Acute Inflammation Flashcards
(23 cards)
Define inflammation
The response of living tissue to injury
List some characteristics of acute inflammation
- stereotyped
- innate
- immediate
- short duration (few hours to a few days)
- limits damage
- controlled
- protective (but can cause local or systemic problems)
What are the causes of acute inflammation?
- 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)
What are the clinical signs of acute inflammation (5 cardinal signs)?
- Rubor (redness)
- Tumour (swelling)
- Dolor (pain)
- Calor (heat)
- Loss of function
What are the two phases of acute inflammation?
1) Vascular phase
2) Cellular phase
What happens during the vascular phase? (Inc. three steps)
- Changes in blood flow; accumulation of exudate
1) Vasoconstriction = trap pathogens
2) Vasodilation = heat and redness
3) Increased permeability = fluid and cells can escape
What is Starling’s law (not CVS)?
Movement of fluid due to the (im)balance between hydrostatic pressure and on oncotic pressure
What is hydrostatic pressure?
Pressure exerted on vessel wall by fluid (draw fluid away)
What is oncotic pressure?
Pressure exerted by proteins; draws fluid towards
What are the two types of interstitial fluid?
- Exudate
- Transudate
Describe Exudate
Protein rich fluid that delivers the proteins to area of injury (from increased permeability; occurs in inflammation)
Describe transudate
Interstitial fluid without proteins from increased capillary hydrostatic pressure and reduced capillary oncotic pressure (occurs in heart failure, hepatic failure, renal failure)
How is the vascular phase effective?
- interstitial fluid dilutes toxins
- delivery of proteins such as fibrin (mesh limits spread) and antibodies
- fluid drains to lymph nodes = stimulate adaptive response
What happens during cellular phase?
Neutrophils are delivered to area of inflammation where they phagocytise pathogens
How do neutrophils leave vessels?
1) Margination = goes to edge of endothelium
2) Rolling = weak bond formation (selectins)
3) Adhesion = binding tightly (integrins)
4) Emigration = diapedesis, escape vasculature
Define chemotaxis
Movement along an increasing chemical gradient of chemoattractants (e.g. bacterial peptides, inflammatory mediators)
How do neutrophils recognise correct material to phagocytose?
Opsonisation = toxin/pathogen covered in opsonins e.g. C3b
They have receptors for the opsonins on their surface
What are the two killing mechanism of neutrophils?
- Oxygen dependent = ROS & RNS
- Oxygen independent = lysozyme, defensins, hydrolytic enzymes
How is the cellular phase effective?
- removes pathogens and necrotic tissue
- releases inflammatory mediators (chemical messengers)
What are the local complications of acute inflammation?
- swelling = compression of tubes such as airways
- exudate compressing on organs
- loss of fluid e.g. burns
- pain = muscle atrophy, psycho-social consequences
What are detrimental systemic consequences of acute inflammation?
- fever = some mediators are pyrogens (e.g. prostaglandins, IL-1)
- septic shock = huge release of chemical mediators causes widespread vasodilation
What are beneficial systemic consequences of acute inflammation?
- leucocytosis = increased production of white cells (level can be measured to monitor)
- acute phase response = malaise, reduced appetite to induce rest
What are the 3 possibilities after acute inflammation?
1) Complete resolution
2) Repair connective tissue
3) Progression to chronic inflammation
