VASCULITIS.

VASCULITIS

Vasculitis = Inflammation of the Blood Vessel
Blood vessel damage Thickening of vessel wall Attenuation of vessel wall Luminal narrowing or occlusion Vessel wall thinning Aneurysm formation or Disruption of the vessel wall with hemorrhage into tissue Tissue or organ ischemia

Vasculitis Is Not One Specific Disease Blood vessel inflammation can be seen in a variety of settings Primary Vasculitides Secondary Vasculitides Vasculitis occurring secondary to an underlying disease or exposure Unique disease entities without a currently identified underlying cause where vasculitis forms the pathological basis of tissue injury Medications Infection Malignancy Transplant Cryoglobulinemia Connective tissue disease (Rheumatoid arthritis, SLE Inflammatory myositis) Giant cell arteritis Takayasu’s arteritis Kawasaki disease Polyarteritis nodosa Wegener’s granulomatosis Microscopic polyangiitis Churg-Strauss syndrome Henoch-Schönlein purpura

Mechanism of vasculitis
1.Immune mediated 2.Direct invasion by infectious agents.

C-ANCA Proteinase 3 (PR3) P-ANCA Myeloperoxidase (MPO)

Patients with Vasculitis have circulating antibodies that react with the Neutrophil cytoplasmic antigens. Immunoflorescent pattern of staining results in C-ANCA shows cytoplasmic localization of staining the antigen is Proteinase (PR3)

P-ANCA perinuclear staining for myeloperoxidase seen in microscopic polyngitis

C-ANCA P-ANCA

Large Vessel Medium Vessel Small Vessel Aorta Capillary Vein
Giant cell arteritis Takayasu’s arteritis Polyarteritis nodosa Kawasaki disease Wegener’s granulomatosis Microscopic polyangiitis Churg-Strauss syndrome

GIANT CELL ARTERITIS It is the most common form of systemic Vasculitis seen in elderly patients and It is a chronic often granulomatous inflammation of large and small sized arteries.

It principally affects the arteries of the head and neck.
Mainly temporal arteries, Vertebral arteries, Ophthalmic arteries and Aorta

“TEMPORAL” ARTERITIS Giant Cell Arteritis, GCA
ADULTS Occurs in people over the age of 50 2:1 women:men Mainly arteries of the head and temporal arteries are the most visibly, palpably, and surgically accessible BLINDNESS most feared sequelae GRANULOMATOUS WALL inflammation diagnostic OFTEN associated with marked ESR elevation

Diagnosis of GCA CBC: anemia, thrombocytosis, leukocytosis
Elevated erythrocyte sedimentation rate (ESR), C-reactive protein Temporal artery biopsy Positive in 50-80% of patients.

TREATMENT Prednisone 40-60 mg daily
- Reduces symptoms and prevents visual loss - Begin immediately while biopsy is being arranged

TAKAYASU ARTERITIS Involves aortic arch and other heavily elastic arteries, i.e., chief thoracic aorta branches, most commonly young Asian women FEMALES <40 “PULSELESS” disease Granulomatous lesion.

Morphology Aortic arch is classically involved sometime aorta and its branches. Irregular thickening of aorta and its branch vessel wall. The orifices of the major arteries to upper body segments leads narrowing and obliteration due to intimal thickening. Mononuclear inflammation in the media.

Clinical features Low blood pressure
Weak pulses in the upper extremities Coldness or numbness in the fingers Ocular disturbances, Retinal hemorrhages, and neurologic deficit If more distal part of aorta involves cause numbness in lower extremities.

USMLE review Takayasu arteritis and temporal arteritis involve arterial vessels of different sizes and locations (aorta and proximal aortic arterial branch involvement versus more distal carotid artery branch involvement, respectively), and have different clinical presentations. Even so, they may share a common pathologic morphology, consisting of granulomatous inflammation of the media.

