INFLAMMATION PART II BY PRO.DR.SOHEIR SAAD

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INFLAMMATION
PROF.SOHEIR SAAD
PART II
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Non suppurative inflammation Includes

• Catarrhal inflammation.
• (2) Serous inflammation
• (3) Sero-fibrinous inflammation.
• (4) Fibrinous inflammation.
• (5) Membranous inflammation.
• (6) Haemorrhagic inflammation.
• (7) Necrotizing inflammation.
• (8) Allergic inflammation.

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NON-SUPPURATIVE INFLAMMATION

• Cattarhal inflammation
• (e.g. rhinitis, gastritis, colitis.)
• When mild inflammation of the mucous membrane
  stimulate excess mucous secretion, the exudate is
  thick and viscid.
• When secondary pyogenic infection supervenes,
  it becomes mucopurulent inflammation.
• The exudate contains mucous and pus

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(1)Cattarhal inflammation
(e.g. rhinitis, gastritis, colitis.)

• When mild inflammation of the mucous membrane
  stimulate excess mucous secretion, the exudate is
  thick and viscid.
• When secondary pyogenic infection supervenes, it
  becomes mucopurulent inflammation.
• The exudate contains mucous and pus

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Produces thin serous exudate with low fibrin
content e.g. blisters of superficial burns.
2. Serous inflammation
By increasing the content of fibrin in the
exudate, you get serofibrinous inflammation
This is a feature of inflammation of serous and
synovial membranes e.g. pericarditis, pleurisy,
arthritis.
4.serofibrinous inflammation
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Still with more fibrin in the exudate, It
results fibrinous inflammation, the best
example for this type is lobar pneumonia. This is
because the invading organisms are virulent
producing severe injury to the vascular
endothelium thus allow more leakage of the large
fibrin molecule.
4.fibrinous inflammation
5. Haemorrhagic
The presence of large number of red cells in the
exudate indicates severe damage to the
blood vessel, so allows more diapedesis of
RBC, and the inflammation is called Haemorrhagic
e.g. plague, and anthrax.
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Anthrax infection in humans presents as a
boil-like skin lesion that eventually forms an
ulcer with a black center (eschar). The black
eschar often shows up as a large,
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6. Pseudomembranous inflammation

• When there is severe damage to the mucous
  membrane caused by the exotoxins liberated from
  the invading organism like the diphtheria
  bacillus, or the chigella chiga (causing
  bacillary dysentery)
• The desquamated epithelium become mixed with the
  fibrinous inflammatory exudate to form a
  pseudomembrane.

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• Occurs whenever the inflammation is severe
  resulting in thrombosis of the
  veins in the area, leading to ischaemic necrosis.
  
• This may be followed by putrefaction and end with
  gangrene e.g. gangrenous appendicitis.

Gangrenous necrotizing inflammation
The fluid is usually serous or
serofibrinous, the cellular component is
characterized by an excess of eosinophils e.g.
hypersensitivity reactions (asthma, urticaria).
8. Allergic inflammation
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Non-suppurative inflammation
Name Occur in Characterized by
Catarrhal Mild inflammation in mucous membrane of respiratory or alimentary tracts e.g. common cold and catarrhal appendicitis Exudates rich in mucous
Serous Mild inflammation in serous surface such as pleural cavity, joint cavity where no damage in endothelium ex. Tuberculosis pleurisy and Common blisters Extensive watery low protein exudates
Fibrinous Outpouring of exudates with high protein and less volume ex. in lobar pneumonia due to Streptococcus pneumonia pericardium inflammation Exudates rich in fibrinogen
Membranous Fibrinous inflammation in which network of fibrin entangling inflammatory cells and bacteria forms pseudo-membrane. Example Diphtheria , Bacillary dysentery. Yellowish grey pseudo membrane rich in fibrin , polymorphs necrotic tissues
Hemorrhagic In blood vessels e.g. in plague Exudates rich RBCs
Gangrenous Acute appendicitis Necrotic tissues resulting from thrombi or emboli
Allergic Result to Ag Ab reaction Hypersensitivity Presence of edema increase in vascularity.
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Chemical Mediators
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The Inflammatory Chemical Mediators

• The inflammatory response is precipitated by
  injury, but it is mediated by chemicals derived
  from plasma, cells or damaged tissue.
• The chemical mediators of inflammation are
  usually present within the body in an inactive
  form that is activated by injury.

