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.