1. Assist. Prof.Dr. Baydaa H. Abdullah
Acute inflammation
Assist. Prof.Dr. Baydaa H. Abdullah

2. The body’s response to injury
Inflammation
Is a protective response
The body’s response to injury
Interwoven with the repair process

3. Inflammation Types Acute (sec, mins, hrs)
Chronic (days, weeks, months, yrs)

4. Causes of inflammation
Bacterial
Viral
Protozoal
Metazoal
Fungal
Immunological
Tumours
Chemicals, toxins etc
Radiation

5. The Cardinal Signs of Acute Inflammation
RUBOR
CALOR
TUMOR
FUNCTIO LAESA

6. Cardinal signs of inflammation

7. Cardinal signs of inflammation

8. Cardinal signs of inflammation

9. Cardinal signs of inflammation

10. Cardinal signs of inflammation

11. Cardinal signs of inflammation

12. Inflammation The basis of the five cardinal signs
Increased blood flow due to vascular dilatation gives redness and heat.
Increased vascular permeability gives oedema causing tissue swelling.
Certain chemical mediators stimulate sensory nerve endings giving pain. Nerves also stimulated by stretching from oedema.
Pain and swelling result in loss of function.
2nd Yr Pathology 2010

13. Components of acute and chronic inflammation
2nd Yr Pathology 2010

14. Cell of the acute inflammatory response
Polymorphonuclear leukocyte

15. The process of inflammation

16. The phases of inflammation
FIRST THERE IS VASCULAR DILATATION followed by exudation of protein-rich oedema fluid which floods the area, dilutes toxins, allows immunoglobulins to opsonise bacteria and provides substrate (fibrinogen) for fibrin scaffold.
SECOND THERE IS ACTIVE EMIGRATION OF POLYMORPHS through vessel wall and along the chemotactic gradient to the site of injury

17. The phases of inflammation
THE VASCULAR PHASE OF INFLAMMATION
Fluid escapes from vessels because of endothelial cell (EC)
retraction, opening up gap-junctions.
The vessels which are normally involved are the post-capillary
venules where the EC have high affinity receptors for histamine.
Severe EC injury leads to leakiness of all vessels
capillaries, venules and arterioles - giving acute local oedema,
e.g. blister formation after a burn.

18. Recognition and attachment
PHAGOCYTOSIS
Recognition and attachment
Foreign objects coated with opsonins IgG and C3b which attach to
receptors on polymorph surface.
Engulfment
Cell membrane fuses around an object: at the some time lysosomes
empty into the vacuole, often before vacuole has time to seal - this gives
rise to 'regurgitation during feeding' and enzymatic damage to surrounding
tissue.
Killing or degradation
H2O2, hypohalous acid (HOC1) produced by myeloperoxidase and
superoxides kill bacteria. Lysozyme digests them.
2nd Yr Pathology 2010

19. Summary of acute inflammation
Stimulated by physical injury, infection, foreign body
Resident macrophages and/or damaged endothelium, mast cells—IL-1, TNF, endothelin, histamine
Vascular response: vasodilation, endothelial contraction, exudation of plasma
Neutrophils: marginate (selectin-glycoprotein), adhere (integrin-CAM), extravasate (CD31), migrate (IL-8, chemotactic stimuli)
Phagocytosis: recognition, engulfment, killing
Phagocytosis receptors bind mannose, oxidized lipids, lipopolysaccharides, lipoteichoic acids, opsonins
Killing is O2-dependent (respiratory burst, NADPH oxidase generated H2O2; myeloperoxidase generated HOCl; iNOS generated NO) or independent (lysozyme, lactoferrin, defensins)
Responding leukocytes cause pain and loss-of-function via prostaglandins, enzymes
Complete resolution; fibrosis, organization or scarring; abcess formation; progression to chronic inflammation
Acute inflammation is a stereotyped response to a septic or sterile stimulus. Circulating neutrophils respond first. Response is receptor-mediated. Outcome varies according to the type and severity of initiating stimulus. Acute inflammation may progress to chronic inflammation, but more often chronic inflammation is not easily associated with an initial bout of acute inflammation.

