Inflammation Flashcards
types of cellular adaptation
atrophy - reduce in size
hyperplasia - increase in numbers
hypertrophy - increase in size
metaplasia - change in morphology and function
dysplasia - increase in numbers and change in cell types
neoplasia - new growth/ uncontrolled cell division
phases of repair in acute wound healing
- haemostasis
- inflammation
- proliferation
- remodelling
briefly describe the haemostasis process
endothelial injury
primary haemostasis - platelet activation; platelet plug
secondary haemostasis - coagulation cascade; fibrinogen –> fibrin
steps in the inflammatory process
tissue injury –> release bradykinin –> stimulate pain receptor
mast cells releast bradykinin and histamine –> subsequent release prostagladins, leukotrienes and chemotactic factors
vascular event: bradykinin and histamine released –> capillary dilation –> redness/heat/swelling/pain
cellular event: neutrophils and macrophages leave bloodstream by chemotaxis –> phagocytose microbes
goal of inflammation
- degradation and removal of necrotic tissue by inflammatory cells: neutrophils and macrophages
- secretion of chemical mediators and growth factors (which are essential for cell division during the proliferation phase) by inflammatory cells and macrophages
acute vs chronic inflammation
acute:
- sudden onset and short duration
- exudation of fluid and plasma protein
- migration of leukocytes (esp neutrophils)
chronic:
- follows acute episode of inflammation with continued tissue destruction
- less swelling and exudate
- presence of more lymphocytes, macrophages, fibroblasts
- more severe/ ongoing tissue destruction
- more collagen and fibrous scar tissue
cause of chronic inflammation
- persistent infection
- persistent indigestible material - endogenous and exogenous
- immune mediated reactions: autoimmune rxn; organ transplant rejection; unregulated immune response; hypersensitivity reactions
- following acute inflammation where the cause persist
- repeated episodes of acute inflammation
effects of corticosteroid
- reduced inflammation
- increase blood sugar
- decrease immunity
- decrease serotonin
- decrease Ca absorption
- regulate metabolism
- retain Na+
what are the 3 Rs of healing
resolution: mild to mod liver injury, superficial skin abrasion, gastric erosion
regeneration: severe liver injury, skin wounds to dermis, gastric ulcer
replacement: myocardiac infarct
cell proliferation process
formation of granulation tissue
collagen synthesis and laydown by fibroblasts
key building blocks of tissue healing
fibronectin and proteoglycans
- glycoprotein of the extracellular matrix
- forming a scaffold that provide tensile strength
- glue substances and cells together
elastin
- cross-linking to frm fibrils - provide elasticity to tissue
collagen
- provide structural support and tensile strength
- key determinant of the structural stability of extracellular matrix
describe the cellular event of the inflammatory phase
- exudate of fluid from blood vessel
- stasis: engorgement of RBC in blood vessel
- margination: leukocyte accumulate and adhere to the vessel wall
- rolling adhesion and tight adhesion
- diapedesis: oozing of WBC out of blood vessel
- chemotaxis: directional migration of WBC to source of injury
pharmacological effects of NSAIDs
anti-inflammatory
- due to decrease synthesis of prostagladin that increases vasodilation
anti-pyretic
- due to inhibition of COX-2 in hypothalamus
analgesic
- due to reduction in peripheral prostagladin synthesis which sensitize nociceptors to inflammatory mediators (such as bradykinin)
anti-inflammatory effects of glucocorticoids
NFkB - regulate inflammatory response
GCS - inhibit NFkB = reduce production of inflammatory cytokines, chemokines and adhesion molecules
GCS - inhibits phopholipase A2 and COX enzyme = decrease production of PG, thromboxane
GCS - increases the transcription of anti-inflammatory proteins: IL-10, lipocortin-1, IL-1 receptor antagonist and neutral endopeptidase
