3. Acute Inflammation Flashcards
What is acute inflammation?
Response of living tissue to injury Immediate Short duration Innate Stereotyped Limits damage
What are the 2 phases?
Vascular phase - changes in blood flow, accumulation of exudate
Cellular phase - delivery of neutrophils
What causes inflammation?
Trauma/foreign body
Microorganisms
Hypersensitivity
Other illnesses (necrosis)
What are the clinical signs of acute inflammation?
Rubor - redness Calor - heat Tumor - swelling Dolor - pain Loss of function
What are the first stages of vascular phase?
Vasoconstriction (seconds)
Vasodilation (minutes) - heat and redness
Increased permeability - fluid and cells can escape
What is starling’s law?
Movement of fluid controlled by the balance of hydrostatic pressure and oncotic pressure
These pressures exist in the vessels and the interstitium
What is hydrostatic pressure?
The pressure exerted on a vessel wall by fluid
Pushes fluid away
What is oncotic pressure?
The pressure exerted by proteins
Draws fluid towards
How does acute inflammation affect pressures?
Vasodilation - increased capillary hydrostatic pressure
Increased vessel permeability - plasma proteins move into interstitium, increased interstitial oncotic pressure
Fluid movement - out of vessel into interstitium (oedema)
What happens because of the change in pressures?
Movement of fluid out of vessel
Increased viscosity of blood - thick and sticky so blood flows slower
Reduced flow through vessel - stasis
What are the 2 types of interstitial fluid?
Exudate
Transudate
What is exudate fluid?
Increased vascular permeability
Protein rich fluid (delivers proteins to area of injury)
Occurs in inflammation
What is transudate fluid?
Vascular permeability unchanged
Fluid movement due to: increased capillary hydrostatic pressure, reduced capillary oncotic pressure
When does transudate fluid occur?
In heart failure
Hepatic failure
Renal failure
How does a vessel wall become permeable?
Retraction of endothelial cells due to histamine, nitric oxide or leukotrienes
Direct injury of endothelial cells
Lecuocyte dependent injury
How is the vascular phase effective?
Interstitial fluid dilutes toxins
Exudate delivers proteins e.g. fibrin mesh limits spread of toxin, immunoglobulins
Fluid drains to lymph nodes
What is the primary WBC involved in acute inflammation?
Neutrophil
How do neutrophils escape vessels?
Margination - neutrophils stick to endothelial cells and bind tightly
Rolling of neutrophils
Adhesion of neutrophils - squeeze through gaps
Emigration of neutrophils outside of vessel
What are the 2 adhesion molecules?
Selectins
Integrins
What are selectins?
Expressed on activated endothelial cells
Cells activated by chemical mediators
Responsible for rolling
What are integrins?
Found on neutrophil surface
Change from low affinity to high affinity state
Responsible for adhesion
What is chemotaxis?
Movement along an increasing chemical gradient of chemoattractants:
- bacterial peptides, inflammatory mediators
- rearrangement of neutrophil cytoskeleton
How do neutrophils recognise what to phagocytose?
Opsonisation
Toxin covered in C3b and Fc (opsonins)
Receptors for C3b and Fc on neutrophil surface
How is the cellular phase effective?
Removal - pathogens, necrotic tissue
Release - inflammatory mediators
