inflammation

1. INFLAMMATION
JOMIN GEORGE
LECTURER
FACULTY OF HEALTH INFORMATION MANAGEMENT
Email: jomin.george@bothouniversity.ac.bw

2.  Inflammation:
 Overview of the process.
 cardinal signs of Inflammation.
 Acute and chronic inflammation.
 Mediators of inflammation(histamine,serotonin,
prostaglandin, Nitric Oxide & cytokines)

3. Definition:
• Inflammation is a local response (reaction) of living
vasculaized tissues to endogenous and exogenous stimuli.
• The term is derived from the Latin "inflammare"
• meaning to burn.
• Inflammation is fundamentally destined to localize and
eliminate the causative agent and to limit tissue injury.

4. • INFLAMMATION – The Sum Of
Host’s Defense To Infectious
Noxious Stimuli.

5. AIMS
To bring defense cells (Immune cells ) to
the area.

6. Cont..
Inactivate or destroy
invaders
or
Begin repair

7. Inflammation clinically denoted by suffix – itis
Example  Dermatitis

9. Histamine
Kinins
Leukotrienes
Prostaglandins
Interleukin -1
Process Injury
WBC
Chemicals

10. Causes
• Injury
Microbial infections
Physical trauma
Allergens (no injury)

11. Inflammatory responses
• 1. Serves to isolate and destroy noxious agents and prepare
the tissue for healing
• Includes: - erythema
Vasodilation
Increase blood
flow to the area

12. Cont..
2. increase capillary permeability
increase movement of antibody proteins
out of the blood stream
H2O
Swelling

13. Cont..
• 3. Activate local pain fibers  Pain
Why
PAIN?????????????

14. Cont..
4. Attract WBCs to the injury & activate
Phagocytosis.
Chemotaxis
A unidirectional attraction of leukocytes from vascular channels towards the site of
inflammation within the tissue space guided by chemical gradients (including
bacteria and cellular debris) is called chemotaxis.
Neutrophils (phagocytes) and monocytes (
macrophages)

15. Summary

16. Injurious agents Cell damage
Capillaries leaky
Heat
Clotting proteins
enter
Remove
dead/pathogens
Neutrophils &
monocytes enter the
area
Release
chemicals
Pain
Too much blood edema
Antibodies enter
Blood vessel dilate
redness
Nutrients & O2
Fibrin barrier
Fever

17. • These signs are:
– rubor (redness)
– tumor (swelling)
– calor (heat)
– dolor (pain)
– functio laesa, or loss of function (In the
second century AD, the Greek physician
Galen added this fifth cardinal sign)
cardinal signs of inflammation.

18. • Inflammation may be acute or chronic
ACUTE OR CHRONIC
Depending on the nature of the
stimulus
Effectiveness of the initial reaction
in eliminating the stimulus
The damaged tissues.

19. Acute Inflammation
Acute inflammation is an immediate and
early response to an injurious agent and it is
……..

20. • Relatively of short duration.
• lasting for minutes.
• several hours or few days.
• It is characterized by exudation of fluids and plasma proteins
• the emigration of predominantly neutrophilic leucocytes to
the site of injury.

21. Major components/ Hallmark
Reaction of blood vessels.
Reaction of Leukocytes.

22. Reaction of blood vessels.
Changes in the vascular flow and caliberIncreased vascular permeability
• Vasodilation & increased blood flow.
• Increased vascular permeability.
• Slow of blood flow.
• Stasis
• Reactions of leukocytes.
• Exudation. ( protein escape)
• Edema. ( Excess fluid )
• Pus. ( rich in neutrophils)

23. • The escape of fluid, proteins, and blood cells from the vascular system into the
interstitial tissue or body cavities is known as exudation.
• Transudate is a fluid with low protein content (most of which is albumin), little or no
cellular material, and low specific gravity. It is essentially an ultra filtrate of blood
plasma that results from osmotic or hydrostatic imbalance across the vessel wall
without an increase in vascular permeability
• Pus, a purulent exudate, is an inflammatory exudate rich in leukocytes (mostly
neutrophils), the debris of dead cells and, in many cases, microbes.

25. Reaction of Leukocytes.
Leukocyte activationExtravasation

26. Mediators of Inflammation
Inflammatory mediators are soluble,
diffusible molecules that act locally at the
site of tissue damage and infection, and at
more distant sites.

