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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
Q

What do alpha granules contain

A

Growth factors like fibrinogen and PDGF

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26
Q

What is the disease caused by a lack of alpha granules called and what does it do

A

Called grey platelet syndrome. It is a rare genetic disorder (autosomal dominant), it will just basically cause reduced clotting

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27
Q

What do dense granules contain

A

Non-protein thinks like thromboxane, serotonin, calcium, ATP and ADP

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28
Q

Describe the coagulation phase

A

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

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29
Q

Describe the events clotting cascade

A

There are two different pathways: intrinsic and extrinsic. These eventually joint to form the common pathway

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30
Q

Where does the intrinsic pathway begin

A

In the blood stream (initiated when blood is exposed to collagen or other damaged surfaces)

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31
Q

Which factor beings the clotting cascade

A

Factor XII beings the cascade, converted to XIIa by the presence of collagen

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32
Q

What triggers the activation of factor XII

A

The presence of collagen

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33
Q

Describe the sequence of events of the intrinsic pathway

A 
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
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34
Q

Where does the extrinsic pathway begin

A

In the vessel wall (damaged endothelial cells will release factor III aka tissue factor)

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35
Q

What does an increase in damage cause

A

An increase in release of factor III (tissue factor)

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36
Q

What is factor III activated by

A

Calcium

37
Q

Describe the sequence of events of the extrinsic pathway

A

Damaged tissue causes III -> IIIa;

IIIa + Ca2+ -> VII-III complex -> common patwhay

38
Q

What does the common pathway begin with

A

X -> Xa (Xa= prothrombinase)

39
Q

What does Xa convert

A

Xa + Ca2+ causes prothrombin -> thrombin

40
Q

What does thrombin convert

A

Fibrinogen to fibrin and XIII to XIIIa

41
Q

What is the role of XIIIa

A

XIIIa and fibrin result in the cross-linking of fibrin

42
Q

Describe the extrinsic pathways production of thrombin

A

Will produce a small amount of thrombin very quickly

43
Q

Describe the intrinsic pathways production of thrombin

A

Will produce a large amount thrombin

44
Q

What is an essential part of the host defense

A

Activation of coagualtion and fibrin deposition as a consequence of inflammation

45
Q

What does cogaulation and fibrin deposition help the body defend against

A

Infectious agents or nonidentical cells, to contain invading entity and keeping the consequent inflammatory response to a limited area

46
Q

What is the link between expression of procoagulant material and coagulation

A

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
Q

How do the inflammation and coagulation systems closely interact

A

Coagulation can substantially modulate inflammatory activity

48
Q

What is an example of coagulation factors

A

Thrombin

49
Q

What is an example of anticoagulant proteins

A

Activated protein C

50
Q

How might cogaulation factors of anticoagulant factors modulate inflammatory activity

A

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
Q

What are 4 processes involved in healing following initial haemostais

A

Inflammation, cell proliferation and migration, angiogenesis and granulation tissue

52
Q

What are the two ways angiogenesis can occur

A

From pre-existing capillaries or formed from EPC (endothelial progenitor cell)

53
Q

Describe angiogenesis from pre-existing vessels

A

Capillary sprouting -> mature network

54
Q

Describe angiogenesis from EPC

A

EPCs mobilised from bone marrow undergo homing to capillary result in formation of capillary plexus and mature network

55
Q

Describe granulation tissue

A

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
Q

When are neutrophils replaced by macrophages

A

At 48-96 hours

57
Q

What functions do macrophages perform

A

Debridement, removal of injured tissue and debris. Antimicrobial activity. Chemotaxis and proliferation of fibroblasts and keratinocytes. Angiogenesis. Deposition and remodelling of ECM.

