Presentation is loading. Please wait.

Presentation is loading. Please wait.

Inflammation and Cell Damage Peer Support 2014 Michael Iveson and Emily Hodgson.

Similar presentations

Presentation on theme: "Inflammation and Cell Damage Peer Support 2014 Michael Iveson and Emily Hodgson."— Presentation transcript:

1 Inflammation and Cell Damage Peer Support 2014 Michael Iveson and Emily Hodgson

2 Give three advantages to inflammation? dilution of toxins entry of antibodies fibrin formation nutrients and oxygen deliver neutrophils stimulation of the immune response entry of drugs

3 Give two problems caused by inflammation? destruction of normal tissue swelling blockage of tubes loss of fluid pain inappropriate inflammation

4 What are the FOUR cardinal signs of acute inflammation? 1.Rubor 2.Tumor 3.Calor 4.Dolor 5.(Functio Laesa)

5 What immune cell is key in acute inflammation? Neutrophils

6 What are the stages of neutrophil recruitment? (IN ORDER) 1. Margination 2. Adhesion 3. Emigration 4. Chemotaxis

7 What are the vascular changes in acute inflammation? Arteriole and capillaries dilate Opening of new capillary beds Increased blood flow Red cell stasis Endothelial cells swell and partially retract – more permeable

8 What is exudate? Inflammatory fluid which has high protein concentration

9 Give the three types of exudate? Fibrinous – large amounts of fibrinogen Purulent – pyogenic bacterial infections Transudate – lower protein content

10 How do neutrophils move through the endothelial wall? Inflammatory mediators increase expression of p- selectin on the endothelial walls Neutrophil attaches to p-selectin Pseudopodia push through the endothelial gaps and digest the basement membranes with proteolytic enzymes Cells enter extravascular space

11 Give three systemic signs and symptoms of acute inflammation. Fever Leukocytosis Malaise Nausea Anorexia Lymphoid hyperplasia CRP, ESR raised

12 Give three mediators of acute inflammation Histamine Prostaglandins Leucotrienes NO PAF Cytokines Complement

13 Give three outcomes of acute inflammation Resolution Suppuration Organisation and repair Calcification Continued acute/ chronic inflammation Septicemia Death

14 What are the three key features of chronic inflammation? Ongoing inflammation Ongoing tissue destruction Ongoing attempts at tissue repair

15 Give two cell types involved in chronic inflammation Macrophages Lymphocytes Plasma cells Eosinophils

16 What do macrophages produce? Proteases Hydrolytic enzymes Reactive O2 species GF Cytokines

17 Give three possible outcomes of chronic inflammation Continued chronic inflammation Change in tissue function Atrophy Metaplasia (= change in cell type) Resolution Damaging stimulus removed, healing can occur Scarring with dysfunction Cirrhosis in viral hepatitis Catastrophe Damaging stimulus increases / tissue healing response weaken > tissue insult worsens E.g. Perforated gastric ulcer

18 What is granulomatous inflammation? A subtype of chronic inflammation Occurs when neutrophil phagocytosis is inadequate to control causative agent Characterised by granulomas = collections of macrophages

19 What cells are present in a granuloma?

20 Make sure you know… Phagocytosis Types of necrosis Differences between apoptosis and necrosis Granulomatous inflammation/granuloma is different to granular tissue

Download ppt "Inflammation and Cell Damage Peer Support 2014 Michael Iveson and Emily Hodgson."

Similar presentations

Ads by Google