Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Exodontia > Wound healing > Flashcards

Wound healing Flashcards

1
Q

Wound healing

A 
Essential
Trauma, injury or surgery
Most commonly skin
Research
Cosmetic industry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Wound healing cost

A

£180M - £2 billion per year to NHS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Healing

A

Follows tissue damage
An attempt to restore integrity to an injured tissue
Follows (often overlaps) the inflammatory process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Resolution definition

A

Return to normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Regeneration definition

A

Lost tissue replaced by same type to restore tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Repair definition

A

Tissue lost replaced by fibrous scar via granulation tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Regeneration vs repair: what determines the type of healing?

A
  1. Cell type involved
  2. Tissue architecture
  3. Amount of tissue lost
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Regeneration vs repair: cell type involved

A

Labile: continual cell division
Stable: infrequent cell division, but can increase e.g. liver cells in injury
Permanent: no cell division possible e.g. nerve cells, cardiac cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Regeneration vs repair: tissue architecture

A

Simple tissues

Complex tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Regeneration vs repair: amount of tissue lost

A

Small

Large - especially if basement membrane/ ECM lost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Repair: organisation: the formation of a fibrous scar via granulation tissue

A

Endothelial cells and fibroblasts at edges
These migrate into area, forming loose CT - granulation tissue
> in BVs and collagen (number of blood vessels eventually decreases again)
Vascularity < and fibrous scar formed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Granulation tissue do not confuse this with granuloma

A

Named such due its appearance in skin
Cells in repair process
-macrophages (phagocytosis & secretion)
-fibroblasts (collagen and other tissue support)
-endothelial cells (nutrition)
Often chronic inflammation is concurrent
!! histology on slides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Shape of fibroblasts

A

Spindle shaped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Macrophages histology

A

Larger, pale staining

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Endothelial cells histology

A

BVs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

3 layers of wound healing

A

Surface: fibrin slough and acute inflammatory cells (blood forms on surface for protection)
Granulation tissue, mostly macrophages and endothelial cells
More mature granulation tissue, more fibroblasts
histology on slides
-over time more macrophages at surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Phases of wound healing

A 
haemostasis
inflammation
proliferation
remodelling
!! pictures on slides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Haemostasis

A

•vessel rupture, bleeding
•activation of coagulation cascade
•vasoconstriction (5-10 mins. serotonin, adrenaline etc.)
•thrombus formation, fibrin & fibrinogen glue wound together
Key cell: Platelets (trapped within clot)
•cytokines & growth factors released (PDGF, TGFβ)
•act as chemo-attractants
•vasodilation (prostaglandins, leukotrienes, histamine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Inflammation

A 
Key cell (early): Neutrophil
•recruited from circulation
•remove bacteria and foreign material
•phagocytosis and enzymes
•short lived (2 days)
Key cell: Macrophage
•recruited from blood monocytes &amp; those already resident
in tissue, proliferate locally
•phagocytosis of remaining debris
Further secretion cytokines &amp; growth factors by both
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Proliferation

A

Granulation tissue formation
Key cell: Fibroblast
-proliferate, migrate & become myofibroblast
Synthesis of matrix proteins e.g. collagen
Proliferation & migration of cells over wound bed
Key cell: Keratinocyte
Re-epithelialisation
Angiogenesis (new BV formation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Remodelling

A

Provisional matrix remodelled
< in cell & capillary density (less red)
Proteases (collagenases) required for remodelling
Wound contraction
Type III collagen replaced by bundles of type I
Strength relies on cross-linked collagen I (Vitamin C)
7-10 days wound = 10% strength
2-3 months=70-80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Phases overlap

A 
Inflammation (early): 0.1-3 days
Inflammation (late): 0.3-10 days
Granulation tissue formation; 3-30 days
Matrix formation and remodelling: 5-100+ days (in which time amount of collagen decreases)
*!*! graph on slide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Primary intention

A

Wound edges are
apposed (brought together) & held in place
by mechanical means (sutures etc.)
-wound is clean, in straight line, with little loss of tissue
-usually rapid healing with minimal scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Secondary intention

