4 - Acute inflammation Flashcards
Acute inflammation response
Basic pathological process
Non-specific initial reaction to tissue damage
Stereotyped irrespective of aetiology
Three options following acute inflammation
Cells can regrow
Cells cannot regrow
Damaging agent persists and so damage continues
Cells can regrow
Healing by regeneration
Cells cannot regrow
Healing by repair
Damage agent persists
Chronic inflammation
Why do we have acute inflammation?
Clear away dead tissues
Locally protect from infection
Allow access of immune system components
Calor
Heat
Rubor
Redness
Dolor
Pain
Tumour
Swelling
Serous inflammation
Copious non-viscous serous fluid release w/o WBCs and so is clear.
Fibrinous inflammation
Occurs when extensive leakage of fluid - fibrinogen coagulates forming fibrin
Purulent (pseudomembranous) inflammation
Made in response to powerful necrotising toxin, characterised by false membrane (of fibrin, necrotic epithelium and leucocytes) formation
Components of the acute inflammatory response
Vascular -> exudative -> cellular
Vascular reaction
Dilatation (=rubor), changes in flow
Exudative reaction
Formation of inflammatory exudate (=tumour)
Cellular reaction
Migration of inflammatory cells out of vessels
Pyrexia definition
Raised body temperature
Acute phase reaction definition
Summary of complex metabolic/neurological/immunological/inflammatory changes that occur after quick onset of injury/infection
Vascular reaction process
Microvascular dilatation
Initially flow up then down
Increased permeability
Mediated vascular reaction hormones
Histamine Bradykinin NO Leukotriene B4 Complement components
Non-mediated vascular reaction hormones
Direct damage to endothelium e.g. toxins, physical agents
Composition of acute inflammatory exudate
Protein rich -> immunoglobulins, fibrinogen
Constantly turning over of loads of agents
Cellular reaction process
Accumulation of neutrophils in extracellular space
In severe cases, accumulation of neutrophils, cellular debris and bacteria forms pus
How neutrophils get through the walls
Axial stream of neutrophils -> margination -> rolling - adhesion (pavementing) -> migration (RBC diapedesis) -> chemotaxis
Mediators of acute inflammation types
Cell derived and plasma derived
Types of cell derived mediators
Stored (histamine)
Synthesised (prostaglandins, leukotrienes, PAF, cytokines, NO, chemokines)
Plasma derived
Kinin system
Clotting pathway
Thrombolytic pathway
Complement pathway
Mediators for vascular dilatation
Histamine PGE2/I2 VIP NO PAF
Mediators for increasing permeability
Histamine Bradykinin NO C5a LTB4 PAF
Mediators for neutrophil adhesion
IL-8 C5a LTB4 PAF IL-1 TNF
Mediators for neutrophil chemotaxis
LTB4
IL-8
Chemokines
Systemic inflammatory response syndrome (SIRS)
Response to immune system for infection but whole body - related to sepsis
Acute (adult) respiratory distress syndrome (ARDS)
Severe, life-threatening inflammation of whole lungs. Triggered by trauma or sepsis.
Chronic granulomatous disease of childhood
Certain compounds in the immune system have problems forming the oxidative compounds needed for the immune response
Hereditary angio-oedema (HAE)
Rare, autosomal dominantly inherited blood disorder causes episodic attacks which swell the face, extremities, genitals, GI tract and upper airways
Amyloidosis
Rare condition where amyloid is deposited in tissues and organs
