MOD 2.1 - Acute Inflammation Flashcards Preview

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Flashcards in MOD 2.1 - Acute Inflammation Deck (44):
1

What are the causes of acute inflammation? (5)

- Microbial infections e.g. Pyogenic organisms (staphylococcus)
- Hypersensitivity reactions (acute)
- Physical agents e.g. Heat
- Chemicals
- Tissue necrosis

2

What are the clinical features of acute inflammation?

- Rubor (redness)
- Tumor (swelling)
- Dolor (pain and loss of function)
- Calor (heat)

3

What are the two phases of acute inflammation?

- Vascular

- Cellular

4

Describe the changes in blood flow during the vascular phase

- Transient vasoconstriction of Arterioles

- Vasodilation of Arterioles and capillaries

- Increased permeability of blood vessels

- Stasis

5

What happens as a result of vasodilation of Arterioles and capillaries during the vascular phase?

Increases blood flow which leads to heat and redness

6

What happens as a result of an increased permeability of blood vessels during the vascular phase?

- Exudation (seeping) of protein rich fluid into tissues from plasma

- Slowing of circulation which leads to swelling

7

What is stasis?

The stoppage or slowing of blood flow

8

What happens as a result of stasis during the vascular phase?

Increased concentration of red blood cells which increases blood viscosity

9

Give an example of a chemical mediator of changes in blood flow

Histamine - released as an early response (first 1/2 hour)

10

What causes a release of histamine and what is it released from?

- Released as a response to stimuli e.g. Physical damage or immunologic reactions

- Released from mast cells, basophils and platelets

11

Describe the changes of histamine (3)

- Vascular dilation

- Transient increase in vascular permeability

- Pain

12

What is acute inflammation?

The response of living tissue to injury that is initiated to limit tissue damage

13

What are the chemical mediators for a persistent response?

Non-specific, there's lots of different types

14

What are the determining factors of fluid flow?

Hydrostatic and colloid osmotic pressure comparing plasma and interstitial fluid

15

What happens as a result of an increase in hydrostatic pressure?

There is an increase in movement of fluid out of the vessel

16

What happens as a result in an increase in osmotic colloid pressure?

There is an increase in flow out pressure therefore increasing the protein concentration in the interstitium

17

What happens due to an increase in vascular permeability?

- Increases concentration of protein in the interstitium therefore causing an outward net flow of fluid

- Leads to oedema (exudate)

18

What is oedema and what are the two types?

- An increase of fluid in tissue spaces

- Transudate and Exudate

19

Describe Transudate oedema

The protein content of the oedema fluid is THE SAME AS the protein content of the plasma

20

Describe exudate oedema

The protein content of the oedema fluid is HIGHER than the protein content of the plasma

21

What are the mechanisms of vascular leakage? (5)

- Endothelial contraction (forms gaps between cells)

- Cytoskeletal reorganisation (forms gaps between cells)

- Direct injury e.g. Toxic burns, chemicals

- Leukocyte dependent injury (enzymatic/ toxic O2 species)

- Increased Transcytosis (movement of macromolecules across a membrane)

22

Describe the cellular phase of acute inflammation

Infiltration of polymorphs (multi lobed nuclei) to the inflamed area

23

What are the four steps in the infiltration of neutrophils?

- Margination
- Rolling
- Adhesion
- Emigration

24

What happens during the Margination step of neutrophil infiltration?

Neutrophils line up at peripheries of blood vessels

25

What happens during the rolling step of neutrophil infiltration?

Neutrophils adhere loosely to endothelium

26

What happens during the adhesion step of neutrophil infiltration?

Neutrophils stick fully to endothelium

27

What happens during the emigration step of neutrophil infiltration?

Neutrophils emigrate through vessel wall

28

How do neutrophils escape from vessels?

- Interendothelial cell junctions relax
- Neutrophils digest basement membrane
- Chemotaxis - neutrophils move along concentration gradients of chemoattractants e.g. C5a

29

What is the significance of dolor?

- Loss of function enforces rest and reduces the chance of further damage

30

What is the role of Serotonin in acute inflammation?

Role is the same as Histamine i.e. stimulates vasodilation and the transient increase in membrane permeability.

Also stimulates fibroblasts for tissue repair

31

What is the role of bradykinin in acute inflammation?

- Produces pain

- Increases vascular permeability

32

What is the role of leukotrienes in acute inflammation?

- Mediation of leukocyte accumulation

(significant in asthma)

33

What is the role of opsonins in acute inflammation?

Coat foreign materials and make them easy to phagocytose

34

What is the process of a neutrophil capturing and killing a bacterium?

- Summoned to the place of injury via chemotaxis

- Become activated by increasing metabolism

- Margination (Stick to the endothelial surface)

- Diapedesis (Crawl through the endothelium)

- Recognition-attachment (Recognise the bacterium and attach to it

- Phagocytosis

35

Why is clotted blood chemotactic?

- Blood clots are made up of a mesh of Thrombin and Fibrin Degredation Products

- Both of which are chemotactic

36

What is diapedesis?

- Digestion of the basement membrane by collagenase produced by Leucocytes (neutrophils)

- Allows neutrophils to move into extravascular space

- Can then move towards target by pulling themselves along collagen fibres of other tissues

37

What is degranulation and when does it occur?

- The movement and fusion of the granules of a neutrophil towards a phagosome during phagocytosis, after which bactericidal substances are injected into the particle.

- Occurs before the particle is completely enclosed in the phagosome

38

What is the function of a complement?

- Formation of a tube (called the membrane attack complex)

- Tube punches holes in bacteria

- Causes bacteria to die

39

Give FOUR examples of local complications of acute inflammation

- Damage to normal tissue

- Pain and loss of function

- Obstruction of tubes e.g. fallopian tubes due to swelling from exudate

- Loss of fluid e.g. from a surface wound

40

Give FOUR systemic effects of acute inflammation

- Fever

- Leucocytosis (increased number of leucocytes in circulation)

- The acute phase response (Change in levels of certain plasma proteins due to a change in protein synthesis in the liver)

- Shock (large drop in blood pressure due to widespread vasodilation and increase in vascular permeability with exudation)

41

Give FOUR examples of exudate

- Pus/abscess - white as is rich in neutrophils, typical of chemotactic bacteria

- Haemorrhagic - enough RBCs to seem bloody. Typical of significant vascular damage from destructive infections/exudate from malignant tumours

- Serous exudate - contains plasma proteins and is typical in blisters e.g. from burns

- Fibrinous exudate - rich in fibrin, common from cuts to the skin

42

What is hereditary angio-oedema?

- Inherited (autosomal dominant) deficiency of C1- esterase inhibitor (a component of the compliment system)

- Rapid oedema of dermis, subcutaneous tissue, mucosa etc.

- Recurrent abdominal pain is also a symptom

43

What is Alpha1-antitrypsin deficiency?

- An autosomal recessive disorder with varying levels of severity

- low levels of alpha-1 antitrypsin which deactivates enzymes released from neutrophils at the site of inflammation

44

What is chronic granulomatous disease?

- Genetic condition where phagocytes are unable to generate the free radical superoxide

- Phagocytes can't kill bacteria as they can't generate an oxygen burst

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