A

Wound left open,
edges come together naturally by means
of granulation and contraction
-large wound with considerable tissue loss
-healing takes longer and results in more scarring
-can’t stitch it up, too big and would cause a lot of stress on the tissue
E.g. tooth extraction, wound on palate (tightly bound mucosa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Intention

A

If you are actively going to do something to help the healing process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Socket healing

A 
Same principles as fracture healing
-inflammation
-proliferation
-remodelling
No calus
27
Q

Tooth socket over time

A

Day 4: residual clot
Day 8: granulation tissue
Day 52: bony infill
Osteoclast rebsorption

28
Q

Factors influencing wound healing

A
  1. Local
    - type, size and location of wound
    - movement within wound
    - infection
    - presence of foreign/ necrotic material
    - irradiation
    - poor blood supply
  2. Systemic
    - age
    - nutrition (VitC, zinc)
    - systemic disease - circulatory, diabetes
    - drugs (esp steroids)
29
Q

How is the healing process controlled?

A 
Different types of cells
-cell-to-ECM interactions (integrins)
-cell-cell interaction
-correct position of cells
Signals (multiple)
-from cells or blood
-growth factors
-cytokines and chemokines
-O2, nutrients etc
-ECM
30
Q

Control of epithelial cells

A 
New cells are required: stimulation
of stem cells in the basal layer
Mitogenic (growth) stimuli are:
-loss of contact inhibition
-growth factor mediated (from
platelets and damaged
endothelial cells):
-> platelet derived growth factor
(PDGF)
-> epidermal growth factor (EGF)
-> keratinocyte growth factor (KCD)
31
Q

Control of epithelial cells

A 
New cells are required: stimulation
of stem cells in the basal layer
Mitogenic (growth) stimuli are:
-loss of contact inhibition
-growth factor mediated (from
platelets and damaged
endothelial cells):
-> platelet derived growth factor
(PDGF)
-> epidermal growth factor (EGF)
-> keratinocyte growth factor (KCD)
32
Q

Control of epithelial cells - movement

A 
Migration of
existing cells at
wound edge
(fibronectin)
Migration stops
when cells meet
Stratification (differentiation) finally occurs
Basement membrane proteins re-appear
33
Q

Control of neutrophils and macrophages

A 
Margination
Adhesion
Emigration
Chemotaxis
Pagocytosis and degranulation
34
Q

Margination

A

Cells line up against the vessel wall

35
Q

Adhesion

A

Adhesion molecule expression on endothelium changed

36
Q

Emigration

A

Pseudopodia push through gaps in endothelium

37
Q

Chemotaxis

A

Movement along a chemical gradient

-bacterial products (exogenous), complement fragments, prostaglandins, leukotrienes, cytokines

38
Q

Phagocytosis and degranulation

A

Free radical, lysozyme

39
Q

Control of angiogenesis

A 
Ingrowth of new BVs
Budding from intact vessels at wound
edge
Macrophages secrete angiogenic
factors in response to low oxygen
Fibroblast growth factor (FGF) &amp;
VEGF stimulate protease secretion &amp;
growth of endothelial cells
Anti-angiogenic factors limit vessel
formation
As inflammation subsides, apoptosis
occurs
40
Q

Control of fibroblasts

A

‘Activated’ to come myofibroblasts (TGFβ)
-fibroblast & smooth muscle features
Proliferation - PDGF, FGF, TGFα, c5a from macrophages, platelets and endothelial cells
Migration - stimulated by fibronectin
Chemoattraction by macrophages
Secretion of collagen and fibronectin: TGFβ

41
Q

Complicated for a reason?

A 
Essential process
Multiple cells types
Multiple control points
Control is key
*diagram on slides
42
Q

Dysregulated healing = cancer?

