1. The document defines and classifies inflammation as either acute or chronic based on duration and predominant cell types. 2. Acute inflammation is short-term, involving increased vascular permeability and neutrophil infiltration, while chronic inflammation lasts weeks to years with lymphocytes and macrophages predominant. 3. Chronic inflammation can lead to tissue damage through macrophage release of reactive oxygen species and is associated with conditions like cancer, fibrosis and impaired tissue function.

1. QPT 10102
Dr.Mohanad
Acute inflammation &
Chronic inflammation

2. Definition
• Inflammation is a defensive process that a living body initiates
against local tissue damage. It takes the form of a complex
reaction of blood vessels, certain plasma components and blood
cells, and cellular and structural components of connective tissue.
• Terms ending in the suffix “–itis” denote inflammation.

3. The classification of inflammation
• According to the course:
• acute,
• subacute,
• chronic
• According to the predominant phase:
• alterative,
• exudative,
• proliferative (productive)
• According to the causative factors:
• Trivial,
• Specific

4. Acute,subacute and chronicinflammation
• Acute inflammation
− Has a short duration, ranging from a few hours to a few days.
• Vascular and exudative processes predominate. Marked clinically by the signs of heat,
redness, swelling, pain, and loss of function. Neutrophils are often predominant;
lymphocytes may be present.
• Exudative-productive inflammation
• Subacute inflammation
• The period between acute and chronic inflammation and may last 2 to 6 weeks
• Chronic inflammation
− Inflammation of prolonged duration, usually weeks to months and even years.
• The response is characterized predominantly by lymphocytes and macrophages, tissue
necrosis, and accompanied by tissue repair, such as healing, fibrosis, and granulation
tissue formation, all of which may occur simultaneous−
• Exudative-productive inflammation

5. How do these changes combat injury?
• Vasodilatation:
• Increases delivery, increases temperature, removes toxins.
• Exudate:
• Delivers immunoglobulins etc., dilutes toxins, delivers fibrinogen, increases lymphatic
drainage.
• Increased lymphatic drainage:
• Delivers bugs to phagocytes and antigens to immune system.
• Cells:
• Removes pathogenic organisms, necrotic debris etc.
• Pain and loss of function:
• Enforces rest, reduces chance of further traumatic damage.
• How is all this brought about?

6. Morphology
Erythema and swelling are present with sparse leukocytic
infiltrate.

7. THE FLUID
Definitions
• A TRANSUDATE has a low protein content, usually caused by
alterations in hydrostatic or oncotic pressure.
Implies a hydrostatic (pressure) problem.
• An EXUDATE has a high protein content, caused by increased
vascular permeability Implies an inflammatory process.

8. Differential characteristic
• Transudate
1. Transparent liquid
2. Origin - congestion
3. Up to 3% protein
4. Isolated mesothelial cells,
accidental single leukocytes and
erythrocytes
• Exudate (serous)
1. Slightly not quiet clear liquid
2. Origin - inflammatory
3. 3-5% protein
4. A small amount of leukocytes
desquamated epithelium,
mesothelium

9. Exudative Inflammations
General definition: inflammations whose principal histologic findings include
exudation of blood serum and extravasation of blood cells into the inflamed
area.
may be classified as follows according to the principal components of the exudate:
• Serous
• Catarrhal
• Fibrinous
• Purulent
• abscess and empyema
• Hemorrhagic

10. Serous Inflammation
Definition: Accumulation of fluid relatively rich in protein on body surfaces, especially
serous surface, represents serous inflammation.
Biologic purpose: Immediate dilution of the harmful agent at the site of
inflammation.
Etiologic factors:
— hypersensitivity reactions;
— bacterial and viral tissue injury;
— physical and chemical tissue injury.

