Lecture 8: Acute inflammation - blood flow

Question 1

Four cardinal signs of inflammation?

Answer 1

Redness (rubor), Heat (calor), Swelling (tumor), Pain (dolor)

Red heads suck p*
Rub Cal’s tummy daily

Question 2

Encapsulation of injury

Answer 2

To limit the spread of harmful agents, abscess walls and fibrin mesh encapsulate the injury, clot it and create a barrrier.

Question 3

Hydralase role in inflammation

Answer 3

Hydralase digest inflammatory exudates following crises.

Question 4

Acute inflammation can lead to:

Answer 4

Complete resolution - successful healing
Abscess/scar formation - failed healing
Chronic inflammation - failed healing.

Question 5

Cell derived mediators

Answer 5

Vasoactive amines, tryptases, lipids

• Control B.V. function. i.e. induce vasopermeability, vasodilation, neutrophil adhesion to endothelial cells, bronchoconstriction, and pain/itching.

Question 6

Damaged cells release and bind to:

Answer 6

Neurons: bioactive peptides
Damaged cells (injury/ischemic): DAMPs
Pathogen in cells: PAMPs

All of them bind to Pattern recognition receptors (PRR) on macrophages and mast cells.

Question 7

What do mast cells and macrophages do after PRR binding?

Answer 7

Degranulation of mast cells and macrophages, and release mediators - histamine, proteases (i.e. tryptases), lipid signals, cytokines (i.e. TNF)

Question 8

Vasodilation

Answer 8

In arterioles due to presence of smooth muscle (relaxtion), increased blood flow and lumen size caused by mediators.

Causes redness and heat in tissues.

Question 9

Vasopermeability

Answer 9

Vasoactive signals bind to receptors of endothelial cells in venules, causing them to reversibly retract, opening up spaces between cells. Plasma leaks through the space into the interstitial space, causing swelling and oedema.

• in mild injury (i.e. insect bite)

Question 10

Oedema

Answer 10

Swelling (oedema) is caused by exudate build up in interstitial space.

Swelling and stretching of tissues causes nerve endings (receptors) to sense pain.

Can cause blisters, swelling, blockage of tubes. i.e. airway constriction or pleural effusion.

Question 11

Vasoactive amines

Answer 11

Degranulation of mast cells/basophils release vasoactive amines (i.e. histamine).

> vasodilation
vasopermeability
neutrophil recruitment
Platelet Activating Factor (PAF) release -> leukocyte adhesion.

Question 12

Platelet Activating Factor (PAF)

Answer 12

Cell derived mediator - allows for platelet aggregation and activation (clotting), leukocyte adhesion, chemotaxis and activation

Question 13

Breakdown of membrane phospholipids (cell derived mediators) to:

Answer 13

Cytokines and chemokines release PLA2 (phospholipase 2).

Membrane phospholipids –PLA2–> arachadonic acid + lysophosphatidylcholine (LysoPC).

Arachadonic acid –COX1,2–> Prostaglandins.

Arachadonic acid –LOX–> Leukotrienes

LysoPC –> Platelet Activating Factor (PAF)

Question 14

Phospholipase A2 (PLA2)

Answer 14

enzyme that cleaves membrane phospholipids to arachadonic acid and lysophosphotidylcholine

Question 15

5’ - lipoxygenase (LOX)

Answer 15

Enzyme that cleaves Arachadonic acid to leukotrienes.

Question 16

Cyclooxygenases (COX-1,2)

Answer 16

Enyme that cleaves arachadonic acid to Prostaglandins

Question 17

Leukotrienes

Answer 17

Cell derived mediating factors

i.e. LTB4 - Neutrophil chemotaxis and activation, vasodilation
i.e. cysLTC4, D4, E4 - vasopermeability, mucus, bronchoconstrictionro

Question 18

Prostoglandins

Answer 18

Cell derived mediators
i.e. Thromboxane - vasoconstriction, platelet aggregation
i.e. Prostacyclin - vasodilation, plately disaggregation, pain
i.e. PG32 - vasodilation, pain

Question 19

Circulating mediators

Answer 19

Present in forms of circulation and are activated via proteolytic cleavage.

• coagulation (bloodclot), fibrinolytic (balances coagulation), kinin (blood flow), complement (blood flow, immune cell attraction, target opsonisation).

Question 20

Complement pathway

Answer 20

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