A 
Wound healing and cancer both:
•keratinocyte proliferation
&amp; migration
•fibroblast ‘activation’
•angiogenesis
•proteases upregulated
•integrin expression
altered
BUT
-Wound healing: reversible changes
-Cancer: irreversible changes
43
Q

Scarring

A

Good healing scarring decreased/ non-healing

44
Q

Scar definition

A 
Macroscopic
disturbance of normal structure &amp; function of skin architecture
resulting from end
product of healed
wound
45
Q

Problems

A 
Burns
Hypertrophic scars
Contractures
Keloids
Neuroma
Loss of function
Restricted growth
Cosmetic (Collagen,
fibroblasts)
46
Q

Hypertrophic scars

A

> incidence of hypertrophic scars/ keloid in those with darker skin
Used as decoration/ tribal identity
Facial scars attractive to opposite sex

47
Q

Contractures

A

Muscle/ tendon shortening

48
Q

Keloid scar histology

A

Thick bundles of collagen, with high levels of type III
Abnormal cross-linkage and high turnover
Altered cytokine levels

49
Q

Keloid scar - prevention and treatment

A

Avoid “cosmetic” procedures in “at risk” individuals
Treat with dressings, cryosurgery, pressure, corticosteroids etc
Excision often results in recurrence
New therapy – intralesional interferon

50
Q

Problems: neuroma

A

Thickening of nerve tissue that may develop
-term also used to refer to any swelling of a nerve, even in the absence of abnormal cell growth. In particular, traumatic neuroma results from trauma to a nerve, often during a surgical procedure

51
Q

Girls dig scars?

A

Females found scarred faces more attractive in the short-term

52
Q

Foetal wounds

A 
‘Scarless’
< inflammation, < neutrophils
Fibroblast phenotype (ECM synthesis, cytokine
production, RTK signalling)
Prompt disappearance of PDGF
VEGF increased (angiogenesis) &amp; FGF
Homeobox genes (transciption factors)
53
Q

Keloid scars

A

People with darker skin more prone with these

Sticks out of wound

54
Q

Wound healing –>

A

Scarless e.g. foetal skin, oral mucosa
Scarring e.g. adult skin
Non-healing e.g. chronic wounds

55
Q

Oral vs skin

A 
Environment: Saliva
Fibroblast are heterogeneous
Oral have > ability to contract
More ‘foetal’ like
‘Younger’ phenotype (telomerase)
> secretion of growth factors (KGF, HGF, VEGF)
> keratinocyte proliferation
56
Q

Oral vs skin

A 
Environment: Saliva
Fibroblast are heterogeneous
Oral have > ability to contract
More ‘foetal’ like
‘Younger’ phenotype (telomerase)
> secretion of growth factors (KGF, HGF, VEGF)
> keratinocyte proliferation
57
Q

Aids to wound healing

A 
Basic wound care
Assisted wound care
-dressings
-hyperbaric oxygen
maggots and Leeches
negative pressure/ vacuum therapy
Recombinant growth factors: EGF, KGF-2,
PDGF
Matrix materials – collagen, hyaluronin
Experimental – cell therapy
58
Q

Cystic / pulmonary/ fibrosis/ scarring of the heart

A

Cystic fibrosis: inherited condition that causes sticky mucus to build up in the lungs and digestive system
-causes lung infections & problems digesting food

59
Q

Maggot therapy

A

Results quite similar to surgical debridement

Eat necrotic and dead material

60
Q

Leech therapy

A

Contain Nitrogen oxygen in saliva - helps circulation

Keeps wound healthy e.g. on flaps after surgery

61
Q

Negative pressure/ vacuum therapy

A

Works quite well for chronic wounds

  • vacuum dressing used to enhance & promote wound healing in acute, chronic and burn wound
  • therapy involves using sealed wound dressing attached to pump to create negative pressure environment in wound
62
Q

Hilotherapy

A

Wearing mask/ bandage which circulates warm water around wound
-reduces swelling, healing time

63
Q

Research - TGFβ

A

TGFβ1 and TGFβ2 low in embryonic and high in adult
TGFβ3 high in embryonic (keratinocytes and fibroblasts) and low in adult
Alter ratio of TGFβ isoforms
Neutralising antibodies to
TGFβ1 and TGFβ2
Enhance TGFβ3
Clinical trials

64
Q

Problems: chronic wounds

A 
'Stuck' in inflammatory phase
Increased proteases (destroy ECM)
Reduced growth factors (PDGS, EGF, FGF)
Fibrin 'cuffs'
Underlying disease (venous insufficiency, diabetes)
Infection
Necrosis

Exodontia (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions