inflammation and cellular responses prof orla sheils
DESCRIPTION
Inflammation and cellular responses Prof Orla Sheils. Inflammation. Is a protective response The body’s response to injury Interwoven with the repair process. Inflammation. Types Acute (sec, mins, hrs) Chronic (days, weeks, months, yrs). Causes of inflammation. Bacterial Viral - PowerPoint PPT PresentationTRANSCRIPT
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2nd Yr Pathology 2010
Inflammation and cellular responses
Prof Orla Sheils
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2nd Yr Pathology 2010
Inflammation
Is a protective response The body’s response to injury
Interwoven with the repair process
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2nd Yr Pathology 2010
Inflammation Types
Acute (sec, mins, hrs) Chronic (days, weeks, months, yrs)
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2nd Yr Pathology 2010
Causes of inflammation Bacterial Viral Protozoal Metazoal Fungal Immunological Tumours Chemicals, toxins etc Radiation
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2nd Yr Pathology 2010
Acute inflammation
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2nd Yr Pathology 2010
Inflammation
The Cardinal Signs of Acute Inflammation
RUBOR
CALOR
TUMOR
FUNCTIO LAESA
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2nd Yr Pathology 2010
Cardinal signs of inflammation
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2nd Yr Pathology 2010
Cardinal signs of inflammation
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2nd Yr Pathology 2010
Cardinal signs of inflammation
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2nd Yr Pathology 2010
Cardinal signs of inflammation
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2nd Yr Pathology 2010
Cardinal signs of inflammation
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2nd Yr Pathology 2010
Cardinal signs of inflammation
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2nd Yr Pathology 2010
Inflammation The basis of the five cardinal signs
Increased blood flow due to vascular dilatation gives redness and heat.
Increased vascular permeability gives oedema causing tissue swelling.
Certain chemical mediators stimulate sensory nerve endings giving pain. Nerves also stimulated by stretching
from oedema.
Pain and swelling result in loss of function.
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2nd Yr Pathology 2010
Components of acute and chronic inflammation
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2nd Yr Pathology 2010
Cell of the acute inflammatory response
Polymorphonuclear leukocyte
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2nd Yr Pathology 2010
The process of inflammation
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2nd Yr Pathology 2010
The phases of inflammation
FIRST THERE IS VASCULAR DILATATION followed by exudation of protein-rich oedema fluid which floods the area, dilutes toxins, allows immunoglobulins to opsonise bacteria and provides substrate (fibrinogen) for fibrin scaffold.
SECOND THERE IS ACTIVE EMIGRATION OF POLYMORPHS through vessel wall and along the chemotactic gradient to the site of injury
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2nd Yr Pathology 2010
THE VASCULAR PHASE OF INFLAMMATIONFluid escapes from vessels because of endothelial cell (EC)retraction, opening up gap-junctions. The vessels which are normally involved are the post-capillaryvenules where the EC have high affinity receptors for histamine.
Severe EC injury leads to leakiness of all vesselscapillaries, venules and arterioles - giving acute local oedema,e.g. blister formation after a burn.
The phases of inflammation
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2nd Yr Pathology 2010
Local vascular manifestations of acute inflammation
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2nd Yr Pathology 2010
Leukocyte migration in inflammation
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2nd Yr Pathology 2010
Molecules modulating endothelial-neutrophil interactions
LFA-1 and MAC-1(activated integrins)
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2nd Yr Pathology 2010
Acute inflammation: tissue effects
Pavementation and diapedesis
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2nd Yr Pathology 2010
Acute inflammation: tissue effects
Inflammatory cells in protein exudate
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2nd Yr Pathology 2010
Acute inflammation: tissue effects
Blood vessel involved in the acute inflammatory process
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2nd Yr Pathology 2010
Acute inflammation: tissue effects
Bronchopneumonia
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2nd Yr Pathology 2010
Acute inflammation: tissue effects
Abscess: collection of acute inflammatory cells
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2nd Yr Pathology 2010
Acute inflammation: tissue effects
Multiple splenic abscesses
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2nd Yr Pathology 2010
Vasoactive amines Histamine Serotonin (5-HT)
Neuropeptides Substance P
Plasma proteases and the complement system Action of Hageman factor
Arachidonic acid metabolites Prostaglandins Leukotrienes Lipoxins
Cytokines IL-1, TNF etc.
