Vascular Pathology — MCQs

A 77-year-old man has had progressive dementia and gait ataxia for the past 9 years. He succumbs to bronchopneumonia. Autopsy shows that the thoracic aorta has a dilated root and arch, giving the intimal surface a "tree-bark" appearance. The microscopic examination of the aorta shows an obliterative endarteritis of the vasa vasorum. Which of the following laboratory findings is most likely to be recorded in this patient's medical history?

Q128Easy

Red infarct is seen in which organ?

Q129Easy

In aortic dissection, through which layer does blood initially enter?

Q130Medium

Pericyte formation occurs in which of the following lesions?

Vascular Pathology Indian Medical PG Practice Questions and MCQs

Question 121: Takayasu arteritis most commonly affects which of the following vessels?

A. Coeliac axis
B. Coronary arteries
C. Radial artery
D. Renal artery (Correct Answer)

Explanation: **Explanation:** **Takayasu Arteritis (TA)**, also known as "Pulseless Disease," is a chronic granulomatous large-vessel vasculitis that primarily involves the **aorta and its major branches** [1]. 1. **Why Renal Artery is Correct:** While the aortic arch is the most frequent site of involvement, among the specific visceral branches, the **renal artery** is the most commonly affected (involved in approximately 30-75% of cases). This often leads to renovascular hypertension, a classic clinical presentation in young females. In the context of this question, it is the most frequent site among the options provided. 2. **Analysis of Incorrect Options:** * **Coeliac axis:** Although it can be involved as a branch of the abdominal aorta, it is affected significantly less frequently than the renal arteries. * **Coronary arteries:** Involvement of the coronary ostia occurs in about 10-25% of patients due to extension of aortic root inflammation, but it is not the most common site. * **Radial artery:** TA typically affects large elastic arteries. The radial artery is a medium-sized muscular artery and is rarely the primary site of involvement; the "pulseless" nature of the disease is usually due to proximal stenosis in the subclavian or axillary arteries. **High-Yield Clinical Pearls for NEET-PG:** * **Demographics:** Most common in females <40 years of age (Asian descent) [1]. * **Pathology:** Characterized by transmural fibrous thickening of the aortic arch and "tree-barking" of the intima. * **Clinical Sign:** Discrepancy in blood pressure between arms and weak/absent upper limb pulses. * **Diagnosis:** Elevated ESR and angiography (showing "string of pearls" or tapered stenoses). * **Key Association:** Often associated with HLA-B52. **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.

Question 122: Kaposi sarcoma is commonly seen in which anatomical location?

A. Upper limbs
B. Lower limbs (Correct Answer)
C. Head and Neck
D. Trunk

Explanation: **Explanation:** Kaposi Sarcoma (KS) is a low-grade vascular neoplasm caused by **Human Herpesvirus-8 (HHV-8)** [2]. The correct answer is **Lower limbs** because of the characteristic presentation of the most common variant, **Classic (European) Kaposi Sarcoma**. 1. **Why Lower Limbs?** Classic KS typically presents in elderly men of Mediterranean or Eastern European descent. It manifests as multiple red-purple skin plaques or nodules, primarily localized to the **distal lower extremities** (feet and legs) [1]. The predilection for the lower limbs is attributed to venous stasis and gravity-dependent vascular pressure, which may promote the proliferation of spindle cells and extravasation of red blood cells. 2. **Analysis of Incorrect Options:** * **Upper limbs & Trunk:** While KS can involve these areas, especially in the **AIDS-associated (Epidemic)** variant where lesions are more widely disseminated and aggressive, they are not the primary or most common initial site [2]. * **Head and Neck:** Involvement of the face or oral mucosa (especially the hard palate) is a hallmark of advanced AIDS-associated KS, but it is statistically less common as the primary site compared to the lower limbs in the general presentation of the disease. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Look for "slit-like vascular spaces" containing RBCs, spindle-shaped cells, and hyaline droplets [1]. * **Variants:** There are four types: Classic (indolent, lower limbs), Endemic (African/lymphadenopathic), Transplant-associated (immunosuppression), and Epidemic (AIDS-defining illness). * **Marker:** HHV-8 (LANA-1) is the definitive diagnostic marker via immunohistochemistry [2]. * **Morphology:** Lesions progress through three stages: **Patch → Plaque → Nodule.** [1] **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 the Immune System, pp. 261-262.

