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Case 1 > Wound Healing > Flashcards

Wound Healing Flashcards

1
Q

What stimulated wound healing

A

Macrophages (therefore it is linked to inflammation)

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2
Q

What has to happen for wound healing to occur

A

Inflammation

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3
Q

What is regeneration

A

Restitution of tissue components identical to those killed/ lost

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4
Q

What regenerates from stem cells

A

Liver, kidney, haematopoietic, skin, GI tract

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5
Q

What is essential for wound healing

A

An intact connective tissue framework, the healing then essentially patches the tissue

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6
Q

Where is scarring

A

At the compact patches of collagen

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7
Q

What is haemostasis

A

Clotting

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8
Q

What three phases occur in conjunction with eachother in haemostasis

A

Vascular phase, platelet phase and coagulation phase

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9
Q

Describe the vascular phase

A

Damage to blood vessel wall causes contraction in that area of the blood vessel (vasconstriction), can last from 30 minutes- few hours.

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10
Q

What does the vascular phase occur as a result of

A

Damage to endothelial cells

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11
Q

What does damage to endothelial cells cause the release of

A

ADP, tissue factor (factor III), prostacyclin, endothelins

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12
Q

What is tissue factor required for

A

Activation of thrombin from prothrombin

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13
Q

Describe the role of prostacylcin

A

Kind of a feedback mechanism, this protein actually causes vasodilation and prevents the formation of the platelet plug

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14
Q

Describe the role of endothelins

A

Primary hormones involved in the vascular phase. They stimulate smooth muscle contraction and stimulate cell division of endothelial cells, smooth muscle cells and fibroblasts this aiding repair of the damaged site

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15
Q

What can occur if damage to the blood vessel is small enough

A

It can be ‘plugged’ by a platelet plug

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16
Q

What is platelet formation controlled by

A

TPO (thrombopoietin)

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17
Q

What is TPO mainly produced by

A

The liver

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18
Q

Describe the platelet phase

A

Platelet formation controlled by TPO. Platelets attach themselves to the collagen of damaged epithelium and begin to aggregate. Fibrin forms threads which stabilise the plug

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19
Q

What is adhesion

A

Platelets attaching themselves to the damaged epithelium

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20
Q

What is fibrin produced by

A

Liver and platelets.

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21
Q

What happens to a platelet when it becomes attached to a damages enothelial surface

A

It will change its own size and shape

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22
Q

Describe the process of a platelet changing its own size and shape when attached to a damaged endothelial surface

A

It will swell and become large and irregular. The contractile proteins contract causing the release of granules. ADP, thromboxane and Ca2+ ions are all released

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23
Q

What is the role of ADP, thromboxane and Ca2+

A

They act on nearby platelets and attract them to the site causing them to adhere to the platelets already present. This creates positive feedback loop causing aggregation of more and more platelets