20. Outcomes of Acute Inflammation
Resolution of tissue structure and function with elimination of stimulus
Tissue destruction and persistent inflammation
Abscess
pus-filled cavity (neutrophils, monocytes and liquefied cellular debris)
walled off by fibrous tissue and inaccessible to circulation
tissue destruction caused by lysosomal and other degradative enzymes
Ulcer
loss of epithelial surface
acute inflammation in epithelial surfaces
Fistula
abnormal communication between organs or an organ and a surface
Scar
Causes distortion of structure and sometimes altered function
Chronic inflammation
Marked by replacement of neutrophils and monocytes with lymphocytes, plasma cells and macrophages
Accompanied by proliferation of fibroblasts and new vessels with scarring

21. Outcomes of Acute Inflammation
Resolution of tissue structure and function with elimination of stimulus
Tissue destruction and persistent inflammation
Abscess
pus-filled cavity (neutrophils, monocytes and liquefied cellular debris)
walled off by fibrous tissue and inaccessible to circulation
tissue destruction caused by lysosomal and other degradative enzymes
Ulcer
loss of epithelial surface
acute inflammation in epithelial surfaces
Fistula
abnormal communication between organs or an organ and a surface
Scar
Causes distortion of structure and sometimes altered function
Chronic inflammation
Marked by replacement of neutrophils and monocytes with lymphocytes, plasma cells and macrophages
Accompanied by proliferation of fibroblasts and new vessels with scarring

22. Outcomes
Resolution
The complete restoration of the inflamed tissue back to a normal status. Inflammatory measures such as vasodilation, chemical production, and leukocyte infiltration cease, and damaged parenchymal cells regenerate. In situations where limited or short lived inflammation has occurred this is usually the outcome.
Fibrosis
Large amounts of tissue destruction, or damage in tissues unable to regenerate, can not be regenerated completely by the body. Fibrous scarring occurs in these areas of damage, forming a scar composed primarily of collagen. The scar will not contain any specialized structures, such as parenchymal cells, hence functional impairment may occur.

23. Outcomes Abscess formation
A cavity is formed containing pus, an opaque liquid containing dead white blood cells and bacteria with general debris from destroyed cells.
Chronic inflammation
In acute inflammation, if the injurious agent persists then chronic inflammation will ensue. This process, marked by inflammation lasting many days, months or even years, may lead to the formation of a chronic wound. Chronic inflammation is characterised by the dominating presence of macrophages in the injured tissue. These cells are powerful defensive agents of the body, but the toxins they release (including reactive oxygen species) are injurious to the organism's own tissues as well as invading agents. Consequently, chronic inflammation is almost always accompanied by tissue destruction.

24. Patterns of Inflammation
Serous Inflammation
Marked by outpouring of thin fluid
From blood serum, e.g. burn blisters
Effusion from mesothelial cells lining the pleural, peritoneal and pericardial cavity
Fibrinous Inflammation
A feature of pericardial and peritoneal inflammation
Vascular permeability allows larger molecules like fibrin to pass or procoagulant stimulus exists in the interstitium (e.g. cancer cells)
Suppurative Inflammation
Characterized by production of large amount of pus composed of neutrophils, necrotic cells and edema fluid
Involves pyogenic bacteria e.g. Streptococci and Staphylococcus aureus
Abscesses are focal localized collections of purulent inflammatory tissue caused by suppuration.
Ulcers
Local defect or excavation of the surface of an organ or tissue by sloughing of inflammatory necrotic tissue
Acute stage - intense polymorphonuclear infiltration and vascular dilation in margin
Chronic stage - margin and base develop fibroblastic proliferation, scarring and accumulation of lymphocytes, plasma cells and macrophages

25. Systemic inflammatory response
Acute Phase Response
Fever
Acute-phase protein secretion from liver
Leukocytosis
Tachycardia, increased blood pressure
Shivering, chills
Anorexia, somnolence, malaise
Septic shock