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Flashcards in Cell Pathology 4 Deck (38):
1

Describe acute inflammation.

1. Transient and early response to injury

2. Chemical mediators released.

3. Vascular and leukocyte response

2

Describe chronic inflammation.

Inflammation of prolonged duration

3

Describe granulomatous inflammation.

Specialised form of chronic inflammation

4

Describe the cardinal signs of acute inflammation.

1. Rubor - redness
2. Calor - heat
3. Tumor - swelling
4. Dolor - pain
5. Loss of function

5

What are the vascular events that cause the cardinal signs?

Calor - heat. Histamine mediated vasolidation

Tumor - swelling. Oedema; caused by histamine mediated increase in vessel permeability

Rubor - blood flow not as fast so redness

Loss of function - due to swelling and pain

6

Describe histamines.

1. Vasoactive amine
2. Produced by mast cells
3. They are packaged into granules that are degranulated when there is cross linking of IgE antibody and antigen.

4. Leads to vasodilation and increased vascular permeability.
5. Dysregulation can cause allergy

7

Name some other important mediators involved in inflammation.

1. Prostaglandins
2. Chemokine
3. Complement
4. Cytokines

8

Name the substances that target inflammatory mediators.

1. Histamines - antihistamines

2. Prostaglandins - aspirin

3. IL-1 and TNF - anti-TNF antibodies

9

What is exudate?

Fluid with high protein content and cell debris. It has escaped from blood vessels and resides in tissues/tissue surfaces, usually due to inflammation.

10

What is transudate?

Caused by disturbances in hydrostatic or colloid osmotic pressure. NOT CAUSED BY INFLAMMATION.

Has low protein content, low specific gravity.

11

What is the function of exudate.

it comprises stuff coming out of leaky vessels (fluid, cells, proteins, antibodies, etc).

Function:
1. Dilutes pathogen and allows soluble mediators to spread

2. Fibrin walls off pathogen - stops it from spreading.
It also gives inflammatory cells a substrate to hold onto/migrate through

12

3 types of exudate?

1. Serous - fluid (e.g. blister). HAS LOWEST PROTEIN CONTENT OF ALL EXUDATES
2. Fibrinous - fibrin (e.g. viral pericarditis). Mostly due to traumatic injury.
3. Purulent - pus. Fibrin + inflammatory cells + debris + fluid. e.g. Peritonitis following bowel perforation

13

What are the cellular events in acute inflammation?

1. Neutrophils enter tissue
2. Chemotaxis to site of injury.
3. Become activated
4. Carry out designated role. 5. Release soluble mediators

14

3 roles of neutrophils?

1. Kill bacteria and recruit more cells.
2. Phagocytosis
3. Degranulation

15

What are the stages of cellular egress.

1. Margination
2. Rolling and adhesion
3. Transmigration/diapedesis
4. Chemotaxis

16

What does phagocytosis consist of?

1. Opsonisation
2. Ingestion
3. Killing

17

How is the inflammatory reaction controlled?

1. Mediators and neutrophils have a short half life.
2. Stimulus removed
3. Mast cells and lymphocytes release anti-inflammatory products (lipoxins)
4. Macrophages release antiinflammatory products

18

What are the histological features of acute inflammation?

1. Lots of neutrophils
2. Lots of mast cells and eosinophils

19

How does acute inflammation become chronic inflammation.

1. Breakdown of myofibres

2. Less neutrophils in chronic inflammation, other cell types present (i.e. macrophages, lymphocytes and plasma cells)

20

What is chronic inflammation?

Inflammation of prolonged duration whereby active inflammation, tissue destruction and attempts at repair occur simultaneously.

21

What causes chronic inflammation?

Persistent damage (e.g. persistent infection, autoimmunity, foreign body, prolonged exposure to toxic agent)

22

What is important about chronic inflammation?

NO EXUDATE

23

Necrosis is not as prominent in chronic inflammation, unlike acute inflammation.

T

24

What is formed in chronic inflammation whilst repair attempts are occurring?

Granulation tissue

25

Describe monocytes/macrophages.

1. Circulate in small numbers as monocytes, become macrophages once in tissue.

2. Live longer than neutrophils.
3. Phagocytosis.
4. Control other inflammatory cells by releasing cytokines
5. Increased in viral/atypical bacterial infections

26

What are the histological features of chronic inflammation?

Macrophages, lymphocytes and plasma cells are abundant.

27

Describe granulomatous inflammation.

1. IT IS A FORM OF CHRONIC INFLAMMATION SHOWING GRANULOMA FORMATION.

2. Involves clusters of macrophages and specific immune reaction T-cells

28

What are the causes of granulomatous inflammation?

1. Infection - TB, fungi
2. Foreign material
3. Reaction to tumours
4. Immune diseases

29

What are the histological features of granulomatous inflammation?

1. Macrophages in the middle and lymphocytes on the outside.
2. Horseshoe shaped nuclei - fused macrophages.

30

Highlight some differences between acute inflammation and chronic inflammation.

1. Neutrophils vs Monocytes/macrophages.
2. Histamines vs cytokines
3. Prominent necrosis vs prominent scar tissue
4. Immediate onset vs delayed onset
5. Can be completely resolved/progress to chronic inflammation vs scar tissue formation vs disability

31

What are the beneficial outcomes of inflammation.

1. Removal of causative agent.
2. Cessation of inflammatory reaction.
3. Healing of tissue damage - preserves integrity and function (resolution)

32

What are negative outcomes of inflammation?

LOCAL:
1. Can cause excess local tissue damage/scarring
2. Secondary effects on nearby tissue

SYSTEMIC:
1. Can evolve into systemic inflammatory reaction and secondary multl-organ failure.

33

What is resolution?

Parenchymal cells are regenerated

34

What is repair?

Connective tissue and scar tissue formation because tissue loss is too great for cells to regenerate

35

When can resolution occur?

1. When tissue contains cells that can regenerate (e.g. liver cells)

2. Little structural damage is done - cells need a framework to build on (basement membrane)

36

Describe how normal tissue is replaced with fibrous scar tissue in repair.

1. Fibroblasts - produce collagen
2. Collagen - strong scar type collagen
3. Remodelling - reorientation of collagen fibres for maximal tensile strength.

37

Name some things that hinder repair.

GENERAL :
1. Poor nutrition
2. Vitamin deficiency
3. Mineral deficiency
4. Suppressed inflammation (e.g. steroids, old age, diabetes, etc)

LOCAL:

1. Poor blood supply
2. Persistent foreign body
3. Movement (e.g. across a fracture site - casts given)

38

What are the complications of repair?

1. Keloid formation - excess collagen deposition
2. Contractures - fibrous scar tissue contracts as it matures. If this occurs at a joint it can cause poor joint mobility
3. Impaired organ function - e.g. fibrous scars in myocardium after heart attack