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The Inflammatory Chemical Mediators

• A) Permeability factors
• 1. Amines.

2. Kinin.
3. Activated fractions. (C3a, C5a
compliment)
4. Prostaglandin.
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B) Chemotactic Factors
(Leucotactic factors)

• 1. Compliment related factors.
• 2. Bacterial factors.

3. Protein stored in PNL granules.
4. Tissue factors.
5. Eosinophilic chemotactic factor of
anaphylaxis.
6. Lymphokines.
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A) Permeability factors These produce
vasodilatation and increased vascular
permeability.

• 1. Amines
• Particularly histamine and serotonin (5
  hydroxytrpytamine) They are stored in granules of
  mast cells, basophils and platelets.
• They are responsible for the early phase of
  acute inflammation (30-90 min).

• 2. Kinin
• They are normally circulating in plasma in an
  inactive form and become activated by the
  presence of antigen antibody complexes, by
  bacterial endotoxin and by polymorph lysosomal
  enzymes.
• The most important of this group is bradykinin.
• Their action is more prolonged, up to 2½ hours.
• They also cause pain

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Activated fractions (compliment)

• They are potent but their action is short lived.
• They cause release of histamine from mast cells.
• C3 component increases vascular permeability.
• C5 component increases vascular permeability
  (more potent than C3). It is also chemotactic for
  neutrophils macrophages
• C5,6,7 complex is chemotactic for neutrophils
  macrophages. It has no permeability effect.

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• It is a long-chain fatty acid present in
  almost all cells, they are rapidly catabolised
  and are not stored in the body.
• Prostaglandin E1 and E2 are thought to be
  important in sustaining the later phases of the
  inflammatory response (3-24 hours).
• They act in part by liberating histamine.
• It also causes pain.
• It is interesting to know that action of
  aspirin and allied drugs as anti-inflammatory,
  antipyretic and analgesic is through inhibiting
  the synthesis of prostaglandin from the injured
  tissue.

4. Prostaglandin
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• (B) Chemotactic (Leucotactic factors)
• They direct the movement of phagocytic cells
  towards the irritant
• Compliment related factors
• (i) Cleavage fragments of C3 and C5, similar but
  not identical with C3a and C5a (anaphylatoxins).
• (ii) C567, an activated component, is chemotactic
  for PNL.
• 2. Bacterial factors
• (i) Soluble low molecular weight products are
  directly chemotactic.
• (ii) Bacterial proteases activate the compliment
  system and cleave C3 and C5.
• 3. Protein stored in PNL granulesHave both
  vasoactive and chemotactic activity.

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4. Tissue factors Tissue injury results in
release of a C3 cleaving enzyme from the damaged
cells. 5. Eosinophilic chemotactic factor of
anaphylaxis Released from sensitized mast cells
on exposure to the specific antigen, e.g. atopic
reaction such as urticaria, hay fever and
asthma. 6. Lymphokines Released by sensitized
lymphocytes in delayed hypersensitivity reactions
is chemotactic for macrophage.
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FATE AND OUTCOME OF ACUTE INFLAMMATION

1. Resolution
2. Healing
3. Spread
4. Chronic inflammation
5. Death
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1. Resolution

• This means complete return of the tissue to
  normal.
• It occurs with mild inflammation provided
  that there
• has been NO tissue destruction.
• The inflammatory exudate reabsorbed and the
  tissues restored to normal, e.g. uncomplicated
  lobar pneumonia.