Chemokines (CXC and CC) Nitric oxide and oxygen-derived free radicals
Chemical mediators of inflammation
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2nd Yr Pathology 2010
Chemical mediators of inflammation
PREFORMEDHistamine, Serotonin NEWLY SYNTHESISEDProstaglandinsLeucotrienesPlatelet activating factorCytokinesNitric oxide
LOCAL AND SYSTEMIC
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2nd Yr Pathology 2010
Chemical mediators of inflammation(local and systemic)
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2nd Yr Pathology 2010
Plasma proteases
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2nd Yr Pathology 2010
The complement system
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2nd Yr Pathology 2010
Arachidonic acid metabolites
HETE = hydroxyeicosatetraenoic acidHPETE = hydroperoxyeicosatetraenoic acid
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2nd Yr Pathology 2010
Cytokines (IL-1 and TNF)
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2nd Yr Pathology 2010
Nitric oxide (NO)
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2nd Yr Pathology 2010
Effects of mediators of inflammationVasodilation:
Prostaglandins, NO
Increased vascular permeability:Histamine, serotonin, C3a, C5a, bradykinin,
Leukotrienes C4, D4, E4, platelet activating factor
Chemotaxis, leukocyte activation:C5a, leukotriene B4, bacterial products, chemokines (IL-8)
Fever:IL-1, IL-6, TNF, prostaglandins
Pain:Prostaglandins, bradykinin
Tissue damage:Neutrophil and macrophage lysosomal enzymes, oxygen metabolites
NO
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2nd Yr Pathology 2010
Phagocytosis
Phagocytosis of bacteria by polymorphs
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2nd Yr Pathology 2010
PHAGOCYTOSIS
Recognition and attachmentForeign objects coated with opsonins IgG and C3b which attach toreceptors on polymorph surface.
EngulfmentCell membrane fuses around an object: at the some time lysosomesempty into the vacuole, often before vacuole has time to seal - this givesrise to 'regurgitation during feeding' and enzymatic damage to surroundingtissue.
Killing or degradationH2O2, hypohalous acid (HOC1) produced by myeloperoxidase andsuperoxides kill bacteria. Lysozyme digests them.
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2nd Yr Pathology 2010
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2nd Yr Pathology 2010
Chronic inflammation
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2nd Yr Pathology 2010
Cells of the chronic inflammatory response
Lymphocytes Monocytes/ macrophages Plasma cells
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2nd Yr Pathology 2010
Maturation of circulating monocytes to macrophages
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2nd Yr Pathology 2010
Macrophage-lymphocyte interactions in chronic inflammation
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2nd Yr Pathology 2010
Cellular interactions in chronic inflammation
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2nd Yr Pathology 2010
Chronic inflammation: tissue effects
Knee joint in rheumatoid arthritis
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2nd Yr Pathology 2010
Chronic inflammation: tissue effects
Chronic cervicitis
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2nd Yr Pathology 2010
Chronic inflammation: tissue effects
Lung abscess
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2nd Yr Pathology 2010
Granulomatous inflammation:
a special form of chronic inflammation
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2nd Yr Pathology 2010
Granuloma Definition
A collection of macrophages, lymphocytes, mononuclear cells and fibroblasts with or without giant cell formation and constitutes a special form of chronic inflammation
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2nd Yr Pathology 2010
Granulomatous inflammation
Bacterial:TB, Leprosy, Syphillis, cat-scratch disease
Parasitic:Schistosomiasis
Fungal:Histoplasma, blastomycosis, cryptococcus
Inorganics, metals, dusts:Silicosis, berrylliosis
Foreign body
Unknown:Sarcoidosis
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2nd Yr Pathology 2010
Granulomatous inflammation: tissue effects
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2nd Yr Pathology 2010
Granulomatous inflammation: tissue effects
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2nd Yr Pathology 2010
Granulomatous inflammation: tissue effects
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2nd Yr Pathology 2010
Granulomatous inflammation: tissue effects
Epithelioid cells
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2nd Yr Pathology 2010
Granulomatous inflammation: tissue effects
Talc granulomas in the lung
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2nd Yr Pathology 2010
Healing and repair
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2nd Yr Pathology 2010
Wound healing: critical steps
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2nd Yr Pathology 2010
The cell cycle
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2nd Yr Pathology 2010
Cyclins, cyclin dependent kinases and cyclin dependent kinase inhibitors
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2nd Yr Pathology 2010
Cell-cell interactions in repair
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2nd Yr Pathology 2010
Cell surface receptors in healing and repair
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2nd Yr Pathology 2010
The major components of the extracellular matrix (ECM) required for
healing and repair
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2nd Yr Pathology 2010 Extracellular matrix re-modelling occurs by the action of
Matrix metalloproteinases
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2nd Yr Pathology 2010
Matrix metalloproteinase regulation
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2nd Yr Pathology 2010
Critical steps in angiogenesis
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2nd Yr Pathology 2010
Major growth factors in wound healing
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2nd Yr Pathology 2010
Wound healing: critical steps
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2nd Yr Pathology 2010
Granulation tissue
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2nd Yr Pathology 2010
Granulation tissue
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2nd Yr Pathology 2010
Scar tissue
Skin
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2nd Yr Pathology 2010
Scar tissue
Lung
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2nd Yr Pathology 2010
Outcome of healing and repair
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2nd Yr Pathology 2010
When healing goes wrong
Keloid scar