Pathology 4 and 5 - Inflammation 2 and 3 Flashcards Preview

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Flashcards in Pathology 4 and 5 - Inflammation 2 and 3 Deck (51)
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1

Why are mediators of inflammation short lived?

They are only produced as long as the stimulus is present

2

How long do neutrophils survive outside of a blood vessel?

A couple of hours

3

What are the 4 possible sequels after acute inflammation`?

ResolutionSuppurationRepair, organisation, and fibrosisChronic inflammation*may not be mutually exclusive

4

what does what one of the 4 possible sequels of inflammation that occurs depend upon? (3)

Site of injury (different organs have different capacities for repair and different vascular supplies)Type of injury (severity, pathogenicity of organism)Duration of injury (can be removed, is it sustained)

5

What is resolution?

Complete restoration of the tissue to normal after removal of inflammatory components

6

How much cell death occurs with resolution?

Minimal amounts

7

What kind of tissues does resolution occur in?

Tissues that have capacity to repair e.g GI tractTissues that have a good vascular supply for delivery of WBCs and removal of injurious agents

8

What is suppuration?

Formation of pus

9

What is pus formed from?

Living, dying and dead cells (neutrophils, bacteria and inflammatory debris (fibrin))

10

What is an abcess?

Collection of pus

11

What is an empyema?

A collection of pus in a body cavity

12

When does repair occur

When a tissue is injured and cannot be wholly regenerated

13

What are the 3 phases of repair?

Phagocytosis to clear debrisOrganisationEpithelial regeneration to cover wound

14

When does repair occur in contrast to resolution? (4)

When injury produces lots of necrosisif injury produces a lot of fibrin that isn't easily clearedif there is a poor blood supply = difficulty removing debrisMucosa where damage goes beyond the basement membrane favours healing by organisation and repair and not resolution (substantial tissue damage meaning the tissue is unable to regenerate and is instead replaced by fibrous tissue - resolution occurs a scaffolding to occur)

15

What is organisation?

Fibroblasts secrete ECM and new vessels grow into region -> formation of granulation tissue

16

What happens in granulation tissue formation? (organisation)

Defect is slowly infiltrated by capillaries and then by myofibroblastsDeposit collagen and smooth muscle cellsHas a very red look

17

What is fibrosis?

Formation of excess fibrous connective tissue in an organ/ tissue in a reparative/ reactive processIf this is in response to injury it is called scarring"patch job"Causes a loss of function

18

When does scarring and fibrosis of the liver occur?

Liver can regenerate but if overwhelmed it undergoes scarring and fibrosis = cirrhosis resulting in liver failure

19

When is chronic inflammation favoured?

SuppurationPersistence of injury e.g. foreign materialPersistence of infectiontype of injury e.g. autoimmune, transplant rejection

20

What is chronic inflammation characterised by?

LymphocyteMacrophage (monocyte within tissue)

21

What is a granuloma?

A collection of immune cells known as histiocytes"aggregate of epithelia histiocytes"

22

What is a histiocyte?

A stationary phagocytic cell present in connective tissue

23

When does a granuloma form?

When the immune system attempts to wall off substances it perceives as foreign but is unable to eliminatee.g. endogenous - keratin, bone, crystalsExogenous - talc, asbestos, suture materials, oil

24

What are some examples of diseases that cause granulomas?

Specific infectionsParasitesWormsEggsSyphilisMycobacterium - including TB

25

What is "cheesy necrosis"?

Tuberculous granulomas - caseous necrosis

26

What is an infarction?

Death of tissue after loss of oxygen

27

Why does muscle need O2?

To produce ATP for energy required to contract

28

What happens if a cell has no ATP?

Na/K ATPase fails = increased K = swellingCalcium pump fails = increased intracellular calciumIncreased calcium stimulates:ATPase (makes things worse)Phospholipase (membrane damage)Proteases (membrane and cytoskeleton damage)Endonuclease (DNA damage and breakdown)Mitochondrial permeability (release pro death factors)

29

What is the time frame for the myocardium being without oxygen but only causing reversible damage?

20 minute window

30

Why is there no point in using clot busting drugs after 30 minutes for clot causing loss of blood supply to myocardium?

After 20 minutes there is non-reversible injury - the cells will die anyway