Question 123: What is the most common cause of pulmonary thromboembolism?

A. Disseminated intravascular coagulation (DIC)
B. Coagulation disorder
C. Deep vein thrombosis (DVT) (Correct Answer)
D. Venous hypertension

Explanation: **Explanation:** **Deep vein thrombosis (DVT)** is the most common cause of pulmonary thromboembolism (PTE), accounting for over **95% of cases** [1]. The underlying mechanism involves the formation of a thrombus in the deep veins of the lower extremities—most commonly the **proximal veins** (popliteal, femoral, and iliac veins). These thrombi dislodge, travel through the right side of the heart, and lodge in the pulmonary arterial circulation [3]. **Analysis of Options:** * **Option A (DIC):** While DIC involves widespread microvascular thrombosis, it typically presents with consumption coagulopathy and bleeding rather than large-scale embolic events like PTE. * **Option B (Coagulation disorders):** Inherited or acquired hypercoagulable states (e.g., Factor V Leiden, Protein C/S deficiency) are significant *risk factors* for PTE, but they act by predisposing the patient to DVT first [4]. * **Option D (Venous hypertension):** This is a clinical feature of chronic venous insufficiency or heart failure. While it can lead to stasis (a component of Virchow’s Triad), it is a physiological state rather than the direct embolic source. **High-Yield Clinical Pearls for NEET-PG:** * **Virchow’s Triad:** The three factors predisposing to thrombus formation are endothelial injury, stasis, and hypercoagulability [4]. * **Saddle Embolus:** A large embolus that straddles the bifurcation of the main pulmonary artery, often causing sudden death. * **Lungs' Dual Circulation:** Most PTEs are clinically silent because the lungs have a dual blood supply (pulmonary and bronchial arteries) [3]. * **Gold Standard Investigation:** CT Pulmonary Angiography (CTPA) is the investigation of choice for PTE [2]. **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. The Lung, pp. 705-706. [3] 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. 144-145. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 136-137.

Question 124: Takayasu arteritis involves which of the following?

A. Small arterioles
B. Medium to large sized arteries with a predilection to branches of the aortic arch (Correct Answer)
C. Femoral and popliteal arteries
D. Abdominal aorta

Explanation: **Explanation:** **Takayasu Arteritis** is a chronic granulomatous vasculitis that primarily affects **medium to large-sized arteries**. It is classically known as "Pulseless Disease" because it has a strong predilection for the **aortic arch and its major branches** (brachiocephalic, carotid, and subclavian arteries) [2]. The inflammatory process leads to transmural scarring, thickening of the vessel wall, and significant luminal narrowing, which results in diminished peripheral pulses and blood pressure discrepancies between limbs. **Analysis of Options:** * **Option A (Incorrect):** Small arterioles are involved in small-vessel vasculitides like Microscopic Polyangiitis or Granulomatosis with Polyangiitis (GPA), not Takayasu. * **Option C (Incorrect):** While the lower body can be affected, the femoral and popliteal arteries are more classically associated with **Buerger’s disease** (Thromboangiitis obliterans) or peripheral arterial disease. * **Option D (Incorrect):** Although the abdominal aorta can be involved in Takayasu arteritis, it is not the *defining* or most characteristic site compared to the aortic arch branches. **High-Yield NEET-PG Pearls:** * **Demographics:** Most common in females under the age of 40 (often of Asian descent). * **Histopathology:** Granulomatous inflammation of the media with mononuclear infiltrates and giant cells (virtually indistinguishable from Giant Cell Arteritis/Temporal Arteritis, but differentiated by age: <40 for Takayasu, >50 for GCA) [1]. * **Clinical Presentation:** Weak/absent upper extremity pulses, ocular disturbances, and "reverse coarctation" (lower BP in arms than legs). * **Diagnosis:** Gold standard is **Arteriography** showing "string of pearls" or tapered narrowing. **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 125: Which of the following are seen in malignant hypertension?

