inflammation Flashcards
inflammation: explain and compare the pathology and histological features of acute, chronic and granulomatous inflammation; list the sequelae of inflammation
purpose of inflammation
protective response removing cause and consequences of injury, setting stage for potential healing
how is inflammation triggered
various cell types and soluble mediators
how is inflammation regulated
leukocyte and vascular responses
what must the tissue be in order for inflammation to occur
vascularised
define acute inflammation
rapid non-specific leukocyte and vascular response to cellular injury, orchestrated by mediators from injured cells
cardinal signs of acute inflammation
rubor (redness), calor (heat), tumour (swelling), dolor (pain), loss of function
process of acute inflammation
alteration in calibre of blood vessels increase flow → structural changes to microvasculature, allowing proteins and leukocytes through → emigration, accumulation and activation of leukocytes at focus of injury
vasodilation in acute inflammation: what introduces it and what follows it
vasodilation (early manifestation causing heat and redness) introduced by mediators including histamine (richest source in mast cells) and nitric oxide, followed by increased permeability (diameter increases and flow decreases, causing stasis)
acute inflammation: mechanism of increasing vascular permeability
histamine causes endothelial cells to contract, increasing interendothelial spacing
define exudate
mass of cells and fluid that has seeped out of blood vessels
contents of exudate
high protein content, purulent (pus formed by suppuration), serous (serum), fibrinous (fibrin), high specific gravity, cells and cell debris (including leukocytes)
functions of exudate
dilutes and “walls off” pathogens, permits spread of soluble inflammatory mediators, provides substrate for inflammatory cell migration
consequence of very high intravascular fluid losses
haemorrhages
2 reasons for leukocyte response in inflammation
recognise and kill bacteria and eliminate foreign and necrotic material by phagocytosis, produce and activate multiple factors and mediators to interact with other cells to amplify inflammatory response
what is the first leukocyte into a damaged area
neutrophil
how do neutrophils enter damaged area
extravasation
function of neutrophils in inflammation
phagocytosis and degranulation
examples of receptors activated by leukocytes during inflammation
cytokines, chemokines, complement proteins
why must the acute inflammatory response terminate
prevent overactivation of leukocytes causing long-term harm
4 ways or contributors for terminating acute inflammatory response
mediators and neutrophils have short half-lives, macrophages release anti-inflammatory products, mast cells and lymphocytes produce anti-inflammatory products (lipoxins), cause of inflammation (e.g. bacteria) removed
what non-specific leukocytes are present in acute inflammation
neutrophils, eosinophils, mast cells
role of macrophages in acute inflammation
phagocytosis (destroy pathogen directly or stimulate another pathway, and once cleared, dies), cytokine release, wound repair and fibrosis, anti-inflammatory effects
define chronic inflammation
prolonged duration of inflammation, where inflammation, tissue injury and attempts at tissue repair coexist
when does chronic inflammation occur
may follow acute inflammation, or arise as insidious, low-grade smouldering inflammation
what causes insidious, low-grade smouldering inflammation
persistent infection, prolonged exposure to toxins, autoimmunity or persistent foreign body
what cells are present in the mononuclear cell filtrate of chronic inflammation
eosinophils, macrophages, T-lymphocytes and plasma B-lymphocytes (antibodies); neutrophils may be present if co-existing with acute inflammation)
following tissue destruction, what is damaged tissue replaced with in chronic inflammation
connective tissue
difference in macrophage presence in chronic inflammation
macrophages persist, causing tissue destruction and can trigger inflammatory cascade
define angiogenesis and prominence in chronic inflammation
formation of new blood vessels; prominent in chronic inflammation
define granulomatous inflammation
distinctive pattern of chronic inflammation showing granuloma formation
what is granuloma formation
aggregate of activated macrophages
why is there an aggregate of activated macrophages
attempts to eliminate resistant pathogen, triggered by strong, specific T-lymphocyte reaction
causes of granulomatous inflammation
infection, foreign material, tumour reaction, diseases (e.g. Crohn’s, TB)
acute vs chronic inflammation: leukocytes
neutrophils vs macrophages
acute vs chronic inflammation: soluble factors
histamine vs cytokines
acute vs chronic inflammation: outcome on cells
prominent necrosis vs prominent scar tissue
acute vs chronic inflammation: onset
immediate vs delayed
acute vs chronic inflammation: duration
a few days vs weeks/months/years
acute vs chronic inflammation: outcomes
complete restoration and progression to chronic inflammation vs scar tissue formation and disability
positive long term consequences of inflammation
removal of pathogen, cessation of inflammatory response, healing of tissue damage
negative long term consequences of inflammation
excessive tissue damage and scarring, systemic involvement with multiorgan failure leading to septic shock
