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Flashcards in Acute inflammation Deck (30):
1

Causes of inflammation

Defense mechanism by the body deals with an insult

- Micro-organism 
- Foreign particles
- Necrotic tissue
- Hypersitivity reactions
- Physical agents
Chemicals

2

What are the cardinal signs of inflammation?

Calor - Hear

Rubor - Redness

Dolor - Pain

Tumor - Swelling

(and loss of function)

3

What are the three types of exudate?

Fibrinous - large amounts of fibrinogen due to increase in vascular permeability

Purulent - pyogenic bacterial infections. Rich in neutrophils, cell debris and bacteria

Transudate - low protein content, caused by alteration in hydrstatic or oncotic pressure

4

Name 5 possible outcomes of an acute inflammatory response

Resolution

Suppuration

Organisation and repair

Calcification

Acute /chronic

Chronic inflammation

Septicaemia

Death

5

Name 6 inflammatory mediators

Histamine

Prostaglandins

Leukotrienes

Platelet activating factor

Cytokines - TNF alpha, ILs

Nitric oxide

Free radicals

Bradykinin

Complement system – esp C5a

6

What is the role of histamine in inflammation?

Causes vascular dilatation, and is the main effector of immediate phase vascular permeability

Released from preformed granules in mast cells in response to trauma, cold, antibodies, cytokines. 
 

7

Role of PAF in inflammation

Released from leukocytes and mast cells. Causes vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst. 1000 times more potent than histamine

8

What is the role of prostaglandins in acute inflammation?

Released from mast cells and leukocytes. Causes vasodilation, pain and fever.

9

What are leukotrienes?

Amino Acid metabolites

Released from mast cells and leukocytes. Vaso-active (increase permeability). 

LTB4 chemotactic & stimulates leukocyte adhesion to endothelium, also generation of free radicals & release of lysosomal enzymes

10

Which cytokines are involved in acute inflammation?

IL-1, TNF-alpha. Released by macrophages, endothelial cells and mast cells. 

Cause local endothelial activation (expression of adhesion molecules)

Chemotaxis of neutrophils

fever/pain/anorexia/hypotension

Decreased vascular resistance (shock)

11

What is the role of complement in inflammation?

Complement products (C5a, C3a, C4a) are produced in liver and secreted into the plasma

Complement can be activated by necrosis, Ag/Ab complexes, endotoxin or fibrinolytic systems. 

Cause leukocyte chemotaxis and activation, vasodilation (mast cell stimulation), cell lysis via the MAC and opsonisation of pathogens

12

What are the problems that are caused by acute inflammation?

destruction of normal tissue
swelling
blockage of tubes
loss of fluid
pain
inappropriate inflammation

13

What are the three stages of acute inflammation?

Increase in blood flow,

Structural changes in the microvasculature that permit plasma proteins and leukocytes to leave the circulation,

Emigration of the leukocytes from the microcirculation to the tissue and activation to eliminate the offending agent

14

What are the systemic effects of acute inflammation?

Fever - enogenous pyrogens e.g IL-2

Leukocytosis - bacterial infections (neutrophils), viral (lymphocytes)

Malaise

Nausea

Anorexia

Acute phase resposne (high CRP, ESR)

15

What are the three steps of extravasation?

Vascular endothelium in its normal, unactivated state does not bind circulating cells or impede their passage.

- Endothelium is activated expresses adhesion molecules which bind to receptors on leukocytes, causing margination, rolling, and adhesion to endothelium. 

- Migration across the endothelium and vessel wall

- Migration in the tissues toward a chemotactic stimulus

16

What is the function of neutrophils?

 In most forms of acute inflammation neutrophils predominate in the inflammatory infiltrate during the first 6 to 24 hours and are replaced by monocytes in 24 to 48 hours. 

Allows destruction of foreign material & removal of damaged tissue

Neutrophils recognise dead tissue and foreign material either directly via mannose receptors or via Opsonins & Fc and C3b receptors, then bind to it

Engulf material (phagocytosis/pinocytosis)

17

Descibe the process of extravasation

Vasodilation slows the blood flow (stasis) and reduces shear stress. Leukocytes redistribute along the endothelial surface (margination).

Endothelial cells are activated by cytokines to express express E-selectin and P-selectin, this binds to receptors expressed on leukocytes and cause adherence which causes the leukocytes to roll along the vessel wall. TNF and IL-1 induce the expression of integrins, which cause leukocytes to adhere tightly to the endothelium (patenting).