58
Q

How does connective tissue remodelling occur

A

Granulation tissue replaced by scar

59
Q

Describe the process of connective tissue remodelling

A

Collagen synthesis, starts 3-5 days post injury (balance between deposition and degradation). Vascular regression begins as scar matures

60
Q

Describe the process of recovery of tensile strength

A

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
Q

What are the 2 types of healing

A

Healing by 1st intention and healing by 2nd intention

62
Q

Describe healing by 1st intention

A

Edges of wound narrow or have been brought together by stitches therefore heals far quicker. Healing by epithelisation results in minimal scarring

63
Q

Describe healing by 2nd intention

A

Heals from the base therefore heals slower. Healing by granulation results in scarring. Wound contraction. Risk of infection

64
Q

What local factors affect wound healing

A

Oxygenation, infection, foreign body, vascularity, location

65
Q

What systemic factors affect wound healing

A

Age/ sex, hormones, stress, diseases (diabetes, jaundice, renal failure), medication, lifestyle (alcohol, smoking, obesity, nutrition)

66
Q

How does old age affect wound healing

A

Decrease in inflammatory response, delayed angiogenesis, decrease in collagen synthesis and degradation, slower epithelialisation

67
Q

How does diabetes affect wound healing

A

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
Q

Describe fetal wound healing

A

Fetal wounds re-epithelialise rapidly. Fetal wounds heal without scarring (small amount of TGF Beta 1), fetal skin rich in metalloproteinases

69
Q

Describe wound contraction

A

Contraction of myofibroblasts (collagen secreting fibroblast cells) attempting to bring edges of wound together

70
Q

Complication

A

Deficient scar formation (dehinscene/ rupture); excessive contraction (avoid this via skin graft); excessive scarring; calcification, pigmentation, pain; incisional hernia

71
Q

Describe the features of a venous leg ulcer

A

Common in elderly, often result of chronic venous hypertension, persistent inflammation, hemosiderin deposits, lipodermatosclerosis

72
Q

Describe the features of an arterial ulcer

A

Reduced blood supply, ischemia and necrosis, little exudate, atrophic skin, common in diabetes, pain

73
Q

Describe the features of a diabetic foot ulcer

A

Common in diabetes, hyperglycaemia, micro/macroangiopathy, neuropathy, infection, foot deformities

74
Q

Describe the features of a pressure sore

A

Area of tissue necrosis, caused by prolonged soft tissue compression, local ischemia and moisture, multi-morbid and elderly

75
Q

Describe the features of a hypertrophic scar

A

Rapid growth, generally regressed in

76
Q

Describe the features of a keloid scar

A

Constant growth, no spontaneous regression, extend beyond margins of tissue damage, genetic predisposition, thick and haphazardly oriented collagen bundles

77
Q

What are the signs of wound infection

A

Erythema, pus/ exudate, abscess, pain

78
Q

What is the role of toxin and enzyme in wound infection

A

Allows spreading of subcutaneous infection- cellulitis, necrotising factors, necrotising fascitis

79
Q

What is the role of bacteraemia in wound infection

A

Seeding, osteomyelitis/ joint infection

80
Q

What are the factors used in classification of wound healing

A

Contamination, colonisation, local infection/ critical colonisation, spreading invasive infection

81
Q

What is contamination

A

Presence of organisms in wound without inflammatory response

82
Q

What is colonisation

A

Replication of organisms in wound without inflammatory response

83
Q

What is local infection/ critical colonisation

A

Organism and tissue response

84
Q

What is spreading invasive infection

A

Organism and organisation spread

85
Q

What are the consequences of wound infection

A

Chronicity, dehiscence, excess scarring, dissemination, gangrene, necrotising faciitis

86
Q

What does microbial cross-talk result in

A

Biofilm development

87
Q

Describe biofilm development

A

Bioflm forms around the wound (no blood vessels). Fibrin, thrombin, albumin, collagen, bacteria. Protects bacteria from immune system. Antiobiotics don’t work

88
Q

Describe a nonhealing phenotype biofilm

A

Nuclear marker present, non-healing tissue within a chronic wound

89
Q

Describe a healing phenotype biofilm

A

Nuclear marker absent, healing tissue within a chronic wound

Case 1 (10 decks)

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