A. Replacement by necrotizing arteriolitis and atherosclerosis (Correct Answer)
B. Atherosclerosis
C. Hyalinised arterioles and replacement by necrotizing arteriolitis
D. Hyalinised arterioles and atherosclerosis

Explanation: In **Malignant Hypertension** (typically defined as BP >200/120 mmHg), the rapid and severe rise in blood pressure leads to acute vascular injury. The hallmark pathological finding is **Fibrinoid Necrosis** (also known as **Necrotizing Arteriolitis**) [2]. 1. **Why Option A is correct:** * **Necrotizing Arteriolitis:** The sudden pressure spike causes plasma proteins to leak into the vessel wall and death of smooth muscle cells, appearing as bright pink, granular material (fibrinoid necrosis) [1]. This is often accompanied by "onion-skinning" (hyperplastic arteriolosclerosis) [1]. * **Atherosclerosis:** While necrotizing arteriolitis is the acute change, patients with malignant hypertension almost always have underlying chronic hypertension, which accelerates **atherosclerosis** in larger and medium-sized arteries. 2. **Why other options are incorrect:** * **Hyaline Arteriolosclerosis (Options C & D):** This is the hallmark of **Benign Hypertension** or diabetes [4]. It involves the leakage of plasma components into vessel walls over a long period, resulting in a homogenous, pink, thickened basement membrane. In malignant hypertension, the process is too rapid for hyalinization; instead, it progresses directly to necrosis. * **Atherosclerosis alone (Option B):** This is a chronic inflammatory process of the tunica intima and does not account for the acute, life-threatening arteriolar changes seen in a hypertensive crisis [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Kidney Appearance:** In malignant hypertension, the kidney shows "flea-bitten" appearances due to pinpoint petechial hemorrhages on the cortical surface. * **Hyperplastic Arteriolosclerosis:** Characterized by concentric, laminated thickening of arteriole walls (onion-skin appearance) due to proliferation of smooth muscle cells [1]. * **Clinical Triad:** Severe hypertension, papilledema, and encephalopathy/renal failure [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 945. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 276-277. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 277-278. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 943-945.

Question 126: What is the commonest site of lodgement of a pulmonary embolus?

A. Right lower lobe
B. Right upper lobe
C. Left lower lobe
D. Left upper lobe (Correct Answer)

Explanation: **Explanation:** The distribution of pulmonary emboli (PE) is primarily determined by the regional blood flow patterns within the lungs. **1. Why Left Upper Lobe is Correct:** In the context of standard medical examinations like NEET-PG, the **Left Upper Lobe** is frequently cited as the most common site for the lodgement of a pulmonary embolus. This is attributed to the anatomical orientation of the pulmonary arteries. The right pulmonary artery follows a more horizontal course, whereas the left pulmonary artery has a more vertical and direct upward trajectory. This hemodynamic pathway facilitates the preferential shunting of embolic material toward the left upper lobe. **2. Analysis of Incorrect Options:** * **Right Lower Lobe (A) & Left Lower Lobe (C):** While the lower lobes generally receive more blood flow in an upright position (due to gravity), they are statistically less common sites for the initial lodgement of an embolus compared to the upper lobes in clinical pathology studies [1]. However, it is important to note that lower lobes are more frequently involved in *pulmonary infarction* if an embolus occurs there [2]. * **Right Upper Lobe (B):** The right pulmonary artery's branching pattern makes it slightly less susceptible to the direct "straight-line" flow that an embolus often follows into the left upper vasculature. **3. High-Yield Clinical Pearls for NEET-PG:** * **Source:** Over 95% of pulmonary emboli originate from **Deep Vein Thrombosis (DVT)** of the lower extremities (specifically proximal veins like the popliteal, femoral, or iliac veins) [1]. * **Saddle Embolus:** A large embolus that straddles the bifurcation of the main pulmonary artery, often leading to sudden death. * **Hampton’s Hump:** A wedge-shaped opacity on a chest X-ray indicating pulmonary infarction (usually in the lower lobes) [2]. * **Gold Standard Investigation:** CT Pulmonary Angiography (CTPA) [2]. * **ECG Finding:** The most common finding is sinus tachycardia; the classic **S1Q3T3** pattern is specific but seen in less than 20% of cases. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 705. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 705-706.

