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    Blood Vessel Diseases LEVEL II

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    David Ogechi Atandi
    1. The document discusses various diseases of blood vessels including inflammatory vasculitides and degenerative conditions like hypertension and atherosclerosis. 2. It describes the pathogenesis of atherosclerosis including formation of atheroma plaques due to accumulation of LDL, VLDL and TG in blood vessel walls. Rupture of plaques can cause thrombosis and clinical symptoms. 3. Several specific vasculitides are mentioned like Wegener's granulomatosis, polyarteritis nodosa, giant cell arteritis and their characteristic clinical features and pathology. Antineutrophil cytoplasmic antibodies are implicated in some vasculitides.

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    Blood Vessel Diseases LEVEL II

    Uploaded by

    David Ogechi Atandi
    30 views33 pages
    1. The document discusses various diseases of blood vessels including inflammatory vasculitides and degenerative conditions like hypertension and atherosclerosis. 2. It describes the pathogenesis of atherosclerosis including formation of atheroma plaques due to accumulation of LDL, VLDL and TG in blood vessel walls. Rupture of plaques can cause thrombosis and clinical symptoms. 3. Several specific vasculitides are mentioned like Wegener's granulomatosis, polyarteritis nodosa, giant cell arteritis and their characteristic clinical features and pathology. Antineutrophil cytoplasmic antibodies are implicated in some vasculitides.

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    1. The document discusses various diseases of blood vessels including inflammatory vasculitides and degenerative conditions like hypertension and atherosclerosis. 2. It describes the pathogenesis of atherosclerosis including formation of atheroma plaques due to accumulation of LDL, VLDL and TG in blood vessel walls. Rupture of plaques can cause thrombosis and clinical symptoms. 3. Several specific vasculitides are mentioned like Wegener's granulomatosis, polyarteritis nodosa, giant cell arteritis and their characteristic clinical features and pathology. Antineutrophil cytoplasmic antibodies are implicated in some vasculitides.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    30 views33 pages

    Blood Vessel Diseases LEVEL II

    Uploaded by

    David Ogechi Atandi
    1. The document discusses various diseases of blood vessels including inflammatory vasculitides and degenerative conditions like hypertension and atherosclerosis. 2. It describes the pathogenesis of atherosclerosis including formation of atheroma plaques due to accumulation of LDL, VLDL and TG in blood vessel walls. Rupture of plaques can cause thrombosis and clinical symptoms. 3. Several specific vasculitides are mentioned like Wegener's granulomatosis, polyarteritis nodosa, giant cell arteritis and their characteristic clinical features and pathology. Antineutrophil cytoplasmic antibodies are implicated in some vasculitides.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    of 33

