ACUTE INFLAMMATION II

Clinicopathological Features
Dr N Williams
Department of Pathology
nadia.williams@uwimona.edu.jm

Lecture Outline

Chemical mediators of acute inflammation

Variations in the acute inflammatory response

The different macroscopic appearances of

acute inflammation in tissues

Specific inflammatory lesions

Mechanisms and causes of an abnormal acute

inflammatory reaction

CHEMICAL MEDIATORS
Exogenous
Bacterial

Source

products

Endogenous

Source

Cells
Plasma
Damaged

tissues

CHEMICAL MEDIATORS
Endogenous

chemicals

Components

of complement

Arachidonic

acid metabolites

Cytokines

CHEMICAL MEDIATORS
Vasoactive

amines (Active)

Histamine*
Serotonin

Plasma
Kinin

proteases (Inactive)

(bradykinin)
Complement (C3a, C5a)*
Plasmin

CHEMICAL MEDIATORS

Arachidonic acid

Nitric oxide

Lysosomal constituents

Oxygen free radicals

(reactive oxygen species)

Neuropeptides
(Substance P)

Prostaglandins
Leukotrienes

Platelet activating factor

Cytokines and
chemokines

Functions of Complement

Inflammation
C3a,

C5a , >C4a

Vasodilatation (anaphylatoxins)
Chemotaxis

Phagocytosis
Opsonin

Cell lysis
Membrane

attack complex

CYTOKINES
[Polypeptide products of activated cells]
Source
Monocytes
Lymphocytes
Non-lymphoid

cells

CYTOKINES
Tumour

necrosis factor (TNF)

Interleukin
Interferon

1 (IL1)

(IFN)

Chemokines

TNF and IL-1

Expression of adhesion molecules on endothelial

cells

Induce the secretion of other cytokines and

chemical mediators

Induce enzymes for matrix remodelling

Fibroblast activation

Systemic inflammatory response (IL-1>TNF)

Mediators of Inflammation

Vasodilation
Prostaglandins
Nitric

oxide

Permeability
Vasoactive

amines

C3a,

C5a
Bradykinin
LT-C4, D4 E4
PAF
Substance

Mediators of Inflammation

Chemotaxis, leucocyte activation

C5a
LTB4
Chemokines
Bacterial

products

Fever
IL-1,

IL-6, TNF
Prostaglandins

Mediators of Inflammation
Pain
Prostaglandins
Bradykinin

Tissue

Damage

Lysosomal

enzymes
Oxygen metabolites
Nitric oxide

Systemic Inflammatory Response

Fever
Myalgia
Arthralgia
Anorexia
Somnolence
Malaise
Rigors and chills

SYSTEMIC INFLAMMATORY RESPONSE

SYNDROME
Hypothalamic Pituitary Adrenal
Fever
Pyrogens

stimulate prostaglandins in vascular and

perivascular cells of hypothalamus reset thermostat

Acute Phase Proteins (ESR)

C-reactive

protein; fibrinogen; serum amyloid A (SSA)

Leucocytosis (neutrophilia with left shift)

pulse and blood pressure

Peripheral vasodilatation (glucocorticoids) Shock

The reaction and the outcome of inflammation

are dependent on :

The nature of the stimulus

The defense capability of the host/ tissue

Variation in Response
Response depends on
Factors related to the type of injurious agent
simplex virus (HSV) blisters
Staph aureus abscesses
Herpes

Factors
HSV

related to the host and tissues

in brain no blisters

Variation in Cellular Component

Typhoid

- monocytes
Parasites - eosinophils
Allergies eosinophils
Polymorphs
Chronic

in chronic inflammation

Helicobacter pylori gastritis

Chronic ulcerative colitis
Chronic osteomyelitis
Fungal granulomas

Variation in Exudate
Serous

- Plasma - serosa
Fibrinous - Fibrin - serosa
Phlegmonous - mucous - mucosa
(Catarrhal)
Suppurative - pus - bacteria
(Purulent)
Haemorrhagic - RBC - vascular tissue/necrosis

Variation in Inflammation

Gangrenous
inflammation + necrosis + putrefaction
(putrefying organisms = Clostridium species in
gut and soil)

Pseudomembranous
inflammation + necrosis + membrane
Diphtheria
Clostridium

difficile

Specific Inflammatory Lesions

Pus

Exudate rich in proteins, polymorphs and

cellular debris
Abscess

Localized collection of pus in tissue, organ or

confines space
Boil (furuncle, carbuncle)
Empyema

Collection of pus in a cavity

Specific Inflammatory Lesions

Ulcer

Circumscribed loss of tissue from the surface

of an organ with surrounding inflammation
Cellulitis

Diffuse area of oedema

Haemolytic streptococcus - hyaluronidase
(spreading factor)

RESOLUTION
Complete restoration of tissues to normal
following acute inflammation.

ORGANIZATION
Replacement of the acute inflammatory infiltrate
by fibrosis/ scar tissues formation

Sequale of Inflammation
Dependent on :
Amount

of

tissue
damaged

Elimination

of
the causative
agent

DEFECTS IN LEUCOCYTE FUNCTION

Decreased numbers

Defects in leukocyte adhesion

Defects in chemotaxis

Defects in phagocytosis

Defects in microbicidal activity

DEFECTS IN LEUKOCYTE FUNCTION

Congenital

Cirrhosis

Malnutrition

Sarcoidosis

Chronic granulomatous disease

Bone marrow failure

Drugs
Viruses

Diabetes

Summary
Acute inflammatory Rxn- mediated by a variety of
exogenous and endogenous chemicals
Reaction relates to aetiology and the tissues
ability to respond

the macroscopic appearances of the exudate vary

in different tissues

Defined specific inflammatory lesions

Aim Resolution
Abnormal reaction may be a congenital defect or
acquired in a variety of diseases.