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Section 1 Surgical Biology > 9 > Flashcards

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1
Q

What are the three stages of wound healing

A
  1. inflammatory
  2. proliferative
  3. maturation
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2
Q

What are the cellular components of wound healing

A 
platelets
neutrophils
macrophages
endothelial cells
fibroblasts
myofibroblasts
keratinocytes
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3
Q

4 mechanisms GF’s cytokines and chemokine act by

A

autocrine
paracrine
juxtacrine
endocrine

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4
Q

cytokines and chemokines are mostly secreted by

A

leukocytes

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5
Q

what is the ECM made up of 1. initially and then 2. latterly

A
  1. fibrin, fibronection, vitonectin

2. large structural proteins such as elastin, collagen saturated with glycoproteins, laminin, hyaluronic acid

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6
Q

what are integrins

A

type of cell surface receptor that are closely associated with cytoskeleton. Crucial for cell motility.

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7
Q

5 roles of the macrophage in wound healing

A 
1.Cell recruitment
2 secrete growth factors
3. Matrix Synthesis
4.Phagocytosis
5. Wound debridement
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8
Q

Broadly, what happens in the inflammatory phase

A
  1. immune barrier
  2. removal of wound contaminants
  3. attracts cells for the next phase (proliferative)
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9
Q

Broadly, what happens in the proliferative phase

A
  1. establishment of vascular supply
  2. Extracellular matrix formed
  3. Epithelial covering
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10
Q

Broadly, what happens in the maturation phase

A
  1. Reorganisation of collagen

2. development of some of pre wound strength

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11
Q

what are the three stages of the inflammatory phase

A

Haemostasis
Early inflammatory phase
Late inflammatory phase

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12
Q

What is the key objective of the haemostats phase of the inflammatory phase?

A

Avoid exsanguination

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13
Q

When the epidermis is disrupted, which cells release which cytokine? (the earliest signal)?

A

Keratinocytes release IL-1

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14
Q

When the vascular endothelium is disrupted what is released?

A

Endothelin, by the endothelial cells

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15
Q

Endothelin acts along with two substances to initiate Haemostasis, what are they ? What is the immediate affect?

A

Epinephrine and Prostglandins.
Profound local arteriolar and capillary vasoconstriction, can prevent haemorrhage in vessels <5mm.
Effect is transient.

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16
Q

After initial haemostatic reflex and reflex local vasconstriction what occurs and why?

A

Passive relaxation due to hypoxia and acidosis

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17
Q

The coagulation cascade is initiated, what collagen types are platelets activated by when contacted? Where is it found?

A

Type IV and V damaged endothelium.

Also require vWG which binds factor VIII

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18
Q

Activation of coagulation cascade affects prothrombin nd fibrinogen how?

A

prothrombin cleaved to thrombin

fibrinogen becomes insoluble fibrin

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19
Q

what do activated platelets release? what does it do?

A

Thromboxane - potent vasoconstrictor.
stimulates further platelet activation and expression of GPIIb and GPIII on the platelet cell membrane.
Fibrin binds GPIIB and GPIII to strength fibrin clot.

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20
Q

What is the purpose of the insoluble fibrin clot>

A
  1. ongoing haemostasis

2. scaffold to facilitate cell migration

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21
Q

Platelets degranulate to reduce which granules? What do theses alphas granules cause the release of (x 8)? in turn which cells are activated?

In addition to alpha granules what are released and what to they do?

A

alpha granules

PDGF, TGFbeta, IGF-1, EGF, fibronectin, fibrinogen thrombpospondin, VWF –> ACTIVATE neutron, macros, endothelial cells + fibroblasts.

Vasoactive amines, (histamine and serotonin) with results in vasodilation and increased vascular permeability.

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22
Q

Give overview of events in haemostasis stage. (x 8 main steps)

A
  1. Endothelin released from endothelial cells (IL-1 released from keratinocytes).
  2. Endothelin + epinephrine + PG’s = vasoconstriction.
  3. hypoxia and acidosis = passive relaxation
  4. coag cascade maintains haemostasis via platelet activation (when exposed to type IV and V collagen in endothelium w add of VWf)
  5. prothrombin -> thrombin
    fibrinogen -> fibrin
  6. activated platelets release thromboxane A2 which is a vasoconstrictor. Also stimulate further platelet activation + expression of GPIIB and GPIII
  7. Fibrinogen binds GPIIB and GPIII to strength fibrin clot
    Fibrin clot = ongoing haemostasis and scaffold for cell migration)
  8. Simultaneous platelet degranulation results in release of alpha granules. Alpha granules stimulate PDGF, TGF, EDGF, IGF-1, fibronectin, fibrinogen, thrombospondin and VWF) which activate neu’s, macrophages, endothelial cells, and fibroblasts.
    Platelets also release serotonin and histamine which cause vasodilation and increase vascular permeability.
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23
Q

what are the effects of histamine and serotonin release at the end of the haemostasis phase?