POLY-(Peri-) ARTERITIS NODOSA (PAN)
ANY MEDIUM or SMALL artery OFTEN visceral arteries Transmural inflammation of the arterial wall Fibrinoid necrosis involving, renal. coronary, mesenteric arteries Spares pulmonary arteries

Clinical features Fever of unknown cause Malaise Weight loss
Hypertension Abdominal pain Melena due vascular lesions in GIT Muscular pains and neuritis Renal artery involvement often cause of death.

About 30% of PAN patients have Hepatitis B antigen in their serum

Polyarteritis Nodosa Laboratories: Elevated ESR
Anemia, mild elevations in WBC and platelets May see LFT abnormalities, microscopic hematuria A PAN-like vasculitis can occur with hepatitis B or C Prednisone + cyclophosphamide Prednisone alone.Antiviral treatment if hepatitis B or C are present

KAWASAKI DISEASE CHILDREN <4 years. CORONARY ARTERIES
LEADING cause of ACQUIRED heart disease in children USA and JAPAN Fatal in only 1%

Pathogenensis The etiology is uncertain, but the vasculitis is thought to result from a delayed-type hypersensitivity response of T cells to an as yet uncharacterized vascular antigen. This leads to cytokine production, with B-cell activation and the formation of autoantibodies to ECs and SMCs.

The autoantibodies precipitate the acute vasculitis.
It is speculated that in genetically susceptible persons, a variety of infectious agents (most likely viral) can trigger the disease.

Approximately 20% of untreated patients develop cardiovascular sequelae, ranging from asymptomatic coronary arteritis, to coronary artery ectasia and aneurysm formation, giant coronary artery aneurysms (7-8 mm)

cardiovascular complications like pericarditis
Also it is called as Mucocutaneous lymphnode syndrome as it involves due to oral, conjuctival erythema and edema of hands and cervical lymphnode enlargement. It is associated with Mycoplasma and HIV infection in some cases. cardiovascular complications like pericarditis ,MI and aneurysm. Immunoglobulin and ASA is the treatment.

To avoid the possibility of inducing Reye syndrome, aspirin should not be administered to children under the age of sixteen except for very specific circumstances where it is indicated for the treatment of a serious illness such as in Kawasaki disease where salicylates are a mainstay of treatment.

Necrotizing Granuloma
Sinusitis Subglottic stenosis Pulmonary nodules Orbital pseudotumor Necrotizing Granuloma Wegener’s Churg-Strauss MPA Pulmonary capillaritis Glomerulonephritis Sensory neuropathy Mononeuritis multiplex Hypereosinophilia Asthma Pulmonary infiltrates Myocarditis

Small Vessel Vasculitis: Cutaneous Vasculitis
Copyright © The McGraw-Hill Companies, Inc. All rights reserved. Cutaneous vasculitis represents the most common vasculitic manifestation encountered in clinical practice

Little or no immunoglobulins in most lesions.
MICROSCOPIC POLYANGIITIS HYPERSENSITIVITY VASCULITIS LEUKOCYTOCLASTIC VASCULITIS SMALL VESSELS OF ALL TYPES, e.g., capillaries and veins too FRAGMENTED NEUTROPHILS Called PAUCI IMMUNE INJURY Little or no immunoglobulins in most lesions. Necrotising GLOMERULONEPHRITIS in 90% of the patients. Most are ALLERGIC reactions to allergens like penicillin or strep

Leukocytoclastic vasculitis

Microscopic polyangiitis is characterized by segmental fibrinoid necrosis of the media with focal transmural necrotizing lesions.

WEGENER GRANULOMATOSIS
More common in males often in 40’s ACUTE NECROTIZING GRANULOMAS OF UPPER an LOWER respiratory tract NECROTIZING GRANULOMATOUS VASCULITIS of SMALL vessels of ALL types Often renal involvement, “crescentic” glomerulonephritis ANTI-NEUTROPHIL-CYTOPLASMIC-AB’s usually present(c-ANCA) Mortality has improved significantly, but flare-ups, i.e., recurrences, are still the main concern.

