INFLAMMATIONS and types of inflammation (3).ppt

A guide to an introductory general pathology for medical students

1. DR Y.D SHAGARI
Depart. Of histopathology
UDUTH

2. 1.(Concept) Understand the chain, progression, or
sequence of vascular and cellular events in the histologic
evolution of acute inflammation
2.Know the three possible outcomes of acute inflammation
3.Visualize the morphologic patterns of acute inflammation
4.Understand the causes, morphologic patterns, principle
cells, minor cells, of chronic and granulomatous
inflammation
Inflammation (OBJECTIVES)

3. Response of vascularized living tissue to sublethal injuries
The responses consist of two main events which are mediated
by chemical mediators
1.Vascular event
2.Cellular events
The aim of the response are
–Elimination of the offending agent by professional
phagocyte
–Neutralization of the offending agent by plasma proteins
INFLAMMATION

4. “PROTECTIVE” RESPONSE
NON-specific
VASCULAR EVENTS
CELLULAR EVENTS (PMN or
PolyMorphonuclearNeutrophil, Leukocyte?,
“POLY”, Neutrophil, Granulocyte, Neutrophilic
Granulocyte
“MEDIATORS”
ACUTE INFLAMMATION

5. ACUTE INFLAMMATION
Neutrophil
Polymorphonuclear
Leukocyte, PMN, PML
“Leukocyte”
Granulocyte, Neutrophilic
granulocyte
“Poly-”
Polymorph

6. Rubor
Calor
Tumor
Dolor
5
th
(functiolaesa)
HISTORICAL HIGHLIGHTS
(Egypt, 3000 BC)

7. INFECTIOUS
PHYSICAL
CHEMICAL
Tissue Necrosis
Foreign Bodies (FBs)
Immune “responses”, or “complexes”
STIMULI ( CAUSES) FOR ACUTE
INFLAMMATION

8. 1.Changes in Vascular Flow and Caliber
2.Increased Vascular Permeability
VASCULAR CHANGES

11. •DILATATION
•Endothelial “gaps”
•Direct Injury
•Leukocyte Injury
•Transocytosis (endo/exo)
•New Vessels
INCREASED PERMEABILITY

12. EXTRAVASATION OF PMNS
1.MARGINATION
(PMN’s go toward
wall)
2.ROLLING
(tumbling and
HEAPING)
3.ADHESION
4.TRANSMIGRATI
ON
(DIAPEDESIS)

13. SECRETINS(from endothelial cells)
INTEGRINS(from many cells)
Secretinsand integrinsare classes of substances to help neutrophils
stick to vessel walls and migrate through the wall. They are Cellular
Adhesion Molecules.
ADHESION MOLECULES
(GLYCOPROTEINS) AFFECTING
ADHESION AND TRANSMIGRATION

14. PMNs going to the site of “injury”
AFTER transmigration
CHEMOTAXIS

15. “triggered” by the offending stimuli for PMNs to:
1) Produce eicosanoids(arachidonicacid
derivatives)
Prostaglandin (and thromboxanes)
Leukotrienes
Lipoxins
2) Undergo DEGRANULATION
3) Secrete CYTOKINES
LEUKOCYTE “ACTIVATION”

16. PHAGOCYTOSIS
RECOGNITION
ENGULFMENT
KILLING
(DEGRADATION)

17. •From plasma or cells
•Have “triggering” stimuli
•Usually have specific
targets
•Can cause a “cascade”
•Are short lived
CHEMICAL MEDIATORS

19. HISTAMINE
SEROTONIN
COMPLEMENT
KININS
CLOTTING FACTORS
EICOSANOIDS
NITRIC OXIDE
PLATELET
ACTIVATING FACTOR
(PAF)
CYTOKINES
CHEMOKINES
LYSOSOME
CONSTITUENTS
FREE RADICALS
CLASSIC MEDIATORS

20. 100% complete RESOLUTION
SCAR
CHRONICinflammation
OUTCOMES OF
ACUTE INFLAMMATION

22. Serous(watery)
Fibrinous(hemorrhagic, rich in
FIBRIN)
Suppurative(PUS)
Ulcerative
MORPHOLOGIC PATTERNS
OF ACUTE INFLAMMATION
(EXUDATE)

23. BLISTER, “Watery”, i.e., SEROUS

24. FIBRINOUS

25. PUS
=
PURULENT
ABSCESS
=
POCKET
OF
PUS
=
NEUTROPHILS

26. NORMAL 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
SEQUENCE OF EVENTS

27. Inflammation of chronic duration (weeks & month)
–Active inflammation
–Tissue destruction
–An attempt at healing
Proceed simultaneously
It may
–Follow acute inflammation
–lung abscess complicating lobar Pneumonia
–Repeated bout of acute inflammation
–Cholecystitis and pyelonephritis
–Begin insidiously as low grade smoldering response
CHRONIC INFLAMMATION

28. CHRONIC NONSPECIFIC INFLAMMATION
CHRONIC GRANULOMATOUS INFLAMMATION
TYPES OF CHRONIC INFLAMMATION

29. It’s a distinctive form of chronic inflammation
cause by
–Certain form of infectious organism
–And non infectious organism
Characterized by formation of granuloma
Accumulation of modified or activated macrophages
Immune reaction are usually involved in the formation of
granuloma
Cellular attempt at containing the offending agent
Activation of macrophage lead to tissue destruction
CHRONIC GRANULOMATOUS
INFLAMMATION

30. Focus of chronic inflammation consisting of
microscopic aggregation of transformed
macrophages Epitheliod cells Surrounded by collar
of lymphocyte and fibrosis
Fusion of the two or more epitheliod cells
gives rise to giant cells
GRANULOMA

31. 1) PERSISTENCEof Infection
2) PROLONGED EXPOSURE to
insult
3) AUTO-IMMUNITY
CAUSES OF
CHRONIC INFLAMMATION

32. LYMPHOCYTES
MACROPHAGES (aka,
HISTIOCYTES)
PLASMA CELLS
EOSINOPHILS
MAST CELLS
CELLULAR PLAYERS

33. INFILTRATION
TISSUE DESTRUCTION
HEALING
MORPHOLOGY

34. GRANULOMAS
GRANULOMATOUS INFLAMMATION
4 COMPONENTS
FIBROBLASTS
LYMPHS
HISTIOCYTES
“GIANT” CELLS

35. GRANULOMAS
GRANULOMATOUS INFLAMMATION
CASEATING (TB)
NON-CASEATING

36. DIFFERENTIAL DIAGNOSIS OF GRANULOMATOUS
LESION

37. •FEVER, CHILLS
•C-Reactive Protein (CRP)
•“Acute Phase” Reactants, i.e., α1-α2
•Erythrocyte Sedimentation Rate
(ESR) increases
•Leukocytosis
•Pulse, Blood Pressure
•Cytokine Effects, e.g., TNF(α), IL-1
SYSTEMIC MANIFESTATIONS
(NON-SPECIFIC)

38. Thank you