P. 1
8 Acute Inflammation IW

8 Acute Inflammation IW

|Views: 12|Likes:
Published by Amy Prom

More info:

Published by: Amy Prom on Oct 29, 2011
Copyright:Attribution Non-commercial

Availability:

Read on Scribd mobile: iPhone, iPad and Android.
download as PDF, TXT or read online from Scribd
See more
See less

01/01/2014

pdf

text

original

Acute Inflammation

Inflammation & Healing
Recognition of injury Removal of injurious stimulus Repair of any damage

Injurious stimuli
Trauma Infection Physical (irradiation, thermal) Chemical Ischaemia (lack of blood i.e. oxygen) Immune reactions

Cell Injury Acute Inflammation Chronic Inflammation Healing & Repair .

.

Acute inflammation Stereotyped response Delivers molecules and cells to site of injury .

exudation of plasma proteins into tissues and emigration of neutrophil polymorphs into tissue .Acute inflammation Vascular reaction leading to increase in blood flow.

.

Acute myocardial infarction .

Vascular changes Vasodilatation & increased blood flow Increased vascular permeability .

Vascular permeability Endothelial cell contraction Direct injury Leukocyte dependent injury Increased transcytosis Vascular neogenesis .

Increase in vascular permeability Loss of oncotic pressure in capillaries as vessels permeable to protein Excess fluid in tissues – oedema fluid (protein rich exudate) – swelling Precursors of protein mediators Fibrin – scaffolding for effector cells Immunoglobulins .

Polymorphonuclear neutrophil granulocytes Mediator cells – release inflammatory mediators Effector cells – kill bacteria and fungi Attracted to site of inflammation and activated by chemotactic factors .

.

How do neutrophil polymorphs get to site of inflammation? Move in marginal zone of blood flow Changes in vessel wall .integrins. ICAM-1 & VCAM-1(leukocytes) & selectins (endothelial cells) induced by IL-1 & TNF Chemotaxis in tissues .

Chemotactic Agents N-formyl–methionine peptides from bacteria C5a Leukotriene B4 IL-8 .

cytokines. C3b & Fc .Leukocyte Activation Production of arachidonic acid metabolites Degranulation & activation of oxidative burst Secretion of cytokines Modulation of adhesion molecules Expression of surface receptors for bacterial products.

C3b.Phagocytosis Recognition – lectins (mannose). Engulfment Killing – oxygen dependent – reactive oxygen intermediates (ROI) (H2O2 & myeloperoxidase) : oxygen independent – lysosyme. Fc. elastase etc .

Chemical Mediators Control Inflammation Cell derived – endogenous and newly synthesised Plasma derived .

increases vascular permeability)– mast cells Serotonin – platelets Lysosomal enzymes – neutrophils .Cell derived – endogenous (pre-formed) Histamine (vasodilator.

immune reactions (IgE). C3a & C5a. trauma). cytokines (IL-1 & IL-8). “Sentinel” cells . etc.Mast cells Found along blood vessels Degranulate in response to physical injury (heat. cold.

.

thromboxanes.Newly synthesised mediators Arachidonic acid metabolites – prostaglandins. IL-1 (macrophages) Nitric oxide (leukocytes) Oxygen metabolites (leukocytes) .(cell membranes) Platelet activating factor (mast cells) Tumour necrosis factor. leukotrienes. lipoxins.

Plasma enzyme cascades preformed in blood Clotting Fibrinolysis Complement Kinin .

Plasma Enzyme Cascades enzyme A Inactive enzyme B Active enzyme B + fragment B Inactive enzyme C Active enzyme C + fragment C Inactive enzyme D Active enzyme D + fragment D .

MAC .XIIa Kinin system: Bradykinin kallikrein Fibrinolysis: Fibrin degradation products plasmin Coagulation: fibrinopeptides thrombin Complement: C3a. C5a.

Vasodilatation Prostaglandins Nitric oxide Histamine .

LTD4.Increased vascular permeability Histamine & serotonin C3a & C5a Bradykinin LTC4. LTE4 PAF .

Chemotaxis C5a LTB4 IL-1. TNF .

Fever IL-1 TNF Prostaglandins .

Pain Prostaglandins Bradykinin .

Tissue damage Neutrophil & macrophage lysosomal enzymes Oxygen metabolites Nitric oxide .

Mast cell Blood vessel Plasma enzyme cascade Neutrophil polymorph Macrophage .

Can you explain signs of acute inflammation? Rubor (redness) Calor (heat) Dolor (pain) Tumor (swelling) Functio laesa (loss of function) .

Outcomes of acute inflammation Resolution Healing by organisation (scarring) Progression to chronic inflammation Death .

Plasma enzyme cascades Mast cells Bacterial products Blood vessels Neutrophil polymorphs vasodilatation oedema Neutrophil polymorphs in tissue .

You're Reading a Free Preview

Download
scribd
/*********** DO NOT ALTER ANYTHING BELOW THIS LINE ! ************/ var s_code=s.t();if(s_code)document.write(s_code)//-->