1 blood vessels
DESCRIPTION
pathologyTRANSCRIPT
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Dr. Muhammad Mudassar Majeed
M.B.B.S, FCPS (HISTOPATHOLOGY)
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Blood vessels
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Before starting the discussion Be ready for questions
from each of you during the session……no body spared…
Don’t fear, just friendly questions………….
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What would we cover MAIN TOPICS
Atherosclerosis
Myocardial infarction
Hypertension
Rheumatic heart diseases
Congenital heart diseases
Aneursysms
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The vascular wall
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Normal structure Endothelial cells
Single cell thick
Continuous lining
Smooth muscle cells
Extracellular matrix Elastin
Collagen
Glycosaminoglycans
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Endothelial cell response to enviornmental stimuli
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Mechanism of intimal thickening Vascular injury stimulates smooth muscle cell growth.
Reconstitution of the damaged vascular wall is a physiologic healing response that includes the formation of neointima in which SMC’s
Migrate from the media to intima
Multiply as intimal SMC
Synthesize and deposit ECM
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Just wait…. What is the difference
between atherosclerosis and arteriosclerosis ?
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Mechanism of intimal thickening
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Before starting atherosclerosis, lets see a clip
Clip no 1
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ARTERIO-SCLEROSIS
GENERIC term for ANYTHING which HARDENS arteries
Atherosclerosis (99%)
Mönckeberg medial calcific sclerosis (1%)
Arteriolosclerosis, involving small
arteries and arterioles, generally regarded as NOT strictly being part of atherosclerosis, but more related to hypertension and/or diabetes
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ATHEROSCLEROSIS (classical)
Etiology/Risk Factors
Pathogenesis
Morphology
Clinical Expression
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MORPHOLOGIC CONCEPTS Intimal Thickening
Lipid Accumulation
Streak
Atheroma
Smooth Muscle Hyperplasia and Migration
Fibrosis
Calcification
Aneurysm
Thrombosis
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PLAQUE
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Risk Factors for Atherosclerosis
Major Minor
NON-modifiable Modifiable
Increasing age Obesity
Male gender Physical inactivity
Family history Stress ("type A" personality)
Genetic abnormalities Postmenopausal estrogen deficiency
High carbohydrate intake
Modifiable
Hyperlipidemia Alcohol
Hypertension Lipoprotein Lp(a)
Cigarette smoking Hardened (trans)unsaturated fat intake
Diabetes Chlamydia pneumoniae
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MAJOR factors
Hyperlipidemia
Hypertension
Cigarette Smoking
Diabetes Milletus
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Who would repeat major factors of atherosclerosis
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HYPERLIPIDEMIA Chiefly CHOLESTEROL,
LDL>>>>HDL HDL mobilizes
cholesterol FROM atheromas to liver
LOW CHOLESTEROL diet is GOOD
UNSATURATED fatty acids GOOD
Omega-3 fatty acids GOOD
Exercise GOOD
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CHOLESTEROL CLEFTS
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CIGARETTES What more
needs to be said?
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PATHOGENESIS SAGA Chronic endothelial injury
LDL, Cholesterol in arterial WALL
OXIDATION of lipoproteins
Monocytes migrate endothelium*
Platelet adhesion and activation
Migration of SMOOTH MUSCLE from media to intima to activate macrophages (foam cells)
Proliferation of SMOOTH MUSCLE and ECM
Accumulation of lipids in cells and ECM
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Who would repeat steps of pathogenesis ?
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Not clear yet ?
Lets have the clip again……. Clip no 4
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Classification of atherosclerosis american heart association
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Lumen in atherosclerosis
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Lumen narrowing in atherosclerosis
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Tear in the wall
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Lumen of the vessel
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Atherosclerosis in aorta
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Atheromatous plaque in coronary artery
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Morphology and complications of Atherosclerosis
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Clinical Scenario Exam question A 65 year old dictator of banana republic, who was an
alcoholic and fond of red meat, suffered a short episode of unexplained chest pain after he was forced to resign and died before he could reach the hospital. At autopsy the pathologist found thickened walls of many arteries including the coronary arteries with luminal narrowing. The lesions consisted of raised plaques having a soft centre with a fibrous cap.
A; what is the process known as and what other arteries it most commonly involves?
B; what are the principal components of these plaques?
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Hypertension
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What is the definition of hypertension ?
