Cell Pathology 3 Flashcards
Causes of inflammation
• Mechanical injury
• Bacteria, viruses, parasites • Ischaemia
• Chemical injury
• Temperature
• Radiation
• Immune mechanism • Foreign body
Inflammation symptoms
Note s
Inflammatory Process
• Microvasculature changes
• Vasodilation → Redness & heat • Permeability → Swelling
• Inflammatory exudate • Fluid
• Cells → Chemical mediators
Immediate-transient response
• Peaking at 5-10 minutes
• Lasts 15-30 minutes
• Produced by chemical mediators
• Nettle stings or insect bits
Immediate-persistent response
• Direct endothelial damage
• Peaking at around 1h
• Lasts until thrombus plugs vessel
• Severe direct injury e.g. burns
Delayed-persistent response
• Subtle endothelial damage
• Leakage starts 18-24hr later
• Last 36h or more
Causes include;
• Sunburn
• Radiotherapy
• Bacterial toxins
Cellular events in inflammation
• ChangesinBloodflow
• White cells fall to edge of
vessels
• Adhesion molecules allow attachments between endothelial cell and leukocyte
Emigration
• Pseudopodiaform
• Push between endothelial cells
• Proteasesreleased
• Digestbasementmembrane
• Leukocytemigratesbetween endothelial cells
• Basementmembraneseals behind them
• Cellsmovetowardschemical signal
• Towardsinflammatory mediator
Phagocytosis
-Phagosome engulfs foreign material
-kill foreign material
-damage to surrounding tissue
Leukocytes order in blood
Neutrophils > lymphocytes>monocytes>eosinophils >basophils
Neutrophils
• Mediatesmajorityofacuteinflammatoryeffects
• Granulecontentsincreasevascularpermeability
• Migrate to damaged area by chemotaxis
• Phagocytic
Granulocytes
> Eosinophils
• Allergic/parasitic conditions
• Granules include major basic protein
Basophils
• Give rise to mast cells
• Granules include histamine
Macrophage
• Derived from monocytes
• Migrate to damaged area (later than neutrophils)
• Low numbers which increase with time
• Survive much longer than neutrophils
Lymphocytes
> TCells
- Antigen recognition and presentation
• Cell killing
•>Bcells
• Give rise to plasma cells
• Synthesize immunoglobulin’s
Chemical mediators;cell derived
• Vasoactive amines (histamine and serotonin)
• Arachidonic acid derivatives (prostaglandin and leukotrienes) • Cytokines (interleukins, interferons, chemokines and GFs)
• Platelet activating factor
• Nitric oxide
• Lysosomal conten
Chemical mediators; Plasma-derived
• Kinin system (bradykinin)
• Coagulation and fibrinolytic system (plasmin/fibrin degradation products)
• Complement system (C3a and C5a)
Systemic effects of inflammation
• Systemic effects
• Leukocyte production
• Fever
• Tachycardia
• lower Blood pressure • lossofappetite
• vomiting
• skeletalweakness • aching
Acute Inflammation
• Short duration
• Minutes to days
• Sequential process
• Neutrophil and macrophage driven
• Protective and reparative mechanism
• Sometimes inflammatory response more harmful than initial
tissue damage/infection
Chronic Inflammation
• Persistent (months or years)
• Defined by type of cell present (Lymphocyte,
macrophage and plasma cell)
• Necrotic cell debris
• Tissue granulation
• Fibrosis
• Balance between repair and continues tissue damage
Macrophage are the main effector cells in chronic inflammation:
• Antigen presentation (to lymphocytes)
• Scavenging
• Phagocytosis
• Giant cell formation
• Harbouring of organisms
• Secretion
• Reactive oxygen metabolites
• Proteases
• Arachidonic acid metabolites
• Cytokines
• Growth factors
Nonspecific chronic inflammation
➢Occurs following infection
➢Lymphocyte and plasma cell
Chronic suppurative chronic inflammation
➢Continued neutrophil production and recruitment
➢Surrounded by fibrous tissue & poorly vascularized
➢Eosinophil-rich
Granulomatus chronic inflammation
➢Agents difficult to destroy using lysosomal enzymes
Granulomatous Inflammation
• Collection of macrophages frequently surrounded by lymphocytes
• Macrophagefuseforming multi-nucleated giant cell or epitheliod cell
• Micro-organismswhichexcite an immune response eg mycobacteria
• Non-living foreign material
Tuberculosis
• Primary
• Never affected before
• Produce lesions
• Neutrophil inflammatory response → macrophage influx
• Macrophage ingest bacilli → present antigen to lymphocytes
• Proliferation of specific T lymphocytes → attract macrophage → Granuloma
• Caseating necrosis
• Secondary
• Patients previously sensitized
• Largely due to reactivation of latent mycobacteria
• More common in immune compromised e.g. steroid treatment, HIV/AIDS
• Miliary
• Extensive caseous necrosis
• Tissue destruction
• Bacilli may enter bloodstream • Granulomas appear in other
organs
Crohn’s Disease
• Chronic inflammation
• Affectsalllayersofthebowelwall
• Unknownaetiology
• Non-caseatinggranulomas
Wound Healing
Four stages in process
1. Haemostasis
2. Inflammation (removal)
3. Cell proliferation (regeneration)
4. Remodelling (replacement)
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