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Flashcards in 4 - Acute inflammation Deck (37):
1

Acute inflammation response

Basic pathological process
Non-specific initial reaction to tissue damage
Stereotyped irrespective of aetiology

2

Three options following acute inflammation

Cells can regrow
Cells cannot regrow
Damaging agent persists and so damage continues

3

Cells can regrow

Healing by regeneration

4

Cells cannot regrow

Healing by repair

5

Damage agent persists

Chronic inflammation

6

Why do we have acute inflammation?

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

7

Calor

Heat

8

Rubor

Redness

9

Dolor

Pain

10

Tumour

Swelling

11

Serous inflammation

Copious non-viscous serous fluid release w/o WBCs and so is clear.

12

Fibrinous inflammation

Occurs when extensive leakage of fluid - fibrinogen coagulates forming fibrin

13

Purulent (pseudomembranous) inflammation

Made in response to powerful necrotising toxin, characterised by false membrane (of fibrin, necrotic epithelium and leucocytes) formation

14

Components of the acute inflammatory response

Vascular -> exudative -> cellular

15

Vascular reaction

Dilatation (=rubor), changes in flow

16

Exudative reaction

Formation of inflammatory exudate (=tumour)

17

Cellular reaction

Migration of inflammatory cells out of vessels

18

Pyrexia definition

Raised body temperature

19

Acute phase reaction definition

Summary of complex metabolic/neurological/immunological/inflammatory changes that occur after quick onset of injury/infection

20

Vascular reaction process

Microvascular dilatation
Initially flow up then down
Increased permeability

21

Mediated vascular reaction hormones

Histamine
Bradykinin
NO
Leukotriene B4
Complement components

22

Non-mediated vascular reaction hormones

Direct damage to endothelium e.g. toxins, physical agents

23

Composition of acute inflammatory exudate

Protein rich -> immunoglobulins, fibrinogen

Constantly turning over of loads of agents

24

Cellular reaction process

Accumulation of neutrophils in extracellular space
In severe cases, accumulation of neutrophils, cellular debris and bacteria forms pus

25

How neutrophils get through the walls

Axial stream of neutrophils -> margination -> rolling - adhesion (pavementing) -> migration (RBC diapedesis) -> chemotaxis

26

Mediators of acute inflammation types

Cell derived and plasma derived

27

Types of cell derived mediators

Stored (histamine)
Synthesised (prostaglandins, leukotrienes, PAF, cytokines, NO, chemokines)

28

Plasma derived

Kinin system
Clotting pathway
Thrombolytic pathway
Complement pathway

29

Mediators for vascular dilatation

Histamine
PGE2/I2
VIP
NO
PAF

30

Mediators for increasing permeability

Histamine
Bradykinin
NO
C5a
LTB4
PAF

31

Mediators for neutrophil adhesion

IL-8
C5a
LTB4
PAF
IL-1
TNF

32

Mediators for neutrophil chemotaxis

LTB4
IL-8
Chemokines

33

Systemic inflammatory response syndrome (SIRS)

Response to immune system for infection but whole body - related to sepsis

34

Acute (adult) respiratory distress syndrome (ARDS)

Severe, life-threatening inflammation of whole lungs. Triggered by trauma or sepsis.

35

Chronic granulomatous disease of childhood

Certain compounds in the immune system have problems forming the oxidative compounds needed for the immune response

36

Hereditary angio-oedema (HAE)

Rare, autosomal dominantly inherited blood disorder causes episodic attacks which swell the face, extremities, genitals, GI tract and upper airways

37

Amyloidosis

Rare condition where amyloid is deposited in tissues and organs