Morphologic Patterns of Acute Inflammation

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Morphologic Patterns of Acute Inflammation

• Dr Shoaib Raza

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Morphologic Patterns of Acute Inflammation

• 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

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Serous Inflammation

• 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

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Fibrinous Inflammation

• 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)

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Suppurative/purulent Inflammation

• 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

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Ulcers

• 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

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Outcomes of Acute Inflammation

• Complete resolution
• Healing by connective tissue replacement
• Fibrosis, organization, scar formation
• Progression to chronic inflammation

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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

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Causes of Chronic Inflammation

• 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

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Morphologic Features

• 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

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Macrophages

• Macrophages are the predominant cells of chronic
  inflammation
• Component of mononuclear phagocyte system
• Liver Kupffer cells
• Spleen Lymph nodes Sinus histiocytes
• Lung Alveolar macrophages
• CNS Microglia
• Bone Osteocytes
• Arise from common precursor in bone marrow
• Monocytes enter tissue differentiate into
  macrophages

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Role of Macrophages in Chronic Inflammation

• Migration begins early in acute inflammation
• Predominant cells after 48 hours
• Macrophages activation occur via
• Microbial products via TLRs
• IFN-? secreted by sensitized T Cells, NK cells,
• Activation results in
• Increased level of lysozyme
• ROS NO production
• Production of cytokines, growth factors, etc

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Role of Macrophages in Chronic Inflammation

• Activation of macrophages result in
• Toxicity to microbes host cells
• Release of protease etc
• Influx of other cell types via cytokines
• Fibroblast proliferation
• Angiogenesis
• Arsenal of mediators make them powerful allies in
  the defense, but the same weaponry can induce
  tissue destruction

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Fate of Macrophages

• 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

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Other cells in Chronic 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

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Other cells in Chronic Inflammation

• 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 FceRI
• Release histamine, prostaglandins, serotonin
• Cytokines production

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Granulomatous Inflammation

• 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

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• Fungal Infections
• Histoplasmosis
• Blastomycosis
• Metal/Dust
• Berylliosis
• Silicosis
• Foreign body
• Splinter
• Suture
• Graft material
• Sarcoidosis

• Bacteria
• Tuberculosis
• Leprosy
• Parasites
• Schistosomiasis

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Systemic Effects of Inflammation

• 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

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Pain is perfect misery, the worst of evils, and
excessive, overturns All patience. - John Milton,
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Inappropriate Inflammatory Responses

• Defective Inflammation
• Increased susceptibility to infections
• Delayed wound healing
• Excessive Inflammation
• Hypersensitivity reactions
• Autoimmune disorders
• Other non-immune related disorders
• AS, CHD, Alzheimers Disease
• Pathology in many infections, metabolic
  disorders, etc.

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