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DEFINITION 140/90
SUSTAINED diastolic >90
SUSTAINED systolic >140
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BP = CO x PR
ALL Hypertension
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Hypertension Elevation of blood pressure is known as hypertension
Hypertension can lead to
Cardiac hypertrophy
Heart failure (hypertensive heart disease)
Aortic dissection
Renal failure
Systolic greater than 140mm and diastolic greater than 90mm is hypertension
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Classification of hypertension Essential hypertension Secondary hypertension
Renal Acute glomerulonephritis Chronic renal disease Renal artery stenosis Renal vasculitis Renin producing tumours
Endocrine Adrenocortical hyperfunction Exogenous horomones Phaeochromocytoma
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Classification of hypertension Acromegaly
Hyperthyroidism
Hypothyroidism
Pregnancy induced
Cardiovascular Coarctation of aorta
Polyarteritis nodosa
Neurologic Pychogenic
Increased intracranial pressure
Acute stress including surgery.
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Hypertension
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Regulation of blood pressure and role of Renin Angiotensin system
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Mutations altering the blood pressure in humans
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Vascular changes in hypertension Hypertension is associated with two forms of
blood vessel disease Hyaline arteriosclerosis
Homogenous pink hyaline thickening of the walls of arterioles with loss of underlying structural detail
Narrowing of the lumen Major characteristic of benign nephrocalcinosis
Hyperplastic arteriosclerosis Characteristic of malignant hypertension Onion skin concentric thickening of walls of arterioles Progressive narrowing of the lumen Deposits of fibrinoid and acute necrosis of vessel wall
(necrotizing arteriolitis)
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HISTOPATHOLOGY of ESSENTIAL HYPERTENSION
“HYALINE” = BENIGN HTN. “HYPERPLASTIC” = MALIGNANT HTN.
SYS>200 1) ONION SKIN 2)“FIBRINOID” NECR.
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What is an aneurysms ?
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Aneurysm
A localized balloon-like enlargement of an artery.
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Aneurysms Is a localized abnormal dilation of blood vessel or the
wall of the heart
True aneurysm: aneurysm bounded by arterial wall components or the attenuated wall of the heart is true aneurysm
False aneurysm is a breach in the vascular wall leading to an extravascular haematoma that freely communicates with the intravascular space (pulsating haematoma)
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Atherosclerotic Abdominal Aortic Aneurysm
Aneurysm with
thrombus
Kidney Kidney
Aorta
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True and false aneurysm
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Aneurysms Abdominal aortic aneurysm
Thoracic and abdominal aneurysms
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Popliteal and cerebral aneurysm Cerebral aneurysm Popliteal aneurysm
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Infarction and aneurysm Infarction and aneurysm Cerebral aneurysm
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Aneurysms According to aetiology they are divided into
Atherosclerotic
Cystic medial degeneration
Traumatic aneurysm
Arteriovenous aneurysms
Congenital aneurysms
Mycotic aneurysms
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Aneurysms According to shape and size
Saccular
Fusiform
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Morphology of aneurysm
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Morphology of abdominal aortic aneurysm
Usually below the renal arteries and above bifurcation of aorta
Saccular or fusiform 15 cm in diameter and variable length
Two variants
Inflammatory abdominal aortic aneurysms
Mycotic abdominal aortic aneurysms
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Atherosclerotic aneurysm Pathogenesis
Atherosclerosis is the major cause
Genetic susceptibility Altered balance of collagen degradation & synthesis
Matrix metalloproteinases
Syphlitic aneurysms
Obliterative endarteritis (tertiary)
Vasa vasorum (syphlitic aortitis)
Cow’s heart
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Abdominal aortic aneurysm
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Aortic disseection Is characterized by dissection of blood between and
along the laminar planes of media with the formation of a blood filled channel within the aortic wall which often ruptures outward causing massive haemorrhage.
Age:
Men between 40 and 60years with hypertension
Younger with connective tissue disorder
Iatrogenic (arterial cannulization
Syphilis
Rarely in pregnancy
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Morphology of aortic dissection In spontaneous dissection the intima is usually 10 cm
of aortic valve.
Tears are transverse or oblique
1-5 cm in length
Sharp and jagged edges
Dissection can extend along the aorta proximally towards the heart or distally to the iliac or femoral vessels
Haemorrhage or double barrelled aorta with false channel. If channel is endothelized :chronic dissection
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Aortic dissection
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Aortic dissection (dissecting haematoma)
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Dissecting aneurysm
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Cystic Medial Necrosis Cystic Medial Necrosis is characterised by
Elastic tissue fragmentation
Separation of elastic and fibromuscular elements of tunica media
Small cleft like spaces
Loss of elastic tissue
Presence of amorphous extracellular matrix
Cysts
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Medial degeneration
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UHS exam question A 55 year old male presents with left sided facial pain
with palpable left temporal artery. Biopsy of the artery reveals fragmentation of internal elastic lamina with granulomas containing Langhan’s and foreign body giant cells?
