Dr.reza2006@gmail.com Dr Reza INFLAMMATION. dr.reza2006@gmail.com.

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dr.reza2006@gmail.com

Dr Reza

INFLAMMATION

Definition of Inflammation:

Inflammation is a complex reaction in living vascularized tissue to injurious agents leading to the exudation and accumulation of protein rich fluid and leucocytes in extravascular tissue, provided the injury does not destroy the tissue.

Reaction of vascularized tissue to injury

Accumulation of protein rich fluid and leucocytes in extravascular tissue

Purposes:

A protective response to-1. to dilute, localize and destroy the

injurious agent2. to limit tissue injury3. to restore the tissue towards

normalityHarmful effect: eg, hypersensitivity

reaction

Acute Inflammation:

Rapid local response of living tissue to injury

Lasts for minutes to a few days Extravascular accumulation of

protein rich fluid and leucocytes, predominantly Neutrophils, ie, Exudative lesion

Stereotype,ie, wide variety of agents share the same basic features

Chronic Inflammation:

Persists for weeks to months Extravascular accumulation of

Lymphocytes and Macrophages Tissue destruction and attempts to

healing by proliferation runs simultaneously, ie, Proliferative lesion

Not stereotype

Cardinal signs of Acute Inflammation

Rubor or redness Calor or heat Tumor or swelling Dolor or pain Loss of function(functio laesa)

Aetiology of Acute Inflammation

1. Infectious agent: Bacteria, virus, fungi, protozoa

2. Immune reaction: Hypersensitivity reaction

3. Trauma: blunt/penetrating4. Physical agent: eg, burn, ionizing

radiation5. Foreign bodies: eg, sutures, dirt6. Chemical agent: acids, alkalies, bile7. Tissue necrosis: eg, infarcts

Events in Acute Inflammation:

1.Vascular changes:• Changes in vascular flow & caliber• Increased vascular permeability(Vascular

leakage)2.Exudation of blood constituents:• Fluid Exudate• Cellular Exudate3.Changes in tissue tissue components

Vascular changes(Flow & Caliber)

Vasodilation, due to-a)Histamineb)Nitric oxide,etcIncreased permeability of

microvasculatureSlowing of circulation/ Stasis, due to-a)Exudationb)Microcirculation packed with red cellc) Increased viscosity of blood

Accounts for warmth and redness

Opens microvascular beds

Increased intravascular pressure causes an early transudate (protein-poor filtrate of plasma) into interstitium (vascular permeability still not increased yet)

Movie- Vasodilation

Vascular changes(Vascular Leakage)

Cellular events:

A) Leucocyte Extravasation1 In the limen-a)Marginationb)Rollingc)Adhesion to endothelium2 Transmigration or diapedesis across

endothelum3 ChemotaxisB) Phagocytosis

leukocytes first roll, then become activated and adhere to endothelium, thentransmigrate across the endothelium, pierce the basement membrane, and

migrate toward chemoattractants

Movie- Leucocyte Rolling

Chemotaxis:Following extravasations, leukocytes

emigrate in tissues toward the site of injury by a process called chemotaxis.

Exogenous chemo attractants:Exogenous chemo attractants: bacterial products, etc.

Endogenous chemo attractants:Endogenous chemo attractants: components of the (LTB4), cytokines, etc.

PhagocytosisRecognition and attachmentEngulfment

PhagosomePhagolysosome

killing and degradationOxydent dependent mechanism:I. H2O2-MPO-Halide systemII.Reactive Oxygen intermediates-

O2- ,H2O2, OH- Oxydent independent mechanism: killing

occur by substances of lysosomal granules- Lysozyme, Lactoferrin, BPI, Defensin

Systemic effects of Acute Inflammation

Fever Sleepiness, poor appetite, chills, rigors,

tachycardia (prolonged inflammation IL-1, TNF increased catabolism of skeletal muscle protein wt loss)

Blood changes Septic shock: Immune response: Ab or cell mediated Lymph node, Liver, Spleen: Enlarged

By Pyrogrns stimulate PG synthesis in Hypothalamus

Exogenous Pyrogrns: bacterial LPS stimulate leucocyte to release of Endogenous pyrogen: IL-1 & TNF

PG produced which act on vasomotor centre skin vasoconstrivtion reduced heat loss fever

Blood changes Leucocyte count:

Leucocytosis(by IL-1 & TNF; also left shift)bacterial infection Neutrophilia most bacterial infection Eosinophilia(by IL-5) allergy & helminths Lymphocytosis viral infection, Tuberculosis

Leucopenia Typhoid, virus, rickettsiae, protozoa Platelet: Thrombocytopenia occur in dengue, measels ESR: Increased Fibrinogen level is responsible for high ESR CRP(C-reactive protein): increased (eg. RF, RA) Acute –phase proteins: liver synthesizes acute phase

protein like C reactive protein(CRP), Fibrinogen and Serum Amyloid A(SAA).

Morphological Variants:1. Suppurative or Purulent inflammation2. Fibrinous inflammation3. Serous inflammation4. Serofibrinous inflammation5. Catarrhal inflammation6. Pseudomembranous inflammation7. Acute inflammatory ulcer8. Haemorrhagic inflammation9. Necrotizing inflammation

Fate of Acute Inflammation:

Resolution Abscess formation Turn into chronic inflammation ulceration

Acute Vs Chronic Inflammation

Exudate Vs Transudate

Movie- Inflammation

Thank You

Dr.reza2006@gmail.com Dr Reza INFLAMMATION. dr.reza2006@gmail.com.

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