Clinical Features Patients present with Chronic Sinusitis, Pnemonitis, Hemoptysis and Hematuria, mucosal ulcerations of the nasopharynx Epistaxis, nasal crusting. Nodular infiltration and Glomerular nephritis .

Pathologically Wegener's Granulomatosis is characterized by three features: Necrotizing granulomatous inflammation of the upper and lower respiratory tracts. Disseminated small vessel necrotizing vasculitis that affects both arteries and veins. Focal necrotizing glomerulonephritis.

Diagnostic criteria for Wegener's Granulomatosis
1) Abnormal urine sediments, like red blood cells or casts, 2) An abnormal chest radiograph. 3) Oral ulcers or nasal discharge and 4) granulomatous inflammation on biopsy. Pathogenesis is believed to be a hypersensitivity reaction to infection with staphylococcus aureus and parvovirus B-19 [

Why is the “necrosis” of Wegener’s not called “caseating”
Why is the “necrosis” of Wegener’s not called “caseating”? Ans: Because, by tradition, rather than objectivity or logic, “caseation” has been attributed to tuberculosis. Yes, we know this is not fair.

CHURG - STRAUSS SYNDROME
Called as Allergic granulomatosis and Angitis. Associated with Bronchial Asthma, Allergic rhinitis, peripheral Eosinophilia, and Necrotising granulomas. Present with cutaneous purpura bleeding from GIT and Focal and glomerulo sclerosis

HLA DRB4 positivity is genetic risk factor for the development of CHRUG STRAUSS SYNDROME

p-ANCAs are present in roughly half the patients
p-ANCAs are present in roughly half the patients. In Churg-Strauss syndrome, and perivascular tissues by eosinophils Coronary arteritis and Myocarditis are main cause for morbidity.

THROMBOANGIITIS OBLITERANS BUERGER(‘s) Disease
100% caused by cigarette smoking MEN commonly affected 30’s, 40’s Often arteries are 100% obliterated, hence the name “obliterans” EXTREMITIES most often involved.

acute and chronic inflammation of medium-sized and small arteries, principally the tibial and radial arteries, with occasional secondary extension into extremity veins and nerves.

Clinical Features The early manifestations are a superficial nodular phlebitis, Resting pain on the forefoot is characteristic, with possible ischemic ulcers or gangrene of foot/ toes; upper limb ischemia [40% to 50% of patients) with ulceration and gangrene; Raynaud's phenomenon. Treatment: smoking cessation essential; intravenous prostaglandin analogue.

Buerger’s Disease

Tumors: Benign, Intermediate (Borderline), Malignant
Raynaud Phenomenon Veins and Lymphatics Varicosities Thrombophlebitis/Phlebothrombosis SVC/IVC syndromes Lymphangitis Lymphedema Tumors: Benign, Intermediate (Borderline), Malignant Vascular Interventions: Angioplasty, Stents, Grafts

Pallor due to vasospasm Cyanosis due to hypoxia-
RAYNAUD’S PHENOMENON. It is a vasospasm in the peripheral arteries due to cold and emotional stimuli. Pallor due to vasospasm Cyanosis due to hypoxia- Rubor due to reactive hyperemia.

Raynaud “Phenomenon” PRIMARY:
Digital PALLORCYANOSISHYPEREMIA (WHITE) (BLUE) (RED) Vasoconstriction usually triggered by COLD, emotion Can be tip of nose, not only digits Self Limited, Gangrene UN-common Arteries often do NOT show diagnostic pathology SECONDARY: (formerly Raynaud “Phenomen.”) Atherosclerosos SLE Buerger Disease

RAYNAUD PHENOMENON There are two types of Raynaud phenomenon. Primary and Secondary Primary Raynaud phenomenon (previously called Raynaud disease) reflects an exaggeration of central and local vasomotor responses to cold or emotion,

Primary Reynaud disease
Structural changes in the arterial walls are absent except late in the course, when intimal thickening can appear. primary Raynaud phenomenon is usually benign, long-standing, chronic cases can result in atrophy of the skin, subcutaneous tissues, and muscles. Ulceration and ischemic gangrene rare.