A. what is the diagnosis?
B. which other condition should be considered in the d/d of a granulomatous vasculitis involves the aorta?
C. List the 3 pathogenetic mechanisms involved in non infectious vasculitides?
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Dr Muhammad Mudassar
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Inflammatory vasculitis Inflammation of the vessel wall is called vasculitis
Clinical features include
Fever
Myalgias
Arthralgias
Malaise
Local ischaemia
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Common Pathogenetic mechanism of vasculitis Direct infection
Bacterial
Rickettsial
Spirochaetal
Viral
Fungal
Immunological Immune complex mediated
Infection induced
Henoch Schonlein purpura
SLE and rheumatoid arthritis
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Common Pathogenetic mechanism of vasculitis Immunological
Antineutrophilic cytoplasmic antibodies
Wegener’s granulomatosis
Microscopic polyangitis
Direct antibody mediated
Good Pasteur’s syndrome
Kawasaki’s disease
Cell mediated
Inflammatory bowel disease
Paraneoplastic vasculitis
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Common Pathogenetic mechanism of vasculitis Unknown
Giant cell arteritis
Takayasu’s arteritis
Polyarteritis nodosa
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Pathogenesis of vasculitis Infectious vasculits
Non infectious vasculitis
Immune complexes
Antineutrophil cytoplasmic antibodies
Anti endothelial cell antibodies
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Vasculitis
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Classification of Vasculitis
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Classification Large vessel vasculitis; (Aorta and Large Branches to
Extremities, Head, and Neck)
Giant cell ( temporal )arteritis
Takayasu arteritis
Medium vessels vasculitis; (Main visceral arteries and their branches)
Polyarteritis nodosa
Kawasaki disease
Small vessels vasculitis; (Arterioles, venules, capillaries, and occasionally small arteries)
Wegener granulomatosis
Churg-Strauss syndrome
Microscopic polyangiitis
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Giant cell or temporal arteritis Most common
Acute and chronic often granulomatous inflammation of arteries of large to small size with multinucleated giant cells
Nodular thickening with reduction of the lumen
May become thrombosed
Fragmentation of the internal elastic lamina
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Temporal arteritis
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Temporal arteritis
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Takayasu’s arteritis Characterized by ocular disturbances and marked
weakening of the pulses in the upper extremities (pulseless disease
Vasculitis with fibrous thickening or obliteration of the lumina.
Classically involves the aortic arch and its branches.
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Takayasu’s arteritis Gross
Irregular thickening of the aortic or the branch vessels with intimal wrinkling
When the aortic arch is involved the orifices to the major arteries to the upper portion of the body maybe markedly narrowed or obliterated
Histological findings
Adventitial mononuclear infiltrate
perivascular cuffing of the the vasa vasorum.
In some cases granulomatous inflammation maybe seen
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Takayasu’s arteritis
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Polyarteritis nodosa PAN Systemic vasculitis of small or medium sized muscular
arteries.
Typically involving the renal and visceral vessels but sparing the pulmonary vessels
Predilection for branching points and bifurcations
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Polyarteritis nodosa Segmental transmural inflammation of arteries of
medium to small size with neutrophils monocytes and eosinophils with fibrionoid necrosis
Lumen may become thrombosed
Acute inflammatory cells disappear and be replaced by fibrous tissue.
All stages of activity may co exist in the same vessel or within different vessels
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A)Polyarteritis nodosa B) leucocytoclastic vasculitis
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Kawasaki’s disease Also known as muco cutaneous lymph node syndrome
Often involves the coronary arteries
Young children and infants less than 4 years of age
Fever
Conjuctival and oral erythema
Erosion
Edema of the hands and feet
Erythema of the palms and soles
Skin rash with desquamation
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Kawasaki’s disease Vasculitis is polyarteritis nodosa like
Inflammation of the entire wall
Fibrinoid necrosis is less common
Complications
Aneurysm
Thrombosis
Myocardial infarction
Aetiology
Immune mediated ( T cell and B cell activation)
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Kawasaki disease
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Kawasaki disease
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Leucocytoclastic vasculitis It is necrotizing vasculitis of arterioles, capillaries and
venules (vessels smaller than PAN)
All lesions tend to be at the same age (in contrast to PAN)
Presents as purpura on skin mucous membranes, lungs brain heart gastrointestinal tract kidneys and muscles
Morphology
Similar to PAN but muscular and larger arteries are spared.
Neutrophils are fragmented as they follow the vessels.
