Wound Repair in Skin Flashcards
Causes of edema
Inflammation, infection, immune, cardio, endocrine
Where is edema located
Accumulation of interstitial fluid in sub epithelial/dermal tissues of the eyelids
Factors that induce edema
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
Medications that cause eyelid edema
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
Inflammatory conditions of the skin can be due to
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
Vertical wrinkles indicate
Chronic edema
Therapies for skin inflammation
Avoid inciting agents Protective eyewear Topical steroid creams Topical antibiotics when needed May need immune modulators
Speed of recovery is impacted by
Depth, size, microbial contamination, genetics and co-morbidities of the patient (ex, DM)
3 phases of wound healing
- Inflammatory / cutaneous neurogenic inflammation
2 Proliferative - Remodeling
What occurs in the Inflammatory / cutaneous neurogenic inflammation stage of wound healing?
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:
- Vascular smooth muscle to cause vasodilation
- Vessel wall to increase permeability and recruit WBC
- 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
Inflammation stage- Nociceptor endothelial cells send a signal to the spinal cord to release neuropeptides. These neuropeptides have which 3 targets?
- Vascular smooth muscle to cause vasodilation
- Vessel wall to increase permeability and recruit WBC
- Mast cell degranulation of histamine, serotonin, and protease. Increases vascular permeability (red and warm) and brings more inflammatory factors to the wound.
Hemostasis process during Inflammation stage
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.
M1 and M2 during Inflammation stage
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
What occurs during the proliferative phase of wound healing?
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
Main cell sending signals during the proliferative stage
MO
Fibroplasia during the proliferative phase
Modulate synthesis and growth of Metalloproteinases and collagen synthesis (yields wound contraction, scar)
Signals keratinocyte/mesenchymal differentiation
Re-Epithelialization during the proliferative phase
Keratinocytes differentiate and establish fibrin clot and dermis.
Suprabasal keratinocytes join and fill in
Angiogenesis during the proliferative phase
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.
Pattern of angio around a wound
Neo forms a ring around the border, then radial connections are made to un-injured skin /vasculature.
Peripheral nerve repair in during the proliferative phase (2)
- Collateral re-innervation
- Factors from the damaged nerve signal nocireceptors to sprout collaterals. - Nerve regeneration
- MO with schwann cells promote nerve regeneration.
- MO release VEGF due to hypoxia
How long does remodeling phase last?
Years
Remodeling phase
Restoring integrity of skin
- Completion of skin remodeling, formation of functional tissues.
- Apoptosis and regression of cellular material that are unneeded.
During which stage of development is there no scarring
Embryonic
End product of wound healing/remodeling phase
Scar
