Lecture 3 Acute inflammation definition, events, signs and morphological patterns

Describes the events sequence of Acute Inflammation

1. General Pathology
Acute Inflammation I
Dr.Emad Ibrahim Osman

2. What is inflammation

The non-specific response of a
vascularized living tissue to
injury.

3. Function of inflammation
Inflammation is a protective response
intended to eliminate theinitial causeof
cell injury as well as the necrotic cells
and tissues resulting from the original
insult and promote healing.
Its apart ofinnate immunity.
Inflammation is fundamental to virtually
all of clinical medicine.

4. Inflammation Term
To indicate inflammation, add the suffix itis
to the organ or tissuewhich mean
inflammation. For example, colitis is
inflammation of the colon.Meningitis, for
inflammation of the meninges.
Carditis, Gastrointeritis, Pharyngitis..ect..
Exceptions, like
Pneumonia
plurisy

5. Types of inflammation
Inflammation can be acute or chronic.
1.Acute inflammation is rapid in onset and of short
duration, lasting from a few minutes to as long as a few
days, and is characterized by fluid and plasma protein
exudation and a predominantly neutrophilicleukocyte
accumulation.
2.Chronic inflammation takes longer duration (days
to years), and is manifested by influx of lymphocytes
and macrophages with associated vascular proliferation
and fibrosis (scarring).

6. The components of inflammation & their
functions

7. Steps of inflammatory response
The steps of the inflammatory response( 5Rs):-
1)Recognition of the injurious agent.
2)Recruitment of leukocytes.
3)Removal of the agent.
4)Regulation (control) of the response.
5)Resolution (repair).

8. Cardinal Signs
The external manifestations of inflammation(cardinal signs)
result from the vascular changes and cell recruitment:
1.Heat (calor).
2.Redness (rubor).
3.Swelling (tumor).
The two additional cardinal features of acute inflammation,
occur as consequences of mediator elaboration and leukocyte-
mediated damage :
4.Pain (dolor).
5.Loss of function (functiolaesa).

10. ACUTE INFLAMMATION
Acute inflammation is a rapid response to injury
or microbes and other foreign substances that is
designed to deliver leukocytesand plasma
proteinsto the sites of injury.
Acute inflammation has two major components:
1)Vascular changes.
2)Cellular events.
The principal leukocytes in acute inflammation are
neutrophils(polymorphonuclearleukocytes).
TheseInflammatory change is induced bychemical
mediatorsthat are produced byhost cells in
response to injurious stimuli

11. Stimuli for Acute Inflammation:
1.Infections(bacterial, viral, fungal, parasitic)are among
the most common and medically important causes of
inflammation.
2.Trauma(blunt and penetrating)
3.Physicaland chemical agents (e.g., thermal injury, such
as burns or frostbite; irradiation; toxicity from certain
environmental chemicals)
4.Foreign bodies(splinters, dirt, sutures, crystal deposit).
5.Immune reactions (hypersensitivity reactions).
6.Tissue necrosis (from any cause), including ischemia (as
in a myocardial infarct)

12. 1-Vascular changes
1.Transient vasoconstrictionfollowedby arteriolar
vasodilation.
2.Increased blood flowand engorgement of the capillary
beds. (erythemaand warmth).
3.The microvasculature becomes more permeable, protein-
rich fluid moves into the extravasculartissues.
4.This causes the red blood cells to become more
concentrated, thereby increasing blood viscosity and
slowing the circulation ( stasis).
5.Leukocytes (principally neutrophils) begin to accumulate
along the vascular endothelial surface, a process called
margination.

13. As arteriolar vasodilationocurrs, increased volume of
blood flow lead to a rise in intravascular hydrostatic
pressure, resulting in movement of fluid from capillaries
into the tissues.
This fluid, called a transudate,it contains little protein.
Increasing vascular permeabilityallows the movement
of protein-rich fluid and even cells into the interstitium.
This fluid, called Exudate,it contains high protein.
The net result is outflow of water and proteins into the
extravasculartissues.
Fluid accumulation in extravascularspaces is called edema

15. Mechanisms contribute to increased
vascular permeability in acute
inflammatory reactions:
Endothelial cell contraction leading to
intercellular gaps in postcapillary venules
Endothelial injury
Increased transcytosis: Transcytosis occurs
through channels formed by fusion of
intracellular vesicles.
Leakage from new blood vessels, as tissue
repair involves new blood vessel formation
(angiogenesis).

16. 2-Cellular Events:
Leukocyte Recruitment and Activation
I.Leukocyte Recruitment
The sequence of events :-
A.Margination, adhesionto endothelium, and rollingalong the
vessel wall(by the binding of complementary adhesion molecules
on leukocytes and endothelial surfaces)
B.Firm adhesionto the endothelium.
C.Transmigration(diapedesis) between endothelial cells.
D.Chemotaxis: Migration in interstitial tissues toward a
chemotacticstimulus.
Chemotaxinsare (1) bacterial products.
(2) cytokines.
(3) complement system,C5a.
(4) products of the arachidonicacid( LTB4).

