventitia individually, selecting only one (A, C, or D) is incomplete. The hallmark of TAO is the **transmural** nature of the inflammation, making "All of the above" the most accurate pathological description. **High-Yield Clinical Pearls for NEET-PG:** * **Strongest Risk Factor:** Heavy tobacco smoking (essential for diagnosis) [1]. * **Demographics:** Young males (usually <45 years) [1]. * **Classic Presentation:** Triad of intermittent claudication, Raynaud phenomenon, and migratory superficial thrombophlebitis. * **Angiographic Finding:** "Corkscrew" appearance of collateral vessels. * **Key Pathology:** Highly cellular, "organized" thrombus with **microabscesses**; the internal elastic lamina remains remarkably intact. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 280-281.

Question 207: A 40-year-old pregnant female in her third trimester presents with bilateral leg swelling. Which type of thrombosis is most likely to develop in this patient?

A. Venous (Correct Answer)
B. Arterial
C. Mural
D. Saddle

Explanation: **Explanation:** The correct answer is **Venous thrombosis**. This patient is in a state of **Virchow’s Triad** [2], specifically characterized by hypercoagulability and stasis, which are the primary drivers of venous thrombi. 1. **Why Venous is correct:** Pregnancy is a classic hypercoagulable state due to increased synthesis of coagulation factors (VII, VIII, X, and fibrinogen) and decreased protein S levels [2]. In the third trimester, the gravid uterus compresses the inferior vena cava (IVC) and iliac veins, causing **venous stasis** in the lower extremities [4]. This combination makes Deep Vein Thrombosis (DVT) the most likely complication, typically presenting with swelling and tenderness [1]. 2. **Why other options are incorrect:** * **Arterial:** These typically occur due to endothelial injury (atherosclerosis) or turbulence [3]. While pregnancy increases risk slightly, venous events are far more common. * **Mural:** These are thrombi that adhere to the walls of heart chambers or the aorta, usually following myocardial infarction or in aneurysms. * **Saddle:** This is a large pulmonary embolus lodged at the bifurcation of the pulmonary artery. While it is a *consequence* of DVT, the question asks for the type of thrombosis *developing* in the patient (the primary event). **NEET-PG High-Yield Pearls:** * **Virchow’s Triad:** Endothelial injury, Stasis, and Hypercoagulability [3]. * **Lines of Zahn:** Microscopic laminations (pale platelet/fibrin layers vs. dark RBC layers) that signify a thrombus formed in **flowing blood** (helps distinguish from post-mortem clots). * **Most common site for DVT:** Deep veins of the leg (above the knee, e.g., popliteal, femoral, and iliac veins) [1]. * **Phlegmasia Alba Dolens:** "Milk leg" associated with third-trimester pregnancy/iliofemoral DVT. **References:** [1] 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. 143-144. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 132-134. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 132-133. [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. 141-142.

Question 208: Atherosclerosis in the coronary circulation most commonly affects which artery?

A. Left anterior descending artery (Correct Answer)
B. Left circumflex artery
C. Right coronary artery
D. All of the above

Explanation: **Explanation:** Atherosclerosis is a chronic inflammatory process characterized by the formation of fibro-fatty plaques in the intima of large and medium-sized arteries [1]. In the coronary circulation, the distribution of these plaques is not uniform; they occur most frequently at sites of **turbulent blood flow and branch points**. **1. Why Option A is Correct:** The **Left Anterior Descending (LAD) artery** is the most common site for clinically significant atherosclerosis. It is often referred to as the "widow-maker" because it supplies the majority of the left ventricle (the apex, anterior wall, and anterior two-thirds of the interventricular septum). The high hemodynamic stress and specific branching pattern at the LAD origin make it highly susceptible to plaque formation. **2. Why Other Options are Incorrect:** * **Options B & C:** While the **Right Coronary Artery (RCA)** and the **Left Circumflex Artery (LCX)** are frequently involved, they follow the LAD in terms of statistical frequency. The typical order of involvement in coronary atherosclerosis is: **LAD > RCA > LCX**. * **Option D:** While atherosclerosis can be diffuse, it does not affect all arteries with equal frequency or severity; the LAD remains the primary site of predilection. **Clinical Pearls for NEET-PG:** * **Order of Arterial Involvement (General):** Lower Abdominal Aorta > Coronary Arteries > Popliteal Arteries [1] > Internal Carotid > Circle of Willis. * **Vessel Sparing:** The **Internal Mammary (Thoracic) Artery** and the **Upper Extremity Arteries** are characteristically spared from atherosclerosis. * **Risk Factors:** The most important modifiable risk factor is **Hyperlipidemia/Hypercholesterolemia**, while the most important non-modifiable risk factor is **Family History**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 507-508.

