W2- Acute Inflammation Flashcards
(46 cards)
What are the characteristics of acute inflammation? Time etc
Innate, immediately, early, stereotyped, short duration (mins-few days)
What are the vascualr and cellular reactions of acute inflam?
Vascular- accumulate fluid exudate, cellular- invasion of neutrophils
What molecules control acute inflam?
Chemical mediators from plasma or cells
What are the causes of acute inflam?
Microbial infections (eg pyogenic- staphylcoccus), acute phase hypersensitivity reactions, physical agents, chemicals, tissue necrosis
What are the clinical features of acute inflam?
Redness (rubor), swelling (tumour), pain (donor), heat (calor), loss of function- LOCAL CHANGES
What 3 changes occur in the tissues during acute inflam?
Changes in blood flow, exudation of fluid into tissues, Infiltration of neutrophils
In the vascular phase of acute inflam, what changes to blood flow occur
Transient vasoconstriction of arterioles (few secs), vasodilation of arterioles and then capillaries- increases blood flow (heat and red), increased permeability of blood vessels causes fluid in tissues and swelling, STASIS
What chemicals mediate the immediate early (1/2 hr) vascular response? Where released from? In response to what?
HISTAMINE, from MC’s, basophils, platelets, in response to trauma, IR, C3a, C5a, Il-1
What effects does histamine have?
Vascular dilation, transient increase in vascular permeability, pain
Give 2 examples of chemical mediators in the persistent vascular response
Leokotrienes, bradykinins
What is the purpose of acute inflammation?
Response of living tissue to injury to limit damage
What is Starling’s Law?
Fluid flow across vessel walls is determined by hydrostatic and colloid osmotic pressure comparing plasma and interstitial fluid
What does increasing the hydrostatic or oncotic pressure in a vessel do?
Increases the fluid flow out of the vessel (protein in interstitium is increased)
Why does fluid exudation occur in acute inflam?
Arteriolar dilation leads to incrased hydrostatic pressure, increased permeability of vessels leads to proteins in interstitium, net flow of fluid out of vessel
Describe what oedema is and what it is characterised by
Excess of fluid in interstitium, transudate or exudate, increased lymphatic drainage.
What is Starling’s Law?
Fluid flow across vessel walls is determined by hydrostatic and colloid osmotic pressure comparing plasma and interstitial fluid
What does increasing the hydrostatic or oncotic pressure in a vessel do?
Increases the fluid flow out of the vessel (protein in interstitium is increased)
Why does fluid exudation occur in acute inflam?
Arteriolar dilation leads to incrased hydrostatic pressure, increased permeability of vessels leads to proteins in interstitium, net flow of fluid out of vessel
Describe what oedema is and what it is characterised by
Excess of fluid in interstitium, transudate or exudate, increased lymphatic drainage.
What is exudate oedema?
Fluid loss in inflammation- high protein content in fluid
What is transudate oedema? Give an example
Fluid loss due to changes in hydrostatic pressure, low protein content of fluid. E.g. Cardiac failure, venous outflow obstruction
What 5 mechanisms can cause vascular leakage? (See with slide 17)
Endothelial contraction and cytoskeletal reorganisation (gaps), direct injury (burns, chemicals), leukocyte dependent injury, increased transcytosis
What is the role of fibrin at a site of injury?
Acts as a mesh work to localise inflam mediators and hold proteins at site of injury
What is the primary type of WBC involved in inflam?
Neutrophil/ polymorph