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Leucocytoclastic vasculitis
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Leucocytoclastic vasculitis
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Wegener’s granulomatosis Necrotizing vasculitis characterized by
Acute necrotizing granulomas of upper respiratory tract
Necrotizing or granulomatous vasculitis
Renal disease crescenteric glomerulonephritis
Pathogenesis
Immunologic mechansim
Hypersensitivity to inhaled or infectious agents
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Wegener’s granulomatosis
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Wegener’s granulomatosis
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Wegener’s granulomatosis
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Wegener’s granulomatosis
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Thromboangitis obliterans Also known as Burger’s disease
Segmental thrombosing acute or chronic inflammation of medium and small sized arteries
Tobacco sensitivity
Morphology
Sharply segmental acute and chronic vasculitis
Thrombosis
Organization and recanalization
Microabscesses with central focus of neutrophils
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Vaculitis associated with other disorders Vasculitis resembling hypersensitivity angitis or classic
PAN may sometimes be associated with some underlying disorder
SLE
Malignancy
Mixed cryoglobulinemias
Henoch Schonlein purpura
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Vasculitis with fibrinoid necrosis (SLE)
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Raynaud’s phenomenon Refers to paroxysmal pallor of finger tips or digits of
hands or feet and infrequently of tips of nose and ears due to cold induced vasoconstriction of digital arteries.
Structural changes in arterial walls are absentexcept late in the course when intimal thickening appears
Secondary Raynaud’s phenomenon is due to arterial insufficiency of the extremities due to SLE, systemic sclerosis atherosclerosis or Buerger’s disease.
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Raynaud’s phenomenon
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Raynaud’s phenomenon
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Varicose veins Common sites
Superficial veins of upper and lower legs
Predisposing factors
Dependence for prolonged periods of time venous pressures are elevated
Long period of standing
Long automobile and air plane rides
Familial tendency
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Varicose veins Morphology
Dilated toruous elongated and scarred
Thinning at points of maximal dilatation
Valvular deformities
Thickening rolling and shortening of cusps
Elastic tissue degeneration
Spotty calcification within the media
Clinical features
Venous congestion edema thrombosis pain,stasis dermatitis ulcerations vulnerability to infections ulcers
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Varicose veins
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Varicose veins
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Dr Muhammad Mudassar
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Tumours of blood vessels Benign tumours and tumour like conditions.
Haemangiomas
Capillary hemangioma
Cavernous hemangioma
Lobular capillary haemangioma
Lymphangioma
Capillary Lymphangioma
Glomus tumour (glomangioma)
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Tumours of blood vessels Vascular ectasia
Nevus flammeus
Spider telangiectasia
Hereditary haemorrhagic telangiectasias
Bacillary angiomatosis
Intermediate Grade (borderline low grade malignant tumours
Kaposi’s sarcoma
Haemangioendothelioma
Malignant tumours
angiosarcomas
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Haemangiomas Capillary haemangiomas
Cavernous haemangiomas
Pyogenic granuloma
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Haemangioma
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Haemangioma Haemangioma of lip Haemangioma on leg
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Haemangioma Haemangioma face Haemangioma face
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Haemangiomas
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Lymphangiomas Are composed of small lymphatic channels and tend to
occur subcutaneously in the head and neck region and in the axilla
Histology
Cystic hygroma
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Lymphangioma/lymphangioma Lymphangioma Lymphangioma
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Lymphangioma
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Glomus tumour benign
Painful
Arteriovenous junction
Distal portion of digits
Microscopy:
Branching vascular channels separated by connective tissue containing glomus cells
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Bacillary angiomatosis Opportunistic infection of immunocompromised
persons by gram negative bacilli of Bartonella family particulary Bartonella henselae.
Red papules or nodules
Proliferation of capillaries that exhibit protuberant epitheliod endothelial cells with nuclear atypia and mitosis.
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Bacillary angiomatosis
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Intermediate grade or borderline tumours Kaposi sarcoma
Classical or European Kaposi’s sarcoma
Lymphadenopathic African or Endemic Kaposi’s sarcoma
Transplant associated kaposi’s sarcoma
KS associated with AIDS
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Kaposi’s sarcoma Morphology
patch
Pink to red purple solitary or multiple macules in the lower limbs
Dilated irregular angulated blood vessels
On the lower limbs
Plaque
Large vilaceous plaques
Spreads proximally
Dialted jagged vascular channels lined by plump spindle cells surrounded by spindle cells
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Kaposi’s sarcoma Nodular
The lesions become nodular
Vessels have slit like spaces with rows of red blood cells
Mitosis are present.
This stage is associated with involvement of lymph nodes and viscera.
Pathogenesis
KS associated herpes virus
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Kaposi’s sarcoma
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Haemangioendothelioma Benign
Borderline
Malignant
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Malignant tumours Angiosarcoma
Are malignant endothelial neoplasms varying from highly differentiated to highly anaplastic lesions
Hepatic angiosarcomas are associated with carcinogens
May arise in setting of lymphoedema
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Angiosarcoma Angiosarcoma abdomen Angiosarcoma breast
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angiosarcoma Angiosarcoma on heel Angiosarcoma abdomen
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Microscopic features Angiosarcoma Angioma
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Angiosarcoma
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Balloon angioplasty stents and restenosis
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Hyperplasia in a graft
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Coronary artery stent with thickened intima
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