Dermis and Subcutaneous Tissue Flashcards
Dermis
ECEM including collagen and elastic fibers for support, strength, elasticity and shape
- has blood vessels, nerves and adnexal structures
- dermal dendrocytes, macrophages, fibroblasts and mast cells
Collagen
braided fibril comprised of 3 alpha chains
- 12 different types in skin for integrity and structure
- type 1 is primary collagen of dermis
Ehlers-Danlos Syndrome (EDS) Type I
Classic EDS
- hypermobility of joints
- excessive stretching of skin with maintenance of elastic recoil
- fragile skin
- atrophic or “fishmouth” scars
EDS Type IV
may involve blood vessels, leading to bruising and gastrointestinal and arterial rupture
-no treatment, avoid contact sports and trauma
Elastic fibers
Elastin and fibrillin
- stretch and recoil
- fibers move across one another readily
- not well replaced after tissue wounding (scar less elastic)
Pseudozanthoma elasticum (PXE)
AR disease from elastic fiber clumping
- affects skin, eyes, CV system
- yellow papules of lateral neck and axillae
- onset in 10s, 20s but not clinically apparent until 30/40s
- ocular involvement almost 100%
- claudication, hypertension, angina and heart attack
Marfan Syndrome
AD disease with disorder of fibrillin
- tall stature with disproportionately long limbs
- ectopia lentis (displacement of the lens of the eye)
- mitral valve prolapse
- aortic root dilation
- aortic dissection
- arachnodactyly (skeletal issues)
Livedo Reticularis (LR)
clinical appearance of reticulated macular erythema of skin
- most common on lower extremities but also trunk and upper
- hypoperfusion of the skin due to cold envi exposure
Leukocytoclastic vasculitis (LCV)
inflammation of blood vessels caused by medications, infection and autoimmune diseases
- palpable purpura, reddish-purple, domed papules that do not blanch with pressure, reflecting vascular origin
- legs, particularly ankles, mostly affected
- renal insufficiency may occur due to inflam of kidney
- treatment is to eliminate causative agent/treat underlying disease
Inflammatory phase
- vasoconstriction and clotting cascade to limit bleeding
- increased vascular permeability leading to edema and pain
- influx of neutrophils and macrophages
Proliferative phase
- fibroblasts stimulate formation of ECM
- angiogenesis to create granulation tissue
- keratinocytes proliferate and migrate to re-epithelialize would (occurs best when moist)
Maturation phase
- wound contraction
- increasing tensile strength (20% final strength 3 weeks post-injury and final wound strength is 70-80% intact skin)
- remodeling (scar maturation may take up to 1 year)
Keloid
excess collagen deposition forming a firm scar extending beyond margins of original wound
- collagen stimulates platelets to undergo activation, adhesion and aggregation
- keloids can be pruritic or painful (mostly asymptomatic)
- intralesional steroid injections, compression and scar massage may promote scar thinning and remodeling
Granular tissue
Neovascularization that provides necessary vascular bed to support nutritional requirement of healing skin
-can impede healing and requires surgical debridement
Pyogenic granuloma
Rapidly growing friable vascular lesion that bleeds easily and often arises in sites of trauma
-proliferating vascular tissue fails to reepithelialize unless lesion cauterized or surgically removed