3) Acute Inflammation Flashcards
What is characteristic of acute inflammation?
Exudation
Neutrophils
Define acute inflammation
The response of living tissue to injury, initiated to limit the tissue damage
It is innate, quick and non-specific
List some possible causes of acute inflammation
- Microbial infection e.g pyogenic organisms
- hypersensitivity reactions
- physical agents
- chemicals
- tissue necrosis
What are some typical LOCAL symptoms of acute inflammation?
- RUBOR (redness)
- TUMOR (oedema/swelling)
- CALOR (heat)
- DOLOR (pain to enforce awareness)
- usually associated with loss of function
What are some SYSTEMIC symptoms associated with acute inflammation
- FEVER, endogenous pyrogens will ^temp (reduced with aspirin)
- LEUKOCYTOSIS, raised WBC count (neutrophils = bacterial)
- ACUTE PHASE (loss of appetite, raised pulse, altered sleep pattern)
- SHOCK due to spread of MO and toxins
Describe the changes in blood vessels that proceed acute inflammation
1.Transient vasoconstriction
2.Vasodilation of Arterioles and capillaries leading to increased flow, RUBOR and CALOR)
3.^permeability
4.
Describe the process of exudation and it’s importance
-Leakage of plasma proteins and slow flow
-imbalance in hydrostatic and oncotic pressures between plasma and interstitium
-leads to oedema
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What is the difference between EXDUATE and TRANSUDATE?
TRANSUDATE is cause by a hydrostatic imbalance only (so low protein content) and is not characteristic of inflammation
Mainly seen in cardiac failure or venous outflow obstruction
Describe neutrophils, their function and derivation
- aka polymorphs
- multi-lobular
- phagocytose MOs and necrotic debris
- release toxic metabolites/enzymes e.g oxidative burst (O2 dependant) release hydrolases or lysosomes (O2 independent during Ischaemia)
- TOB
Describe the process of neutrophil infiltration
- Caused by CHEMOTAXIS (conc grad+ of chemoattractants)
- receptor-ligand binding, rearrangement of cytoskeleton and production of pseudopods
- STASIS caused neutrophils to marginate along endothelium
- they roll sticking intermittently until more avid adhesion
- EMIGRATION through blood vessels via relaxation of cell junctions and localised digestion of basement membrane
What chemical mediators are important during acute inflammation and how are they produced?
- initially, HISTAMINE released from mast cells, basophils and platelets: acts to vasodilate and increase vascular permeability
- in response to physical damage, immunological reactions, clotting factors (3a/5a) and IL-1
What are some complications associate with acute inflammation?
- Swelling may block tubes e.g bile duct/intestine
- exudate may compress e.g cardiac tamponade
- loss of fluid leading to dehydration e.g burns
- pain and eventual permanent loss of function
What are the possible outcomes following acute inflammation?
- Resolution
- continued acute inflammation with chronic inflammation
- chronic inflammation with fibrous repair (scarring) or tissue regeneration if tissue architecture is not destroyed
- Death due to shock
Features of acute inflammation resolution?
Reversal of acute inflammation:
1) No margination of neutrophils
2) Reduce blood vessel permeability
3) Drain exudate using the lymphatic system
4) Neutrophils - die and are phagocytosed
5) Fibrin degraded by proteases
6) Mediators have short half life - inhibited, degraded, diluted or become unstable
Give some examples of when acute inflammation is important
- Bacterial meningitis leading to poor cerebral perfusion and thrombus
- lobar pneumonia, exudate in alveoli
- skin blister, fluid collects and strips off overlying epithelium
- abscess, in solid tissue where exudate forces part two tissue with liquefactive necrosis in between
- pericarditis, exudate effuses into cavity causing tamponade and fibrin deposits
- liver abscess
