Acute Inflammation 2

Question 1

What is inflammation in the lungs called?

Answer 1

pneumonia

Question 2

What is inflammation in the pleural cavity called?

Answer 2

pleurisy

Question 3

What do neutrophils do?

Answer 3

-Recognise a foreign antigen, move towards it and adhere to organism.
-Granules possess oxidants (H2O2) and enzymes (proteases)
Release granule contents
-Phagocytose and destroy foreign antigen

Question 4

What are the consequences of neutrophil action?

Answer 4

• Neutrophils die when granule contents released
• Produce pus filled with bits of cell, organisms and endogenous proteins
• Inflammation might progress if extension into other tissues

Question 5

What is the role of plasma proteins in inflammation?

Answer 5

• Fibrinogen is a coagulation factor which forms fibrin and clots exudate. This localises the inflammatory process
• Immunoglobulins provide a humoural immune response, plasma specific for antigen

Question 6

What are mediators of acute inflammtion

Answer 6

• molecules on endothelial cell surface membrane
• molecules released from cells
• molecules in the plasma

Question 7

What are the collective effects of mediators?

Answer 7

• vasodilation
• increased permeability
• neutrophil adhesion
• chemotaxis
• itch and pain

Question 8

What does ICAM-1 do?

Answer 8

Helps neutrophils to stick

Question 9

What does P-selectin do?

Answer 9

Interacts with neutrophil surface

Question 10

What molecules are released from cells?

Answer 10

• histamine
• 5-hydroxytryptamine (serotonin)
• prostaglandins (arachidonic acid metabolites via lipoxygenase pathway)
• leukotrienes (arachidonic acid metabolites via cyclo-oygenase pathway)
• omega-3 polyunsaturated fatty acids
• platelets activating factor
• cytokines and chemokines
• nitric oxide
• oxygen free radicals

Question 11

Histamine

Answer 11

• It is preformed in mast cells beside vessels, platelets, basophils]
• It is released as a result of local injury: IgE mediated reactions
• Causes vasodilation and increased permeability
• Acts via H1 receptors on endothelial cells

Question 12

Serotonin

Answer 12

-Preformed in the platelet
Released when platelets degranulate in coagulation
-Cause vasoconstriction

Question 13

Prostaglandins

Answer 13

• Released by many cells (endothelium and leukocytes).
• Many promote histamine effects and inhibit inflammatory cells.
• Thromboxane A2 promotes platelet aggregation and vasoconstriction- the opposite effect to PGD2, PGE2 etc.. -Latter: effectiveness of non-steroidal anti-inflammatory drugs.

Question 14

Leukotrines

Answer 14

• Released by neutrophils especially

- Vasoactive-dynamic effort on vessels to increase permeability and constrict smooth muscle

Question 15

Omega-3 polyunsaturated fatty acids

Answer 15

Decrease synthesis of arachidonic acid derived inflammatory response?

Question 16

What is platelet activating factor?

Answer 16

• Produced by cell membranes of activated inflammatory cells

- Reduces permeability by enhancing platelet degranulation at site of injury

Question 17

Cytokines and Chemokines

Answer 17

• small molecules produced by macrophages, lymphocytes and endothelium in response to inflammatory stimuli
• they attract inflammatory cells

Question 18

Nitric Oxide

Answer 18

• Released by various cells

- Cause relaxation of smooth muscle, anti platelet, regulate leukocyte recruitment to inflammatory response

Question 19

Oxygen Free Radicals

Answer 19

• Released by neutrophils on phagocytosis

- They amplify other mediator effects

Question 20

What are the 4 enzymes cascades that take place in the plasma?

Answer 20

• blood coagulation pathways
• fibrinolysis
• kinin system
• complement cascade

Question 21

Blood Coagulation Pathways

Answer 21

• clots fibrinogen in the exudate

- interacts widely with other systems

Question 22

Fibrinolysis

Answer 22

• breaks down fibrin to help maintain blood supply

- products of fibrin breakdown are vasoactive

Question 23

Kinin System

Answer 23

Bradykinin responsible for pain

Question 24

Complement Cascade

Answer 24

• Ties inflammation with the immune system

- Active components stimulate increased permeability, chemotaxis, phagocytosis and cell breakdown

Question 25

What are the immediate systemic effects of inflammation?

Answer 25

- pyrexia - feeling unwell including malaise, anorexia, nausea, abdominal pain and vomiting - neutrophilia- released by bone marrow

Question 26

What are the longer term effects of acute inflammation?

Answer 26

- lymphadenopathy - weight loss - anaemia

Question 27

What are the outcomes of acute inflammation?

Answer 27

- resolution - suppuration - organisation - dissemination - chronic inflammation

Question 28

What is suppuration?

Answer 28

- Formation of pus | - Pyogenic membrane surrounds pus and walls it off

Question 29

What is an abscess?

Answer 29

- A collection of pus under pressure - Can be single locule or multi-loculated - It points and discharges before collapsing and healing

Question 30

How are multiloculated abscesses formed?

Answer 30

Pus bursts through pyogenic membrane and forms new cavities

Question 31

What is an empyema?

Answer 31

Pus in a hollow viscous such as the gall bladder or the pleural cavity

Question 32

What is pyaemia?

Answer 32

When pus is discharged into the bloodstream

Question 33

What is organisation?

Answer 33

Organisation is healing and repair. Characterised by granulation tissue and leads to fibrosis and formation of a scar.

Question 34

What is granulation tissue?

Answer 34

It is a universal patch formed of new capillaries, fibroblasts, collagen and macrophages.

Question 35

What is dissemination?

Answer 35

-Spread to the bloodstream which results in patients becoming septic

Question 36

Bacteraemia

Answer 36

bacteria in the blood

Question 37

septicaemia

Answer 37

growth of bacteria in blood

Question 38

toxaemia

Answer 38

toxic products in blood

Question 39

What are the effects of systemic infection?

Answer 39

- shock=inability to perfuse tissues | - early septic shock

Question 40

What are the symptoms of early septic shock?

Answer 40

- peripheral vasodilation - tachycardia - hypotension - pyrexia - sometime haemorrhagic skin rash

Question 41

What is the pathogenesis of septic shock?

Answer 41

- There is a systemic release of chemical mediators from cells into plasma - Mediators cause vasodilation causing loss of systemic vascular resistance - Results in catecholamine release - Tachycardia follow to maintain CO because increased heart rate compensates CO=SV x HR - bacterial endotoxin released - activation of coagulation

Question 42

What does interleukin-1 do?

Answer 42

When released it acts on the hypothalamus and causes pyrexia

Question 43

How does the activation of coagulation result in a haemorrhagic skin rash?

Answer 43

- Disseminated intravascular coagulation - Vasoactive chemical causes vasodilation - Results in haemorrhagic skin rash

Question 44

What happens when a raised HR is insufficient to maintain cardiac output?

Answer 44

- SVR is low so BP falls. - There is reduced perfusion of tissues which results in tissue hypoxia and leads to loss of cell tissue and organ function

Question 45

What are the outcomes of septic shock?

Answer 45

- proves rapidly fatal - tissue hypoxia -cell death - haemorrhage - requires urgent intervention and support- admittance to ICU