Untitled Deck

Question 1

What is inflammation?

Answer 1

A reaction of vascularised living tissue to injury or infection, involving movement of fluid and leukocytes into tissue.

Question 2

What are the two main types of inflammation?

Answer 2

Acute and chronic.

Question 3

What triggers acute inflammation?

Answer 3

Injury, infection, or foreign bodies.

Question 4

What are the cardinal signs of inflammation?

Answer 4

Redness, heat, swelling, pain.

Question 5

What causes redness and heat?

Answer 5

Hyperaemia (increased blood flow due to vasodilation).

Question 6

What causes swelling?

Answer 6

Exudation of protein‑rich fluid into tissues.

Question 7

What causes pain?

Answer 7

Sensitisation of pain receptors by prostaglandins and other mediators.

Question 8

What is hyperaemia?

Answer 8

Increased blood flow through tissue due to arteriolar vasodilation.

Question 9

Which vessels mediate exudation?

Answer 9

Post‑capillary venules.

Question 10

What is exudate?

Answer 10

Protein‑rich oedema fluid caused by increased vascular permeability.

Question 11

What is pus?

Answer 11

Exudate containing neutrophils, microbes, debris, protein, DNA.

Question 12

What is the purpose of exudation?

Answer 12

Dilute toxins, deliver antibodies/complement/fibrin, recruit neutrophils.

Question 13

What are the main vasoactive mediators?

Answer 13

Histamine, prostaglandins, leukotrienes, kinins, complement fragments (C3a, C5a).

Question 14

What does histamine do?

Answer 14

Causes vasodilation and increased vascular permeability.

Question 15

What enzyme releases arachidonic acid?

Answer 15

Phospholipase A2.

Question 16

What blocks phospholipase A2?

Answer 16

Corticosteroids.

Question 17

What blocks cyclo‑oxygenase?

Answer 17

NSAIDs (aspirin, indomethacin, celecoxib).

Question 18

What do prostaglandins do?

Answer 18

Cause vasodilation and sensitise pain receptors.

Question 19

What do leukotrienes do?

Answer 19

Increase vascular permeability and act as chemoattractants.

Question 20

What do C3a and C5a do?

Answer 20

Increase vascular permeability and recruit neutrophils.

Question 21

What is the stereotypic nature of acute inflammation?

Answer 21

Different injuries produce the same sequence of vascular + cellular events.

Question 22

What is the role of inflammation?

Answer 22

Defence, elimination of damaged tissue, initiation of healing.

Question 23

Does acute inflammation usually progress to chronic?

Answer 23

No — this is rare.

Question 24

What is the first leukocyte to arrive in acute inflammation?

Answer 24

Neutrophils.

Question 25

What is the timeline of acute inflammation?

Answer 25

Seconds → mediators; minutes → vasodilation; hours → neutrophils; days → healing.

Question 26

What are the main roles of neutrophils?

Answer 26

Kill microbes and release chemoattractants.

Question 27

Where are neutrophils produced?

Answer 27

Bone marrow (~1.5 million/sec).

Question 28

How long do neutrophils live?

Answer 28

~12 hours in blood, ~24 hours in tissues.

Question 29

Can neutrophils proliferate?

Answer 29

No — terminally differentiated.

Question 30

What are the steps of neutrophil emigration?

Answer 30

Margination → rolling → adhesion → emigration (diapedesis).

Question 31

What mediates rolling?

Answer 31

Selectins.

Question 32

What mediates firm adhesion?

Answer 32

Integrins.

Question 33

What is chemotaxis?

Answer 33

Directed movement of neutrophils up a chemoattractant gradient.

Question 34

What structural change allows neutrophil movement?

Answer 34

Polarisation (lamellipodium front, uropod rear).

Question 35

What are the two types of neutrophil granules?

Answer 35

Primary (azurophilic) and secondary (specific).

Question 36

What is the main energy source for neutrophils?

Answer 36

Anaerobic glycolysis (glycogen).

Question 37

What are the steps of phagocytosis?

Answer 37

Recognition → engulfment → phagosome → phagolysosome → killing.

Question 38

What enzyme generates ROS?

Answer 38

NADPH oxidase.

Question 39

Where does the oxidative burst occur?

Answer 39

Inside the phagolysosome.

Question 40

What are NETs?

Answer 40

Neutrophil extracellular traps made of DNA + antimicrobial proteins.

Question 41

What do NETs do?

Answer 41

Trap and kill microbes extracellularly.

Question 42

What is a clinical downside of NETs?

Answer 42

Can promote cancer progression and autoimmune disease.

Question 43

What are the main roles of macrophages?

Answer 43

Kill microbes, phagocytose debris, produce cytokines, regulate inflammation.

Question 44

How long do macrophages live?

Answer 44

Months to years.

Question 45

Can macrophages proliferate?

Answer 45

Yes.

Question 46

What are macrophage extracellular traps (METs)?

Answer 46

DNA‑based traps similar to NETs; can contribute to autoimmunity.

Question 47

What are cytokines?

Answer 47

Proteins that modify activity of immune/inflammatory cells.

Question 48

What are the modes of cytokine action?

Answer 48

Autocrine, paracrine, endocrine.

Question 49

What are the key pro‑inflammatory cytokines?

Answer 49

IL‑1 and TNF.

Question 50

What do IL‑1 and TNF do?

Answer 50

Increase adhesion molecules, induce fever, stimulate leukocyte production.

Question 51

What are PAMPs?

Answer 51

Pathogen‑associated molecular patterns (microbial components).

Question 52

What are PRRs?

Answer 52

Pattern recognition receptors that detect PAMPs.

Question 53

What are TLRs?

Answer 53

Toll‑like receptors — major PRR family.

Question 54

What does TLR4 recognise?

Answer 54

LPS.

Question 55

What does TLR5 recognise?

Answer 55

Flagellin.

Question 56

What does TLR3 recognise?

Answer 56

Double‑stranded RNA.

Question 57

What does TLR9 recognise?

Answer 57

CpG DNA.

Question 58

What are DAMPs?

Answer 58

Damage‑associated molecular patterns released from injured cells.

Question 59

Examples of DAMPs?

Answer 59

ATP, DNA, RNA, HMGB1, S100 proteins, uric acid, ECM fragments.