Question 127: A 77-year-old man has had progressive dementia and gait ataxia for the past 9 years. He succumbs to bronchopneumonia. Autopsy shows that the thoracic aorta has a dilated root and arch, giving the intimal surface a "tree-bark" appearance. The microscopic examination of the aorta shows an obliterative endarteritis of the vasa vasorum. Which of the following laboratory findings is most likely to be recorded in this patient's medical history?

A. Antibodies against Treponema pallidum (Correct Answer)
B. Double-stranded DNA titer positive at 1 :512
C. Ketonuria of 4+
D. P-ANCA positive at 1 :1024

Explanation: ### Explanation The clinical and pathological findings described are classic for **Tertiary Syphilis (Cardiovascular Syphilis)**. **Why Option A is Correct:** The patient presents with **obliterative endarteritis** of the vasa vasorum [1], which is the hallmark of syphilitic aortitis. The vasa vasorum (vessels of the vessels) supply the outer media of the aorta. Inflammation and narrowing of these vessels lead to ischemic injury of the aortic media, causing loss of elastic fibers and smooth muscle [1]. This weakening results in aneurysmal dilation of the aortic root and arch. The resulting scarring and contraction of the intima create the characteristic **"tree-bark" appearance**. Furthermore, the patient’s dementia and gait ataxia suggest **Neurosyphilis** (General Paresis and Tabes Dorsalis), which often coexists with cardiovascular involvement in late-stage syphilis [1], [2]. Diagnosis is confirmed by antibodies against *Treponema pallidum*. **Why Other Options are Incorrect:** * **Option B (dsDNA):** This is highly specific for Systemic Lupus Erythematosus (SLE). While SLE can cause vasculitis, it does not typically cause "tree-bark" aortitis or obliterative endarteritis of the vasa vasorum. * **Option C (Ketonuria):** This indicates Diabetic Ketoacidosis. While diabetes causes macrovascular disease (atherosclerosis) and microangiopathy, it does not present with these specific aortic findings. * **Option D (P-ANCA):** This is associated with Microscopic Polyangiitis or Churg-Strauss syndrome, which affect small vessels, not the elastic fibers of the large aorta. **Clinical Pearls for NEET-PG:** * **Syphilitic Aortitis:** Primarily involves the **ascending aorta** (unlike atherosclerosis, which favors the abdominal aorta) [1]. * **Complications:** Aortic regurgitation (due to ring dilation), coronary ostial stenosis, and thoracic aortic aneurysm [1]. * **Pathogenesis:** "Vasa vasorum of the vasa vasorum" involvement leads to medial necrosis. * **Neurosyphilis Triad:** Argyll Robertson pupil ("Prostitute's pupil"), Tabes Dorsalis (ataxia), and General Paresis (dementia) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 386-389. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1276-1277.

Question 128: Red infarct is seen in which organ?

A. Liver
B. Kidney
C. Brain
D. Lung (Correct Answer)

Explanation: **Explanation:** Infarcts are classified into two types based on their color and the amount of hemorrhage: **Red (Hemorrhagic)** and **White (Anemic)** [1]. **Why Lung is the Correct Answer:** Red infarcts occur in tissues with a **dual blood supply** or loose textures that allow blood to collect in the infarcted area [1]. The lung has a dual blood supply from the **Pulmonary arteries** and **Bronchial arteries** [2]. When a pulmonary artery branch is obstructed, the bronchial arteries continue to pump blood into the necrotic area, but the damaged capillaries cannot contain it, leading to extensive hemorrhage [1]. This results in a firm, red-colored wedge-shaped infarct. **Analysis of Incorrect Options:** * **Kidney (Option B):** This is a classic example of a **White (Anemic) Infarct**. It occurs in solid organs with **end-artery circulation**, where the density of the tissue limits the amount of hemorrhage into the area of ischemic necrosis [1]. * **Liver (Option A):** While the liver has a dual blood supply (Portal vein and Hepatic artery), true infarction is **rare** due to this protective mechanism. When it does occur, it is usually pale or variegated, but it is not the classic textbook example of a red infarct compared to the lung. * **Brain (Option C):** Brain infarcts typically undergo **liquefactive necrosis**. While they can sometimes be hemorrhagic (especially after an embolic stroke with reperfusion), the primary classification for **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 140. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 137-138.

