Cell Pathology 4

Question 1

Describe acute inflammation.

Answer 1

1. Transient and early response to injury
2. Chemical mediators released.
3. Vascular and leukocyte response

Question 2

Describe chronic inflammation.

Answer 2

Inflammation of prolonged duration

Question 3

Describe granulomatous inflammation.

Answer 3

Specialised form of chronic inflammation

Question 4

Describe the cardinal signs of acute inflammation.

Answer 4

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

Question 5

What are the vascular events that cause the cardinal signs?

Answer 5

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

Question 6

Describe histamines.

Answer 6

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

Question 7

Name some other important mediators involved in inflammation.

Answer 7

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

Question 8

Name the substances that target inflammatory mediators.

Answer 8

1. Histamines - antihistamines
2. Prostaglandins - aspirin
3. IL-1 and TNF - anti-TNF antibodies

Question 9

What is exudate?

Answer 9

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

Question 10

What is transudate?

Answer 10

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

Has low protein content, low specific gravity.

Question 11

What is the function of exudate.

Answer 11

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

Question 12

3 types of exudate?

Answer 12

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

Question 13

What are the cellular events in acute inflammation?

Answer 13

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

Question 14

3 roles of neutrophils?

Answer 14

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

Question 15

What are the stages of cellular egress.

Answer 15

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

Question 16

What does phagocytosis consist of?

Answer 16

1. Opsonisation
2. Ingestion
3. Killing

Question 17

How is the inflammatory reaction controlled?

Answer 17

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

Question 18

What are the histological features of acute inflammation?

Answer 18

1. Lots of neutrophils

2. Lots of mast cells and eosinophils

Question 19

How does acute inflammation become chronic inflammation.

Answer 19

1. Breakdown of myofibres

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

Question 20

What is chronic inflammation?

Answer 20

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

Question 21

What causes chronic inflammation?

Answer 21

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

Question 22

What is important about chronic inflammation?

Answer 22

NO EXUDATE

Question 23

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

Answer 23

T

Question 24

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

Answer 24

Granulation tissue

Question 25

Describe monocytes/macrophages.

Answer 25

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

Question 26

What are the histological features of chronic inflammation?

Answer 26

Macrophages, lymphocytes and plasma cells are abundant.

Question 27

Describe granulomatous inflammation.

Answer 27

1. IT IS A FORM OF CHRONIC INFLAMMATION SHOWING GRANULOMA FORMATION. 2. Involves clusters of macrophages and specific immune reaction T-cells

Question 28

What are the causes of granulomatous inflammation?

Answer 28

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

Question 29

What are the histological features of granulomatous inflammation?

Answer 29

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

Question 30

Highlight some differences between acute inflammation and chronic inflammation.

Answer 30

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

Question 31

What are the beneficial outcomes of inflammation.

Answer 31

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

Question 32

What are negative outcomes of inflammation?

Answer 32

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.

Question 33

What is resolution?

Answer 33

Parenchymal cells are regenerated

Question 34

What is repair?

Answer 34

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

Question 35

When can resolution occur?

Answer 35

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)

Question 36

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

Answer 36

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

Question 37

Name some things that hinder repair.

Answer 37

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)

Question 38

What are the complications of repair?

Answer 38

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