T3 Acute Inflammation Flashcards
List a range of situations in which an acute inflammation can occur.
- Physical agents - burns, frostbite etc.
- Infections
- Hypersensitivity
- Chemical
- Tissue necrosis - for example in MI
What are the main stages of acute inflammation?
- Increase in vessel calibre - there is and transient initial vasoconstriction but then a vasodilation of the capillaries. Mediated by histamine and nitrous oxide in vascular smooth muscle to increase blood flow.
- Increased vascular permeability and formation of fluid exudate
- Formation of cellular exudate
What are the main characteristics of an acute inflammatory response? (5)
Why do these occur?
Calor - Hot to touch - due to hyperaemia resulting in vasodilation and the delivery of warm blood to the area. Systematic fever also contributes to this.
Rubor - Red - due to vasodilation.
Dolor - Pain - due to stretching and situation of the tissues due to inflammatory oedema and the pressure from the exudate in an abscess cavity. Cytokines such as bradykinin, prostoglandins and serotonins cause pain.
Tumour - Swelling due to oedema and to a much lesser extent the mass of inflammatory cells.
Functio lasea - Loss of function - This is conscious and reflexly inhibited by pain. Severe inflammation may also immobilise the tissue.
What is the role of neutrophil polymorphs in acute inflammation?
- Movement towards the source
- Adhesion to microorganisms - this is through opposition by C3b and antibodies
- Phagocytosis
- Intracellular killing of microorganisms by oxygen dependent and oxygen independent pathways (bleach)
- Release of lysosomal products attracting other leucocytes to the area
What is an exudate?
Extracellular fluid with high protein concentration, containing cellular debris. Its presence implies inflammation.
What are the clinical effects and sequelae of acute inflammation?
Resolution
Repair
Regeneration
Suppuration - formation of pus, a mixture of living and dead neutrophils, cellular debris.
Define transudate.
Low protein fluid with little or no cellular component.
What is oedema?
Excess fluid in the interstitial tissue/serous cavities. It can be either exudate or transudate.
How does fluid exudate form?
Increased permeability of microvasculature results in escape of protein rich fluid into tissue. These proteins include immunoglobulins, coagulation factors and fibrinogen.
Causes include:
- Chemical mediators such as histamine, nitrous oxide and leukotriene
- Direct vascular injury e.g. trauma
- endothelial injury - bacteria and toxins
How does cellular exudate form?
- Margination of neutrophils - normally cells are confined to the central stream (axial) and do not flow in the peripheral (plasmatic zone) near the endothelium. Loss of intravascular fluid and increase in viscosity means neutrophils move in the plasmatic zone.
- Adhesion of neutrophils - this is known as pavementing.
- Neutrophil emigration - leukocytes move by active ameboid movement through the walls of venules and small veins. They can insert puesodpodia between endothelial cells and migrate the through gap.
- Diapedesis - red cells escape by diapedesis. This is and passive process and depends on hydrostatic pressure.
What is the effects of fluid exudate?
- Dilution of toxins
- Entry of antibodies
- Transport of drugs
- Fibrin formation
- Delivery of nutrients and oxygen
- Stimulation of the immune response
- High turnover
Give examples of cell derived mediators of acute inflammation.
- Histamine
- Prostaglandins
- Lysosomal components
- Leukotrienes
- Cytokines
Give examples of plasma derived mediators of acute inflammation.
- Complement system
- Coagulation system
- Fibrinolytic system
- Kinin System
What are possible harmful affects of acute inflammation?
· Digestion of normal tissues e.g. abscess cavities
· Swelling e.g. acute epiglottitis - inflammation of the epiglottis is potentially dangerous
Inappropriate inflammatory response e.g. hay fever - type I hypersensitivity reaction.
What are general effects of inflammation?
- Pyrexia
- Lymph node enlargement - due to reactive hyperplasia of the reticular endothelial reticulum. Local and systemic enlargement is very common. Some can even get splenomegaly.
- Nausea, malaise, anorexia - non-specific side effects
- Leukocytosis - raised white cells. In allergic disorders and parasitic infections you get raised eosinophils. In chronic such as tuberculosis, you get lots of lymphocytes. Increase in neutrophils is seen in pyogenic infections and acute inflammation.
- Amyloidosis - long standing chronic inflammation by elevation of serum amyloid A protein may cause amyloid to deposit in various tissue resulting in secondary amyloidosis.
- Increased erythrocyte sedimentation rate