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BED Revision Lecture
IC1 2013
Prof Mary LeaderBED
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Acute Inflammation
Definition response of tissue to cell damage
Professor Mary LeaderProfessor of Pathology
Royal College of Surgeons
Dublin and Bahrain
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Causes of Cell Necrosis
Ischaemia
Micro-organisms
Radiation
Hypersensitivity
Cold
Heat
Trauma
Chemicals
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Role of Inflammation
1. Contain and isolate injury
2. Destroy microorganisms
3. Inactivate Toxins
4. Prepare for tissue repair and healing
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Inflammation
Acute- minutes to days Immediate and early response to injury
Characterized by
fluid protein
Polymorphonuclear cells (neutrophils)
Chronic- weeks to years Cells (Lymphocytes and macrophages)
Granulation tissue
Define Granulation tissue? 6
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Acute inflammation Vascular & Cellular
Response
Components of acute inflammation
Vascular
Vasodilatation
Increased endothelial permeability. This allows
protein, fluid, polymorphs and monocytes into
the area of tissue damage
Cellular
Extravasation of neutrophils and monocytes
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Cellular response-
Leucocyte Function
Opsonisation-coating a bacterium or a particle
to facilitate its phagocytosis
Phagocytosis (to engulf and destroy cells and cell
constituents)
Release of leucocytes products/mediators with
effects on surrounding tissue (tissue injury)
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Exudate- Extravascular fluid with high protein
concentration
Exudate is the characteristic fluid of acuteinflammation
Transudate -Extravascular fluid with low proteinconcentration
Vascular permeability- osmotic
pressure
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Signals that attract leucocytes
Products of invading micro-organisms
Endogenous Compounds
4 plasma systems eg Complement, Kinin, Clotting,
Fibrinolytic
Vasoactive Compounds
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Chemical mediators of inflammation
Vasoactive amines eg histamine & heparin
Phospholipid-derived products
Arachnoid Acid metabolites
Platelet activating factor
Cytokines
Nitric oxide
Lysosomal enzymes
Oxygen derived free
radicals No need to know functionof each, just know they
are pro inflammatory 11
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Plasma Proteases:These are 4 interrelated
systems that are activated in inflammation
Complement system
Kinin system
Clotting system
Fibrinolytic System
What are the functions of complement and
kinins?
What activates complement?
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The Complement System
Cascade of 20 proteins activated by 2 Pathways
ClassicalAg/Ab
ComplexAlternate
1. Lipopolysaccharide from cell wall
2. Ig A
3. Ig E
4. Plasmin
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Functions of Complement proteins
Chemotaxis
Opsonization
PhagocytosisCell Lysis
Vascular permeability
Anaphalotoxins
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The Kinin System
Function: Change the tone of the blood vessel
wall
Cascade commences with activation of
Hageman Factor
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Beneficial effects of inflammation
Contain and isolate injury
Destroy microorganisms
Dilute toxins
Arrival of antibodies to the site ofinflammation
Drug transport
Delivery of nutrients and oxygen
Prepare for healing and repair
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Outcome of Acute Inflammation
Complete Resolution
Healing by Scarring
Abscess Formation
Progression to Chronic Inflammation
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Chronic Inflammation
Definition:
Inflammation of prolonged duration in whichactive inflammation, tissue destruction and
attempts at repair are proceeding
simultaneously.
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Chronic Inflammation
Tissue infiltrated by:
LymphocytesPlasma cells
Macrophages
Granulation tissue
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What is granulation tissue?
Newly formed blood vessels and chronicinflammatory cells.
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Causes of Chronic Inflammation
Progression from Acute Inflammation
Following repeated bouts of Chronic Inflammation
Primary Chronic Inflammation
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Macrophages
Central character in Chronic Inflammation.
Functions Phagocytosis
Secretion : oxygen metabolites,
proteases, cytokines, chemotacticfactors, growth factors.
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LymphocyteMacrophage Relationship
Lymphocytes are activated by antigen presentedby macrophages.
Lymphocytes consequently producelymphokines.
Lymphokines stimulate macrophages to further
stimulate macrophages to present antigen and
secrete mediators
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Granulomas
Localised collection of Histiocytes and macrophages.
Causes of granuloma formation.
o TB
o Fungal infections
o Sarcoidosis
o Foreign material
o Response to tumourso Type IV Hypersensitivity reactions.
