Acute Inflammation Flashcards

1
Q

Define inflammation

A

The response of living tissue to injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List some characteristics of acute inflammation

A
  • stereotyped
  • innate
  • immediate
  • short duration (few hours to a few days)
  • limits damage
  • controlled
  • protective (but can cause local or systemic problems)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the causes of acute inflammation?

A
  • microbial infections (e.g. viruses)
  • hypersensitivity reactions (e.g. parasites)
  • physical agents (e.g. trauma, heat, cold)
  • chemicals (e.g. corrosives, acids)
  • tissue necrosis (e.g. is had mic infarction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the clinical signs of acute inflammation (5 cardinal signs)?

A
  • Rubor (redness)
  • Tumour (swelling)
  • Dolor (pain)
  • Calor (heat)
  • Loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the two phases of acute inflammation?

A

1) Vascular phase

2) Cellular phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What happens during the vascular phase? (Inc. three steps)

A
  • Changes in blood flow; accumulation of exudate
    1) Vasoconstriction = trap pathogens
    2) Vasodilation = heat and redness
    3) Increased permeability = fluid and cells can escape
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is Starling’s law (not CVS)?

A

Movement of fluid due to the (im)balance between hydrostatic pressure and on oncotic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is hydrostatic pressure?

A

Pressure exerted on vessel wall by fluid (draw fluid away)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is oncotic pressure?

A

Pressure exerted by proteins; draws fluid towards

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the two types of interstitial fluid?

A
  • Exudate

- Transudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe Exudate

A

Protein rich fluid that delivers the proteins to area of injury (from increased permeability; occurs in inflammation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe transudate

A

Interstitial fluid without proteins from increased capillary hydrostatic pressure and reduced capillary oncotic pressure (occurs in heart failure, hepatic failure, renal failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is the vascular phase effective?

A
  • interstitial fluid dilutes toxins
  • delivery of proteins such as fibrin (mesh limits spread) and antibodies
  • fluid drains to lymph nodes = stimulate adaptive response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens during cellular phase?

A

Neutrophils are delivered to area of inflammation where they phagocytise pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do neutrophils leave vessels?

A

1) Margination = goes to edge of endothelium
2) Rolling = weak bond formation (selectins)
3) Adhesion = binding tightly (integrins)
4) Emigration = diapedesis, escape vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define chemotaxis

A

Movement along an increasing chemical gradient of chemoattractants (e.g. bacterial peptides, inflammatory mediators)

17
Q

How do neutrophils recognise correct material to phagocytose?

A

Opsonisation = toxin/pathogen covered in opsonins e.g. C3b

They have receptors for the opsonins on their surface

18
Q

What are the two killing mechanism of neutrophils?

A
  • Oxygen dependent = ROS & RNS

- Oxygen independent = lysozyme, defensins, hydrolytic enzymes

19
Q

How is the cellular phase effective?

A
  • removes pathogens and necrotic tissue

- releases inflammatory mediators (chemical messengers)

20
Q

What are the local complications of acute inflammation?

A
  • swelling = compression of tubes such as airways
  • exudate compressing on organs
  • loss of fluid e.g. burns
  • pain = muscle atrophy, psycho-social consequences
21
Q

What are detrimental systemic consequences of acute inflammation?

A
  • fever = some mediators are pyrogens (e.g. prostaglandins, IL-1)
  • septic shock = huge release of chemical mediators causes widespread vasodilation
22
Q

What are beneficial systemic consequences of acute inflammation?

A
  • leucocytosis = increased production of white cells (level can be measured to monitor)
  • acute phase response = malaise, reduced appetite to induce rest
23
Q

What are the 3 possibilities after acute inflammation?

A

1) Complete resolution
2) Repair connective tissue
3) Progression to chronic inflammation