WHITE BLUE RED

Raynaud’s Disease

Secondary Raynaud phenomenon
See around 30 year age groups. Common in males. Usually common in persons with electrical drilling tool users. Also associated with SLE, Atherosclerosis, Burger disease and scleroderma. Ulcers and ischemia are common and gangrene in later stages.

“Varicose” Veins 20% of population, Female 30% male 20%
Related to increased venous pressure, age, valve dysfunction Superficial veins of lower extremities most common PATH: 1) DILATED, 2) TORTUOUS, ) ELONGATED, 4) SCARRED (phlebosclerosis), 5) CALCIFICATIONS, 6) NON-UNIFORM SMOOTH MUSCLE Conceptually like varices or hemorrhoids

. Varicose veins . 1. Abnormally distended, lengthened, and tortuous veins 2. Locations a. Superficial saphenous veins (most common site) b. Distal esophagus (due to portal hypertension) c. Anorectal region (e.g.. hemorrhoids) d. Left scrotal sac (e.g., varicocele)

Esophageal varices. Liver cirrhosis causes portal vein hypertension Portal hypertension leads to the opening of porto-systemic shunts, increasing blood flow into veins at the gastroesophageal junction forming esophageal varices. Esophageal varices rupture can lead to massive upper GI hemorrhage.

Exacerbated by pregnancy, prolonged standing, obesity, oral contraceptives, Advanced age Familial tendency Secondary to deep venous thrombosis

Hemorrhoids Hemorrhoidal plexus undergo vericose dilation and rupture. Due to prolonged pelvic congestion by the gravid uterus in pregnant women.

(1) Nonpharmacologic Graded compression stockings (2) Chronic treatment (a) Compression sclerotherapy (b) Ligation and stripping (e) Endovenous obliteration using radiofreqency (diathermy) or laser.

VERICOSE VEINS INCOMPETENT . VENOUS VALVES
Incompetent venous valves in the lower extremities allow retrograde blood flow from deep to superficial veins. This increases the pressure in the superficial veins leading to their dilation (varicose veins).

SEVERE VARICOSITIES

SKIN ULCERS ARE MORE COMMON
VERICOSE VEINS Venous stasis ulcers are very common and often occur over the medical malleolus. SKIN ULCERS ARE MORE COMMON

Phlebothrombosis 1. Thrombosis of vein with out inflammation. Causes Phlebothrombosis. a. Stasis of blood flow b. Hypercoagulability-(e.g.. antithrombin III deficiency) 3. Location a. Most often occurs in the deep vein of the calf muscles. b. Less common sites includes portal vein, hepatic vein, dural sinuses,

(1) Swelling (2) Pain on dorsiflexion of foot (Homans' sign) and compression of the calf muscles. (3) Pitting edema distal to the thrombosis (increased hydrostatic pressure) Unilateral sometime bilateral either impaired venous or lymphatic return.

Migratory thrombophlebitis (Trousseau sign).
In patients with cancer, particularly adenocarcinomas, hypercoagulability occurs as a paraneoplastic syndrome related to tumor elaboration of procoagulant factors. Venous thromboses classically appear in one site, disappear, and then reoccur in other veins, so-called migratory thrombophlebitis (Trousseau sign).

Migratory thrombophlebitis
Also called as Trousseaus' sign several episodes of Thrombophlebitis involving different sites Commonly seen in patients with Colon cancer Pancreatic cancer Or any visceral cancers

Phlegmasia alba dolens
Painful white leg due to iliofemoral venous thrombosis occur in pregnant women due to gravid uterus initiates phlebitis and lymphatic blockage and painful white leg.