Question 129: In aortic dissection, through which layer does blood initially enter?

A. Intima
B. Media (Correct Answer)
C. Adventitia
D. Any of the above layers

Explanation: **Explanation:** **Core Concept:** Aortic dissection is defined as the separation of the layers of the aortic wall by blood. The fundamental pathology involves an **intimal tear** that allows blood to track into the **tunica media** [1]. Once inside the media, the blood creates a "false lumen" by cleaving the laminar planes of the elastic and muscular tissue [2]. Therefore, the layer through which the blood actually travels and dissects is the **Media**. **Analysis of Options:** * **B. Media (Correct):** The dissection occurs specifically within the outer third of the media [2]. The presence of blood in this layer creates the characteristic false lumen [1]. * **A. Intima (Incorrect):** While an intimal tear is the most common *entry point* (trigger), the blood does not "enter through" the intima in the sense of the dissection's location; the intima is the layer that is breached to reach the media. * **C. Adventitia (Incorrect):** If blood reaches the adventitia, it usually results in an external rupture (hemopericardium or hemothorax), which is often fatal [1], [2]. The adventitia acts as the outer boundary, not the site of dissection. * **D. Any of the above (Incorrect):** Dissection is anatomically specific to the medial layer. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Hypertension (most common) and connective tissue disorders like **Marfan Syndrome** (associated with cystic medial necrosis) [1]. * **Classification:** * **Stanford Type A:** Involves ascending aorta (Surgical emergency). * **Stanford Type B:** Involves descending aorta only (Medical management). * **Classic Presentation:** Sudden onset "tearing" or "ripping" chest pain radiating to the back. * **Radiology:** Gold standard is CT Angiography showing an **intimal flap** [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 272-273. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 512-513.

Question 130: Pericyte formation occurs in which of the following lesions?

A. Kaposi sarcoma
B. Glomus tumor
C. Hemangiopericytoma (Correct Answer)
D. Myopericytoma

Explanation: **Explanation:** **1. Why Hemangiopericytoma is correct:** Hemangiopericytoma is a rare vascular neoplasm classically described as arising from the **Zimmermann’s pericytes**, which are contractile cells wrapped around capillaries and post-capillary venules. Histologically, it is characterized by a "staghorn" or "antler-like" branching vascular pattern. While modern pathology often reclassifies many of these as Solitary Fibrous Tumors (SFT) based on *NAB2-STAT6* fusion, the classic association with **pericyte proliferation** remains a high-yield fact for competitive exams. **2. Analysis of Incorrect Options:** * **Kaposi Sarcoma:** This is a spindle-cell tumor caused by **HHV-8** [1]. It originates from **endothelial cells** (lymphatic or blood vessel), not pericytes [1]. It presents with slit-like vascular spaces containing extravasated RBCs. * **Glomus Tumor:** This arises from the **glomus body**, a specialized arteriovenous anastomosis involved in thermoregulation. While glomus cells are modified smooth muscle cells similar to pericytes, they form distinct nests around vessels rather than the classic pericyte formation seen in hemangiopericytoma. * **Myopericytoma:** This is a distinct entity where tumor cells show a circumferential, perivascular growth pattern with **myoid (smooth muscle) differentiation**. While related, "pericyte formation" as a classic descriptor is traditionally linked to Hemangiopericytoma in standard pathology curricula. **3. High-Yield Clinical Pearls for NEET-PG:** * **Staghorn/Antler vasculature:** Pathognomonic histological feature of Hemangiopericytoma/SFT. * **Silver Stain (Reticulin):** Used to highlight the basement membrane, showing that tumor cells are located outside the vascular endothelium. * **Glomus Tumor Triad:** Severe pain, localized tenderness, and sensitivity to cold (typically subungual/under the fingernail). * **Kaposi Sarcoma Marker:** CD34 and HHV-8 (LANA-1) positivity [1]. **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.

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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