Term Test 1 - Jeff Flashcards

1
Q

what are the three phases of CT healing

A

inflammatory phase, proliferative phase, remodelling

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1
Q

How does CT heal

A
  1. fibrin scaffold (minutes)
  2. necrotic tissue removed via phagocytosis and proteases from macrophages and neutrophils (days)
  3. macrophages and platelets secrete chemical mediators (hours)
  4. angiogenesis and fibroblasts invade along fibrin scaffold (after 2-3 days)
  5. fibroblasts secrete collagen (AFTER 4-5 DAYS)
  6. remodelling and contraction (weeks-months)
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2
Q

formation of the fibrin scaffold occurs within

A

minutes

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3
Q

by what two mechanisms is fibrin removed

A

secretion of proteases; phagocytosis

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4
Q

for large wounds, what might be required to remove necrotic debris

A

debridement

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5
Q

what 4 factors are released from macrophages and platelets

A

PDGF, VEGF, bFGF, TGF-β

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6
Q

what growth factors stimulate angiogenesis

A

VEGF, bFGF

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6
Q

what growth factors stimulate fibroblast infiltration along the fibrin scaffold

A

bFGF, PDGF, TGF-β

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7
Q

fibroblasts start secreting collagen after….

A

4-5 days

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8
Q

what is granulation tissue

A

tissue containing fibroblasts, new blood vessels and newly synthesized collagen

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9
Q

T/F granulation tissue and granulomatous inflammation are the same thing

A

VERY FALSE

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10
Q

what is the significance of 4-5 days

A

the time at which fibrous tissue is starting to be formed and we will start seeing issues such as contractures, strictures, adhesions, etc.

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11
Q

what does maturing of collagen involve

A

change from type III -> type I
crosslinking

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12
Q

what is responsible for contraction of wounds

A

myofibroblasts (after 4-14 days)

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13
Q

wound strength (%) after:
- 3 weeks
- 6 weeks
- 6 months

A
  • 3 weeks: 20%
  • 6 weeks: 70%
  • 6 months: 80%
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14
Q

T/F after tissue injury, over time, the collagen will eventually always return to a normal histological appearance

A

F; may never return to normal appearance, but will be functional

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15
Q

fibrin vs fibrous tissue

A

fibrin = polymerized fibrinogen (elastic, loosely adherent)
fibrous tissue = fibroblasts, newly synthesized bvs, collagen

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16
Q

T/F fibrous tissue and granulation tissue are the same (for the sake of this course)

A

T

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17
Q

granulation tissue vs granulomatous inflammation

A

granulation tissue: fibroblasts, collagen, new bvs
granulomatous inflammation: type dominated by activated macrophages, +/- giant cells, T cells and fibrous tissue

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18
Q

how does EPITHELIAL tissue heal (3)

A
  1. rapid sliding
  2. delayed hyperplasia and migration
  3. differentiation into normal epithelial phenotype (ex. stratified squamous)
19
Q

what are the requirements for epithelial tissue repair

A
  1. intact CT framework
  2. adequate blood supply
  3. mitotically active cells
20
Q

epithelial repair takes approximately how many hours

21
Q

abrasion vs incision

A

abrasion only goes through epidermis; incision goes through epidermis, BM, and dermis

22
Q

would an abrasion or incision take longer to heal and why

A

incision; have to first repair the CT framework

23
what are the three main reasons that epithelial tissue might fail to heal
1. lack of CT framework 2. no mitotically active cells 3. ischemia (loss of blood supply)
24
name other reasons a wound may fail to heal
infection, extensive tissue damage, poor nutrient availability, movement malnutrition, corticosteroid therapy
25
adverse consequences of tissue repair
cosmetic; impaired nutrient/gas exchange; altered organ perfusion; adhesions; stricture/contratures; impaired electrical activity
26
what is ankylosis
joint fixation
27
what is contracture
fixation of a joint in flexion
28
collagen stains what colour histologically
blue
29
who came up with the cardinal signs of inflammation? who added loss of function ot the list?
Celsus; Virchow
30
what two MAIN changes define inflammation
1. alterations in blood vessels 2. leukocyte infiltration of tissues
31
inflammation is linked with (3)
tissue repair, coagulation, immunity
32
T/F inflammation is phylogenetically old and conserved across species
F; species differences but conserved otherwise
33
what are 3 adverse consequences of inflammation
1. systemic effects (SIRS, Sepsis, APR) 2. temporary loss of function 3. scarring - permanent loss of function
34
why is inflammation beneficial (2)
1. contain/eliminate inciting cause 2. tissue repair
35
what are the 3 stages of inflammation
1. serous or fibrinous effusion 2. leukocyte infiltration 3. repair
36
vascular changes are responsible for what cardinal signs of inflammation? (specific)
vasodilation: warmth, redness increased vasc. perm: swelling (edema)
37
what are 4 inflammatory mediators
histamine, cytokines (IL-1, IL-6, TNFα), eicosanoids, complement
38
what is a common source of all inflammatory mediators
plasma, local cells
39
effects of inflammatory mediators are typically ____________ and usually ____________
transient; localized
40
redundancy vs pleiotropy
redundancy: many mediators, one function pleiotropy: one mediator, many function
41
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...
42
what cell produces fibrin protein
hepatocytes
43
describe the elicitation phase of a type I hypersensitivity reaction
1. allergen binds IgE 2. IgE crosslinked 3. mast cells degranulate 4. release of inflammatory mediators (ex. histamine) causes immediate vasodilation and increased vascular permeability (also bronchoconstriction, pruritis) 5. late phase reaction dominated by eosinophils, macrophages, lymphocytes
44
what type of T cells are involved in type I hypersensitivity (allergic reactions)
Th2
45
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
46
neutrophil responses to inflammation only occur in (veins or arteries)
VEINS