SVC SYNDROME Usually from bronchogenic CA or mediastinal lymphoma
“DUSKY CYANOSIS” of: Head Neck Arms

Pathogenesis Extrinsic compression of the superior vena cava Due to a primary lung cancer (90% of cases) • Usually a small cell carcinoma of the lung Mediastinal mass 2. Clinical findings a, "Puffiness" and blue to purple discoloration of the face, arms, and shoulders b. Retinal hemorrhage, stroke 3. Treatment • Radiation; stent to bypass obstruction.

IVC SYNDROME Secondary to: Bilateral leg edema
NEOPLASMS (external compression) ASCENDING THROMBOSIS from FEMORALS, ILIACS AAA, Gravid uterus Bilateral leg edema Massive proteinuria if renal veins involved (like nephrotic syndrome)

LYMPHANGITIS From regional infections
Group-A beta-hemolytic strep most common Lymphatics dilated, filled with WBCs Cellulitis usually present too Lymphadenitis also usually follows

Diseases of veins and lymphatics
E) Lymphangitis and Lymphedema Primary diseases – extremely uncommon. Secondary processes – develop in association with inflammation or cancer. Lymphangitis: bacterial infections spreading into and through the lymphatics.

Obstructive lymphedema:
Occlusions of lymphatic drainage by tumor,  by postradiation fibrosis,  by filariasis,  trauma or  by inflammatory thrombosis which is accompanied by abnormal accumulation of interstitial fluid in the affected part.

Vascular TUMORS BENIGN (NEVER metastasize, in fact some are not even TRUE neoplasms, but hamartomas) INTERMEDIATE (rarely metastasize) MALIGNANT (FREQUENT and EARLY metastases, like any other sarcoma lung) Vascular tumors generally follow the same diagnostic patterns of other mesenchymal (i.e., “soft” tissue) tumors. Often the KEY difference is that “endothelium” lined blood filled spaces, or identification of endothelial cells by antigenic markers, such as factor VIII, is usually present.

Vascular tumors can be endothelium derived or
Arise from the cells support and or surrounds the vessel. Benign tumors produce obvious vascular channels filled with blood cells or lymph lined by normal endothelial layer Malignant are more cellular and show atypia.

HEMANGIOMA CAPILLARY (small vascular spaces)
Often a generic term for ANY benign blood vessel tumor very common tumor. 7% of infants and childhood tumor. CAPILLARY (small vascular spaces) Also called “juvenile”, present from birth” Usually regress with age CAVERNOUS (LARGE vascular spaces) Also called “adult” Usually do NOT regress Small spaces = often small people, i.e., kids Large spaces = often large people, i.e., adults

Capillary hemangioma Most commonly seen skin, subcutaneous tissues, and mucous membranes of the oral cavities and lips, as well as in the liver, spleen, and kidneys (JUVENILE HEMANGIOMA)

A Hemangioma and D Pyogenic granuloma B Juvenile capillarty hemangioma C Cavernous hemangioma

Strawberry or juvenile hemangioma of the skin of the newborn is extremely common.

Cavernous hemangioma These are larger and involve the deeper structures. well circumscribed tumor.

Cavernous hemangioma Cavernous hemangioma is the most common benign liver tumor typically presenting in adults aged years. These benign tumors are thought to be congenital malformations that enlarge by ectasia

Cavernous hemangioma Microscopically these tumors consist of cavernous, blood-filled vascular spaces of variable size lined by a single epithelial layer.

von Hippel-Lindau disease
Cavernous hemangiomas are a component of von Hippel-Lindau disease occurring within the cerebellum or brain stem and eye grounds, along with similar angiomatous lesions or cystic neoplasms in the pancreas and liver; von Hippel-Lindau disease is also associated with renal neoplasms.

Von Hippel—Lindau disease
A rare autosomal dominant condition characterized by the presence of capillary hemangioblastomas in the retina and/or cerebellum, as well as congenital cysts and/or neoplasms in the kidney, liver, and pancreas. Patients are also at increased risk for renal cell carcinoma, which can be bilateral.