    diseases of blood vessels-Vaculitides

    and degenerative
    27th may 2009
    Objectives
    • Understand the classification of BV dx
    • List the causes
    • Be able to describe the pathogenesis and
    possible complications
    Broad classification
    • 1. Inflammatory- vasculitides, vasculitis
    • 2. Degenerative- hypertension and
    atherosclerosis
    Causes of athero and arteriosclerosis
    • Arteriosclerosis
    • Atherosclerosis
    • Modifiable causes- diet high in salt, cholesterol,
    cigarette smoking, diabetes, hyperlipidemia,
    hypertension, C-reactive protein
    • Non-modifiable-genes, environment, familial
    history, gender, increasing age
    atherosclerosis
    • Coronary atherosclerotic heart disease-more
    pathologically correct. IHD-non-specific
    • This accounts for 80-90% of cardiac mortalities in
    the west
    • The commonest cause of myocardial ischaemia is
    atherosclerotic coronary arteriole disease
    • Cardiac ischaemia may also be observed in
    hypertensive heart dx, anaemia, chronic
    obstructive airway disease, and cyanotic
    congenital heart disease
    atheroma
    • Athero-porridge
    • The factors leading to coronary
    insufficiency are:
    a) -the plaque size- 75% cause
    symptoms when stressed, 90% at
    rest
    -the plaque integrity-ulceration,
    thrombosed or haemorrhage
    atheroma
    • These events lead to gradual increase on the
    luminal occlusion and sudden acute
    symptomatology
    • 66% MI due to plaque rupture and
    thrombosis had < 50% narrowing while
    80% had <70% narrowing
    Pathogenesis of atheroma
    • Plaque formation- LDL, VLDL, TGS- endothelial damage,
    absorption by macrophages
    • Depostion in the tunica media
    • Smooth muscle proliferation and inflammation and
    degeneration
    atheroma
    • Plaque rupture occurs due to intrinsic and extrinsic
    factors, extrinsic=adrenergic stimulation in stress and
    hypertension, hence increase in deaths after stress
    and uncontrolled hypertension-e.g.homo case
    • Intrinsic= position of the plaque in relation to
    1.turbulence, 2.the thinnest part of the shoulder, the
    junction between the plaque and normal
    endothelium, 3. amount of inflammatory cell
    aggregates and inflammatory process,
    • 4. number of smooth muscles.
    atheroma
    • coronary thrombus- following a plaque rupture a
    thrombus forms due to platelet aggregation; may
    be mural thrombus or complete occlusive
    thrombus; formed as a result of exposure of sub-
    endothelial collagen, stimulating platelet
    aggregation and de-granulation releasing
    thromboxane A2, Serotonin and platelet factor 3
    and 4. (intrinsic coagulation pathway)
    • Extrinsic coagulation pathway also activated
    • The thrombus may dislodge and cause a embolus
    atheroma
    • Inflammatory processes-the plaque formation is an
    inflammatory process. The endothelial cells
    release chemotactic factors and adhesins-ICAM-
    1 , VCAM-1 E-selectin and P-selectin.
    • The chemokines attract macrophages and T-
    lymphocytes. The T-lymphocytes release-TNF,
    IFN-gamma, and IL-6 which stimulate endothelial
    cells and macrophages to engulf oxidized LDL
    • C-reactive proteins also increase
    atheroma
    • Rupture
    • Aneurysm
    • Arrthymias due to scar formation
    • Mural thrombus
    • Arteriole thrombo-embolism
    • Cerebral infarcts
    • Renal infarcts
    • death
    Systemic arteriole hypertension
    • Small and medium sized BV
    • The kidneys
    • Eyes
    • brain
    hypertension
    Primary and secondary
    The pathology similar
    Effects on the media
    Diffuse hyalinization
    Or medial proliferation- hyperlastic medial
    degeneration,
    PATHOLOGY IN VARIOUS
    ORGANS
    • Retinal – copper wire and cotton wool
    changes
    • Kidneys- onion skin appearance of the
    arterioles
    • Glomerulosclerosis, flee beaten appearance,
    granular scars, shrinkage
    • Complications- brain, eyes, heart- LVH,
    KIDNEYS
    vasculitides
    • Introduction:
    – Vasculitides=Inflammation of blood vessel wall.This
    may affect any of the blood vessels , from large to the
    large arteries to arterioles.
    – They are as a result of direct effects of infections and
    indirect effects as a result of immune complexes and
    immune response there after.
    – Generally these diseases present with local and
    constitutional symptoms ( fever, myalgia, arthritis and
    malaise)
    Classification
    Immune complex mediated-
    Direct infection hep B/C, SLE, RA,
    • Bacterial-N.gonorrhoea Henoch-Schonlen purpura,
    • Rickettsiae-rocky mt. spotted Drugs, cryoglobulinaemia,
    fever
    • Fungal-aspergillosis
    serum sickness
    • Viral-herpes zooster
    • Spirochaets-Syphillis

    Anti-nutrophil cytoplasmic antibody Antibody-mediated


    (ANCA-c or p) • Good Pastures syndrome
    • Wegeners granulomatosis
    • Kawasakis disease
    • Microscopic polyangitis/arteritis
    Cell mediated
    • Churg-Straus syndome
    Organ allograft rejection
    classification
    Immune-
    Paraneoplastic syndrome
    Inflammatory bowel disease-eg ulcerative
    colitis
    Unknown-giant cell temporal arteritis,
    Takayasus disease, polyarteritis nodosa
    Pathogenesis

