L7 - Acute Inflammation Flashcards
what causes the formation of fluid exudate?
- chemical mediators; histamine, NO, leukotriene
- direct vascular injury (trauma)
- endothelial injury (bacteria and toxins)
what are the effects of fluid exudate?
- dilution of toxins
- entry of antibodies
- transport of drugs
- fibrin formation
- delivery of nutrients and oxygen
- stimulation of immune response
- high turnover
how is cellular exudate formed?
- loss of fluid into tissues and increased calibre of vessels = slower blood flow and increased viscosity of blood (stasis).
- Neutrophils line up along vascular endothelium and migrate through vessel wall into tissues
- margination of neutrophils
- pavementing of neutrophils (adhere)
- diapedesis/transmigration
- migration into adventitia.
what is acute inflammation?
- initial tissue reaction to injury
- lasts minutes-days
- characteristic cell: neutrophil
Physical characteristics of acute inflammation?
RCTDF
Rubor (redness) Calor (heat) Tumour (swelling) Dolor (pain) Functio laesa (loss of function)
causes of acute inflammation?
physical agents
infection
hypersensitivity reactions
chemicals
tissue necrosis
what chemically mediates acute inflammation?
- vasodilation
- migration of neutrophils
- chemotaxis
- increased vascular permeability
general effects of acute inflammation?
- pyrexia (fever)
- lymph node enlargement
- nausea, malaise, anorexia
- leukocytosis
harmful effects of acute inflammation?
- digestion of normal tissues e.g abscess cavities
- swelling e.g epiglottis
- inappropriate inflammatory response e.g hayfever
what changes in vessel calibre occur in acute inflammation?
Vasodilation ([after] initial transient vasoconstriction)
- Early change (15 mins to several hours)
- Increases blood flow (<10x) - Heat and redness
- Mediated by histamine and NO on vascular smooth muscle
characteristics of neutrophils.
- produced in bone marrow
- most common WBC
- increased in acute inflammation
- motile/amaeboid, can move into tissues
- directional chemotaxis
- short lifespan (hours)
major components/features of acute inflammation?
- changes in vessel calibre
- increased vascular permeability
- fluid ad cell exudate
what is exudate?
Implies inflammation
extravascular fluid with high protein concentration, containing cellular debris.
what is transudate?
low protein, little or no cellular component
what is oedema?
excess fluid in interstitial tissue / serous cavities – exudate or transudate
what is pus?
inflammatory exudate rich in neutrophils, dead cell debris and microbes
what affect does histamine have on the CNS?
NONE
[Different tissues have different susceptibility e.g. CNS is insensitive to
histamine but skin, conjunctiva & bronchial mucosa are sensitive →
hayfever]
how is fluid exudate formed?
Increased permeability of microvasculature results in escape of protein rich fluid into tissue
- hydrostatic pressure
list cell derived mediators of acute inflammation
- histamine
- prostaglandins
- lysosomal componenents
- leukotrienes
- cytokines
list plasma derived mediators of acute inflammation
- complement system
- kinin system
- coagulation system
- fibrinolytic system
what does phospholipase do in the Arachidonic acid, prostaglandins and leukotriene pathway?
converts cell membrane phospholipid into arachidonic acid
what do steroids inhibit? what physiological effect does this have?
phospholipase
prevent vasodilation
what does cycloxygenase do in the Arachidonic acid, prostaglandins and leukotriene pathway?
converts arachidonic acid to prostaglandins
what physiological effect do prostaglandins have?
vasodilation
oedema
what inhibits cycloygenase? what physiological effect does this have?
Aspirin & indomethacin inhibit cyclooxygenase
reduces the inflammation
what does 5-Ilpoxygenase do in the Arachidonic acid, prostaglandins and leukotriene pathway?
converts arachidonic acid to leukotrienes
what physiological effect do leukotrienes have?
vasoconstriction
bronchospasm
increased vessel permeability
what are the general effects of acute inflammation?
➢Pyrexia
➢Lymph node enlargement
➢Nausea, malaise, anorexia
➢Leukocytosis
what are the harmful effects of acute inflammation?
- digestion of normal tissues e.g abscess cavities
- swelling eg epiglottis
- inappropiate inflammatory response eg swelling of lips
what happens if acute inflammation is not resolved?
- excessive exudate (suppuration and formation of pus)
- excessive necrosis (repair or fibrosis)
- chronic inflammation
what effect do Anti-inflammatory glucocorticoid steroids have?
stabilize membranes and prevent phospholipid
hydrolysis thereby inhibiting both prostaglandins and leukotriene pathway
what effect do Aspirin and other NSAIDs have on the prostaglandins and leukotriene pathway?
inhibit cyclooxygenase
but not lipoxygenase
what effect do Leukotriene receptor antagonists (LTRAs) have on the prostaglandins and leukotriene pathway?
inhibit the bronchoconstrictive and
inflammatory mechanisms of leukotrienes
what would you see on a blood test (full blood count) if inflammation was apparent?
Full blood count – significant increase in lymphocyte levels
higher erythrocyte sedimentation rate (increases with the higher the level of inflammation)
increase in C-reactive Protein (CRP)
What are the possible complications of pneumonia (inflammation of the lungs)
Bacteria in the bloodstream (bacteremia)
Difficulty breathing.
Fluid accumulation around the lungs (pleural effusion)
Lung abscess.
what is systemic inflammatory response syndrome?
systemic inflammation, organ dysfunction/failure
Abnormal regulation of various cytokines (cytokine storm)
What is Acute (adult) respiratory distress syndrome?
wide spread inflammation of the lungs
triggered by various pathologies such as pneumonia and sepsis
what is chronic granulomatous disease of childhood?
hereditary disease
phagocytes cannot form reactive oxygen compounds (required to kill infections)
= long term (chronic) and repeated infections
what is Hereditary angio-oedema?
rare, autosomal dominant
Inherited blood disorder
causes episodic attacks of swelling
what is Amyloidosis?
Amyloidosis is when an abnormal protein called amyloid builds up in your tissues and organs. When it does, it affects their shape and how they work.
Caused by accumulation of amyloid fibrils (abnormal insoluble proteins) within extracellular space of tissues
Can be local or systemic = inflammation
how would acute inflammation present under a microscope?
[Neutrophils are seen and some necrotic and dead cells and sometimes microbial agents]
how is fluid exudate formed?
Increased permeability of microvasculature results in escape of protein rich fluid into tissue
what are some chemical mediators of acute inflammation?
➢ Vasodilatation
➢ Migration of neutrophils
➢ Chemotaxis
➢ Increased vascular permeability
what are the outcomes of acute inflammation?
- resolution (body goes back to normal)
OR:
● Excessive exudate
● Excessive necrosis
● Persistent causal agent → Chronic inflammation