Cavernous hemangioma Microscopically, these tumors consist of cavernous, blood- filled vascular spaces of variable size lined by a single epithelial layer. is the most common benign liver tumor typically presenting in adults aged years. These benign tumors are thought to be congenital malformations that enlarge by ectasia, not hyperplasia or hypertrophy. Hemangiomas may occur singly or in multiples and are well-circumscribed masses of spongy consistency, typically measuring less than 5 cm in width.

CHERRY HEMANGIOMAS The small, vascular, bright-red papular lesions shown on the image above are called cherry hemangiomas and are the most common benign vascular tumors in adults. Cherry hemangiomas appear during the third or forth decade of life. They do not regress spontaneously, and their number often increases with age which is why they are also referred to as senile.

Pyogenic granuloma It is a form of capillary hemangioma.
Seen after a trauma usually reach in size about 2 to 3 cm after 6 weeks. There is also pregnancy tumor( granuloma gravidarum) They undergo fibrosis. Or need excision.

LYMPHANGIOMA Small 1-2 mm Simple or capillary type and Cavernous
90% Head and neck region in kids <2 Generally……RARE When large size and/or spaces present often called “CYSTIC HYGROMA”

Cystic Hygroma Common sites are Neck or axilla of children and, rarely, Retroperitoneum; Cavernous lymphangiomas of the neck are common in Turner syndrome (≤15 cm in diameter) and may fill the axilla or produce gross deformities about the neck.

Tumors are composed of massively dilated lymphatic spaces lined by ECs and separated by intervening connective tissue stroma containing lymphoid aggregates. The tumor margins are not discrete and the lesions are not encapsulated, making resection difficult.

Cystic hygroma

Glomus Tumor (Glomangioma)
It is a benign but painful tumors arising from modified SMCs of the glomus body, a specialized arteriovenous structure involved in thermoregulation. They are most commonly found in the distal portion of the digits, especially under the fingernails. Excision is curative.

Glomus tumor(Glamnagioma)

Vascular Ectasias Are common lesions characterized by local dilation of preexisting vessels; they are not true neoplasms. Telangiectasia is a term used for a congenital anomaly or acquired exaggeration of preformed vessels-usually in the skin or mucous membrane.

Nevus flammeus It is an ordinary birth mark present over the head and neck anf flat lesion and the color deep purple to light pink. Dilation of the vessels in the demis. Majority of them fade and regress.

Sturge-Weber syndrome
Port wine stain

Sturge-Weber syndrome
Port wine stain in a trigeminal nerve distribution are occasionally associated with the Sturge-Weber syndrome (also called encephalotrigeminal angiomatosis). Associated with venous angiomatous masses in the cortical leptomeninges and Ipsilateral facial port wine nevi; mental retardation, seizures, hemiplegia, and skull radio-opacities.

The so-called port wine stain is a special form of nevus flammeus; these lesions tend to grow with a child, thicken the skin surface, and demonstrate no tendency to fade.

Spider Telangiectasia non-neoplastic vascular lesion grossly resembles a spider; there is a radial, often pulsatile, dilated subcutaneous arteries or arterioles (resembling legs) about a central core (resembling a body) that blanches when pressure is applied to its center.

It is commonly seen on the face, neck, or upper chest
Causes. Hyper estrogenic states such as pregnancy or Cirrhosis.

Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu Disease)
Autosomal dominant disorder Distributed over the skin and oral mucous membranes present. Lesions rupture and can cause Hematuria and Epistaxis.

Capillary malformations

MISC. “BENIGN” TUMORS -ectasias, telangiectasias
Nevus Flammeus,, port wine stain---- Spiders (spider telangiectasias), ass. W. pregnancy, cirrhosis  Osler-Weber-Rendu Disease (Hereditary Hemorrhagic Telangiectasia)  Bacillary Angiomatosis, in HIV patients, caused by bacilli of Bartinella species “-ectasia” is a generic term meaning dilation and is primarily used with regard to veins rather than arteries.

