wound healing Flashcards

1
Q

What are the 5 wound healing models?

A
  • Superficial wound healing: only affects epidermis
  • Primary intention-surgical;
  • Delayed primary intention-surgical;
  • Partial-thickness wound healing: epidermis destroyed, wound into dermis
  • Full-thickness wound healing
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2
Q

What do Rete Pegs do?

A

Prevent shearing of dermis

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3
Q

The Simplified phases of healing

A
  • inflammatory: platlets, fibrin, neutrophils, macrophages, mast cells
  • Proliferative: fibroblasts, myofibroblasts, endothelial cells, keratinocytes
  • Remodeling: collagen
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4
Q

What are platlets, neutrophils, & monocytes

A
  • Platlets: small fragments in blood involved in homeostasis
  • Neutrophils: phagocytic, clean up debris/bacteria
  • Monocytes: WBC in response to inflammation will differentiate into macrophage
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5
Q

What are Endothelial cells, fibroblasts, myofibroblasts?

A
  • EC: form endothelium, lining of blood vessels
  • Fibro: produce protein fibers (collagen) and ECM
  • Myofib: cell differentiated from fibroblast, contains actin/myosin system.
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6
Q

What are keratinocytes, mast cells?

A
  • Ker: main cell in epidermis

- Mast cells- specialized secretory cell that helps promote fibroblast proliferation

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7
Q

What are Cytokines?

A
  • Signaling molecules (peptides, proteins; essential for cell communication
  • Play role during inflammation: attract immune cells for defense
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8
Q

Growth Factors?

A
  • Proteins that are able to effect cell reproduction, movement, and function
  • Can act on distant cells (endocrine stimulation), adjacent cells (paracrine stim), or on themselves (autocrine)
  • Released in response to homeostatic control signals
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9
Q

What are Chemokines?

A
  • Regulate trafficking of leukocyte population during normal health/development
  • Direct activation of neutrophils, lymphocytes, macrophages, during inflammation.
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10
Q

What are MMP’s?

A
  • Matrix metalloproteinases
  • Family of 20 proteolytic enzymes; critical in achieving tissue degradation
  • Require Ca ions for structural conformation; Zinic to function
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11
Q

What are TIMPS?

A
  • Tissue inhibitors of metalloproteinase

- Synthesized by same cells that produce MMPs

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12
Q

What are some initial characteristics of the inflammatory phase?

A
  • Begins at time of injury; lasts 3-7 days
  • Clotting takes place hemostasis; factors released to rid debris, bacteria, damaged tissue
  • Redness, warmth, pain, edema, dec ROM
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13
Q

What are the first initial steps in the inflammatory phase?

A
  • Clotting & vasoconstriction to reduce BF
  • Break down pre-existing tissue scaffolding; clean up debris
  • Epidermal barrier disrupted; platelets are activated by collagen exposed by the injury (trigger vasoconstriction)
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14
Q

What is Hemostasis?

A
  • Clot is formed made of cytokines, GF’s, fibrin, fibronectin, thrombosponinds (clotting cascade)
  • Serves as scaffolding for migration of leukocytes, keratinocytes, fibroblasts, and endothelial cells (foundation for collagen deposition)
  • Reservoir of GF’s
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15
Q

What do platelets secrete during the inflammatory phase?

A
  • Multiple cytokines and GF’s: EGF, PDGF, TGF-B, IL-1
  • Attract neutrophils to wound
  • Monocyotes are transformed into macrophages
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16
Q

Describe wound space hypoxia during inflammatory phase?

A
  • Vasoconstriction= dec O2; hypoxia controls wound healing
  • Neutrophils, macrophages; stimulates endothelial cells- angiogenesis
  • Shift to anaerobic glycolysis= inc lactate; wound becomes hyperlactic
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17
Q

The role of Neutophils during inflammatory phase

A

-Cleanse the wound; there w/in 24 hours; like hypoxic environment; part of pus

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18
Q

The role of Macrophage during inflammatory phase?

A
  • Initiate angiogenesis & granulation tissue formation during proliferation
  • Phagocytosis of debris (excrete lactic acid)
  • Secrete collagenases- help break down damaged collagen that is there, being to lay new collagen
  • Produce NO, secrete GF’s
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19
Q

Mast Cells during inflammatory phase

A
  • Promote fibroblast proliferation- TNF-a

- Release histamines (vascular dilation-edema), produce heparin, accelerate activity of neutophils

20
Q

Nitric Oxide?

A

-Vasodilatation; role in angiogenesis, most abundant during first 10-14 days

21
Q

Complement system?

A
  • Noncellular group of substances that are responsible for acute inflammation
  • Facilitate bacterial destruction; antibodies IgG & IgM activate it
22
Q

Temperature during inflammatory phase

A
  • Vasodilatation of surrounding tissue- perfusion aids in moving cells to the injury (inc temp)
  • Injured nerve endings cause hyperemia (inc temp)
  • Inc cell metabolism (inc temp)
  • If no dec in temp by 4th day possible infection
23
Q

Current of injury

A

-Cells posses currents of ion movement; current flowing b/t normal and injured tissue is stimulus for repair process

24
Q

What are the initial characteristics of proliferative phase?

A
  • Begins around 3rd-5th day, can last up to 21 days
  • Angiogenesis, granulation tissue formation, collagen deposition, epithelialization, wound contraction
  • Fill in tissue defect with shiny new tissue
  • Restore integrity of skin (collagen syn (fibroplasias), angiogenesis, contraction
  • Macrophages releases GF/cytokines- attract fibroblasts to wound (produce collage/elastin (foundation of connective tissue
  • Act as scaffolding that will support blood vessel growth by endothelial
25
Q

Describe elastin/collagen

A
  • Elastin: form network of fibers that stretch/recoil; gives ECM elasticity
  • Collagen: predominate fiber; resists stretching forces
  • Ground substance- fills space b/t cells/fibers, high water content, GAGS/proteoglycans/glycoproteins
26
Q

Examples of collagen in Proliferative phase?

