Morphologic Patterns of Acute Inflammation

Dr Shoaib Raza

•

Acute inflammation is morphologically characterized by – Dilatation of small blood vessels – Slowing of blood flow – Leukocyte infiltration – Fluid accumulation in interstitial space

•

Special morphologic patterns are seen – Severity of reaction – Specific cause of reaction – Particular tissue/site involved

 Marked

by

• Outpouring of thin fluid derived from  Plasma  Secretions of mesothelial cells • Accumulation of fluid in these cavities is called

as EFFUSION • Skin blister represent accumulation of serous fluid

• •

Characterized by deposition of fibrin in the extracellular spaces Fibrinous exudate develops when – Vascular leaks are large, or – Local procoagulant stimulus

•

Fibrinous exudate is characteristic of: – Inflammation in the lining of body cavities

•

Conversion to fibrous tissue (organization) within pericardial sac leads to fibrous thickening (Fibrinous pericarditis)

•

Characterized by production of large amounts of pus (purulent exudate), consist of – PMN, liquefactive necrosis, edema fluid

• •

Pyogenic bacteria produce this Abscess are localized collection of purulent inflammatory exudate – Suppuration buried in an organ, tissue or confined

space

• Central necrotic area • Preserved PMN around this necrotic focus • Vascular dilatation, parenchymal and fibroblastic proliferation occurs peripherally

•

• •

A local defect or excavation, of the surface of an organ or tissue, produced by the sloughing (shedding) of inflamed necrotic tissue Occur when tissue necrosis and inflammation exist on or near a surface Encountered in – Mouth, stomach, intestine, genital or urinary tract – Skin & subcutaneous tissues

 Complete

resolution  Healing by connective tissue replacement • Fibrosis, organization, scar formation  Progression

to chronic inflammation

 Inflammation

of the prolonged duration (weeks or months) in which inflammation, tissue injury and attempts at repair coexist  It may • Follow acute inflammation • Begin insidiously as low grade smoldering

response without any manifestation of the acute reaction

 Chronic

inflammation arises in following

settings: • Persistent infection by microorganism  Mycobacteria, fungi, viruses, parasites etc

• Immune mediated inflammatory diseases  Autoimmune diseases (Allergic disorders) • Prolonged exposure to potentially toxic agents  Exogenous  Silica, carbon

 Endogenous  Atherosclerosis

 Chronic

inflammation is characterized

by: • Infiltration with mononuclear cells  Macrophages, lymphocytes, plasma cells • Tissue destruction  Induced by persistence of offending agent • Attempts at healing by connective tissue

replacement of damaged tissue  Proliferation of small blood vessels (Angiogenesis)  Fibrosis

 Macrophages

are the predominant cells of chronic inflammation • Component of mononuclear phagocyte system     

Liver Spleen & Lymph nodes Lung CNS Bone

Kupffer cells Sinus histiocytes Alveolar macrophages Microglia Osteocytes

• Arise from common precursor in bone marrow • Monocytes enter tissue & differentiate into

macrophages

 Migration

begins early in acute inflammation  Predominant cells after 48 hours  Macrophages activation occur via: • Microbial products via TLRs

• IFN-γ secreted by sensitized T Cells, NK cells,  Activation

results in:

• Increased level of lysozyme • ROS & NO production • Production of cytokines, growth factors, etc

 Activation of macrophages result • Toxicity to microbes & host cells • Release of protease etc • Influx of other cell types via cytokines • Fibroblast proliferation • Angiogenesis  Arsenal of mediators make them

in:

powerful allies in the defense, but the same weaponry can induce tissue destruction

 In

acute inflammation:

• If irritant is eliminated, macrophages disappear  Either dying off  Drain to regional lymph nodes via lymphatics  In

chronic inflammation:

• Accumulation of macrophages persists  As a result of continuous recruitment from the circulation and local proliferation at the site of inflammation

 Lymphocytes:

• Cell mediated or antibody mediated reactions • Selectins, integrins and chemokines help in their

recruitment • TNF, IL-1, etc promote leukocyte recruitment,  Persisting the inflammatory response

• Macrophages present antigens to T Cells  Plasma

cells

• May transform the inflammatory site into tertiary

lymphoid organ



Eosinophils: • Abundant in immune reaction mediated by IgE and parasitic

infestations (infections) • Eotaxin is a potent chemotactic agent for eosinophil • Eosinophil produce:  Major Basic Proteins 

Mast Cells: • Widely distributed in connective tissue • Participate in both acute & chronic inflammation

• Express FcεRI • Release histamine, prostaglandins, serotonin • Cytokines production

   

Distinctive (Specific) pattern of chronic inflammation Immune reactions are usually involved in granuloma formation Granuloma is an attempt to contain an offending agent Granuloma composed of: • Modified macrophages (epitheliod cells)

• Collar of lymphocytes • Giant cells (multinucleated cells) • + Necrosis (caseous) 

Granulomas are of two main types: • Foreign body granuloma • Immune granulomas  Delayed type hypersensitivity reactions

Fungal Infections:

Bacteria:

• Histoplasmosis • Blastomycosis

• Tuberculosis • Leprosy

Metal/Dust • Berylliosis • Silicosis

Foreign body • Splinter • Suture • Graft material Sarcoidosis

Parasites: • Schistosomiasis

 Acute

Phase Response (systemic inflammatory response syndrome) • Fever:  Usually seen in infections  Pyrogens stimulate hypothalamus to form PG

• Acute Phase proteins:  CRP, Fibrinogen, Serum Amyloid A (SAA)

• Leukocytosis:  Leukemoid reactions, leukopenia

• Others:  Increased pulse rate, Increased blood pressure, decreased sweating, rigors, chill, anorexia, somnolence, malaise

 Defective

Inflammation:

• Increased susceptibility to infections • Delayed wound healing  Excessive

Inflammation:

• Hypersensitivity reactions • Autoimmune disorders • Other non-immune related disorders  AS, CHD, Alzheimer’s Disease

• Pathology in many infections, metabolic disorders,

etc.