INFLAMMATION

DEFINITION

INFLAMMATION IS A HOST RESPONSE TO LOCAL INJURY IN VASCULARISED TISSUES.

CARDINAL SIGNS OF INFLAMMATION

•

INFLAMMATION- CARDINAL SIGNS: CELSUS

RUBOR-REDNESS

CALOR-HEAT

TUMOR-SWELLING

DOLOR- PAIN

5TH SIGN DESCRIBED BY VIRCHOW-LOSS OF FUNCTION

(FUNCTIO LAESA)

INFLAMMATION-TYPES

ACUTE CHRONIC

Onset Rapid Slow

Duration Short Longer

Predominant cells

Neutrophil Lymphocytes and macrophages

Chief pathological event

Exudation of fluid and plasma proteins

Proliferation of blood vessels and fibrosis

INFLAMMATION-STIMULI

Infection- bacterial, viral , parasitic

Trauma

Physical/chemical injury- burns, irradiation

Tissue necrosis

Foreign body

Immune reaction

ACUTE INFLAMMATION

VASCULAR CHANGES:

Vascular caliber alteration.

Change in vascular structure.

CELLULAR EVENTS:

leucocyte emigration

ACUTE INFLAMMATION- VASCULAR CHANGES

IMPORTANT TO BRING ANTIBODIES AND LEUCOCYTES

1. VASODILATATION EARLIEST EVENT

ARTERIOLES- OPENING OF CAPILLARIES

INCREASED BLOOD FLOW- RUBOR AND CALOR

2. INCREASED PERMEABILITY

3. STASIS

Increased Vascular Permeability (Vascular Leakage)

Contraction of endothelial cells resulting in increased interendothelial spaces is the most common mechanism of vascular leakage.

VASCULAR CHANGES-INCREASED PERMEABILITY-MECHANISMS

FORMATION OF ENDOTHELIAL GAPS IN VENULES

RAPID,SHORT LIVED

Agent: Histamine,bradykinin

MECHANISM: Phosphorylation Of Cytoskeletal

Proteins Contraction

IMMEDIATE TRANSIENT RESPONSE

Endothelial injury, resulting in endothelial cell necrosis and detachment

VASCULAR CHANGES-INCREASED PERMEABILITY-MECHANISMS

DIRECT INJURY

IMMEDIATE SUSTAINED RESPONSE

ALL LEVELS

NECROTIZING INJURIES (e.g.SEVERE BURN)

VASCULAR CHANGES-INCREASED PERMEABILITY-MECHANISMS

DELAYED PROLONGED LEAKAGE

VENULES,CAPILLARIES

THERMAL INJURIES,X-RADIATION

AFTER 2-12 HOURS,LASTS FOR HOURS OR DAYS

Neutrophils that adhere to the endothelium during inflammation may also injure the endothelial cells and thus amplify the reaction.

VASCULAR CHANGES-INCREASED PERMEABILITY-MECHANISMS

LEUCOCYTE MEDIATED ENDOTHELIAL INJURY

DELAYED PROLONGED RESPONSE

COMMON IN GLOMERULI AND LUNGS

VASCULAR CHANGES-INCREASED PERMEABILITY-MECHANISMS

INCREASED TRANSCYTOSIS

ACROSS ENDOTHELIAL CYTOPLASM

INCREASE IN NO: AND SIZE OF TRANSENDOTHELIAL CHANNELS

LEAKAGE FROM NEW BLOOD VESSELS

IMPORTANT DURING EARLY PHASES OF HEALING

VASCULAR CHANGES-INCREASED PERMEABILITY

ESCAPE OF PROTEIN RICH FLUID AND BLOOD CELLS - FORMATION OF EXUDATE

TRANSUDATE FLUID WITH LOW PROTEIN

DUE TO OSMOTIC OR HYDROSTATIC IMBALANCE

VASCULAR PERMEABILITY INTACT

Transcytosis:

may involve channels consisting of interconnected, uncoated vesicles and vacuoles called the vesiculovacuolar organelle: located close to intercellular junctions.

EXUDATE Vs TRANSUDATE

Exudate Transudate

Protein content High Low

Cells & debris High Low

Specific gravity > 1.020 < 1.012

Cause vascular

permeability

hydrostatic

pressure;

osmotic pressure

Associated with Inflammation

Exudate Transudate

Responses of Lymphatic Vessels

lymph flow is increased and helps drain edema fluid, leukocytes, cell debris, as well as microbes.

Lymphatic vessels also proliferate.

+/-(lymphangitis),+/-(lymphadenitis).

Inflamed lymph nodes are often enlarged because of hyperplasia of the lymphoid follicles and increased numbers of lymphocytes and macrophages. This constellation of pathologic changes is termed reactive, or inflammatory, lymphadenitis

summary

Inflammation-acute and chronic

Acute - cardinal sign

stimuli

changes -vascular & cellular

•vascular- vasodilation;

increased vascular permeability

transcytosis