A
  • Type 1- dermis, bone, tendon, fascia, disk
  • Type 2- hyaline & elastic cartilage
  • Type 3- smooth muscle, arteries, lung, uterus, kidney
27
Q

Angiogenesis during Proliferative phase

A
  • Restores vascular integrity; macrophages induce this by releasing TNF-a, VEGF
  • New capillary buds arise from intact blood vessels- supply O2/nutrients; capillary loops have appearance of granulation tissue, are fragile
  • Endothelial cells proliferate and grow into wound space
28
Q

Contraction during Proliferative phase

A

-Myofibroblasts connect the wound margin to pull epidermal layer inward; closes wound

29
Q

-Re-epithelialization during Proliferative phase

A
  • Re-establishment of intact epidermis over newly formed tissue
  • Keratinocytes near basal lamina migrate across the granulation tissue
  • Epithelial migration from intact hair follicles and sebaceous glands
30
Q

Remodeling phase

A
  • Occurs 6 mongths-3 years post injury
  • Collagen becomes parallel & creates stronger bonds, most endothelial cells, macrophages, myofibroblasts undergo apoptosis
31
Q

Collagen during remodeling phase?

A
  • Type 3 was laid down during proliferative
  • Type 3 is lysed and replaced with type 1 (stronger)
  • Collagen lysis: collagenase produced during inflammatory/proliferative phases cleave topocollagen molecules aiding in resorption
32
Q

Stress on remodeling?

A
  • Stress affects shape, strength, pliability
  • Collagen, elastin, and ground substance are affected by the direction and magnitude of mechanical stress applied to scar (Wolfe’s Law)
  • Laid in response to lines of stress
  • Tension causes inc in collagen fibers
  • Stress will increase population of connective tissue cells to remodel the tissue, too much stress can pull scar apart
33
Q

Scar formation during remodeling phase

A
  • Vascularity/ cellularity diminish; becomes less red and flattens out
  • Ratio of collagen breakdown to production determines type of scar
  • —>Break down > production= flat pliable scar
  • —–>Breakdown < production= hypertrophic scar (red, elevated, itchy, confined to original area of injury (pictures in slides)
34
Q

Keloid scar

A

-Type of hypertrophic scar, extends outside the area of injury, tumor like appearance

35
Q

Scar- Remodeling phase

A
  • Essential & hindrance; begins highly vascular and becomes aceullar/avascular
  • Changes to collagen- basket weave= small parallel bundles
  • Intact skin: collagen (basket weave), elastin fibers, Ground substance
  • Scar tissue- Collagen (bundles), Ground Substance
  • Mature scar 80% of strength- rete pegs lost with scar
  • Heals centipedially
36
Q

Chronic Wound- Factors that affect wound healing

A
  • Wound that deviates from the expected sequence of repair (time, appearance, response to tx)
  • Inflammatory phase: stimulus for repair; inside-out; inadequate perfusion (vascular insufficiency)
  • Proliferative phase: diminished keratinocyte migration lack of moisture, large surface area, rolled edges, thickened edges, hypergranulation tissue
  • Proliferative phase: repeated trauma/infection, long term hypoxia (dec fibroblast production, negative effect on collagen production
  • Remodeling phase: imbalance b/t collagen synthesis. Over production (hypertrophic) or underproduction (wound breakdown)
37
Q

Intrinsic factors that affect wound healing

A

-Related to medical status of patient: Age, chronic disease, perfusion, immunosuppressant, neuropathy

38
Q

-Extrinsic factors that affect wound healing

A

-Those that come from environment that affect body: medications (anticoagulants, immunosuppressant’s), nutrition (protein intake), irradiation, chemotherapy, psychological, wound bioburden & infection

39
Q

Iatrogenic Factors

A
  • Related to way wound is managed
  • Local ischemia (pressure from bony prominence, compression)
  • Inappropriate wound care; trauma, time to heal
40
Q

Transforming Growth Factor β

A
  • TGF-β1: platlets –> chemotatic for fibroblasts
  • TGF-β2 : fibroblasts–> promote ECM formation
  • TGF-β3: Machrophages–> inc collagen/TIMP syn, dec MMP syn. Reduce scarring ( Dec collagen/fibronectin
41
Q

-Platelet-Derived GF

A
  • PDGF-AA, PDGF-BB: platlets –> activates immune cells and fibroblasts
  • VEGF: macrophages (promote ECM formation), Keratincocytes (inc collagen/TIMP syn), fibroblasts (dec MMP syn, inc angiogenesis)
42
Q

Fibroblast GF

A
  • Acidic FGF, basic FGF: macrophages (inc angiogensis)

- KGF: endothelial cells ( inc keratinocyte proliferation/migration) & fibroblasts (inc ECM deposition)

43
Q

Insulin-Like GF

A
  • IGF-I, IGF-II: liver –> inc keratinocyte/fibroblast proliferation
  • Insulin: skeletal mm (inc angiogenesis), fibroblasts (inc collagen syn), macrophages (inc ECM formation), neutrophils (inc cell metabolism)
44
Q

Epidermal GF

A

-EGF, HB-EGF, TGF-α: keratinocytes –>inc Keratinocyte proliferation and migration

45
Q

Connective Tissue Growth Factor

A

-CTGF: fibroblasts (inc collagen syn), endothelial cells (mediates action of TGF-βs on collagen syn)

46
Q

Table in Wound healing lecture

A

slide 32