11. Catarrhal Inflammation
Definition: Exudative inflammation occurring exclusively on the mucous
membranes of the respiratory and gastrointestinal tracts and producing a
watery exudate of serum and mucus.
Grossly the surface appears reddened and swollen and may be covered with
or contain, a clear to slightly opaque, thick fluid
Etiologic factors:
— hypersensitivity reactions;
— bacterial and viral tissue injury;
— physical and chemical tissue injury.

12. Morphology
The mucosa and submucosa appear reddened and
swollen, with a slight degree of lymphocytic infiltration.

13. 13

14. Fibrinous Inflammation
Definition: Exudative inflammation with exudation of fibrinogen- containing
serum that polymerizes to fibrin outside the blood vessels.
Biologic purpose: Immediate temporary barrier against additional
effects of inflammation.
Etiologic factors:
— Infectious toxic tissue injury;
— Tissue injury from physical trauma;
— Chemical and toxic tissue injury;
— Excretion of toxic metabolites (uremic toxins);
— Ischemic tissue injury.

16. 16

17. Purulent Inflammation
General definition: Inflammation with exudate consisting primarily of died neutrophils
and cellular debris.
The predominant feature of the exudate is the formation of pus, a creamy liquid
Biologic purpose: Damaged tissue is dissolved along with the pathogen.
Etiologic factors – pyogenic bacteria:
•Staphylococci
•Streptococci
Types: empyema, phlegmon, abscess, pus

18. Empyema
Definition: Suppurative inflammation in a
body cavity.
Pathogenesis: An empyema usually occurs when a
suppurative inflammation of an organ breaks through into
an adjacent cavity.
Examples:
• Pericardial, peritoneal, and pleural empyema
• Gallbladder and appendiceal empyema;
• Middle ear and nasal sinus empyema;
• Pyosalpinx (pus in the uterine tube);
• Pyocephalus (pus in the cranial cavity);
• Hypopyon (pus in the anterior chamber of the eye).

19. Hemorrhagic Inflammation
Definition: Exudative inflammation involving microvascular injury with massive
microvascular bleeding, producing an exudate with a high erythrocyte content.
Biologic purpose: Exudative inflammation due to severe vascular
injury.
Morphology: The inflamed area is usually necrotic and filled with blood.
Etiologic factors:
— bacterial exotoxins and endotoxins;
— viral cytopathic effect on endothelium;
— proteolytic tissue destruction;
— cytotoxic injury in hypersensitivity type III.

21. Different morphological patterns of acute inflammation can be found
depending on the cause and extend of injury and site of inflammation
Serous inflammation
Fibrinous inflammation
Purulent inflammation
ulcers

22. SYSTEMIC EFFECTS OF ACUTE
INFLAMMATION
• Acute phase response
• Decreased appetite, altered sleep patterns and changes in
plasma concentrations of:
• C-reactive protein (CRP) (Clinically useful)
• 1 antitrypsin
• Haptoglobin
• Fibrinogen
• Serum amyloid A protein

23. ACUTE INFLAMMATION:
RESOLUTION.
• What may happen after the development of acute inflammation?
1) Complete resolution.
2) Continued acute inflammation with chronic inflammation; chronic suppuration.
3) Chronic inflammation and fibrous repair, probably with tissue regeneration.
4) Death.

24. RESOLUTION OF ACUTE INFLAMMATION
• Morphology
• Changes gradually reverse.
• Vascular changes stop:
• neutrophils no longer marginate
• vessel permeability returns to normal
• vessel calibre returns to normal.

25. RESOLUTION OF ACUTE INFLAMMATION
MECHANISMS
• Therefore:
1. Exudate drains to lymphatics
2. Fibrin is degraded by plasmin and other proteases
3. Neutrophils die, break up and are carried away or are phagocytosed
4. Damaged tissue might be able to regenerate.
• Note that if tissue architecture has been destroyed, complete
resolution is not possible.