Chemokines produced at the site of injury activate the leukocytes and stimulate migration through endothelial spaces toward the sie of infection. After traversing the endothelium, leukocytes pierce the basement membrane, by secreting collagenases and enzymes, and enter the extravascular tissue.

Once inside the tissue, cells migrate to areas of inflammation by chemotaxis. 

18

What is the purpose of inflammation?

Inflammation is a protective response, designed to rid the organism of both the initial cause of cell injury (e.g. microbes, toxins) and the consequences of such injury (e.g., necrotic cells and tissues).

19

What factors comprise the anti-oxidant defence system?

Vitamin C

Vitamin E

beta-carotene

20

What is the effect of aspirin on inflammation?

Aspirin irreversible acetylates and inhibits COX-1 and COX-2 enzymes. These convert arachadonic acid to PGH2 which is a precursor for other prostaglandins. 

Prostaglandins are involved in the vascular and systemic reactions of inflammation, particularly TXA2 which is a potent platelet activator. 

21

How do corticosteroids modify acute inflammation?

Corticosteroids suppress the immune system. 

 Produces an anti-inflammatory response. Can act by reducing the transcription of genes encoding COX-2, phospholipase A2, pro-inflammatory cytokines (such as IL-1 and TNF), and iNOS.

22

How does inflammation help produce an effective response to injury?

Inflammation causes cellular reactions (stimulates the immune response), which promote destuction and removal of the damaging agent.

Increased vascular permeability increases delivery of antibodies, nutrients and oxygen to cells. 

 destroys and removes dead or foreign material and promotes repair process. 

23

What are the microscpic features of acute inflammation? How do they occur?

Oedema, fibrin and neutrophil infiltration 

Causes by haemodynamic changes (vasodilation slow blood flow)

Increased vascular permeability (leading to the escape of a protein-rich exudate into the extravascular tissue) 

Recruitment and migration of neutrophils

24

What are the underlying processes that result in the signs of inflammation?

Rubor (redness) is caused by increased circulation and vasodilation in the injured tissues

calor (warmth) is the heat given off by the increased flow of blood;

tumor (swelling) is caused by increased fluid escaping into the tissues;

dolor (pain) is caused by the stimulation of nerve endings.

Combined, these events often cause the temporary loss of function of the afflicted tissue (functio laesa)

25

Name one inherited disorder of acute inflammation

Inherited angio-oedema: defective gene means immune system not regulated causing spontanous angioedema 

Chronic granulamous disesase

26

Describe 3 possible outcomes of acute inflammation

Resolution: Once the injurious agent has been neutralised, the site of acute inflammation is restored to normal. This is the usual outcome when the injury is limited or short-lived or when there has been little tissue destruction and the damaged parenchymal cells can regenerate. Resolution involves removal of cellular debris and microbes by macrophages, resorption of fluid by lymphatics, fibrin degraded by plasmin, apoptosis of neutrophils. 

Suppuration: Pus formation due to resistant organism. Results in abscess formation, empyema and fistulae 

Organisation: This occurs after substantial tissue destruction, when the inflammatory injury involves tissues that are incapable of regeneration, or when there is abundant fibrin exudation in tissue or serous cavities (pleura, peritoneum) that cannot be adequately cleared. In all these situations, connective tissue grows into the area of damage or exudate, converting it into a mass of fibrous scar tissue.

Chronic inflammation: If acute inflammation cannot be resolved or if the injury persists the healing process is impaired. Causes fibrosis and long term tissue damage

27


What are the three main funciton sof the acute inflammatory response?

Transport of cells and proteins from local blood vessels which promote a defensive response.

Destruction and removal of foreign agent (e.g. bacteria, material)

Destruction and removal of damaged tissue and debris

28


What are the contents of acute inflammatory exudate?

Fluid: containing salts, Ig, proteins

Fibrin: filamentous protein which polymerises into form clots

Cells: neutrophils, lymphocytes, macrophages

 

29

What are the underlying processes that produce the cardinal signs of inflammation?

The redness and heat of acute inflammation are the result of vesel dilation and icnreased blood flow into the inflamed part.

Swelling is caused by the accumulation of exudate, particularly the fluid component.

Pain is due to the direct effects of certain chemical mediators and pressure on the nerve endings caused by swelling

When swelling is marked, there is a loss of function of the inflamed structure.

30


What is an abscess?


A mass of necrotic tissue with dead and viable neutrophils, suspended in the fluid products of tissue breakdown.

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