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Cell pathology > Inflammation > Flashcards

Flashcards in Inflammation Deck (40):
1

What is inflammation?

Reactions of living vascularised tissue to sub-lethal cellular injury. Evolutionary development to protect against infection and trauma. Can be local/systemic, tightly regulated and involves many cell types/mediators.

2

What is acute inflammation?

Short and early response to injury
- Hours/few days
- Involves release of chemical mediators
- Vascular and leukocyte response

3

What is chronic inflammation?

Inflammation of prolonged duration in which active inflammation, tissue destruction and attempts at repair occur simultaneously.
- Weeks/months/years
- Usually due to persistent injury causing agent

4

What are the main components of the inflammatory response and healing?

- Cells
- ECM
- Soluble factors
- Vessels

5

Which cells are involved in inflammation and healing?

Neutrophils, macrophages, lymphocytes, eosinophils, mast cells

6

Which components of the ECM are involved in inflammation and healing?

- collagen
- proteoglycans
- fibroblasts

7

What is the role of vessels in inflammation and healing?

- immediate supply of cells and soluble factors

8

Which soluble factors are involved in inflammation and healing?

- Antibodies
- Cytokines
- Complement system
- Coagulation system

9

What are the cardinal signs of inflammation?

- RUBOR: redness (slowed blood flow and vasodilation by histamine)
- CALOR: heat (vasodilation by histamine)
- DOLOR: pain
- TUMOUR: swelling (oedema due to increase in permeability by histamine)
- FUNCTIO LAESA: loss of function (due to swelling and pain)

10

What is histamine?

- Vasoactive amine
- Produced by mast cells
- Packaged into granules inside mast cells - when antigen binds to IgE on the surface of mast cells - causes cross-linking and degranulation

11

What are the two main effects of histamine?

Vasodilation
Increased Vascular Permeability

12

What does dysregulation of histamine result in?

Allergy (Type 1 Hypersensitivity)

13

What are some other important mediators in inflammation and what do they do?

Prostaglandins: PGE2 causes vasodilation, pain and fever
PGI2 causes vasodilation

Chemokines: activate neutrophil chemotaxis

Complement: variety of proteins and actions including stimulating mast cell degranulation, neutrophil chemotaxis and osponisation

Cytokines (Interleukins and TNF): actions include pro and anti inflammatory signalling, inducing fever, weight loss and malaise

14

How are histamines, prostaglandins and IL-1 and TNF targeted?

prostaglandins- aspirin
histamine - anti-histamine
IL-1, TNF - anti TNF antibodies

15

What is exudate?

A fluid with a high content of protein and cellular debris which has escaped from blood vessels and has been deposited in tissues or on tissue surfaces, usually as a result of inflammation. FLUID LEAKS

16

What is transudate?

Caused by disturbances in hydrostatic and colloid osmotic pressure, not caused by inflammation.
FLUID FORCED OUT

17

What is the composition of transudate?

- low protein
- few cells
- low specific gravity: ratio of density of substance to reference substance

18

What is the function of exudate?

It contains cells, fluid, proteins and antibodies etc.

Fluid - dilutes pathogen and allows soluble mediators to spread

Fibrin - walls off pathogen to stop it spreading. Gives inflammatory cells substrate to hold on to/migrate through

19

What are the types of exudate?

Serous = fluid filled
Lowest protein content of all the exudates. E.g. blister

Fibrinous = High fibrin content
More due to traumatic injury
E.g. Viral Pericarditis

Purulent = pus filled
Combination of fibrin, inflammatory cells, debris and fluid
E.g peritonitis following bowel perforation

20

What are the cellular events that occur during acute inflammation and what is the main cell involved?

NEUTROPHILS
1) Enters into tissues
2) Migrate via chemotaxis
3) They become activated
4) They carry out phagocytosis
5) They release mediators and interact with other cells

21

What is the main role of neutrophils?

- Kill bacteria and recruit more cells
- Phagocytosis
- Degranulation

FIRST CELLS TO SITE

22

How do phagocytes kill the engulfed material?

