Wound Repair in Skin Flashcards

1
Q

Causes of edema

A

Inflammation, infection, immune, cardio, endocrine

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2
Q

Where is edema located

A

Accumulation of interstitial fluid in sub epithelial/dermal tissues of the eyelids

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3
Q

Factors that induce edema

A

Medications if allergic
Allergies- conjunctivitis or contact dermatitis
Rosacea- blepharitis
General body edema- cardiac, lymphatic or renal disease
Systemic and connective tissue disease- thyroid
Conjunctival edema

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4
Q

Medications that cause eyelid edema

A

Acetaminophen/Ibuprofen have eyelid edema through angioedemtous disease.

Brimonidine may cause local allergic response

Corticosteroids/NSAIDs cause general fluid retention

Hormonal therapies cause fluid retention

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5
Q

Inflammatory conditions of the skin can be due to

A

Periocular contact dermatitis- causes type 4 hypersensitivity. Edema, erythema, itching, scaling. Consider allergy testing.

Periorbital dermatitis- Redness, Papule and microvessicles. More common in adult women. Associated with makeup and contraceptives (hormonal impact)

Periorbital psoriasis- Red, flaky, crusty patches covered by silvery skin. Reaction due to trauma, burns, insect bites. Less common at eyelid. Shiny.

Periocular atopic dermatitis (eczema)- genetic change to a filaggrin protein. Propensity for dryness. Susceptibility to allergens.

CT disorders- graves, scleroderma (may see telangiectasia)

Periorbital infections- Zoster, cellulitis

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6
Q

Vertical wrinkles indicate

A

Chronic edema

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7
Q

Therapies for skin inflammation

A
Avoid inciting agents 
Protective eyewear 
Topical steroid creams 
Topical antibiotics when needed 
May need immune modulators
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8
Q

Speed of recovery is impacted by

A

Depth, size, microbial contamination, genetics and co-morbidities of the patient (ex, DM)

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9
Q

3 phases of wound healing

A
  1. Inflammatory / cutaneous neurogenic inflammation
    2 Proliferative
  2. Remodeling
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10
Q

What occurs in the Inflammatory / cutaneous neurogenic inflammation stage of wound healing?

A

Peripheral nervous system is first response.
Sensory neurons up regulate activity in keratinocytes, mast cells, dendritic cells, and endothelial cells.

Dendritic cells function as nocireceptors and send an impulse to the spinal cord to release neuropeptides.

The neuropeptides have 3 main targets:

  1. Vascular smooth muscle to cause vasodilation
  2. Vessel wall to increase permeability and recruit WBC
  3. Mast cell degranulation of histamine, serotonin, and protease.

Hemostasis occurs- platelet aggregation, thrombin activity, and coagulation cascade.
Neutrophils, monocytes, and lymphocytes arrive
M1 and M2

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11
Q

Inflammation stage- Nociceptor endothelial cells send a signal to the spinal cord to release neuropeptides. These neuropeptides have which 3 targets?

A
  1. Vascular smooth muscle to cause vasodilation
  2. Vessel wall to increase permeability and recruit WBC
  3. Mast cell degranulation of histamine, serotonin, and protease. Increases vascular permeability (red and warm) and brings more inflammatory factors to the wound.
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12
Q

Hemostasis process during Inflammation stage

A

Platelets bind to activated collagen exposed on the injured vessel wall–> Aggregation –> Thrombin activity –> Coagulation cascade. Fibrin is attracted to the free collagen, trapping RBC to form clot.

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13
Q

M1 and M2 during Inflammation stage

A

M1- Present early in the wound repair. Phagocytic activity and release pro-inflammatory mediators.

M2- Later in wound repair. Make anti-inflammatory mediators, promote fibroblast proliferation, update angiogenesis. Clean up the other cells by phagocytosis

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14
Q

What occurs during the proliferative phase of wound healing?

A

Fibroplasia to cause wound contracture

Re-epithelialization

Angiogenesis- vessel wall repair and new vessel growth

Peripheral nerve repair- regeneration. Can regrow in the periphery.

*MO are the main cell signaling different aspects

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15
Q

Main cell sending signals during the proliferative stage

A

MO

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16
Q

Fibroplasia during the proliferative phase

A

Modulate synthesis and growth of Metalloproteinases and collagen synthesis (yields wound contraction, scar)

Signals keratinocyte/mesenchymal differentiation

17
Q

Re-Epithelialization during the proliferative phase

A

Keratinocytes differentiate and establish fibrin clot and dermis.

Suprabasal keratinocytes join and fill in

18
Q

Angiogenesis during the proliferative phase

A

MO interacts with endothelial cells, fibroblasts, keratinocytes, ECM, and peripheral nerves.

Hypoxia from injury causes release of VEGF from MO.
Endothelial cells induce angiogenesis.
Growth factors cause breakdown of vascular BM so new vessels can sprout.

19
Q

Pattern of angio around a wound

A

Neo forms a ring around the border, then radial connections are made to un-injured skin /vasculature.

20
Q

Peripheral nerve repair in during the proliferative phase (2)

A
  1. Collateral re-innervation
    - Factors from the damaged nerve signal nocireceptors to sprout collaterals.
  2. Nerve regeneration
    - MO with schwann cells promote nerve regeneration.
    - MO release VEGF due to hypoxia
21
Q

How long does remodeling phase last?

A

Years

22
Q

Remodeling phase

A

Restoring integrity of skin

  • Completion of skin remodeling, formation of functional tissues.
  • Apoptosis and regression of cellular material that are unneeded.
23
Q

During which stage of development is there no scarring

A

Embryonic

24
Q

End product of wound healing/remodeling phase

A

Scar

25
Q

Scar vs keloid

A

Scar is deformity across the joint of the wound

Keloid is deformity beyond the joint of the wound

26
Q

Scar characteristics

A

Replacement of original skin with collagenous tissue, more densely packed and not reticular/fine, packed network

Lacking hair follicle and sebaceous glands

Originally more red due to higher capillary density, which will regress.

27
Q

Difference between normal skin and scar tissue collagen

A

Normal skin- 3D basket weave orientation, giving elasticity

Scars- Densley packed and parallel layered collagen. Altered appearance and less elasticity.

28
Q

Excessive (hypertrophic) scars and keloids could be due to

A

Sustained inflammation. Excessive MO activity and poor signaling to other tissues.

Fibrosis. Overproduction of collagen.

Hypertrophic scar does not go beyond the original wound border, but it is raised/red/itchy. Could be due to excessive tension across the joints. Do PT. May flatten over time. Develop soon after surgery.

Keloids do not regress. Tend to progress over time, beyond the wound boarder. Collagen is very disorganized vs parallel in a scar. May develop months after trauma. Rare, associate with dark skin color.

29
Q

Non healing wounds

A

Vascular ulcers, pressure sores, diabetic foot ulcers

Due to persistent M1 and less M2

30
Q

How to reduce scars in surgery

A

Make incisions parallel to natural skin tension lines (langer lines)

Sharply defined and well aligned wound edges.

Infection management

Wound closure

reduce sun exposure

Additional: Skin grafting, silicone gel sheeting or ointments to prevent scar, steroid injections for keloid.

31
Q

Langer lines

A

Tension lines