Acute inflammation Flashcards
(31 cards)
what is inflammation?
the response of living tissue to injury
what is acute inflammation?
- immediate
- short duration
- innate response
- stereotyped - the same for all injuries
- limits chronic inflammation
what are the 2 phases of acute inflammation?
Vascular phase:
* changes in blood flow
* accumulation of exudate
Cellular phase:
* delivery of neutrophils
how is acute inflammation controlled?
chemical mediators
what causes acute inflammation?
- trauma
- micro organisms
- hypersensitivity reactions
- other illness (e.g. necrosis)
what are the clinical signs of acute inflammation?
The 5 cardinal signs:
1. rubor
2. tumor
3. dolor
4. calor
5. loss of function
what happens in the vascular phase in the acute inflammatory response?
- blood vessels undergo vasoconstriction (few seconds)
- then blood vessels undergo vasodilation and this causes rubo and dolor (lasts a few minutes)
- blood vessels become more permeable
- exudate forms and the blood in vessels becomes viscous and stasis
- fluid drains into lymph nodes and presents antigens to antigen presenting cells triggering an immune response
what is Starling’s law?
fluid movement is based on 2 pressure:
1. hydrostatic pressure - pressure exerted on vessel walls by fluid (forces fluid out of vessels)
2. oncotic pressure - pressure exerted by proteins (draws fluid back into vessels)
what are the impacts of acute inflammation on Starling’s law?
- vasodilation - increases hydrostatic pressure
- increased vessel permeability - plasma proteins move into interstitial space which decreases oncotic pressure
net movement of water out of vessels causes oedema which gives rise to tumor
what happens to the blood after fluid moves out?
blood becomes more viscous (sticky)
this results in stasis of blood
what are the 2 types of interstitial fluid?
Exudate:
* increased vascular permability
* protein rich fluid
* occurs in inflammation
Transudate:
* vascular permeability unchanged
* fluid movement is due to - increased capillary hydrostatic pressure and reduced capillary oncotic pressure
* occurs in heart failure
how do vessel walls become leaky?
- endothelial cells shrink so spaces between endothelial cells increases
- injury to endothelial cells as a result of trauma
- WBC release enzymes and free radicals which damage endothelial cells
how is the vascular phase effective?
- interstitial fluid dilutes toxins
- exudate delivers proteions and immunoglobulins
- fluid drains into lymph nodes - when this occurs antigens are delivered to antigen presenting cells (triggers immune response)
what happens in the cellular phase of the acute inflammatory response?
neutrophils are the main cells involved in the cellular phase:
* WBC’s involved in acute inflammation
* trilobed nucleus
how do neutrophils escape blood vessels?
- margination - neutrophils move to periphary of vessels
- rolling - weak intermitent bonds (selectins) form between the neutrophils and endothelial cells
- adhesion - strong bonds (integrins) formbetween neutrophils and endothelial cells
- emigration - neutrophils move out of vessels into interstitial space
what are the different adhesion molecules?
selectins:
* involved in forming weak intermitent bonds between endothelial cells and neutrophils allowing rolling
Integrins:
* when selectins bind then integrins enter a high affinity state which allows for the formation of stronger bonds between the endothelial cells and neutrophils allowing adhesion
how do neutrophils move through interstitial space to area of injury?
Chemotaxis - movement along an increasing electrochemicla gradient of chemoattractants
neutrophils move towards the bacterial peptides, inflammatory mediators etc.
what do neutrophils do?
Phagocytosis:
* neutrophils rearrange cytoskeleton to form around a pathogen forming a phagosome
* phagosomes fuse with lysosme to form phagolysosome
Neutrophils also release inflammatory mediators
how do neutrophils recognise pathogens?
Opsonisation:
* toxin is covered in C3b + Fc (opsonins on the surface of pathogens)
* neutrophils have receptors specific to these opsonins so can bind to them
how do neutrophils actually kill pathogens?
2 proccesses occur in the phagolysosome
Oxygen dependent:
* uses free radicals
* hydrogen peroxide
* nitric oxide
Oxygen independent:
* enzymes in the lysosomes
* defensins
how is the cellular phase effective?
- removes pathogens + necrotic tissue
- neutrophils release inflammatory mediators which can stimulate or inhibit inflammation
what are the different inflammatory mediators?
chemical messangers which control + co-ordinate the inflammatory response
originate from:
* activated inflammatory cells
* platelets
* endothelial cells
* toxins
which chemical mediators cause vasodilation?
histamine
serotonin
prostaglandins
nitric oxide
which chemical mediators cause increased vessel permeability?
histamine
bradykinin
leukotrienes
C3a + C5a