Question 209: A lesion composed of microscopic vessels is called as:

A. Haemangioma
B. Angioma
C. None of Haemangioma and Angioma
D. Haemangioma and Angioma (Correct Answer)

Explanation: ### Explanation **Concept Overview** The correct answer is **D (Haemangioma and Angioma)** because, in medical terminology, these terms are often used interchangeably to describe benign tumors or malformations composed of blood vessels [1]. 1. **Why the Correct Answer is Right:** * **Haemangioma:** This is the specific pathological term for a benign neoplasm of blood vessels [1]. Depending on the size of the vascular channels, they are classified as **Capillary** (small, microscopic vessels) or **Cavernous** (large, dilated channels) [2]. * **Angioma:** This is a broader, generic term used to describe any tumor composed of vascular tissue (blood vessels or lymphatics) [1]. Since a lesion of microscopic blood vessels fits this definition, "Angioma" is also technically correct. * In many standard pathology textbooks (like Robbins), the terms are used synonymously when referring to benign vascular proliferations. Therefore, both A and B are correct, making D the most appropriate choice. 2. **Why Other Options are Incorrect:** * **Option A & B:** While both are correct individually, selecting only one would be incomplete given that they represent the same pathological entity in this context. * **Option C:** This is incorrect as both terms accurately describe the lesion. 3. **High-Yield Clinical Pearls for NEET-PG:** * **Capillary Haemangioma:** Most common type; often occurs in the skin, subcutaneous tissues, and mucous membranes. * **Strawberry Hemangioma:** A subtype of capillary hemangioma found in newborns; it grows rapidly for a few months but typically **regresses spontaneously** by age 7 [1]. * **Pyogenic Granuloma:** A pedunculated capillary hemangioma that often occurs on the gingiva of pregnant women (Granuloma gravidarum) [2]. * **Kasabach-Merritt Syndrome:** A rare complication where a large hemangioma leads to platelet sequestration and consumptive coagulopathy. * **Von Hippel-Lindau (VHL) Disease:** Associated with hemangioblastomas in the cerebellum and retina. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 481-482. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 524-525.

Question 210: The defect in Berry aneurysm lies in which layer of the artery?

A. Degeneration of the internal elastic lamina
B. Degeneration of the media/muscle cell layer (Correct Answer)
C. Deposition of mucoid material in the media
D. Low-grade inflammation of the vessel wall

Explanation: **Explanation:** **Berry (Saccular) Aneurysms** are the most common cause of non-traumatic subarachnoid hemorrhage [1]. The fundamental pathogenesis involves a **congenital focal weakness** in the arterial wall, specifically at the branching points of the Circle of Willis [2]. **Why Option B is Correct:** The primary defect is the **absence or degeneration of the tunica media (muscle layer)** [1]. In a normal artery, the media provides structural integrity against luminal pressure. At the site of a Berry aneurysm, the muscle layer is either congenitally thin or entirely missing. Under the constant stress of pulsatile blood flow, the remaining layers (intima and adventitia) bulge outward, forming a sac [1]. **Why Other Options are Incorrect:** * **Option A:** While the **internal elastic lamina** is often fragmented or absent within the aneurysmal sac itself, this is usually a *consequence* of the bulging rather than the primary initiating defect [1]. * **Option C:** Deposition of mucoid material (cystic medial necrosis) is the hallmark of **Marfan Syndrome** and typically leads to **Aortic Dissection**, not Berry aneurysms. * **Option D:** Berry aneurysms are **non-inflammatory** and non-atherosclerotic in origin [2]. Inflammation is characteristic of vasculitides or mycotic aneurysms. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Site:** Junction of the **Anterior Communicating Artery (A-com)** and Anterior Cerebral Artery [2]. * **Associated Conditions:** Autosomal Dominant Polycystic Kidney Disease (**ADPKD**), Ehlers-Danlos Syndrome (Type IV), and Coarctation of the Aorta. * **Clinical Presentation:** "Thunderclap headache" or "worst headache of my life." * **Risk Factors:** Hypertension and smoking (which accelerate the degeneration of the media). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1272-1273. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, p. 1272.

Practice by Chapter

Atherosclerosis

Practice Questions

Hypertensive Vascular Disease

Practice Questions

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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