Pathology 3 - Acute Inflammation Flashcards Preview

CJ: UoL Medicine Semester Two (ESA2) > Pathology 3 - Acute Inflammation > Flashcards

Flashcards in Pathology 3 - Acute Inflammation Deck (48):
1

What is the definition of acute inflammation?

"The response of living tissue to injury".

- innate, immediate, early, stereotyped
- short duration
- initiated to limit the tissue damage

2

What is acute inflammation generally controlled by?

A variety of chemical mediators derived from plasma or cells

3

Give some causes of acute inflammation

- microbial infections eg. pyogenic organism
- hypersensitivity reactions
- physical agent (heat, light etc)
- chemicals
- tissue necrosis

4

What are the main clinical signs of acute inflammation?

Rubor, tumor, calor, dolor, loss of function

5

What is the general pattern of acute inflammation?

1) changes in blood flow
2) exudation of fluid into tissues
3) infiltration of inflammatory cells

6

What are the 4 stages of changes in the blood flow during the inflammory response?

- transient vasoconstriction of arterioles
- vasodilatation of arterioles then capillaries, leading to increase in blood flow to area
- increased permeability of blood vessels, leading to exudation of protein-rich fluid into tissues and slowing of circulation
- concentration of RBCs in small vessels and increased viscosity of blood ('stasis')

7

What is histamine released from?

Mast cells, basophils and platelets

8

What does histamine cause?

Vascular dilatation, transient increase in vascular permeability, pain

9

True or false - histamine mediates the persistent response?

False - histamine lasts for around half an hour, and is therefore the 'immediate early response'. The persistent response is controlled by other mediators eg leukotrienes, bradykinin

10

What does Starling's Law state?

Fluid flow across vessel walls is determined by the balance of hydrostatic and colloid osmotic pressure, comparing plasma and interstitial fluid.

11

How does acute inflammation lead to oedema?

- Arteriolar dilatation leads to increase in hydrostatic pressure
- increased permeability of vessel walls leads to loss of protein into interstitium
- net flow of fluid out of vessel leads to oedema

12

Define 'oedema'

Excess of fluid in the interstitium

13

What is the difference between transudate and exudate?

Fluid loss due to inflammation will have a high protein content and is referred to as an EXUDATE, while fluid loss due to hydrostatic pressure imbalance will have low protein content and is a TRANSUDATE

14

Give some examples of mechanisms of vascular leakage

- endothelial contraction
- cytoskeletal reorganisation
- direct injury, eg toxic burns, chemicals
- leukocyte dependent injury
- increased transcytosis

15

Why does plasma contain fibrin?

It produces a meshwork which localises the inflammation and prevents it from spreading to the entire serosa cavity

16

What is the main cell involved with the cellular phase of acute inflammation?

Neutrophil leukocyte (aka 'polymorph')

17

Outline the four stages of infiltration of neutrophils into tissue

1) Stasis causes neutrophils to line up at the edge of blood vessels along the endothelium ('margination')
2) neutrophils roll along endothelium, sticking intermittently ('rolling')
3) they then stick more effectively ('adhesion')
4) neutrophils move through blood vessel wall ('emigration')

18

How do cell adhere in neutrophil migration?

They use proteins called selectins and integrins to adhere to the cell wall

19

How do neutrophils manage to get through the blood vessels?

- relaxation of inter-endothelial cell junctions
- digestion of vascular basement membrane
- movement

20

Define 'chemotaxis'

Movement of chemoattractants along concentration gradients

21

How do neutrophils 'move'?

Chemotaxins eg. C5a, LTB4, bacterial peptides bind to receptors on the neutrophils. When the receptor is activated, the neutrophil moves towards the chemotaxin by rearranging its cytoskeleton and producing a pseudopod

22

What do neutrophils do once they reach the tissues?

They phagocytose substances in three stages - contact, recognition and internalisation. Opsonins (Fc and C3b) facilitate this. They then fuse with lysosomes to produces secondary lysosomes.

23

What are the two methods of killing cells?

O2 dependent and O2 independent

24

Why may neutrophils sometimes cause inflammation to tissue?

They release toxic metabolites

25

Which chemical mediators are responsible for increased blood flow?

Histamine and prostaglandins

26

Which chemical mediators are responsible for vascular permeability?

Histamine and leukotrienes

27

Which chemical mediators are responsible for neutrophil chemotaxis?

C5a, LTB4, bacterial peptides

28

Which chemical mediators are responsible for phagocytosis?

C3b

29

What are proteases?

Plasma proteins synthesised in liver. Three large families - kinins, complement system (C3a, C5a), coagulation/fibrinolytic system

30

What are the two hallmarks of acute inflammation?

Exudate of oedema fluid, and infiltrate of inflammatory cells

31

How does exudation of fluid combat injury?

- Delivers plasma proteins to area of injury eg. immunoglobulins, inflammatory mediators, fibrinogen.
- dilutes toxins
- increases lymphatic drainage (this delivers microorganisms to phagocytes and antigens to immune system)

32

How does infiltration of cells combat injury?

Removes pathogenic organisms and necrotic debris

33

How does vasodilatation combat injury?

Increases delivery, increases temperature

34

How does pain and loss of function combat injury?

Enforces rest, reduces chance of further traumatic damage

35

Give some local complications of acute inflammation

- swelling can block tubes (eg bile duct)
- exudate can cause compression (cardiac tamponade) and serositis
- loss of fluid eg burns
- pain and loss of functions

36

Why is fever associated with inflammation?

IL-1 and TNF alpha are important cytokines that also function as endogenous pyrogens. Prostaglandins are also endogenous pyrogens and can be combated with aspirin

37

Why is leukocytosis associated with acute inflammation?

IL-1 and TNF alpha produce an accelerated release from marrow

38

What are the symptoms of acute phase response?

Decreased appetite, raised pulse rate, altered sleep patterns and changes in plasma concentrations of acute phase proteins

39

What are the acute phase proteins?

- C-reactive proteins
- alpha1 antitrypsin
- haptoglobin
- fibrinogen
- serum amyloid A protein

40

What is the name given to the process which occurs once neutrals are no longer marginating, and vessel permeability and calibre has returned to normal?

Resolution

41

Give some mechanisms for how resolution can occur

- degradation may inactivate
- inhibitors may bind
- may be unstable
- may be diluted in exudate
- may be specific inhibitors of acute inflammatory changes

42

What is bacterial meningitis?

Acute inflammation in meninges which can cause vascular thrombosis and reduce cerebral perfusion

43

What are the symptoms of lobar pneumonia?

Worsening fever, prostration, hypoxaemia over a few days, dry cough and breathlessness

44

Why is exudate from a blister clear?

There are relatively few inflammatory cells involved

45

Why os there sometimes pain associated with an abscess?

Can cause high pressure

46

Give some features of acute inflammation in serous cavities

- Ascites, pleural or pericardial effusion
- respiratory/cardiac impairment
- localised fibrin deposition

47

Give some sequelae of acute inflammation

- complete resolution
- continued acute inflammation with chronic inflammation (abscess)
- chronic inflammation and fibrous repair, with tissue regeneration
- death

48

Give some examples of disorders of acute inflammation

- hereditary angio-oedema
- alpha-1 antitrypsin deficiency
- inherited complement deficiencies
- defects in neutrophil function
- defects in neutrophil numbers

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