Bacillary Angiomatosis
Bacillary angiomatosis is an opportunistic infection in immunocompromised persons that manifests as vascular proliferations involving skin, bone, brain, and other organs. First described in patients with acquired immunodeficiency syndrome, Causative organism gram-negative bacilli of the Bartonella hensle

Skin lesions are red papules or nodules rounded subcutaneous masses.
Capillary proliferation due to VEGF production by HIF 1 alpha. Nuclear atypia and mitosis also lesions contain neutrophils and bacteria.

Kaposi Sarcoma Kaposi sarcoma (KS) common in patients with acquired immunodeficiency syndrome (AIDS) prior to the advent of effective antiretroviral therapy; indeed, its presence is used as a criterion for diagnosing AIDS.

1.Chronic KS also called classic European KS
They usually present red to purple nodules on the skin on the lower extremities. Due to malignancy or altered immunity. Not seen with AIDS patients.

2.Lymphedenopathic KS called African or endemic KS
Skin lesions are less. Visceral involvement is more and aggressive.

3.Transplant-associated KS occurs in the setting of solid-organ transplantation with its attendant long-term immunosuppression. It tends to be aggressive with nodal, mucosal, and visceral involvement; . Lesions occasionally regress when immunosuppressive therapy.

4.AIDS-associated (epidemic) KS was originally found in a third of AIDS patients, particularly male homosexuals. However, with current regimens of intensive antiretroviral therapy, KS incidence is now less than 1%.

Pathogenesis of KS KS human herpes virus 8 KSHV proteins disrupt the cell cycle and viral genes produce P53 inhibitors and prevent apoptosis

Malignant tumors Angiosarcoma are malignant endothelial tumor.

Angiosarcoma is common in both sex.
More common in older adults. Site any part f the body involved, commonly in the skin, soft tissue, breast and liver.

Hepatic angio sarcoma following environmental exposure Plastic factory workers(Vinayl chloride) Arsenic pesticides Radio contrast( Thorotrast)  Induced by radiation

Lymphangiosarcoma Angiosarcoma can arise from lymphatic edema. Typically seen after 10 years following radical mastectomy for breast cancer.

They present as red nodules
Locally invasive and metastasize readily. Aggressive tumors.

Hepatic angiosarcoma Hepatic angiosarcoma is associated with exposure to carcinogens such as Arsenic, Thorotrast, and Polyvinyl chloride. Tumor cells express CD 31, an endothelial cell marker.

Angiosarcoma of breast is known as
Female with breast cancer after radical mastectomy chances of developing a type of angiosarcoma over 10years of period is known as Lymphangiosarcoma

VASCULAR INTERVENTIONS
ANGIOPLASTY STENTS GRAFTS Autologous (saphenous v., internal mammary a.) Synthetic (Teflon) 133

PATHOLOGY OF VASCULAR INTERVENTION
Morphologic changes that occur in vessels following therapeutic intervention (i.e., balloon angioplasty, stenting, or bypass surgery) typically recapitulate many of the changes that occur in the setting of any vascular insult.

Local EC trauma (e.g., due to a stent),
vascular thrombosis (after angioplasty), and abnormal mechanical forces (e.g., a saphenous vein inserted into the arterial circulation as a coronary artery bypass graft) As with atherosclerosis, the traumas of vascular intervention tend to induce a concentric intimal thickening composed of recruited SMCs and their associated matrix deposition.

STENTS Metallic mesh Permanently placed
Stays patent longer than angioplasty OFTEN DRUG COATED Goals: Prevent thrombosis Prevent spasm Delay RE-stenosis

What is angioplasty? PT CA Percutaneous transluminal Coronary AGP Premedications Antithrobotic Prevent Vasospasm

GRAFTS 400,000 CABG grafts per year in USA
Saphenous v. vs. Internal mammary a. (internal thoracic a.) 50% patent after 10 years, for saphenous v. 90% patent after 10 years, for mammary a.

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