Acute Inflammation 2 Flashcards
What is inflammation in the lungs called?
pneumonia
What is inflammation in the pleural cavity called?
pleurisy
What do neutrophils do?
-Recognise a foreign antigen, move towards it and adhere to organism.
-Granules possess oxidants (H2O2) and enzymes (proteases)
Release granule contents
-Phagocytose and destroy foreign antigen
What are the consequences of neutrophil action?
- Neutrophils die when granule contents released
- Produce pus filled with bits of cell, organisms and endogenous proteins
- Inflammation might progress if extension into other tissues
What is the role of plasma proteins in inflammation?
- Fibrinogen is a coagulation factor which forms fibrin and clots exudate. This localises the inflammatory process
- Immunoglobulins provide a humoural immune response, plasma specific for antigen
What are mediators of acute inflammtion
- molecules on endothelial cell surface membrane
- molecules released from cells
- molecules in the plasma
What are the collective effects of mediators?
- vasodilation
- increased permeability
- neutrophil adhesion
- chemotaxis
- itch and pain
What does ICAM-1 do?
Helps neutrophils to stick
What does P-selectin do?
Interacts with neutrophil surface
What molecules are released from cells?
- histamine
- 5-hydroxytryptamine (serotonin)
- prostaglandins (arachidonic acid metabolites via lipoxygenase pathway)
- leukotrienes (arachidonic acid metabolites via cyclo-oygenase pathway)
- omega-3 polyunsaturated fatty acids
- platelets activating factor
- cytokines and chemokines
- nitric oxide
- oxygen free radicals
Histamine
- It is preformed in mast cells beside vessels, platelets, basophils]
- It is released as a result of local injury: IgE mediated reactions
- Causes vasodilation and increased permeability
- Acts via H1 receptors on endothelial cells
Serotonin
-Preformed in the platelet
Released when platelets degranulate in coagulation
-Cause vasoconstriction
Prostaglandins
- Released by 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.
Leukotrines
- Released by neutrophils especially
- Vasoactive-dynamic effort on vessels to increase permeability and constrict smooth muscle
Omega-3 polyunsaturated fatty acids
Decrease synthesis of arachidonic acid derived inflammatory response?
What is platelet activating factor?
- Produced by cell membranes of activated inflammatory cells
- Reduces permeability by enhancing platelet degranulation at site of injury
Cytokines and Chemokines
- small molecules produced by macrophages, lymphocytes and endothelium in response to inflammatory stimuli
- they attract inflammatory cells
Nitric Oxide
- Released by various cells
- Cause relaxation of smooth muscle, anti platelet, regulate leukocyte recruitment to inflammatory response
Oxygen Free Radicals
- Released by neutrophils on phagocytosis
- They amplify other mediator effects
What are the 4 enzymes cascades that take place in the plasma?
- blood coagulation pathways
- fibrinolysis
- kinin system
- complement cascade
Blood Coagulation Pathways
- clots fibrinogen in the exudate
- interacts widely with other systems
Fibrinolysis
- breaks down fibrin to help maintain blood supply
- products of fibrin breakdown are vasoactive
Kinin System
Bradykinin responsible for pain
Complement Cascade
- Ties inflammation with the immune system
- Active components stimulate increased permeability, chemotaxis, phagocytosis and cell breakdown
What are the immediate systemic effects of inflammation?
- pyrexia
- feeling unwell including malaise, anorexia, nausea, abdominal pain and vomiting
- neutrophilia- released by bone marrow
What are the longer term effects of acute inflammation?
- lymphadenopathy
- weight loss
- anaemia
What are the outcomes of acute inflammation?
- resolution
- suppuration
- organisation
- dissemination
- chronic inflammation
What is suppuration?
- Formation of pus
- Pyogenic membrane surrounds pus and walls it off
What is an abscess?
- A collection of pus under pressure
- Can be single locule or multi-loculated
- It points and discharges before collapsing and healing
How are multiloculated abscesses formed?
Pus bursts through pyogenic membrane and forms new cavities
What is an empyema?
Pus in a hollow viscous such as the gall bladder or the pleural cavity
What is pyaemia?
When pus is discharged into the bloodstream
What is organisation?
Organisation is healing and repair. Characterised by granulation tissue and leads to fibrosis and formation of a scar.
What is granulation tissue?
It is a universal patch formed of new capillaries, fibroblasts, collagen and macrophages.
What is dissemination?
-Spread to the bloodstream which results in patients becoming septic
Bacteraemia
bacteria in the blood
septicaemia
growth of bacteria in blood
toxaemia
toxic products in blood
What are the effects of systemic infection?
- shock=inability to perfuse tissues
- early septic shock
What are the symptoms of early septic shock?
- peripheral vasodilation
- tachycardia
- hypotension
- pyrexia
- sometime haemorrhagic skin rash
What is the pathogenesis of septic shock?
- There is a systemic release of chemical mediators from cells into plasma
- Mediators cause vasodilation causing loss of systemic vascular resistance
- Results in catecholamine release
- Tachycardia follow to maintain CO because increased heart rate compensates CO=SV x HR
- bacterial endotoxin released
- activation of coagulation
What does interleukin-1 do?
When released it acts on the hypothalamus and causes pyrexia
How does the activation of coagulation result in a haemorrhagic skin rash?
- Disseminated intravascular coagulation
- Vasoactive chemical causes vasodilation
- Results in haemorrhagic skin rash
What happens when a raised HR is insufficient to maintain cardiac output?
- SVR is low so BP falls.
- There is reduced perfusion of tissues which results in tissue hypoxia and leads to loss of cell tissue and organ function
What are the outcomes of septic shock?
- proves rapidly fatal
- tissue hypoxia -cell death
- haemorrhage
- requires urgent intervention and support- admittance to ICU
