superficial introduction to the topic for bachelor level

2. Introduction
O Local response of living tissues to injury.
O Causes:
O Infective agents – bacteria, virus, fungi,
toxins, parasites.
O Immunological agents
O Physical agents – heat, cold, radiation,
mechanical trauma
O Inert materials like foreign bodies.
O Prefix –itis (except – boils, abscess,
pneumonia, etc)

4. Signs of inflammation
O Cardinal signs (celsus in 1st century AD)
O Rubor (redness)
O Tumor (swelling)
O Calor (heat)
O Dolor (pain)
O Functio laesa (loss of function) – virchow
Purpose of inflammation
O To dilute, localize and to destroy the injurious
agent.
O To limit tissue injury
O To restore the tissue towards normality.

5. Types
O Acute –
O Short duration (<2 weeks)
O Early body reaction (exudative lesion)
O Resolves quickly
O Usually followed by healing
O Fulminant acute inflammation (severe form)
O Chronic –
O Longer duration
O Occurs if the cause of acute inflammation persists for
a long time. (proliferative lesion)
O Subacute inflammation – phase between acute and
chronic inflammation
O Chronic active inflammation (acute exacerbation)

6. Acute vs. Chronic
Inflammation
Feature Acute chronic
Common cause Pyogenic
organism
Tubercle bacilli,
lepra bacilli, etc
Duration Hours to days Weeks to months
to years
Character Exudative Proliferative
Vascular
phenomenon
Prominent Non prominent
Fluid exudates Marked Scanty
Cellular exudates Earl PMN then
macrophages
Mononuclear cells
in most cases
Repair process Follows it Starts concurrently

7. Acute inflammation
O Aetiology:
O Infection
O Physical injury
O Chemical injury
O Immunologic injury
O Necrosis associated injury
O Idiopathic
O Events:
O Vascular events
O Cellular events

8. Vascular events
1. Haemodynamic changes
O Immediate transient vasoconstriction
O Persistent progressive vasodialation
O Increased local hydrostatic pressure  transudation of
fluid (edema)
O Stasis  leucocytic margination (cellular events)
2. Altered vascular permeability
Mechanisms:
O Contraction of endothelium
O Retraction of endothelium
O Direct injury to endothelium
O Leucocyte mediated endothelial injury
O Leakiness and neovascularization

9. Lewis’ experiment of triple
response
1. Red line within few seconds (local
vasodilation of capillaries and venules)
2. Flare (bright reddish appearance/ flush)
d/t vasodilation of adjacent arterioles.
3. Wheal (swelling/ oedema) d/t
transudation

10. Cellular events
O Change in formed elements of blood 
margination
O Rolling and adhesions
O Selectins, integrins and Ig gene superfamily
adhesion molecules
O Emigration
O WBC + RBC escape (diapedesis)
O Chemotaxis
O Chemokines (leukotrine, complements, cytokines,
soluble bacterial products)
O Phagocytosis
O Recognition and attachment (opsonins)
O Engulfment (via cytoplasmic pseudopods)
O Killing and degradation

12. Outcomes of acute
inflammation
O Resolution
O Abscess formation (suppuration)
O Healing (regeneration/ scarring)
O Chronic inflammation

14. Chemical mediators
O Cell derived mediators
O Vasoactive amines
O Histamine
O 5-HT / serotonin
O Neuropeptides
O Arachidonic acid metabolites (eicosanoids)
O Via cyclo-oxygenase pathway – PGs, TXA2, prostacyclin, resolvins
O Via lip-oxygenase pathway – 5 HETE, LT (leukotrienes), LX (lipoxins)
O Lysosomal components
O Granules of neutrophils
O Granules of monocytes & tissue macrophages
O Platelet activating factor (PAF)
O Cytokines
O Free radicals
O Plasma derived mediators (plasma proteases)
O The kinin system
O The clotting system
O The fibrinolytic system
O The complement system

15. O Platelet activating factor (PAF)
O Released from IgE sensitised basophils or mast cells,
leucocytes, endothelium and platelets
Actions of PAF:
• Increased vascular permeability
• Vasodilation in low concentration; otherwise constriction
• Bronchoconstriction
• Adhesions of leucocytes to endothelium
• chemotaxis
O Cytokines
O Polypeptides produced by lymphocytes and monocytes
(activated)
O IL-1, TNF-alpha and beta, IFN- gamma and chemokines
O Free radicals
O Oxygen derived metabolites
O Nitric oxide

16. Plasma derived mediators
(plasma proteases)
O The kinin system
O Activation by factor XIIa generated bradykinin from kallikrein.
Actions:
• Smooth muscle contraction
• Vasodilation
• Increased permeability
• pain
O The clotting system
O Factor XIIa fibrinogen  fibrin and fibropeptides.
Actions:
• Increased vascular permeability
• Chemotaxis for WBC
• Anticoagulant activity
O The fibrinolytic system
O Activated by plasminogen activator
Actions:
• Activation of factor XII
• Complement C3 C3a (permeability factor)
• Degradation of fibrin to degradation products  chemotaxis + permeability
O The complement system
O C3a, 5a,4a (anaphylatoxins); C3b (opsonin); C5a (chemotaxis), C5b- C9 (membrane
attack complex – MAC)

17. Regulators of inflammation
1. Acute phase reactants:
O Cellular protection – Alpha 1 antitrypsin, alpha 1
chymotrypsin, alpha 2 antiplasmin
O Coagulation proteins – Fibrinogen, plasminogen, VW factor,
Factor VIII
O Transport proteins (ceruloplasmin, haptoglobin)
O Immune agents (sr amyloid A and P, CRP)
O Stress proteins (HSP)
O Antioxidants (ceruloplasmin)
2. Glucosteroids:
O Anti inflammatory action
3. Free cytokine receptors
4. Anti-inflammatory chemical mediators
O PGE2, prostacyclin

18. Giant cells
O Multinucleate giant cells formed when
macrophages fail to deal with the particles to be
removed.
O Giant cells in inflammation:
• Foreign body giant cells – chronic infective
granulomas, TB and leprosy.
• Langhan’s giant cells – tuberculosis and sarcoidosis
• Touton giant cells – xanthoma
• Aschoff giant cells – rheumatic nodules
O Giant cells in tumors:
• Anaplastic cancer GC – carcinoma of liver, soft
tissue sarcoma, etc.
• Reed-stenberg cells – Hodgkin’s lymphoma
• Ginat- cell tumor of bone – osteoclastic giant cells

20. Chronic inflammation
O Prolonged process of tissue destruction,
inflammation and repair occur
simultaneously.
Causes:
1. Following acute inflammation
2. Recurrent attacks of acute inflammation
(recurrent UTI  chronic pyelonephritis)
3. Chronic de novo (e.g. in TB)

21. General features

22. Systemic effects
O Fever
O Anaemia
O Leucocytosis
O ESR elevated
O Amyloidosis (group of diseases/ disorders
characterised by extracellular deposition
of fibrillar proteinaceous substance called
amyloid)

23. THANK YOU