week 1: acute inflammation Flashcards
define parenchyma
specialised cells of an organ
define stroma
network supporting and holding together the specialised cells of an organ (collagen and fibroplasts)
define endothelial cells
specialised cells lining the internal aspects of blood vessels
define epithelial cells
cells that line organs, ducts, airways
define pathophysiology
the physiology (process) behind pathological behaviours
define pathogenesis/aetiology
the causal factors of a pathology
- smoking = emphysema
define necrosis
death of most or all of the cells in an organ or tissue due to disease, injury, or failure of the blood supply.
define the 2 types of cell injury
reversible:
- cellular adaptation
- alterations in structure and function
irreversible
- lethal
- cell death
- necrosis
what can reversible injury cause to a cell (DAHHM)
- atrophy: reduction in size and function
- hypertrophy: increasd in size and output
- hyperplasia: increase in cell number
- metaplasia: changes from one cell type to another cell type (notable in smokers epithelial cells)
- dysplasia: abnormal growth or development of cells or organs (most smokers develop dyplastic changes)
how does loss of blood lead to cell death
- ischemia (blood flow is restricted to part of the body)
- decreased oxygen in the cells
- not enough o2 fo aerobic respiration
- decreased ATP due to anerobic glycolis increase
- lack of ATP to sodium potassium pump
- too many sodium/potassium ions enter cell
- water will follow sodium
- leads to loss of function
how do injurous agents lead to cell death
- any injurous agents enters cell
- either damages plasma membrane or ATP production which allows ions into the cell
- increased calcium (damage to mitochondria)
- increased calcium (activate intracellular enzymes which damges cell membrane and production of phospholipids)
- cell death
how do stressors (hypoxia, poison) lead to cell death
- increased production of reative oxygen species as well as o2 for ATP
- free radicals are produced
- ions grab onto electrons from other molecules and damage others
- dirupts cell membrane water and electrolytes
- cell damgage (mitochondria)
-cell death
what/how does hypoxia lead to cell death
hypoxia: preprogrammed cell death that happens all day everyday
- cell breaks down into small lipid enclosed packages
- therfore lysosomal enzymes (digestive enzymes) are contained
can cell death cause inflammation
yes, except pre-programmed cell death
-un-programmed cell death releases digestive enzymes causing localised inflammation
-necosis follows this: it is the clean up process
what is the main componenent of inflammation
blood:
- it contains all the neccessary elements
- eg. neutrophiuls
- lymphocytes
- monocytes
define: nuetrophils, monocytes (macrophages), nuetrophils, T cells and B cells
- nuetrophils: first responders that phagocytose
- monocytes: turn into macrophges that become primary phagocytosers
lymphocytes: recruited when there is viruses/bacteria
- Killer T cells: kill and ingest
- Helper T cells: release chemical mediators driving response
- B cells: things that pump out antibodies
what are the 2 types of immunity
innate: non-specific, no memory
- defence mechanism that you were born with
aquired: has specificity and memory
- cell mediated: T-cells recognise pathogens
- humoral: B cells produce antibodies mediators when presented with pathogen
- chemical mediators produce inflammatory response
- anti bodies lock onto pathogens
- destrohys pathogen by “revealing it to toher cells, cause blood protiens to lock onto pathogen, or covers all receptor cites of pathogen
define accute inflammation
an immediate, adaptive response with limited specificity caused by several noxious stimuli, such as infection and tissue damage
what are the 2 phases of accute inflammation
vascular
cellular
steps of vascular inflammation
- chgemical mediatos released by phagocytosis
- vasoconstricton
- vasodilation (nitroxcide relaxes smooth muscle)
- hyperaemia (increased blood to area)
- increase in hydrostatic pressure
- increase of fluid/plasma loss (transudate)
- increased concentation of cells
- increased blood flow/ blood slows becuase of high cellular concentration
steps of cellular inflammation
- increased activation of endothelial cells
- inceased adhesiveness
- WBC’s marginate and aggregate at injuy site
- gaps develop between endothelial cells
- diapedisis: WBC moving across chemical gradient
- transudate: plasma moveing across
- exudate: cells moving across
- edema occurs (swelling)
- phagocytosis of offending agent (nuetrophils, monocytes-macrophages)
- release of cytokines (MMP’s) for further destruction, also destructs surrounding material (not much in acute)
- if it is viral/bacterial T-cells and B-cells will move in (not regular for acute inflamm)
what are the outcomes of acute inflammation
- slight tissue damge but removal of agent (back to normal)
- siubstantial tissue damage, or in non regenerative tissue, or lots of fibrin exudate (healing by scarring)
- necrosis + bacterial/fungal inffection (formulationf of granulation tissue, absess)
- tissue damge and persistance of agent (chronic inflammation)
