Acute inflammation Flashcards
Describe the principle causes, physical characteristics Describe the difference between vascular and exudative phases Recognise the macroscopic and microscopic appearances of acute inflammation Describe the beneficial, harmful and systemic effects of acute inflammation
Causes of acute inflammation
- Microbial infection
- Allergic reaction
- Physical causes
- Chemical causes
Characteristics
Rubor – red – dilation of blood vessels
Calor – hot – peripheral inc in temp – due to inc blood flow
Tumor – swelling – mainly to oedema – some contribution from inflammatory cells
Tender – stimulation of nerve endings by pressure and chemical mediations
loss of function
common examples
acute appendicitis and cellulitis
Phases of acute inflammation
Initial reaction of tissue to injury
Vascular phase – dilation and increased permeability INC PERM
Exudative phase – fluid and cells escape from permeable venules ESC FROM PERM VEN
Neutrophil polymorph is the characteristic cell – weird nucleus so easy to spot – most common white blood cell – 70% of wbc are neutrophils
Normal vs acute inflammation
Capillary beds start to occupy cells and fluid bc of the now open precapillary sphincter
Normal vs acute inf net flow – due to hydrostatic pressure the proteins escape the cell
No net flow – some hydrostatic pressure that relieves once some net flow is released by out flow is compensated by in flow – good balance
With net flow bc of permeable wall – this hydrostatic pressure compromises proteins to go to damaged area and fluid is secreted from the walls causing swelling in the tissue
Features of exudate
Features of an exudate – the secretion
High protein content – 50 times more content
Proteins include immunoglobulins ( antibodies ) – may be important for destruction of invading organisms
Fibrinogen -> fibrin
- On extravascular contact
- Acutely inflamed organ surfaces commonly covered by fibrin
High turnover
- Continuously removed via lymphatics
Exudate vs transudate
Exudate - acute inf processes
- Net flow out
- Inc vascular perm
- High protein content
Transudate – normal inf processes
- No net flow
- Normal vasc perm
- Low protein content
What causes vascular permeabilty
- Produced by chemical mediators including histamine, bradykinin
- Involves stimulation of endothelial cell cytoskeleton by chemical mediators
- Confined to post capillary venules
- Transient intercellular gaps ( 0.1-0.4 microns ) appear
- Endothelial cells are not damaged in this process which is good, gaps go BETWEEN cells – tighten up again after inflammation
Lymphatic system in inflmmation
- Lymphatics dilated
- Drain fluid from exudate
- Antigens carried to lymph nodes
- Recognised by lymphocytes
Cellular component of acute inflammation
Neutrophil accumulation in the extracellular space is the diagnostic feature of acut inf
Neutrophils
- Kill orgs
- Degrade necrotic dissue
- Ingest offending agents
- Produce chem mediators
- Produce toxic oxygen radicals
- Produce tissue damaging enzymes
pavementation and margination
Immune cells move out of blood vessels into inflamed area
And do, attaching to vessel walls through margination and moving along to find a gap through pavementation in a process called diapedesis
The vessel wall expresses certain molecules during inf time, proteins like selectins and integrins which inc in number and they interact with receptors on the immune cell membrane causing a higher affinity allowing them to move along and across to the inf site
neutrophil chemotaxis
Neutrophil chemotaxis – smelling socks
Chemotactic compounds include:
Bacterial products
Some complement components
Products of neutrophil activity
How do neutrophils do it?
Movement – chemotaxis
Recognition of and adhesion to microorganisms
Phagocytosis
Intracellular killing of microorganisms
Chemical mediators of acute inflammation
- The spread of acute inflammatory response following injury suggests chemical substances released from the injured tissues spread outwards into uninjured areas
- Derived from cells and extra cellular sources eg plasma
- These endogenous chemical mediators cause
- Vasodilation
- Emigration of neutrophils
- Chemotaxis
- Increased vascular permeability
- Itching and pain
Plasma factors of acute inflammation
Plasma contains 4 enzymatic cascade systems – argents that get triggered
Complement system
The kinins
Coagulation factors
Fibrinolytic system
Recognition and adhesion in acute inflammation
- Most microorganisms are not recognised for phagocytosis until they are coated in opsonins
- These opsonins bind to specific receptors on leuccocytes and greatly enhance phagocytosis
- Major opsnonins – IgG – C3b ( a fragment of C3 generated by complement activation ) – collectins – plasma proteins that bind to microbial cell walls
Phagocytosis
Phagocytosis – process whereby cells such as neutrophils and macrophages ingest solid particles is termed phagocytosis
what does acute inflammation tend to look like?
serous - protein rich fluid exudate
cattarhal - mucus hypersecretion
fibrinous - exudate contains plentiful fibrin
haemmorrhagic - extreme vascular injury
suppurative - production of pus
Membranous - epithelium coated by fibrin
Pseudomembraenous - superficial mucosal slough
suppuration
- formatio of pus - neutrophils, bacteria, cellular debris
- causative stimulus virtually always infective agent
- a collection of pus surrounded by a membrane of sprouting capillaries , neutrophils and occasional fibroblasts is called an abscess
- on draining , the absecc cavity collapses and is obliterated by organisation and fibrosis
- deep seated abcesses may drain along a sinus tract or fistula
ulceration
- an ulcer is a local defect or excavation of the surface of an organ or tissue that is produced by the sloughing of inflammatory necrotic tissue
Most commonly encountered
- inflammatory necrosis of the mucosa - mouth, stomach,intestine
- Chronic leg ulcers in those with circulatory disturbance
Beneficial affects of circulation
- Dilution of toxins – allows them to be carried away by lymphatics
- Entry of antibodies – due to inc vasc permeability
- Fibrin formation – impedes movement of microorgansims
- Transport of drugs – eg antibiotics
- Delivery of nutrients and oxygem – aided by inc fluid flow
- Stimulation of the immune response – fluid exudate containg antigens reaches local lymph nodes
Harmful affects of acute inflammation
Harmful effects of acute inflammation
- Digestion of normal tissues
- Swelling – eg laryngeal odema, brain swelling
- Inappropriate inflammatory response eg type 1 hypersensitivity
Systemic affects of acute inflammation
Systemic effects of acute inflammation
Pyrexia – IL1-IL6 – cyotkytes – resets temp gage
Infectious agents can drive pyrogens to the brain that produce the drive forward and uptake the thermoregulatory mechanisms that push up the temperature which lead to a fever which means skin vasoconstriction and reduced heat dissipation
Elevation In temperature of even a few degrees may improve the efficiency of leukocyte killing and probably impairs the replication of many offending micro-organisms
Is fever a good thing or a bad thing?
Is fevera good thing or a bad thing – fever is a good sign as it’s a sign that your body is recognising and taking actions to defeat infections – not dangerous but there is some exceptions like infants where it can trigger seizures, or sudden fevers which could indicate meningitis
Symptoms of acute inflammation
Constitutional symptoms including malase, anorexia and nausea
Weight loss due to negative nitrogen balance, particularly when there is extensive chronic inflammation
Reactive hyperplasia of the reticuloendothelial system
Haematological changes
Increased erthrpocytes sedimentation rate
Anemia
Leukcytosis
