Inflammation

Question 1

What is inflammation?

Answer 1

• Response of living tissue to injury/insult, can be physical/chemical/infective/hypersensitive
• Protective reaction: dilute/destroy/isolate/initiate repair
• Potentially harmful - componments can injury bystander normal tissue

Question 2

Two types of inflammation

Answer 2

Acute and chronic

Question 3

Signs of infection

Answer 3

Heat/redness/swelling/pain/loss of function

Question 4

Characteristics of acute inflammation

Answer 4

Fast
Mainly neutrophils
Usually mild and self-limited
Prominent symptoms

Question 5

Characteristics of chronic inflammation

Answer 5

Slower
Mainly monocytes/macrophage and lymphocytes
Severe and progressive tissue injury
More subtle symptoms

Question 6

Vascular response of acute inflammation

Answer 6

Vasodilation, leaky capillaries

Question 7

Cellular response of acute inflammation

Answer 7

Margination, adhesion, emigration and activation of neutrophils

Question 8

Is the complement cascade activated in acute inflammation?

Answer 8

Yes

Question 9

How is vasodilation stimulated?

Answer 9

Histamines and NO act on smooth muscle

Question 10

What is stasis?

Answer 10

Shortened blood flow, hyperviscosity

Question 11

Characteristics of vasodilation

Answer 11

Increased permeability of vasculature: formation of early transudate (protein-rich filtrate of plasma) gives rise to exudate (protein rich filtrate) into extracellular tissues

Question 12

Which molecules cause endothelial cell contact to widen intercellular gaps of venues?

Answer 12

Histamines, bradykinins, leukotrienes

Question 13

Process of vascular leakage

Answer 13

• Histamines, bradykinins, leukotrienes cause endothelial cell contraction that widens intercellular gaps of venules
• Outpouring of exudate into extracellular tissue leads to reduction of intravascular osmotic pressure and increase in extravascular, interstitial osmotic pressure
• Increase of interstitial osmotic pressure leads to edema (water and ions)

Question 14

How can leukocytes leave vasculature?

Answer 14

Margination and rolling
Activation and adhesion
Transmigration

Question 15

How is CRP produced?

Answer 15

Interleukins stimulate liver to produce CRP

Question 16

What impact does TNF have on the heart?

Answer 16

Negative - stops it beating as strongly

Increases risk of thrombosis

Question 17

Symptoms of systemic infection

Answer 17

Lower blood pressure, change in heart rate, fatigue, depression, fever

Question 18

What happens to [albumin] in inflammation?

Answer 18

Goes down

Question 19

Factors impacting would healing

Answer 19

Infection/pressure /nutrition/ age/ immunocompromised/diabetes /BMI

Question 20

Factors aiding wound healing

Answer 20

Oxygen, maggots, Manuka honey, general good health, antibiotics

Question 21

Symptoms of acute inflammation

Answer 21

Malaise, fever, pain, rapid pulse

Question 22

Laboratory investigations for acute inflammation

Answer 22

Increased neutrophils, increased erythrocyte sedimentation rate, increased concentration of acute-phase proteins
CRP begins to rise and peak at 36-50 hours after infection
ESR shows slower rise and return to normal than CRP

Question 23

Components of chronic inflammation

Answer 23

Lymphocytes, plasma cells, macrophage infiltration

Question 24

How are cells repaired after chronic inflammation?

Answer 24

Fibrosis and angiogenesis

Question 25

Through which routes can chronic inflammation occur?

Answer 25

May progress from acute inflammation or repeated episodes of acute inflammation or occur 'de novo' if the causative agent produces only a mild acute response

Question 26

Chemicals stimulating vasodilation

Answer 26

Prostaglandins, NO

Question 27

Chemicals stimulating increased vascular permeability

Answer 27

Histamines, serotonin, C3a, C5a, bradykinin, leukotrienes (C4, D4, E4), platelet activating factor

Question 28

Chemicals stimulating chemotaxis and leukocyte activation

Answer 28

C5a, leukotriene B4, bacterial products, chemokines (IL-8)

Question 29

Chemicals stimulating fever

Answer 29

IL-1, IL-6, TNF, prostaglandins

Question 30

Chemicals stimulating pain

Answer 30

Prostaglandins, bradykinin

Question 31

Chemicals stimulating tissue damage

Answer 31

Neutrophil and macrophage lysosomal enzymes, oxygen metaboplites, NO

Question 32

Where can chemical mediators arise from?

Answer 32

May be derived locally at the site of inflammation or may be derived from circulating inactive precursors that are activated at the inflammation site

Question 33

When are cell-derived mediators created?

Answer 33

Normally sequestered in intracellular granules, they are rapidly secreted when activated or are synthesised 'de novo' in response to stimulus

Question 34

What are plasma protein-derived mediators?

Answer 34

Complement proteins/kinins which circulate in an inactive form and undegro proteolytic cleavage to acquire biologic activities