Chapter 2

(1) Discuss types of inflammation.

(2) Outline molecular and cellular events in inflammation.
(3) Discuss systemic inflammatory response.
(4) Discuss pathological types and features of chronic inflammation.

(1) Acute Inflammation

a. Short duration. Repair with early body reaction.

Chronic Inflammation
a. Longer duration, over 6 months. Either caused by agent or the stimulus.

Signs of inflammation

1. Redness Rubor
2. Heat Calor
3. Swelling Tumor
4. Pain Dolor
5. Loss of Function (Functio laesa)

(2) Acute Inflammation

I. Vascular Events
b. Increased vascular permeability:
a. Changes in vascular flow and caliber
During inflammation, endothelium lining of microvasculature
• Transient vasoconstriction for a few seconds.
becomes more leaky resulting in escape of protein
• Progressive vasodilatation involving mainly arterioles.
rich fluid into the interstitial compartment and this
Increase blood flow heat and redness.
fluid is known as exudate.
• Progressive vasodilatation  hydrostatic pressure transudation.
• Next occurs slowing or stasis of microcirculation. Increased hydrostatic pressure increased vascular permeability edema
(transudation) (exudation).
Lewis’s triple response
- The flush appears immediately following stroking as
a dull red line and is due to capillary dilatation.
- The flare is a bright red irregular surrounding
due to arteriolar dilatation.
- The wheal is a swelling or edema of surrounding
skin occurring due to transudation of fluid into
extravascular space.

II. Cellular Events

a. Leukocyte extravasation b. Phagocytosis

a. Leukocyte extravasation b. Phagocytosis

escape
Leukocytes  the interstitial tissue  Inflammation It is the process by which polymorphs and macrophages ingest
(from the lumen of microvasculature) microorganisms and other foreign particles.
Steps of leukocyte extravasation include: It is similar to feeding process of amoeba and involves
following steps:
- Stasis of blood and changes in axial flow of blood. - Recognition and attachment.
- Margination of leukocytes and pavementing. - Engulfment.
- Rolling and adhesion to endothelium. - Killing and degradation.
- Emigration through inter-endothelial gaps by ameboid movements into
extravascular space.
- Red cells also escape by passive movements (Diapedesis).
- Chemotaxis: It is movement of leukocytes towards the site of injury and is
defined as locomotion oriented along a chemical gradient.

(3) SYSTEMIC INFLAMMATORY RESPONSE

Involves neuroendocrine, immunological and metabolic alterations.

Endocrine Response Metabolic Response Immune Response

There is increased release of i. There is increased lipolysis resulting in elevated i.Innate Response ii. Acquired Response
hormones namely: ACTH, levels of plasma fatty acids and glycerol.
cortisol, growth hormone, epinephrine, ii. There is increased nitrogen excretion leading to Occurs early and is Occurs later after antigen processing
norepinephrine,glucagon, renin rise in blood urea levels. not antigen specific. It and clonal expansion of T- and B-cells.
and aldosterone. iii. There is increased production and decreased depends on It is antigen specific.
utilization of glucose by tissues leading to functioning of natural
hyperglycemia. killer (NK) cells.

During innate response to injury, mediators release Cytokines.(small proteins or lipids)

Cytokines appear very rapidly after injury, influence by proinflammatory or anti-
inflammatory response.
systemic inflammatory response syndrome(SIRS)- fever, tachycardia,
leukocytosis(by Cytokines)
Pre-existing cytokine production multiple organ failure (MOF) and mortality.

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Various cytokines related to inflammatory response are: Tumor Necrosis Factor-alpha (TNF-α) (most potent mediator of inflammation)
Interleukin-1 (IL-1) (extremely potent mediator of inflammation)
IL-6, IL-8, IL-11 (other proinflammatory cytokines)
IL-4, IL-10 and IL-13 ( anti-inflammatory cytokines produced by T-helper cells )
Interferon-γ (IFN-γ ) ( central role in innate immune response to microbial invasion)
Inducible Nitric Oxide Synthase (NOS-2) and Cyclooxygenase-2 (COX-2)

(4) I. Pathological Features of Chronic Inflammation

- Infiltration by mononuclear cells.
- Presence of tissue macrophages, epithelioid cells (modified macrophages) and multinucleated giant cells.
- Tissue necrosis, e.g. central caseation necrosis in tuberculosis.
- Proliferation of granulation tissue comprising blood vessels and fibroblasts.
- Collagen formation and healing by fibrosis.

II. Types of Chronic Inflammation Chronic Specific Inflammation

Chronic Nonspecific Inflammation
When irritant substance produces nonspecific inflammation
with formation of granulation tissue and healing
by fibrosis, e.g. chronic osteomyelitis.
When the causative agent leads to characteristic
histological tissue response like ‘granuloma formation’.
It is also called as chronic granulomatous inflammation.
The granuloma is a circumscribed tiny lesion about 1 mm
in diameter. It consists of epithelioid cells, lymphoid cells and giant cells
along with necrosis and fibrosis. Examples are: tuberculosis, leprosy,
syphilis, actinomycosis. (Details in Chapter 4, Specific
infections).

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