Acute Inflammation Flashcards
List the causes of acute inflammation.
- micro-organisms such as bacteria since pathogenic organisms cause infection
- mechanical (trauma) injury to tissue even sterile (eg surgery)
- chemical - upset stable environment such as pH
- physical - extreme conditions such as temperature or ionising radiaton.
- dead tissue as cell necrosis irritates adjacent tissue
- hypersensitivity have several classes of reaction
Recognise the benefits of acute inflammation.
- Effects of exudation
- oedema formed - accumulation of fluid formed in the
- Rapid response to non-specific insult
- Cardinal signs and loss of function through swelling of - extravascular provides transient protection of inflamed area
- Neutrophils destroy organisms and denature antigen for macrophages
- Plasma proteins localise process
- Resolution and return to normal
where does acute inflammation take place
in the microcirculation (series of microscopic events are localised to affected tissue)
name the cardinal signs of inflammation
(local effects include) rubor - redness calor - heat tumor - swelling dolor - pain loss of function
All of these are explained by the sequence of Pathological events taking place
what is flush, flare and wheal
Transient arteriolar constriction - occurs for few moments, probably protective Local arteriolar dilatation - active hyperaemia Relaxation of vessel smooth muscle - ?autonomic NS or mediator derived
exudation is
endothelial leak - fluid and protein not held in vessel lumen (imbalance of Starling forces)
localised vascular response
exudate contains
fluid rich in protein - plasma - includes immunoglobulin and fibrinogen
what is microcirculation
capillary beds, fed by arterioles and drained by venules
- lymphatic channels and drainage
Describe the sequence of microvascular change.
what is flush, flare and wheal
Transient arteriolar constriction - occurs for few moments, probably protective Local arteriolar dilatation - active hyperaemia Relaxation of vessel smooth muscle - ?autonomic NS or mediator derived
exudation is
endothelial leak - fluid and protein not held in vessel lumen (imbalance of Starling forces)
localised vascular response
net movement of plasma from capillaries to extravascular space
exudate contains
fluid rich in protein - plasma - includes immunoglobulin and fibrinogen
migration and neutrophils
neutrophils move to endothelial aspect of lumen
step 1
pavementing and neutrophils
neutrophils adhere to endothelium
step 2
migration of neutrophils
neutrophils move to endothelial aspect of lumen
step 1
pavementing of neutrophils
neutrophils adhere to endothelium
step 2
emigration of neutrophils
neutrophils squeeze between endothelial cells - active process - to extravascular tissues
(step 3)
outcomes of cute inflammation
resolution
suppuration
organisation
chronic inflammation
outcomes of acute inflammation
resolution suppuration organisation dissemination chronic inflammation
list mediators of acute inflammation and describe functions
Molecules on endothelial cell surface membrane (sticky) Molecules released from cells Molecules in the plasma Molecules inside cells effects include: - vasodilatation - increased permeability - neutrophil adhesion - chemotaxis - itch and pain
inflammation of peritoneal cavity
peritonitis
immediate systemic effects of acute inflammation
pyrexia - raised temperature
- endogenous pyrogens from white cells act centrally
feel unwell
- malaise, anorexia, nausea
- abdominal pain and vomiting in children
neutrophilia - raised white cell count
- bone marrow releases/produces
explain the outcomes of acute inflammation - suppuration
Pus formation
- dead tissue, organisms, exudate, neutrophils, fibrin, red cells, debris
Pyogenic membrane surrounds pus
- capillary sprouts, neutrophils, fibroblasts
- walls off pus
Abscess
- collection of pus (suppuration) under pressure
- single locule, multiloculated
- “points” and discharges
- collapses - healing and repair
Explain the systemic effects of acute inflammation.
shock - inability to perfuse tissues clinical picture of early septic shock - peripheral vasodilatation - tachycardia - high heart rate - hypotension - low blood pressure - often pyrexia - sometimes hemorrhagic skin rash
Describe the complications of acute inflammation.
raised HR insufficient to maintain cardiac output
SVR low; so BP falls
- BP = CO x SVR
- increasing heart rate insufficient (CO = SV x HR)
reduced perfusion of tissues
- tissue hypoxia
- loss of cell tissue and organ function
Summarise the mediators of acute inflammation.
histamine
maybe add more later?
Prostaglandins (arachidonic acid metabolites via cyclo-oxygenase pathway) and inflammation
- many cells (endothelium and leukocytes)
- many promote histamine effects and inhibit inflammatory cells
- thromboxane A2 promotes platelet aggregation and vasoconstriction – the opposite effect to PGD2, PGE2, etc
- latter: effectiveness of non-steroidal anti-inflammatory drugs
Types of signalling in molecules inside cells:
pattern associated molecular patterns
- microbial antigen
- genetically hard wired to recognise
- innate and adaptive immunity
Types of signalling in molecules inside cells:
danger associated molecular patterns
- substances released in response to stimulus
Other types of signalling in molecules inside cells:
- stimulate pattern recognition receptors on cell membranes
- activate inflammatory response
Types of signalling in molecules inside cells:
pattern associated molecular patterns
- microbial antigen
- genetically hard wired to recognise
- innate (non-specific) and adaptive immunity
long term systemic effects of acute inflammation
lymphadenopathy - regional lymph node enlargement
- immune response
weight loss - catabolic process
anaemia
what does 5-hydroxytryptamine (serotonin) do in inflammation
- preformed in platelets
- released when platelets degranulate in coagulation
- vasoconstriction
Pus in other places
empyema - in a hollow viscus
- gall bladder
- pleural cavity
pyaemia - discharge to bloodstream
Outcomes of acute inflammation - organisation
- granulation tissue characteristic
- healing and repair
- leads to fibrosis and formation of a scar
What is granulation tissue?
“universal patch” – repair kit – for all damage formed of: - new capillaries - angiogenesis - fibroblasts and collagen - macrophages
Outcomes of acute inflammation - dissemination
- spread to bloodsteam - patient “septic”
- bacteraemia - bacteria in blood
- septicaemia - growth of bacteria in blood
- toxaemia - toxic products in blood
Pathogenesis of septic shock
Systemic release of chemical mediators from cells into plasma
Increased heart rate compensates - CO = SV x HR
Bacterial endotoxin released
Activation of coagulation
Systemic release of chemical mediators from cells into plasma causes
- mediators cause vasodilation causing loss of systemic vascular resistance (SVR) - BP = CO x SVR
- results in catecholamine release
- tachycardia (increased heart rate) follows to maintain (CO)
Bacterial endotoxin release causes
- interleukin-1 released
- acts on hypothalamus - pyrexia
Activation of coagulation causes
- disseminated intravascular coagulation
- vasoactive chemical - vasodilatation
- hemorrhagic skin rash
Systemic release of chemical mediators from cells into plasma causes
- mediators cause vasodilation causing loss of systemic vascular resistance (SVR) - BP = CO x SVR
- results in catecholamine release
- tachycardia (increased heart rate) follows to maintain (CO)
reduced perfusion of tissues in septic shock can lead to
tissue hypoxia
loss of cell tissue and organ function
