Acute Inflammation (4) Flashcards Preview

EMS - Mechanisms of Disease > Acute Inflammation (4) > Flashcards

Flashcards in Acute Inflammation (4) Deck (33):
1

Causes

Tissue death - Ischaemia, trauma, toxins, chemical insults, thermal injury, radiation

Infection - pus forming (pyogenic) bacterial

2

What is the purpose?

- Clear away dead tissues
- Locally protect from infection
- Allow access of immune system components

3

Cardinal signs

Calor - heat - vascular dilatation
Rubor - redness - vascular dilatation
Dolor - pain
Tumor - swelling - inflammatory exudate into surrounding tissues
Function laesa - disturbance of function

4

Serous inflammation

Abundant protein-rich fluid exudate, non-viscous serous fluid

5

Fibrinous inflammation

Exudate of coagulated fibrin

6

Purulent inflammation

Pus formation

7

Pseudomembranous inflammation

Response to a powerful necrotising toxin, formation on a mucosal surface of a false membrane composed of fibrin, necrotic epithelium and inflammatory leukocytes

8

Vascular reaction

Dilatation (rubor), changes in flow

9

Exudative reaction

Formation of inflammatory exudate (tumour)

10

Exudate

Mass of cells and fluid that has seeped out of a blood vessel/organ, especially in inflammation

11

Cellular reaction

Migration of inflammatory cells out of vessels

12

Pyrexia

(Systemic effect of inflammation) Increase body temperature and fever

13

Acute phase reaction

(Systemic effect of inflammation) Changes to the synthesis of certain protein within the serum during an inflammatory response, provides rapid protection for host against microorganisms through non-specific defence mechanisms

14

Markers of acute phase reaction

- C-reactive protein
- Erythrocyte sedimentation rate

15

Vascular reaction

- Microvascular dilatation
- Initially flow increases, then decreases
- Increased permeability
(Mediated - histamine, bradykinin, NO, leukotriene B4, complement components)
(Non-mediated - direct damage to endothelium e.g. toxins, physical agents)

16

Exudative reaction

- Protein rich (50g/l) - immunoglobulins and fibrinogen
- Constantly turning over - dilution of noxious agents, transport to lymph nodes, supply to nutrients O2, spread of inflammatory mediators, spread of antibodies, spread of drugs

17

Pericarditis

Inflammation of pericardium (fibrous from fibrin in inflammatory exudate)

18

Cellular reaction

- Accumulation of neutrophils in extracellular space
- If Severe > accumulation of neutrophils, cellular debris and bacteria > pus

19

Neutrophils

- Produced in bone marrow
- Commonest WBC
- Increase in acute inflammation
- Motile, amoeboid (crawling-like motion), can move into tissues
- Directional chemotaxis
- Short lifespan (hours in tissues)
- Phagocytotic and microbicidal (destructive to microorganisms)

20

O2 dependent phagocytosis

Myeloperoxidase, H2O2, Cl-, O2-, OH-

21

O2 independent phagocytosis

Lysozyme, lactoferrin, cationic proteins

22

Neutrophil process

1) Margination - align themselves on the wall e.g. selectin
2) Rolling - adhesion
3) Migration - out of vessel
4) Chemotaxis

23

Cell derived mediators of acute inflammation

- Histamine (stored)
- Prostaglandins (synthesised)
- Leukotrienes (synthesised)
- PAF (synthesised)
- Cytokines (synthesised)
- NO (synthesised)
- Chemokines (synthesised)

24

Plasma derived mediators of acute inflammation

- Kinin system
- Clotting pathway
- Thrombolytic pathway
- Complement pathway

25

Mediators of vascular dilatation

- Histamine
- PGE2/I2
- VIP
- NO
- PAF

26

Mediators of increased permeability

- Histamine
- Bradykinin
- NO
- C5a
- LTB4
- PAF

27

Mediators of neutrophil adhesion

Upregulation:
- IL-8
- C5a
- LTB4
- PAF
- IL-1
- TNF

28

Mediators of neutrophil chemotaxis

- LTB4
- IL-8
- Chemokines

29

Drugs that interfere

- Glucocorticoid steroids
- NSAIDs
- LT receptor antagonists

30

Minimal tissue damage

Resolution

31

Some tissue damage

Fibrosis

32

Marked neutrophil reaction with tissue damage

Suppuration - abscess

33

Damaging agent persists

Chronic inflammation