A

increase vascular permeability–> Extravasation of plasma and vasodilation –> increases blood flow to wound bed.

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24
Q

Which leukocyte migrate to wound first?
when are the numbers of these cells highest?
which methods do they get to wound? ( x 3)

A

Neutrophils
24-48 hours post injury
Adherence, migration, chemoattraction

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25
What is the function of neutrophils in early inflammatory phase? x 4
1. Prolong inflammatory phase by releasing cytokines 2. Kill bacteria through the release of reactive oxygen species 3. Phagocytose degraded bacteria 4. Breakdown extracellular matrix through proteolytic enzymes
26
Neutrophils have IgG and complement receptors. Activation of complement leads to (x2)
1. bacteria opsonised and bound to neuts--> RECOGNITION AND PHAGOCYTOSIS 2. after phagocytosis, NADPH uses o2 to catalyse formation of bacterial superoxides, superoxides increase killing capacity
27
below what partial pressure of oxygen is neutrophil killing impaired and therefore wounds more susceptible to infection? Why is neutrophil killing oxygen sensitive?
40mmHg
28
Lactate is produced during the inflammatory phase, why? and why is lactate important at this stage?
inflammatory cells consume a lot of o2 resulting in local hypoxia. Lactate stimulates angiogenesis and collagen synthesis required for proliferation.
29
Angiogenesis and collagen synthesis is stimulated by GFs expressed by which cells, amplified by what?
macrophages, keratinocytes and fibrioblasts. | Neutrophils chemotaxis amplified by TNF alpha.
30
main role of early inflamm phase
establish immune barrier
31
Main role of the late inflammatory phase?
Establish macrophages in the wound
32
How long after injury do monocytes arrive in the wound?
48-72hours
33
what doe TGF beta influence in the late inflammatory phase?
Monocytes --> macrophages
34
What influences monocytes turn to macrophages
TGF beta
35
during which phase of inflammation do we clinically see oedema and at wound edges
late inflammatory phase
36
which cells dominate the late inflammatory phase
Macrophages
37
what are roles of the macrophage in the late inflammatory phase? (such delayed reteeince perm memeor)
1. Further release of Signalling molecules 2. Debride wound 3. Release Cytokines 4. Phagocytose degenerating neutrophils so that by 48-96 hours post injury are primary leukocyte 5. MMP release to degrade ECM to facility cell movement through wound
38
how long does the late inflammatory phase last?
3-5 days
39
what are the 5 stages of the proliferative phase
``` Angiogenesis Fibroplasia Collagen Synthesis Contraction Epitheliazation ```
40
what is the product of the proliferative phase?
granulation tissue
41
when post injury does the proliferative phase occur?
4-12 days
42
proliferative phase? when do they enter the wound bed?
Macrophages, endothelial cells, fibroblasts, epithelial cells Enter during the inflammatory phase
43
what GF causes proliferation of endothelial cells? What is the secreted by? What is the response to this GF dependant on ?
VEGF secreted by keratinocytes. Endothelial response dependant on Pp02.
44
how many days post injury is there an invading vascular network?
4-6
45
What are the 4 steps of angiogenesis?
1. activated endothelial cells degrade basal lamina of existing vessels via proteases 2. Activated endothelial cells migrate into provsional ECM under influence of GF's 3. Endothelial cells proliferate ( under influence of VEGF) and make tubular structure. Response to VEGF dependant on pp02 4. basal lamina laid down
46
which cells precede the speciallzed fibroblasts? what leads them to differentiate? when do they differentiate?
Mesenchymal cells differentiate under the influence of PDGF, TGF and epidermal growth factor, secreted by macrophages and platelets. at 3-5 days post injury.
47
what do specialised fibroblast synthesise?
definitive ECM. --> type III and IV collagen. | also HA, proteoglycans, GAG's elastin and fibronectin
48
what are there three steps of fibroplasia?
1. mesenchymal cells become specialised fibroblasts under VEGF that is dependant on PP02. 2. specialised fibroblast migrate into ECM under chemotactic influence 3. fibroblasts synthesise ECM - type III and IV collagen mainly. plus proteoglycans, GAGs, elastin, fibronectin
49
What types of collagen are found in normal dermis and what is dominant in healing dermis?
Normal is 80% type I and 20% type III. | Type III is dominant in healing tissue.
50
when does FGFb peak? what does it do? What does TGF beta do? when is fibroblast recruitment limited and by what?
7-14 days post. Directs ECM production and degradation. TGFbeta - increases synthesis go type I collagen Ltd at 5-6 weeks any IP10
51
what makes up granulation tissue?
newly vasculairized ECM, fibroblasts, macrophages, fibroblast collagen and HA. results in lower wound exudate and lower risk infection. may become player as increased collagen content w fibroplasia