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24
Q

What are the two types of granules released by the platelets

A

Alpha and dense

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25
What do alpha granules contain
Growth factors like fibrinogen and PDGF
26
What is the disease caused by a lack of alpha granules called and what does it do
Called grey platelet syndrome. It is a rare genetic disorder (autosomal dominant), it will just basically cause reduced clotting
27
What do dense granules contain
Non-protein thinks like thromboxane, serotonin, calcium, ATP and ADP
28
Describe the coagulation phase
Begins at about 30 seconds after the injury. It incolves a complex sequence of events that ultimately lead to the activation of fibrin from fibrinogen
29
Describe the events clotting cascade
There are two different pathways: intrinsic and extrinsic. These eventually joint to form the common pathway
30
Where does the intrinsic pathway begin
In the blood stream (initiated when blood is exposed to collagen or other damaged surfaces)
31
Which factor beings the clotting cascade
Factor XII beings the cascade, converted to XIIa by the presence of collagen
32
What triggers the activation of factor XII
The presence of collagen
33
Describe the sequence of events of the intrinsic pathway
``` Exposed collagen + XII -> XIIa; XIIa + HMX kininogen cause XI -> XIa; XIa + Ca2+ causes XI -> XIa; VIII + thrombin -> XIIIa; XIa + VIIIa + platelet phosphlipids -> factor X activator complex -> common pathway ```
34
Where does the extrinsic pathway begin
In the vessel wall (damaged endothelial cells will release factor III aka tissue factor)
35
What does an increase in damage cause
An increase in release of factor III (tissue factor)
36
What is factor III activated by
Calcium
37
Describe the sequence of events of the extrinsic pathway
Damaged tissue causes III -> IIIa; | IIIa + Ca2+ -> VII-III complex -> common patwhay
38
What does the common pathway begin with
X -> Xa (Xa= prothrombinase)
39
What does Xa convert
Xa + Ca2+ causes prothrombin -> thrombin
40
What does thrombin convert
Fibrinogen to fibrin and XIII to XIIIa
41
What is the role of XIIIa
XIIIa and fibrin result in the cross-linking of fibrin
42
Describe the extrinsic pathways production of thrombin
Will produce a small amount of thrombin very quickly
43
Describe the intrinsic pathways production of thrombin
Will produce a large amount thrombin
44
What is an essential part of the host defense
Activation of coagualtion and fibrin deposition as a consequence of inflammation
45
What does cogaulation and fibrin deposition help the body defend against
Infectious agents or nonidentical cells, to contain invading entity and keeping the consequent inflammatory response to a limited area
46
What is the link between expression of procoagulant material and coagulation
Expression of procoagulant material by inflammatory cells in the unstable plaque (particularly tissue factor) may initiate the activation of coagulation and the thrombin generated will both activate platelets and result in the formation of a platelet-fibrin thrombus.
47
How do the inflammation and coagulation systems closely interact
Coagulation can substantially modulate inflammatory activity
48
What is an example of coagulation factors
Thrombin
49
What is an example of anticoagulant proteins
Activated protein C
50
How might cogaulation factors of anticoagulant factors modulate inflammatory activity
Thrombin or activated protein C may activate specific cell receptors on mononuclear cells or endothelial cells which may affect cytokine production or inflammatory cell apoptosis
51
What are 4 processes involved in healing following initial haemostais
Inflammation, cell proliferation and migration, angiogenesis and granulation tissue
52
What are the two ways angiogenesis can occur
From pre-existing capillaries or formed from EPC (endothelial progenitor cell)
53
Describe angiogenesis from pre-existing vessels
Capillary sprouting -> mature network
54
Describe angiogenesis from EPC
EPCs mobilised from bone marrow undergo homing to capillary result in formation of capillary plexus and mature network
55
Describe granulation tissue
New connective tissue and tiny blood vessels that form on the surfaces on a wound during the healing process. Granulation tissue typically grows from the base of a wound and is able to fill wounds of almost any size
56
When are neutrophils replaced by macrophages
At 48-96 hours
57
What functions do macrophages perform
Debridement, removal of injured tissue and debris. Antimicrobial activity. Chemotaxis and proliferation of fibroblasts and keratinocytes. Angiogenesis. Deposition and remodelling of ECM.
58
How does connective tissue remodelling occur
Granulation tissue replaced by scar
59
Describe the process of connective tissue remodelling
Collagen synthesis, starts 3-5 days post injury (balance between deposition and degradation). Vascular regression begins as scar matures
60
Describe the process of recovery of tensile strength
10% by end of week 1 (sutures are removed). 70-80% after 3 months (3 month plateau). Initial excess collagen synthesis over degradation. Structural modification (fiber size, cross link)
61
What are the 2 types of healing
Healing by 1st intention and healing by 2nd intention
62
Describe healing by 1st intention
Edges of wound narrow or have been brought together by stitches therefore heals far quicker. Healing by epithelisation results in minimal scarring
63
Describe healing by 2nd intention
Heals from the base therefore heals slower. Healing by granulation results in scarring. Wound contraction. Risk of infection
64
What local factors affect wound healing
Oxygenation, infection, foreign body, vascularity, location
65
What systemic factors affect wound healing
Age/ sex, hormones, stress, diseases (diabetes, jaundice, renal failure), medication, lifestyle (alcohol, smoking, obesity, nutrition)
66
How does old age affect wound healing
Decrease in inflammatory response, delayed angiogenesis, decrease in collagen synthesis and degradation, slower epithelialisation
67
How does diabetes affect wound healing
Diabetic ulcers- neuropathy (unable to sense and relieve cutaneous pressure), ischaemia secondary to vascular disease, prone to infection- impaired granulocyte function and chemotaxis, prolonged inflammation, impaired neovascularisation, decreased collagen synthesis, increases levels of proteinases, defective macrophage function
68
Describe fetal wound healing
Fetal wounds re-epithelialise rapidly. Fetal wounds heal without scarring (small amount of TGF Beta 1), fetal skin rich in metalloproteinases
69
Describe wound contraction
Contraction of myofibroblasts (collagen secreting fibroblast cells) attempting to bring edges of wound together
70
Complication
Deficient scar formation (dehinscene/ rupture); excessive contraction (avoid this via skin graft); excessive scarring; calcification, pigmentation, pain; incisional hernia
71
Describe the features of a venous leg ulcer
Common in elderly, often result of chronic venous hypertension, persistent inflammation, hemosiderin deposits, lipodermatosclerosis
72
Describe the features of an arterial ulcer
Reduced blood supply, ischemia and necrosis, little exudate, atrophic skin, common in diabetes, pain
73
Describe the features of a diabetic foot ulcer
Common in diabetes, hyperglycaemia, micro/macroangiopathy, neuropathy, infection, foot deformities
74
Describe the features of a pressure sore
Area of tissue necrosis, caused by prolonged soft tissue compression, local ischemia and moisture, multi-morbid and elderly
75
Describe the features of a hypertrophic scar
Rapid growth, generally regressed in
76
Describe the features of a keloid scar
Constant growth, no spontaneous regression, extend beyond margins of tissue damage, genetic predisposition, thick and haphazardly oriented collagen bundles
77
What are the signs of wound infection
Erythema, pus/ exudate, abscess, pain
78
What is the role of toxin and enzyme in wound infection
Allows spreading of subcutaneous infection- cellulitis, necrotising factors, necrotising fascitis
79
What is the role of bacteraemia in wound infection
Seeding, osteomyelitis/ joint infection
80
What are the factors used in classification of wound healing
Contamination, colonisation, local infection/ critical colonisation, spreading invasive infection
81
What is contamination
Presence of organisms in wound without inflammatory response
82
What is colonisation
Replication of organisms in wound without inflammatory response
83
What is local infection/ critical colonisation
Organism and tissue response
84
What is spreading invasive infection
Organism and organisation spread
85
What are the consequences of wound infection
Chronicity, dehiscence, excess scarring, dissemination, gangrene, necrotising faciitis
86
What does microbial cross-talk result in
Biofilm development
87
Describe biofilm development
Bioflm forms around the wound (no blood vessels). Fibrin, thrombin, albumin, collagen, bacteria. Protects bacteria from immune system. Antiobiotics don't work
88
Describe a nonhealing phenotype biofilm
Nuclear marker present, non-healing tissue within a chronic wound
89
Describe a healing phenotype biofilm
Nuclear marker absent, healing tissue within a chronic wound

Case 1 (10 decks)

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