By free radicals, lysozyme, lactoferrin (binds iron and stops bacteria reproducing), major basic protein (produced by eosinophils - cytotoxic to helminth parasites)

23

How is the inflammation reaction controlled?

- Mediators and neutrophils have short half life
- Stimulus (e.g. bacteria) removed
- Mast cells and lymphocytes release anti-inflammatory products (lipoxins)
- Macrophages release anti-inflammatory products

24

Can tissue damage occur during acute inflammation?

Yes, the body responding tot the agent causing inflammation can lead to necrosis.

25

What are the histological features of acute inflammation?

- Lots of neutrophils
- Mast cells
- Eosinophils

26

How does acute inflammation differ to chronic?

- fewer neutrophils in chronic
- other cell types involved in chronic e.g. macrophages, lymphocytes and plasma cells
- time period
- no exudate in chronic inflammation
- necrosis isn't as prominent in chronic
- formation of granulation tissue while repairing in chronic

27

What are the causes of chronic inflammation?

- Persistent infection
- Prolonged exposure to toxic agent
- Autoimmunity
- Foreign body

28

What are the histological features of chronic inflammation?

Macrophages, lymphocytes and plasma cells will be abundant

29

What is granulomatous inflammation, its features and what are its causes?

Form of chronic inflammation characterised by granuloma formation

- Clusters of macrophages
- Involves specific immune reaction T cells

Causes:
- Infection
- Foreign Material
- Reaction to tumours
- Immune Diseases (e.g. Crohn's)

30

What are the histological features of granulomatous inflammation?

- macrophages in the middle and lymphocytes around the outside
- horse-shoe shaped nuclei - fused macrophages seen during later stages

31

What are the differences between acute and chronic inflammation?

Acute:
- neutrophils
- histamine
- necrosis
- exudate
- immediate onset
- lasts a few days
- complete resolution
- may progress to chronic

Chronic:
- macrophages
- cytokines
- scar tissue
- delayed onset
- lasts weeks/months/years
- scar tissue
- disability

32

What are the good long term outcomes of inflammation?

- removed causative agent
- inflammation stops
- resolution

33

What are the bad outcomes of inflammation?

Local:
- excess damage and scarring
- secondary effects on nearby tissue

Systemic:
- systemic inflammation
- secondary multi-organ failure e.g. septic shock

34

What is resolution and when can it occur?

regeneration of normal functional parenchymal cells

- tissue is capable of regeneration e.g. liver cells
- little structural damage is done as a framework is needed e.g. BM

35

What is repair?

connective tissue and scar tissue formation
happens when tissue loss is too great and cannot be regenerated

36

Example of resolution

Pneuomococcal lobar pneumonia:

- initially you get exudation
- red hepatisation (erythrocytes move into alveolar cells and it become like liver)
- erthrocytes break down causing grey hepatisation
- as long as BM is intact the body can resolve the problem

37

What is the process of repair?

- fibroblasts make collagen
- collagen is a string scar type
- then remodelling of collagen fibres for maximal tensile strength

38

Which factors hinder repair?

General:
- Poor nutrition (protein needed for collagen production)
- Vitamin Deficiency (C needed by fibroblasts to make collagen, A needed for epithelial regeneration)
- Mineral Deficiency
- Suppressed Inflammation

Local:
- Poor blood supply
- Persistent foreign body
- Movement (e.g. broken bones)

39

What are some of the complications of repair?

Keloid Formation:
Excess collagen deposition ( can result in scar tissue formation other than at the site of original injury).

Contractures:
Fibrous scar tissue contracts as part of its maturing process. If this happens across a joint, you can get reduced joint mobility.

Impaired Organ Function:
Fibrous scars forming in organs will cause loss of functional tissue which can affect organ function.

40

Stages of wound healing

1) hemostasis (stop bleeding)
2) inflammation (vessel growth and remove pathogens)
3) proliferation (wound closed)
4) remodelling