26. MECHANISMS OF RESOLUTION
5. All mediators of acute inflammation have short half-lives.
6. May be inactivated by degradation, e.g. heparinase
7. Inhibitors may bind, e.g. various anti-proteases.
8. May be unstable e.g. some arachidonic acid derivatives
9. May be diluted in the exudate, e.g. fibrin degradation products.
10. Specific inhibitors of acute inflammatory changes
e.g. lipoxins, endothelin...

27. Hepatic abscess

28. Tissue oedema Neutrophil margination …. And emigration

29. CHRONIC INFLAMMATION
Chronic inflammation is inflammation of prolonged duration (weeks to months to years) in which
active inflammation, tissue injury, and healing proceed simultaneously.
CAUSES OF CHRONIC INFLAMMATION
• Chronic inflammation arises in the following settings:
• Persistent infections by microorganisms (mycobacteria)
• Excessive and inappropriate activation of the immune system (autoantigens evoke
a self-perpetuating immune reaction)
• Prolonged exposure to potentially toxic agents, either exogenous or endogenous
(asbestosis)
• What is chronic inflammation?
• Characterised by the microscopic appearances.
• Most important characteristic is the type of cell present.

30. Chronic inflammation: tissue effects
Knee joint in rheumatoid arthritis

31. Chronic inflammation: tissue effects
Chronic cervicitis

32. Granulomatous inflammation: tissue
effects

33. Chronic inflammation = tissue damage
• Chronic inflammation - macrophages in the injured tissue.
• Macrophages release toxins (including reactive oxygen
species or ROS) that injure tissues
• chronic inflammation is almost always accompanied by tissue
destruction.
Normal tissue
Tissue : chronic inflammation

34. Chronic inflammation and tissue damage
Reduce
d tissue
functio
n
Tissue
damage
Chronic
inflammatio
n
Activation
of immune
cells
Killing of host cells

35. Chronic inflammation and Cancer
ROS
O2
-
OH- DNA
Mutatio
n
Cancer

36. Cells of the chronic inflammatory response
• Lymphocytes
• Monocytes/ macrophages
• Plasma cells

37. Macrophages
• Derived from blood monocytes. Various levels of ‘activation’.
• Functions:
• Phagocytosis and destruction of debris & bacteria
• Processing and presentation of antigen to immune system.
• Control of other cells by cytokine release
• Synthesis; not only cytokines, but also complement components, blood
clotting factors, proteases, ....

38. Macrophages

39. Lymphocytes

40. Lymphocytes
• Sometimes called ‘chronic inflammatory cells’
(but note they are a normal component of some tissues)
• Functions:
• Complex, mainly immunological.
• B lymphocytes differentiate to produce antibodies.
• T lymphocytes involved in control & some cytotoxic functions.
(See Immunology teaching)

41. Other cells involved in chronic inflammation
• Plasma cells:
• Differentiated antibody-producing B lymphocytes. Implies
considerable chronicity.
• Eosinophils:
• Allergic reactions, metazoal infestations, some tumours.
• Fibroblasts / Myofibroblasts:
• Recruited by macrophages; make collagen. See next lecture.

42. Eosinophils
Plasma cells

43. ‘Giant’ Cells
• Multinucleate cells made by fusion of macrophages. Several
types.
• Morphology of most chronic inflammatory reactions is non-specific,
BUT proportions of each cell type may vary in different conditions.
• For example:
• Rheumatoid arthritis: Mainly plasma cells.
• Chronic gastritis: Mainly lymphocytes.
• Leishmaniasis (a protozoal infection): Mainly macrophages.
• Giant cell type may be a help to diagnosis.

44. Langhans type giant cell - Tuberculosis

45. EFFECTS OF CHRONIC INFLAMMATION
• Fibrosis
• (see next lecture)
• e.g. gall bladder (chronic cholecystitis), chronic
ulcers..
• Impaired function
• e.g. chronic inflammatory bowel disease
• Rarely, increased; e.g. mucus secretion,
thyrotoxicosis
• Atrophy
• e.g. gastric mucosa, adrenal glands
• Stimulation of immune response
• Macrophage - lymphocyte interactions