2. Healing
When the tissues have been destroyed, healing
occur by either repair or regeneration.
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• Direct Spread through tissue spaces e.g.
  cellulitis.
• (ii) Lymphatic Spread Through producing
  lymphangitis and lymphadenitis.
• (iii) Blood spread producing Bacteraemia,
  Toxemia, Septicemia and Pyaemia.

3. Spread
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• Occurs when the organisms are not
• completely destroyed by the defensive
• mechanisms of the host.
• They remain in the body and provoke chronic
  inflammatory and immunologic reactions.
• From toxaemia or involvement of vital organs e.g.
  heart (myocarditis), the brain

4. Chronic inflammation
5. Death
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Outcome of Acute inflammation
spread
Death
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CHRONIC INFLAMMATION
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Chronic INFLAMMATION
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Chronic Inflammation
Chronic Non-Specific
Chronic Specific

• chronic abscess
• chronic sinus
• chronic fistula,
• chronic ulcer.

GRANULOMA
NON Infective Sarcoidosis Forgein body
Infective e.g T.B ,S,B
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• Chronic inflammation occurs when the body cannot
  get rid of the irritant and remains in the body
  in rather a state of equilibrium with the bodys
  defensive mechanisms
• It is a prolonged process in which tissue
  destruction and inflammation are proceeding at
  the same time as attempts at repair i.e..
• 1.Local tissue damage.
• 2. Inflammation response.
• 3. Attempts at healing and repair.

Chronic inflammation
Definition of chronic inflammation
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Causes of chronic inflammation

• (1) Persistence of the agent, which caused the
  acute inflammatory response, e.g. unevacuated
  abscess.
• (2) Insoluble irritant, foreign bodies such as
  silica particles, talc powder, asbestos, catgut
  suture etc.
• (3) Poor local circulation as associated with
  varicose veins of leg.
• (4) Immunologic injury such as Rheumatoid
  arthritis, Crohns disease.
• (5) Resistant microorganisms such as T.B., Lepra
  bacilli.

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General characteristics of chronic inflammation

• Although the histologic appearance vary according
  to the causative factor, yet they all share in
  the following
• The reaction is more proliferative (productive)
  than exudative exudation of fluid
• (2) The cellular reaction is a pleomorphic one,
  consisting mainly of macrophage, lymphocytes and
  plasma cells and sometimes eosinophils, PNL are
  found in considerable number ONLY in chronic
  suppurative lesions, such as chronic abscess,
  chronic osteomyelitis.
• (3) The arterioles show thick walls and narrow
  lumens (endarteritis obliterans) in contrast to
  the changes seen in acute inflammation.
• (4) Fibrosis is a common feature, preceded by
  granulation tissue.
• (5) The chemical inflammatory mediators are
  mainly the lymphokines.

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• In Case of Non-Specific Chronic Inflammation
• The microscopic appearance gives no indication of
  the cause.
• Follows acute inflammation.
• The inflammatory cells are present in a diffuse
  manner with more concentration around blood
  vessels (perivascular infiltration), e.g. chronic
  abscess, chronic sinus, chronic fistula, chronic
  ulcer.

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Chronic Specific Inflammation (Granulomatous
Inflammation)

• It has distinctive histologic appearance
  characteristic of its causal agent, so in most
  cases, it is easy to name the exact causative
  irritant e.g. T.B., Bilharziasis.
• Usually chronic from the start.
• Usually characterized by granuloma formation
  and so called chronic granulomatous inflammation.

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Granuloma

• Is defined as collection of chronic
  inflammatory cells composed largely of
  macrophage, starts as tiny granules, then
  coalesce to form a mass hence the suffix oma
  (tumour).
• Are caused by insoluble particles that induce
  cell mediated immune response.
• The macrophages engulf the foreign material
  and present them to T-lymphocytes which become
  activated to which secrete cytokines, such as
  IL-2 which activate other lymphocytes and IFN-d
  which transform macrophages into epithelioid
  cells and giant cells.