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Systematic Effects of Inflammation.
o Pyrexiapolymorphs and macrophagesproduce pyrogens which act on thehypothalmus
o Constitutional symptomsmalaise, anorexia,nausea
o Weight Loss
o Reactive hyperplasia of mononuclearphagocytic systemnodes
o Haematological changesincreased ESR,wcc, anaemia, amyloidosis.
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Morphologic patterns in acute and
chronic inflammation
Serous inflammation
Fibrinous inflammation
Suppurative inflammation Ulcers
Sinus
Fistula
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Serous inflammation
Accumulation of thin fluid derived from the blood
serum or secretion of mesothelial lining
Effusion
Peritoneal Pleural
Pericardial
Skin blisters
Viral infection
Burn
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Fibrinous inflammation
Accumulation of fluid and fibrin
Body cavities
May be removed by fibrinolysis (resolution) Organisation
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Suppurative inflammation
Characterised by large amounts of pus
Can be seen in association with certain
organisms (staphylococcus)
May lead to abscess formation
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Abscess
Localised collection of pus
Dead and degenerate leucocytes
Dead and degenerate host tissue cells
Oedema fluid
Dead microorganisms
Empyema
Localised collection of pus in a cavity eg pleura,
gallbladder
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Ulcer
Local defect in an epithelial surface
They are distinguished from erosions by the
extent of tissue loss
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Sinus
Is a tract lined by granulation tissue leading
from a chronically inflamed cavity to a surface
eg
Sinuses associated with osteomyelitis
Pilonidal sinus
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Fistula
Is a track open at both ends, with abnormal
communication between two surfaces
Gastrointestinal fistula in Crhons disease
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Wound healing
Types of wound healing
Primary intention
Secondary intention
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Wound with apposed edges Minimal loss of tissue
Surgical incision or clean wound
Primary intention
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Large gaping wound
Extensive loss of cells
Infarction Ulcer
Abscess
Secondary intention
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Pathologic aspects of wound healing
Deficient scar formation
Wound rupture
Excessive scar formation
Keloid
Contracture deformity
Malignant transformation (v. very rare)
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Factors that influence healing
Local factors
Systemic factors
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Factors which impair bone healing
Movement
Poor approximation
Poor blood supply
Infection
Steroids
Poor nutrition Interposition of soft tissue
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Systemic factors
Age
Nutrition (protein, Vit. C)
Metabolic status (Diabetas Mellitus)
Hormones (steroids)
Malignancy
Chemotherapy Radiotherapy
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Steps in Repair
Formulation of new vessels, migration andproliferation of fibroblasts.
Deposition of extra cellular matrix.
Maturation and organisation of fibrous tissue.
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Necrosis
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Necrosis
Definition: cell death in living tissue
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Atoptosis
Programmed cell death in living tissue
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Causes of Necrosis
Ischaemia
Microorganisms
High or low temperature
Chemicals
Hypersensitivity
Radiation Drugs
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Inflammation is the bodys response to
Necrosis
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Types of Necrosis
Coagulativecell outlines visible
Caseousno cell outlines
Liquifactivebrain
Fibrinoidassociated with fibrin deposition
Fat Necrosis
Gangrenous (ischaemia and anaerobic organisms)
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Bodys response to Apoptosis no
inflammation
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Ischaemia Reperfusion Injury
Causes
Oxygen radicals during reoxygenation damage
the mitochondrial membrane Xss Oxygen radicals are toxic to the cell
Cytokines from adjacent dead cells attract
polymorphs
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OEDEMA (EDEMA)
Definition is an increase in interstitial water.
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ECF
l m
3 litres 9 litres of
Intravascular fluid Interstitial fluid
(plasma high ) (low protein
content) content)
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ECF contains practically all body sodium,
whereas intracellular fluid has a high
potassium and magnesium concentration.
Interstitial fluid has a low colloidal osmotic
pressure.
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Fluid collections in body cavities
Hydrothorax
Hydropericardium
Hydroperitoneum (ascites)
More commonly referred to as effusions
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Hydrostatic pressure pushes fluid out of vessel
Oncotic pressure -due to high protein in vessel
-pulls fluid into vessel. Lymphatics also play a
role in removal of interstitial fluid.
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Factors which cause oedema
Inflammation
Increased Hydrostatic Pressure in Vessels
Local or generalised venous obstruction
Na & Water retention
Lymphatic Obstruction
Low intravascular protein levels
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Reduced plasma osmotic pressure
Liver Failure
Nephrotic Syndrome
Protein losing enteropathy
Starvation
Malabsorption
Burns