Case 1 - cutaneous wound healing Flashcards

1
Q

what are the 4 stages of healing?

A

1)Haemostasis

2)Inflammation – occurs after a few hours up until a few days

3)Proliferation – we lost tissue so we need to get the tissue back

4)Remodelling

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2
Q

when does haemostasis occur post injury?

A

immediately after injury

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3
Q

when does inflammation occur post injury?

A

Begins within minutes, typically within the first hour, and becomes fully active in the first 24–48 hours

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4
Q

when does proliferation occur post injury?

A

generally begins around day 3 to day 5 post-injury and can last up to 2 weeks, depending on the severity and type of injury.

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5
Q

when does remodelling occur post injury?

A

Remodeling after an injury typically occurs in the later stages of the healing process. It is part of the healing phase known as the maturation and remodeling phase. This phase follows the initial inflammatory and proliferative stages and can last anywhere from several weeks to months, or even years, depending on the severity of the injury

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6
Q

what cells are involved in haemostasis?

A

Platelets

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7
Q

what cells are involved in inflammation?

A

Neutrophils,
Macrophages

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8
Q

what cells are involved in proliferation?

A

Macrophages,
Lymphocytes,
Fibroblasts

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9
Q

what cells are involved in remodelling?

A

Fibrocytes

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10
Q

what is the function/activity of haemostasis?

A

Clotting

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11
Q

what is the function/activity of inflammation?

A

Phagocytosis

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12
Q

what is the function/activity of proliferation?

A
  • Fill defect
  • Re-establish
    skin function
  • Closure
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13
Q

what is the function/activity of remodelling?

A

Develop
tensile
strength

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14
Q

what happens in the vascular stage of haemostasis?

A

▪ Cellular damage causes endothelial cells to
release cytokines and endothelin, which
stimulate smooth muscle contraction, bringing
about vasoconstriction.
▪ Cytokines additionally stimulate the division of
endothelial cells, smooth muscle cells, and
fibroblasts.
▪ The endothelial plasma membranes become
“sticky”

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15
Q

what are the 3 principal components of haemostasis?

A
  1. The vessel wall (vascular phase)
  2. Platelets (primary hemostasis; platelet phase)
  3. Fibrin (secondary hemostasis; coagulation phase)
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16
Q

what are platelets

A

▪ Are disc-shaped anucleate cell fragments that are shed from megakaryocytes in the bone marrow into the bloodstream.
[▪ Their function depends on several glycoprotein
receptors:
▪ Platelet Gplb receptors to vWF
▪ GPIIb/IIIa receptors on activated
platelets form bridging cross-links with
fibrinogen, leading to platelet
aggregation.
▪ A contractile cytoskeleton]

17
Q

what are the inhibitors that regulate the size of the primary hemostatic plug or soft clot?

A

Prostacyclin – this is released by endothelial cells

Circulating enzymes – these break down ADP

ADMTS13: a plasma metalloprotease that proteolyses vWF and thereby helps limit further platelet adhesion

18
Q

what is fibrin?

A

Fibrin is a protein polymer, which has a high tensile strength and reinforces, anchors and stabilises the primary hemostatic plug

19
Q

what are macrophages?

A

Macrophages are large, irregular shaped, agranulated cells with a
large bean-shaped nucleus

20
Q

what are the primary roles of macrophages?

A

Primary
roles of macrophages:
▪ Phagocytosis of neutrophils
▪ Phagocytosis of fragments of ECM

21
Q

what do you know about macrophages and MMP’s?

A

▪ Macrophages secrete extracellular enzymes, called Matrix Metallo Proteases (MMPs), to degrade necrotic tissue at the wound site.
▪ MMPs require Calcium to form a functional shape & Zinc for the active site.
▪ Uncontrolled MMPs can degrade newly formed tissue or destroy growth factors.
▪ MMPs are balanced by tissue inhibitors of metalloproteases (TIMPs), which are released locally by cells and inactivate MMPs by reversibly binding to them.

22
Q

what’s the difference between what M1 macrophages are for and what M2 macrophages are for?

A

M1 Macrophages - macrophages involved in the initial inflammation response and
removal of dead tissue and debris
M2 Macrophages - macrophages involved in tissue repair

23
Q

what is granulation tissue?

A

Granulation tissue is a new connective tissue with microscopic blood vessels and myofibroblasts that develop at the wound site in the process of healing. It’s made up of fibroblasts, collagen type III fibres, blood vessels

24
Q

what does epethelialisation require?

A

Epithelialization requires the migration of epithelial cells across the granulation tissue, to close the epidermal defect.

25
what factors drive re-epithelialization of a wound surface?
Re-epithelialization of a wound surface is driven by many growth factors: ▪ Epidermal Growth Factor (EGF) ▪ Transforming Growth Factor-β (TGF-β) ▪ Keratinocyte Growth Factor (KGF)
26
when does Re-epithelialization start?
Re-epithelialization starts when keratinocytes, located at the wound edges, start to proliferate.
27
what happens after the wound surface is covered by a monolayer of keratinocytes?
After the wound surface has been covered by a monolayer (one layer) of keratinocytes, a new stratified squamous epithelium is established from the margins of the wound towards the centre.
28
Name some wound healing complications (you don't need to list all the ones listed)
▪ Rupture due to deficient scar formation ▪ Excessive contraction ▪ Excessive formation of repair components - excessive scaring: ▪ Hypertrophic scar ▪ Keloid scar formation ▪ Wound calcification, pigmentation, pain ▪ Incisional hernia
29
Describe healing by primary intention
The wound is with opposed edges; clean, uninfected surgical incision Clean incision into the wound Early suture (Glue the scar with certain therapeutic glues or staple them.) Such wounds heal with a clean, neat and thin scar - hairline scar
30
Describe healing by secondary intention
Wounds with separated edges Extensive loss of tissue (large defect) Care is needed to ensure that debris is removed (wound left open) Inflammatory reaction is more intense - Much larger amounts of granulation tissue Such wounds heal with substantial scar formation