Inflammation II 2024.PDF

Chronic inflammation and outcomes ◼ ◼ ◼ ◼ ◼ Introduction Causes Processes and morphology Systemic effects Outcomes Learning outcomes ◼ ◼ ◼ ◼ To demonstrate knowledge on the concept and causes of chronic inflammation To understand the processes involved in chronic inflammation and its morphology To d...

Chronic inflammation and outcomes ◼ ◼ ◼ ◼ ◼ Introduction Causes Processes and morphology Systemic effects Outcomes Learning outcomes ◼ ◼ ◼ ◼ To demonstrate knowledge on the concept and causes of chronic inflammation To understand the processes involved in chronic inflammation and its morphology To describe its systemic effects To know its main outcomes Chronic inflammation and outcomes ◼ ◼ ◼ ◼ ◼ Introduction Causes Processes and morphology Systemic effects Outcomes Chronic inflammation ◼ Can be a consequence of acute inflammation ◼ Not characterised by the 5 signs of acute inflammation ◼ Prolonged duration – months, years ◼ Simultaneous injury and healing ◼ May occur without acute inflammation Chronic inflammation and outcomes ◼ ◼ ◼ ◼ ◼ Introduction Causes Processes and morphology Systemic effects Outcomes Causes of chronic inflammation ◼ Persistent infection by microorganisms that are difficult to eliminate ◼ Immune-mediated inflammatory diseases autoimmune disease allergic diseases ◼ Prolonged exposure to potentially toxic agents exogenous endogenous Chronic inflammation Chronic inflammation and outcomes ◼ ◼ ◼ ◼ ◼ Introduction Causes Processes and morphology Systemic effects Outcomes Morphology of chronic inflammation ◼ Infiltration of mononuclear cells: ❑ ❑ ❑ macrophages lymphocytes plasma cells ◼ Tissue destruction ◼ Attempts at healing by connective tissue replacement ❑ ❑ Angiogenesis Fibrosis Lung tissues Chronic inflammation Structural destruction Fibrosis Chronic inflammatory cells Acute inflammation Neutrophils fill the alveolar spaces and blood vessels congestion Cells in chronic inflammation ◼ Macrophages ❑ ❑ ◼ Dominant cell type activated Products of activated macrophages can cause tissue damage and fibrosis Lymphocytes ❑ produce cytokines: IFN ◼ Plasma cells developed from activated B lymphocytes ◼ Eosinophils ◼ Mast cells Macrophage-lymphocyte interactions Changes in chronic inflammation ◼ Persistent inflammatory stimulus ◼ Absence of neutrophils ◼ Predominately lymphocytes ◼ Macrophages present to clear debris, presentation of antigen materials and granuloma formation ◼ Angiogenesis ◼ Proliferation of fibroblasts - fibrosis Granuloma formation ◼ Granuloma: special type of chronic inflammation ◼ Caseating (mycobacterial infection) and non-caseating (autoimmune) ◼ Caused by resistance to phagocytosis ◼ For infective organisms this include TB, leprosy, syphilis or exogenous materials such as asbestos, silica ◼ Some of unknown aetiology such as sarcoidosis Epitheloid granuloma Typical granuloma seen with TB Chronic inflammation ◼ Contains the injurious agent and attempts to eradicate it ❑ ❑ ❑ ◼ Can be harmful ❑ ❑ ◼ with antibodies from plasma cells direct killing by lymphocytes phagocytosis by macrophages Tissue necrosis Fibrosis Associated with systemic signs of low grade fever, weight loss, anaemia Chronic inflammation and outcomes ◼ ◼ ◼ ◼ ◼ Introduction Causes Processes and morphology Systemic effects Outcomes Systemic effects of inflammation ◼ Fever: usually 1-4°C higher Acute phase protein: C-creative protein (CRP) Fibrinogen Serum amyloid A (SAA) Systemic effects of inflammation Leukocytosis: a feature of bacterial infection Leukocyte count: 15000-20000, but can be 100,000/μL Other manifestations: Increased pulse and blood pressure Decreased sweating, chills Chronic inflammation and outcomes ◼ ◼ ◼ ◼ ◼ Introduction Causes Processes and morphology Systemic effects Outcomes Inflammation outcomes Fibrosis – loss of function Acute vs. chronic inflammation Acute Chronic Duration Hours/days Days/months/year Cell Types Neutrophils/Macr ophage Macrophage, plasma cells, lymphocytes Vasc Change Oedema None Sequence Inflammation, then repair Infl. and concurrent repair; fibrosis Damage Some A lot In lecture question and discussion True or False The following are correctly paired: A) B) C) D) E) Granulomatous inflammation – mycobacterium tuberculosis Plasma cells – phagocytosis Pus – collection of neutrophils Eosinophils – parasitic infection Langerhan’s cells – mycobacterium tuberculosis