Term Test 1 - Jeff Flashcards
what are the three phases of CT healing
inflammatory phase, proliferative phase, remodelling
How does CT heal
- fibrin scaffold (minutes)
- necrotic tissue removed via phagocytosis and proteases from macrophages and neutrophils (days)
- macrophages and platelets secrete chemical mediators (hours)
- angiogenesis and fibroblasts invade along fibrin scaffold (after 2-3 days)
- fibroblasts secrete collagen (AFTER 4-5 DAYS)
- remodelling and contraction (weeks-months)
formation of the fibrin scaffold occurs within
minutes
by what two mechanisms is fibrin removed
secretion of proteases; phagocytosis
for large wounds, what might be required to remove necrotic debris
debridement
what 4 factors are released from macrophages and platelets
PDGF, VEGF, bFGF, TGF-β
what growth factors stimulate angiogenesis
VEGF, bFGF
what growth factors stimulate fibroblast infiltration along the fibrin scaffold
bFGF, PDGF, TGF-β
fibroblasts start secreting collagen after….
4-5 days
what is granulation tissue
tissue containing fibroblasts, new blood vessels and newly synthesized collagen
T/F granulation tissue and granulomatous inflammation are the same thing
VERY FALSE
what is the significance of 4-5 days
the time at which fibrous tissue is starting to be formed and we will start seeing issues such as contractures, strictures, adhesions, etc.
what does maturing of collagen involve
change from type III -> type I
crosslinking
what is responsible for contraction of wounds
myofibroblasts (after 4-14 days)
wound strength (%) after:
- 3 weeks
- 6 weeks
- 6 months
- 3 weeks: 20%
- 6 weeks: 70%
- 6 months: 80%
T/F after tissue injury, over time, the collagen will eventually always return to a normal histological appearance
F; may never return to normal appearance, but will be functional
fibrin vs fibrous tissue
fibrin = polymerized fibrinogen (elastic, loosely adherent)
fibrous tissue = fibroblasts, newly synthesized bvs, collagen
T/F fibrous tissue and granulation tissue are the same (for the sake of this course)
T
granulation tissue vs granulomatous inflammation
granulation tissue: fibroblasts, collagen, new bvs
granulomatous inflammation: type dominated by activated macrophages, +/- giant cells, T cells and fibrous tissue
how does EPITHELIAL tissue heal (3)
- rapid sliding
- delayed hyperplasia and migration
- differentiation into normal epithelial phenotype (ex. stratified squamous)
what are the requirements for epithelial tissue repair
- intact CT framework
- adequate blood supply
- mitotically active cells
epithelial repair takes approximately how many hours
24-48
abrasion vs incision
abrasion only goes through epidermis; incision goes through epidermis, BM, and dermis
would an abrasion or incision take longer to heal and why
incision; have to first repair the CT framework
what are the three main reasons that epithelial tissue might fail to heal
- lack of CT framework
- no mitotically active cells
- ischemia (loss of blood supply)
name other reasons a wound may fail to heal
infection, extensive tissue damage, poor nutrient availability, movement malnutrition, corticosteroid therapy
adverse consequences of tissue repair
cosmetic; impaired nutrient/gas exchange; altered organ perfusion; adhesions; stricture/contratures; impaired electrical activity
what is ankylosis
joint fixation
what is contracture
fixation of a joint in flexion
collagen stains what colour histologically
blue
who came up with the cardinal signs of inflammation? who added loss of function ot the list?
Celsus; Virchow
what two MAIN changes define inflammation
- alterations in blood vessels
- leukocyte infiltration of tissues
inflammation is linked with (3)
tissue repair, coagulation, immunity
T/F inflammation is phylogenetically old and conserved across species
F; species differences but conserved otherwise
what are 3 adverse consequences of inflammation
- systemic effects (SIRS, Sepsis, APR)
- temporary loss of function
- scarring - permanent loss of function
why is inflammation beneficial (2)
- contain/eliminate inciting cause
- tissue repair
what are the 3 stages of inflammation
- serous or fibrinous effusion
- leukocyte infiltration
- repair
vascular changes are responsible for what cardinal signs of inflammation? (specific)
vasodilation: warmth, redness
increased vasc. perm: swelling (edema)
what are 4 inflammatory mediators
histamine, cytokines (IL-1, IL-6, TNFα), eicosanoids, complement
what is a common source of all inflammatory mediators
plasma, local cells
effects of inflammatory mediators are typically ____________ and usually ____________
transient; localized
redundancy vs pleiotropy
redundancy: many mediators, one function
pleiotropy: one mediator, many function
what is a potential long term consequence of increased vascular permeability
fibrosis (due to exudation of fibrin; becomes fibrotic after 4-5 days) - subsequent issues such as stricture, adhesions, ankylosis, contractures…
what cell produces fibrin protein
hepatocytes
describe the elicitation phase of a type I hypersensitivity reaction
- allergen binds IgE
- IgE crosslinked
- mast cells degranulate
- release of inflammatory mediators (ex. histamine) causes immediate vasodilation and increased vascular permeability (also bronchoconstriction, pruritis)
- late phase reaction dominated by eosinophils, macrophages, lymphocytes
what type of T cells are involved in type I hypersensitivity (allergic reactions)
Th2
give one example of allergic disease in all species, dogs, cats, horses, and cows
all: anaphylaxis
dogs: allergic gastroenteritis
cats: feline asthma
horses: heaves
cows: milk allergy
neutrophil responses to inflammation only occur in (veins or arteries)
VEINS