Granulomas
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Activated lymphocytes MQ influence each other
release inflammatory mediators that affects other
cells.
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• Classification of Granuloma-
• Infective caused by
• Bacteria, T.B., leprosy, syphilis, actinomycosis,
  rhino-scleroma.
• b) Parasites e.g. Bilharzia, Leishmania.
• c) Fungi and other microorganism e.g. Madura
  foot.
• 2. Non-infective Foreign body granuloma
• Usually caused by foreign body.
• Endogenous like fat (fat necrosis), cholesterol
  crystal.
• b) Exogenous like silica, asbestos, talc powder,
  insoluble ligatures.
• c) Granuloma of immunologic origin like Aschoff
  body (rheumatic carditis), Crohns disease.

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• Role of Inflammatory Cells in Inflammation
• Phagocytic cells
• Polymorphs
• Engulf bacteria and to a lesser extent
  products of necrotic tissue,
• redominate in the acute inflammatory
  reaction.
• Macrophage predominate in chronic granulomatous
  inflammation, he macrophage is derived from
  blood monocytes, tissue histiocytes,.
• Giant cells They are formed either from fusion
  of many macrophage or by repeated amitotic
  division of one histiocyte. They clean and clear
  the area for repair process. They are responsible
  for the so called demolition phase.

• Types of Giant Cells
• Foreign body giant cells seen in cases of foreign
  body granuloma.
• 2. Langhans giant cells in T.B.
• 3. Aschoff cells of Rheumatic fever.
• 4. Tumour giant cells e.g. Reed-Sternberg cell in
  Hodgkins disease and giant osteoclast in bone
  tumours

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• 2. Cells responsible for the immune reaction
• Lymphocytes
• B-cells for humeral immunity(undergo
  transformation into
• plasma cell (antibody
  producing cell).
• T-cells (CD4 CD8 ) for the cell-mediated
  immune response
• NK). Under antigenic stimulation, the
  B-lymphocytes
• Mast cells which are responsible for the
  secretion of chemical mediators early in the
  inflammatory lesions.
• Eosinophils seen in Allergic and Helminthic
  infection. They also secrete eosinophilic
  chemotactic factor of anaphylaxis.
• Fibroblast They have a major role in the
  process of repair.

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Name Neutrophil Eosinophil Basophil Monocyte Lymphocyte Plasma cell
Microphage Acidophile Basophil Macrophage Histocytes lymphocyte Plasmacyte
Shape Pale pink to blue, Minimal granulation. Red with eosin, Coarse granulation. Blue with eosin, Coarse granulation 1.5 to 2 times larger, Abundant fine granulation Agranular non-granulated, Large round nucleus Basophilic, Encentric nucleus
of WBCs 60-70 1-2 (50 in allergy) 1 4-6 30 Found in tissue only
Function Phagositic 1st defense Unknown but could neutralize histamine, serotonin and other kinins Unknown but contain histamine heparin Phagocytic 2nd defense element engulf bacteria, dead cells, debris dead neutrophils (pus cells) Antibodies production Late stage of the inflammation Primary source of specific Antibodies
Monocytes
Plasma cell
Plasma cell
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Chronic Inflammation
Acute Inflammation

Presence of lymphocytes

• Is rapid in onset
• (typically minutes)

• insidious in onset

• Short duration
• lasting for hours or a few days

• Longer duration

• Characterized by
• exudation of fluid
• plasma (edema)
• emigration of PNLs

• Characterized by

Macrophageproliferation of bl.v. fibrosis
tissue necrosis.
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Comparison between acute and chronic
inflammation
chronic acute
Delayed for months or years Immediate for few days Onset Duration
Persistent infections by microorganisms , Immune-mediated inflammatory diseases,Prolonged exposure to potentially toxic agents Infections Tissue necrosis from any cause, Etiology
The reaction is more proliferative (productive) than exudative predominantly cells lymphocytes Macrophages plasma cells fibroblasts vascular changes, edema, and predominantly neutrophilic infiltration,,and Macrophages Tissue reaction
lymphokines Vasoactive amines mediators
Tissue destruction with attempts for healing and fibrosis. Resolusion,healing,abscess,chronic inflammation outcome
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