27. It can be…
Platelets, Neutrophils, monocytes and mast cell .
(histamine, serotonin, prostaglandin, Nitric oxide &
cytokines
????????????
Cell
Plasma
protein
TABLE 2-4 -- The Actions of the Principal Mediators of
Inflammation

28. Cell Mediated

30. Chronic Inflammation
Chronic inflammation can be defined as a prolonged
inflammatory process (weeks or months) in which active
inflammation, tissue damage and healing occurs at same time.
hi

31. Causes of chronic
inflammation:

32. 1. Persistent infections
• Infection such as tuberculosis, leprosy, certain fungi etc
• These organisms are of low toxicity and evoke delayed
hypersensitivity reactions.

33. 2. Progression from acute inflammation: Acute inflammation
almost always progresses to chronic inflammation following.
• Persistent suppuration as a result of uncollapsed abscess
cavities, foreign body materials (dirt, cloth, wool, etc),
sequesterum in osteomyelitis.

34. 3. Prolonged exposure to toxic substances  either
endogenous lipid components which result in atherosclerosis or
exogenous substances such as silica, asbestos.

35. 4. Autoimmunity. Autoimmune diseases such as rheumatoid
arthritis and systemic lupus erythematosis are chronic
inflammations from the outset.

37. Differences Between Acute and Chronic
Inflammation
Features Acute Inflammation Chronic Inflammation
Onset
Rapid onset Insidious/delayed onset
Duration of Course Short (Days) Long (Weeks to Months)
Specificity Non-specific Specific as it involves Acquired
Immunity
Cardinal Signs Pain (Dolor)
Heat (Calor)
Redness (Rubor)
Swelling (Tumor)
Loss of Function (Functio Leasa)
Absent in any of cardinal signs

38. Classification of chronic inflammation:
• Nonspecific chronic inflammation: This involves a diffuse
accumulation of macrophages and lymphocytes at site of
injury that is usually productive with new fibrous tissue
formations. E.g. Chronic cholecystitis.

39. • Specific inflammation (granulomatous inflammation):
• Granulomatous inflammation is a distinctive pattern of chronic
inflammation. It is produced by limited number of infectious and
some noninfectious conditions and involves immune reaction.
• Granulomatous inflammation is characterized by the presence of
granuloma.

40. Granuloma
• Granuloma is an inflammation found in many diseases. It is a
collection of immune cells known as macrophages.
Granulomas form when the immune system attempts to wall
off substances that it perceives as foreign but is unable to
eliminate.

42. Consequences of defective &excessive
inflammation
• Defective inflammation typically results in increased
susceptibility to infections.
• The inflammatory response is a central component of the
early defense mechanisms.

43. So what will happen..
• Delayed wound healing, because inflammation is essential for
clearing damaged tissues and debris.
• Provides the necessary stimulus to get the repair process
started.

44. • Excessive inflammation is the basis of many types of human
disease.
• Allergies  immune responses develop against normally
tolerated self-antigens.

45. Morphologic types of acute inflammation:
• Serous Inflammation  Serous inflammation is marked by the outpouring of a
thin fluid that may be derived from the plasma or from the secretions of
mesothelial cells lining the peritoneal, pleural, and pericardial cavities.
• Accumulation of fluid in these cavities is called an effusion.
• The skin blister resulting from a burn or viral infection

46. Fibrinous Inflammation
• The exudate which is rich in fibrin is called fibrinous exudate.
• It develops when the vascular leakage allows exudation of
fibrinogen which is then converted to fibrin.
• Eg: Fibrinous pericarditis  Bread and butter pericarditis.

47. SUPPURATIVE OR PURULENT
INFLAMMATION; ABSCESS
• This type of inflammation is characterized by the production
of large amounts of pus or purulent exudate consisting of
neutrophils, liquefactive necrosis, and edema fluid. Certain
bacteria (e.g.staphylococci) produce this localized
suppuration and are therefore referred to as pyogenic (pus-
producing) bacteria.

48. • A common example of an acute suppurative inflammation is
acute appendicitis.
• Abscesses are localized collections of purulent inflammatory
tissue caused by suppuration buried in a tissue, an organ, or a
confined space.

49. ULCERS
• An ulcer is a local defect, or excavation, of the surface of an
organ or tissue that is produced by the sloughing (shedding)
of inflamed necrotic tissue.
• It is most commonly encountered in the mucosa of the
mouth, stomach, intestines