Broad descriptions of Acute inflammation
- fast
- mainly consists of neutrophils
- usually mild and does not destroy self tissues
- has prominent local & systemic signs
Broad descriptions Chronic inflammation
- slow
- produces monocytes/macrophages and B/T cells
- usually severe and damages self tissue
- little systemic & local signs
Calor
Heat
Rubor
Redness
Tumor
Swelling
Dolor
Pain
Functio laesa
Loss off. Function
Specific descriptions of acute inflammation
Dilation of small vessels
Increase permeability of microvasculature
Emigration of leukocytes from microcirculation to the focus of injury
Exudate
Extravascular fluid that contains cellular debris and lots of proteins
- presence implies increased permeability of small blood vessels
Purulent inflammation
Accumulation of exudate that forms pus
- high concentration of leukocytes/ dead cell debris
- caused by pyogenic pathogens.
Ulcer
Shedding “stuffing” of surface of organ
Outcomes of acute inflammation
- complete resolution/regeneration
- progression to chronic inflammation
- healing via scarring/fibrosis
Labile tissues
Tissues containing cells that are ALWAYS undergoing self-replication
Stable tissues
Tissues containing cells that are capable of regeneration, but not always undergoing it
Permanent tissues
No regeneration of cells.
Steps of scar tissue formation
- inflammation
- angiogenesis
- formation of granulation tissue
- ECM remolding/ scar formation
TNF-B
Most importation cytokine to granulation tissue formation
Primary union
Regeneration w/ mild scaring
Secondary union
Regeneration w/extensive scarring
keloid
Excessive ECM production causes large boundary-less scars
Factors that impair tissue repair
Infection (most impactful) Diabetes Steroids Poor nutrition Poor perfusion Location, type and extent of injury
Matrixmetalloproteinases (MMPs)
Most important molecule in formation and shrinkage of scars overtime
Autophagy
Self digestion of intracellular organelles via lysosomes
-done in times of nutrient deprivation
Mechanisms of intracellular accumulation
Abnormal metabolism
Mutations in protein folding/transport
Lysosome enzyme deficiencies
Inability to degrade phagocytosis pigments (carbon)
Steatosis
Accumulation of triglycerides in parenchyma cells
Alpha-1 antitrypsin deficiency
Mutation causing significant slowing of protein folding.
unfolded protein intermediates build up in ER
Glycogenoses
Enzymes cant break down glucose
Most common exogenous pigment
Carbon
- build up called (anthracosis)
Transudate
Fluid with low protein content & little or no cellular material.
- presenceimplies hydrostatic imbalance across vessels w/normal permeability