52
at what day does contraction start and what cells initiate? | when do these cells undergo apoptosis?
day 6, fibroblast differentiate to myofibroblasts. | Die at weeks 5-6
53
Describe epithelization
1. basal layer keratinocytes at wound edges detach from basal lamina 2. activated keratinocytes express integrin, cells mobilise across wound by interaction with ECM 3. kerationocytes release processes to breakdown ECM in path of migration 4. migrating cells phagocytes debris 5. continue until contact inhibition. nb keratinocyte proliferation cont into maturation phase.
54
in what time period is the total collagen produced?
6 weeks. matures over 6-18 months
55
which collagen fires are resorbed and which fibres persist in the maturation phase?
fibres in line with tension persist and those not in line are resorbed.
56
why is type III collagen weaker?
is more glycosylated with more fibrils
57
what per centage of final scar is made of type III collagen?
10%
58
how strong is the scar as a per cent of unwounded tissue?
70-80%
59
what happens if the mechanical lands endures across a scar?
collagen synthesis continues, myofibroblasts contract and forms a CONTRACTURE
60
how long does a GI mucosal injury take to heal?
3 days
61
In the GI, which cells make collagen? (compared to the skin?)
GI collagen made by smooth muscle cells and fibroblast. | skin fibroblasts only.
62
Collagenases activity is not significant in skin, what is it effect in the GI? In was situation is its activity increased?
Activity increased at easy 0-3 which means overall weakening of wound/anastomisis in that time. Collagenases have increased activity in sepsis.
63
what types of collagen are present in the GI?
I, III AND V (just I and III in skin)
64
is healing in the GI more or less affected by perfusion? why? which pressure of 02 are important.
MORE. GI perfusion down regulated by shock. pp02<40mmg = failure of mature collagen in the GI, <10mmhg = failure of angiogenesis and epitheliazation.
65
critical components for healing of enterotomies are
1. maintainCO 2. optimize o2 sat 3. avoid tension 4. preserve blood supply
66
when suturing fascia where should sutures be placed?
>3mm from wound edge (outside inflammatory zone)
67
Fascial healing 1. failure often due to? 2. how can avoid failure? 3. where should sutures be placed?
1. failure due to high tense forces 2. use in absorbable/slowly absorbable cont. suture 3. place sutures >3mm from edge
68
Is bladder peak collagen level earlier or after skin?
5 days so earlier. skin is 7-14 days.
69
does the bladder return to 100% pre injury streggnth?
yes - 100% at 21 days
70
at what time point do nerves and smooth muscle infiltrate the matrix in bladder injury?
4 weeks.
71
What is the role of BMP's in bone healing?
1. stimulate undifferentiated cells in the periosteum, marrow, endosteum and surrounding muscles to become chondroblasts and osteoprogenitor cells. 2. callular compeonte in marrow differentiate to osteoblastic phenotype within 24 hours.
72
whcih collagen plays a role in bone healing? what does it do?
type III, in osteoblast differentiation and remodelling
73
how long may the maturation phase of bone last?
up to 1 year
74
4 ways that healing is different i the cat to the dog
1. 7 day breaking strength of line alba sig less in cat 2. tissue granulate in 6.3 days in cat vs 4.5 days in dog 3. contraction and epitheliazation faster in dogs cf cats 4. cats more affected by removal sc tissues than dogs
75
loose skin is more likely to heal by ..... where are tight skin more likely to heal by ....
loose skin = contractino, | tight skin = epithelization
76
females or males show superior healing? why?
females are faster, healing probably negatively affected by androgen.
77
6 local factors influence wound healing
``` Perfusion Tissue Viability Fluid Accumulation Wound Infection Mechanical Envenomatino ```
78
How does infection affect the inflammatory phase?
1. consumption of complement = decreased chemotaxis 2. depleted platelets 3. impaired leucocyte function 4. tissue damage by free radicals and toxic enzymes
79
how does infection affect the proliferative phase?
1. Endotoxin and protease damages granulation bed 2. fibroblast proliferation = disorganised collagen 3. bacterial endotoxin reduce cross lining of collagen 4. increased collagen breakdown and decreased wound strength 5. metabolites inhibit keratinocyte migration and digest dermal protein 6. proteases damage endothelium
80
what bacterial load is significant in a wound and how does it infect the wound infection rate?
>10e5 / g tissue - infection rate 50-100%
81
3 major effects glucocortioinds on wound healing
decreased fibroblast activity +collagen synthesis decreased macrophage activity declared MMP
82
what percentage collagen is present in unwounded dermis?
80% type I 20% type III
83
what is percentage of collagen type on ht eGI submucosa
Type I68%, Type III 20%, type V 12%

Section 1 Surgical Biology (3 decks)

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