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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
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)
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
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
Fever
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