18. II.Leukocyte Activation
Leukocytes express on their surface different kinds of
receptorsthat sense the presence of microbes and
lead to their activation.
Leukocyte activation results in the
enhancement of the following functions:
• Phagocytosis of particles and microbes
• Liberation of enzymes & toxinsthat destroy
extracellular microbes and dead tissues
(e.g. NETs).
• Production of mediators, including arachidonic
acid metabolites and cytokines.

19. Phagocytosis
Phagocytosisconsists of three steps:-
(1) Recognitionand attachmentof the
particle to the ingesting leukocyte.
(2) Engulfment, with subsequent formation
of a phagocyticvacuole.
(3) killingand degradation of the ingested
material.

20. A recently discovered mechanism by which neutrophils
destroy extracellular microbes is the formation of
extracellular “traps.”(NETs)

21. Sequence of Events
NORMAL TISSUE HISTOLOGY
VASODILATATION
INCREASED VASCULAR PERMEABILITY
LEAKAGE OF EXUDATE
MARGINATION, ROLLING, ADHESION
TRANSMIGRATION (DIAPEDESIS)
CHEMOTAXIS
PMN ACTIVATION
PHAGOCYTOSIS: Recognition, Attachment, Engulfment,
Killing (degradation or digestion)
TERMINATION
100% RESOLUTION, SCAR, or CHRONIC inflammation

22. MORPHOLOGIC PATTERNS OF
ACUTE INFLAMMATION

23. MORPHOLOGIC PATTERNS OF ACUTE INFLAMMATION
1)Serous inflammation
Is characterized by a relatively protein-poor fluidthat,
depending on the site of injury, derives either from the
serum or from the secretions of mesothelialcells lining
the peritoneal, pleural, and pericardial cavities.
Example: The skin blister resulting from a burn or viral
infection .
Fluid in a serous cavity is called an effusion.

26. 2) Fibrinousinflammation:-occurs as a consequence of
more severe injuries,resulting in greater vascular
permeability that allows large molecules (such as
fibrinogen) to pass the endothelial barrier.
Example: inflammation of meninges, pericardium, and
pleura.
Fate of it, is either degradation by fibrinolysis
(resolution) or failure to completely remove the fibrin
results in the in growth of fibroblasts and blood vessels
(organization) leading ultimately to scarring .

28. 3)Suppurative(purulent) inflammation & Abscess
formation:-
Is characterisedby the presence of large amounts of
purulent exudate(Pus) consisting of neutrophils, necrotic
cells, and edema fluid.
Abscessesare focal collections of pus.
Abscesses typically have a central, largely necrotic region
rimmed by a layer of preserved neutrophils.

30. 4) An ulcer:-
Is a local defect of the surfaceof an organ or tissue that is
produced by necrosis of cells and shedding of inflammatory
necrotic tissue .
It is most commonly encountered in:-
1)Inflammatory necrosis of the mucosa of the mouth, stomach,
intestines, or genitourinary tract.
2)Tissue necrosis and subcutaneous inflammation of the lower
extremities in older persons who have circulatory
disturbances.
During the acute stagethere is polymorphonuclear
infiltration and vascular dilation in the margins of the defect.
In chronic stage, the margins and base of the ulcer develop
scarring with accumulation of lymphocytes, macrophages,
and plasma cells.

32. 5) Phlegmonous (Cellulitis) :-
-it’s a diffuse inflammation of soft
tissues resulting from spreading
effects of substances like
hyaluronidase released by some
bacteria (Streptococcus).

34. 6) Pseudomembranous inflammation
• It’s a inflammatory response of the mucous
surface to toxins of diphtheria or irritant
gases.
• Necrosis & denudation of the epithelium
• Plasma exudates on the surface where it
coagulates & together with the necrosed
epithelium forms a false membrane
Pseudomembranous Colitis (Antibiotic
Associated C.difficile infection)

36. 7) Haemorrhagic inflammation
• Sufficient vascular damage lead to
haemorrhages
-In the bladder: hemorrhagic cystitis,
caused by chemotherapy or Gram-ve
bacteria; the bladder mucosa is swollen,
hyperemic and displays focal hemorrhages
> haematuria
-In the lungs: if influenza virus infects the
alveoli > severe alveolar damage lead to
hemorrhagic pneumonia; frequently fatal.
-(Where else???)

37. Acute hemorrhagic
cystitis:
the bladder mucosa is
swollen, hyperemic
and
displays focal
hemorrhages

38. Outcome of acute inflammation
In acute inflammation there is either:-
1.Eliminationof the stimulus followed by decline of
the reaction and repair of the damaged tissue, or..
2.Persistentinjury resulting in chronic inflammation.

39. Acute inflammation may have one of the four
outcomes:
-Complete resolution
-Scar :Healing by connective tissue replacement
(fibrosis)
-Abscess formation
-Progression of the tissue response to chronic
inflammation

41. The End
Thanks