    Imuune mediated vasculitis

    1. IMMUNE COMPLEX 2. ANCA-Cytoplasmic or


    3. Antiendothelial cell antibodies
    AB+AG perinuclear
    Immune complex mediated
    Formation of antibody-antigen complex- TYPE III Hypersensititvy
    • Following introduction of a foreign protein or endogenous
    protein,immune competent cells recognise them and change into
    plasma cells and start AB production to mop out the antigens.
    • Large complexes are easily mopped out by macrophages
    • The small and intermediate complexes deposit easily onto the
    endothelium.
    • The avidity and the affinity of the AB to the AG, the affinity of the
    AG to tissues, the shape of the complexes and the haemodynamic
    factors influence the binding to the endothelium
    Immune complex mediated
    vasculitis
    • Some of the complexes bind to NEUTROPHILS
    through the FC portion of the AB or C3b receptors
    • This triggers release of vaso-active factors such as
    serotonin, C3a and C5a(anaphylatoxins)
    • This leads to an increase in permeability- with
    chemotaxis of macrophages and more neutrophils
    • SLE-DNA and nucleoproteins; PAN-hep B
    Surface AG; Arthus Disease and serum sickness –
    various foreign proteins eg anti thymocyte
    globulin
    Mediators of Inflammatory damage
    of the BV wall
    • Prostaglandins
    • Proteases
    • Lysosomes
    • Vasodilators
    • Chemotactic factors
    • Release of free radicals-superoxides from neutrophils
    Lead to digestion of collagen, elastin, and basement
    membrane
    Platelet aggregation and release of Hageman factor-leads to
    thrombosis, necrosis and more vasculitis
    Chronic exposure to AG eg in SLE leads to chronic
    immunecomplex vasculitis
    Morphology –mainly microscopic

    • Fibrinoid necrosis-deposits of eosinophilic


    protein
    • Immunoflourescent granular lumpy deposits
    on the basement membrane(BM)
    • EM-electron dense deposit on the BM
    Antineutrophil cytoplasmic
    antibodies (ANCA) mediated
    •
    vasculitis
    The exact mechanism is unknown
    • Its postulated that the presence of an antigen leads to cytokine release-
    eg TNF and GCSF and MCSF
    • These lead to neutrophil expression of Proteinase (PR3)-
    CYTOPLASMIC AG in the neutrophil granules and (MPO)-
    Myeloperoxidase.
    • These lead to production of c-ANCA and p-ANCA respectively
    (c=cytoplasmic; p=perinuclear)
    • The ANCAS react with circulating neutrophils leading to
    degranulation leading to endothelial damage
    • Seen in sclerosing cholangitis, RA, Autoimmune liver disease and
    inflammatory bowel disease
    • The level of Serum ANCAS can give an indication of the activity of
    the disease
    Anti-endothelial cell antibodies
    • Thought to cause damage in SLE and
    Kawasakis disease
    Temporal (giant cell arteritis)
    • Common in the Nordic countries
    • Affects the aorta, temporal and ophthalmic
    arteries. May be a medical emergency-
    blindness or aneurysm
    • Associated with HLA-DR and responds
    well to steroids therefore thought to be
    immune-related
    Polyarteritis nodosa (PAN)
    • DX of young adults but also seen in
    children and elderly
    • Presents with fever, weight loss,
    hypertension and meleana
    • 30% show hep Bs AG
    PAN
    • Medium and small vessel disease
    • Transmural necrotising arteritis, fibrinoid
    necrosis,
    • Segmental affecting mainly the bifurcations
    • Complicated by aneurysms, renal failure
    and haemorrhage
    Takayasus arteritis (pulseless Dx)
    • Young females dx., weak pulse, hypotension,
    numbness and visual impairment
    • Japanese show HLA-a24, B52, DR-52
    • Aorta and the brances mainly affected leading to
    pulseless – in the upper limbs
    • Transmural necrotising granulomatous arteritis,
    not easy to distinguish from giant cell arteritis
    before the age of 40 years. Narrowing of the
    lumen
    Wegener granulomatosis
    • Middle aged males, with pneumonitis, pulmonary nodules, cavitation,
    sinusitis and nasopharyngeal ulcers
    • Acute necrotising ganulomatous arterits, in the ENT/Sinuses,
    • Focal crescenteric glomerulonephritis
    • Pulmonary Dx
    • Morphology-granulomas, necrotising, giant cells, plasma cell ,
    lymphocytes, numerous eosinophils, may cavitate and alveolar
    congestion and haemorrhage,
    • To exclude TB and fungi-special stains-ZN and Grocots methenamine
    silver respectively
    • C-ANCA positive, used for follow up
    • Necrotising glomerulonephritis-haematuria and proteinuria
    Bacillary angiomatosis
    • Bartonela spp
    • HIV patients- presents as a nodular skin
    lesion, numerous neutrophil infiltrate with
    capillary proliferation, has granular
    particles of bacteria
    refer
    • Thromboangitis obliterans
    • thrombophlebitis,
    • tumors- haemangiomas,
    • arteriovenous malformations,
    • Kaposis sarcoma,
    • haemangiopericytoma,
    • lymphangiomas
    Giant cell arteritis

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