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Flashcards in Acute Inflammation Deck (40)
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1

What is inflammation

Response of living tissue to injury

2

Compare the vascular and cellular phase
How is inflammation controlled

Cellular: Delivery of neutrophils
Vascular: Blood flow changes, accumulation of exudate

Chemical mediators

3

Name 5 major causes of acute inflammation

Microbial infections
Hypersensitivity reactions
Physical agents (trauma)
Chemicals
Tissue necrosis

4

Name 5 clinical signs of acute inflammation

Rubour
Tumour
Calor
Dolor
Loss of Function

5

How does vascular flow change during acute inflammation

Vasoconstriction in first few seconds
Vasodilation in first few minutes
Increased vessel permeability

6

Regarding fluid movement, what is Starling’s Law?

Movement of fluid is controlled by the balance of Hydrostatic Pressure and Oncotic Pressure

7

How does inflammation cause swelling by altering vascular flow

1. Vasodilation increases hydrostatic pressure

2. Increased vessel permeability allows plasma proteins to enter interstitium, thus increased interstitial oncotic pressure

3. Fluid moves out of vessel, into Intersitium

8

How does fluid leaving vessel affect the contents that remain

Increased viscosity of blood
Reduced flow (Stasis)

9

Compare Exudate and Transudate

- Vascular permeability
- Protein content of fluid
- When do they occur

Exudate:
- Increased vascular permeability
- Protein rich fluid
- In inflammation

Transudate:
- Unchanged vascular permeability
- No protein in fluid
- Heart/ hepatic/ renal failure

10

State 3 ways vascular permeability can be increased

1. Direct injury (Burns, trauma)
2. Retraction of endothelial cells
3. Leukocyte dependent injury (Enzymes/ toxic oxygen species released by inflammatory cells)

11

How is the vascular phase effective
Give 3 ways

More interstitial fluid= Toxins diluted

Exudate delivers proteins such as antibodies and fibrinogen (Mesh limits toxins spread)

Fluid drains to lymph nodes, antigens presented to immune system

12

How do Neurophils leave vessels in 4 steps

1. Margination (Move towards endothelia)
2. Rolling (Move along endothelia via weak bonds)
3. Adhesion (Tight bonds formation)
4. Diapedesis/ Emigration (Move through endothelia)

13

Compare the 2 adhesion molecules response for “rolling” and “adhesion” in Neutrophil Emigration

- Selectins on Activated endothelial cells are responsible for Rolling

- Integrins on Neutrophil surface change from Low to High affinity state, responsible for Adhesion

14

What is Chemotaxis
How do neutrophils move in this way

Movement along an increasing chemical gradient of chemoattractants

Re-arrangement of cytoskeleton

15

How do Neutrophils recognise pathogens

Give an example

Opsonins

Pathogen covered in C3b and Fc opsonins
Neutrophil surface has C3b and Fc receptors

16

How is the cellular phase effective in 3 ways

Removal of pathogens
Removal of necrotic tissue
Release of inflammatory mediators

17

What are inflammatory mediators

Name 4 ways they originate

Chemical messengers that control and co-ordinate inflammatory response

Activated inflammatory cells
Platelets
Endothelial cells
Toxins

18

Name 4 Mediators that cause vasodilation

Histamine
Serotonin
Prostaglandins
Nitric Oxide

19

Name 5 mediators that increase vascular permeability

Histamine
Serotonin
Bradykinin
Leukotrienes
Nitric Oxide

20

Name 4 mediators that stimulate chemotaxis

C3a, C5a
IL-1
TNF-Alpha
Leukotrienes

21

Name 3 mediators that cause pain

Bradykinin
Histamine
Prostaglandins

22

Name 3 pyrogens (Mediators cause fever)

Prostaglandins
IL-1
IL-6

23

Mediators;

Name 2 vasoactive amines
name 1 vasoactive peptides
Name 2 complement proteins

Amines: Histamine, Serotonin
Peptides: Bradykinin
Complement: C3a and C5a

24

Mediators;

Name 2 derived from phospholipids
Name 1 Cytokines/ chemokine
Name 1 exogenous mediator

Prostaglandins and Leukotrienes
TNF (Tumour Necrosis Factor)
Endotoxins from pathogens

25

What are the 2 types of Complications from Acute Inflammation

Name 4 examples of each

Local
- Obstruction of tubes/ compression of organs
- Loss of fluid
- Pain
- Normal tissue damaged

Systemic
- Fever
- Leucocytosis (Increased WBC production)
- Acute Phase Response (Malaise, Lethargy, Altered sleep) induces rest
- Septic shock (Huge release of mediators)

26

What are NSAIDs
How do they work?

Non-Steroidal Anti Inflammatory drugs
Block mediators that cause fever

27

What are Acute Phase Proteins
Name one that is measured as a marker for inflammation

Name 1 protein made in smaller amounts during Acute Phase Response. Name 2 made in larger amounts

Proteins released due to inflammation
C-Reactive Protein

Albumin- made less
Alpha-1 antitrypsin and Fibrinogen- made more

28

Name 4 outcomes of Septic Shock

Hypotension
Tachycardia
Multi-organ failure
Death

29

What are the 3 possible outcomes of Acute Inflammation

1. Complete resolution
2. Fibrosis (Repair with connective tissue)
3. Chronic inflammation (With repair)

30

When does Acute Inflammation result in Fibrosis
When does it result in Chronic Inflammation

Fibrosis- If there is substantial tissue destruction
Chronic- When Acute isn’t enough to combat cause