Dermis and Subcutaneous Tissue Flashcards

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1
Q

What are the structural components of the dermis?

A

the extracellular matrix includes collagen, elastic fibers and glycoportiens, proteoglyans and hyaluraonic acid

blood vessels, nerves

adnexal structures: hair, eccine, sebaceous and apocrine glands

cells including dermal dentrocytes, fibroblasts, macrophages, mast cells

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2
Q

What is the function of the dermis?

A

provide support, strength, elasticity and shape of the skin, allows the subcutaneous tissue to resist outside forces and underlying structures such as muscle and bone against trauma

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3
Q

Which is the primary collagen of the dermis, how is it organized?

A

type I collagen is primary collagen of the dermis, each subtype has 3 polypeptide a-chhains which wrap into one triple helix

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4
Q

What is the clinical presentation of Ehlers-Danlos Syndrome?

A

hyper extensible skin and joints while the skin still retains normal elasticity with skin fragility, caused by mutations in collagen fibers, classic fish mouth scars (genetic disease causes mutations in post-translational modifications of collagen)

NOTE type IV may also involve blood vessels and lead to bruising or gastrointestinal and arterial rupture

No treatment, just minimize trauma

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5
Q

What is the clinical presentation of pseudoxanthoma easticum?

A

yellow papules of neck and axiallae and decreased visual acuity, clumping of elastic fibers affecting the skin, eyes and cardiovascular system (caudication, hypertension, angina or MI) caused by autosomal dominant recessive disease of elastin

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6
Q

What is the clinical presentation of Marfan Syndrome?

A

tall stature, long limbs and digits, scoliosis and flexible joints stretch marks, aortic dilation, and myopia and dystopia lentis or detached retina (caused by autosomal dominant mutation in fibrillin which impairs the structural integrity of skeletal, ocular and CV systems)

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7
Q

Describe the arrangement of cutaneous vasculature.

A

anastomosing “net-like” vascular plexus at three levels (superficial, deep dermal and fascial

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8
Q

What is the clinical presentation and causes of livedo reticularis?

A

reticulate macular erythema that accentuates with cold weather, arising from hypo perfusion of medium-sized vessels, may be associated with autoimmunidiseases or coagulation disorders

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9
Q

What is the clinical presentation and causes of vaculitis?

A

presentation varies with the caliber of vessel affected, cutaneous presents with palpable purpura, necrotizing libedo reticular is and ulcerations; systemic with weight loss, fever, headache and a TON of other random symptoms

both are due to inflammation of the blood vessels

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10
Q

What is the clinical presentation of leukocytoclastic vaculitits?

A

common on legs, specifically a reactive inflammation of the small cutaneuous vessels resulting in palpable purport that is triggered by medication, infection, connective tissue disease or autoimmune disease

NOTE may affect renal vasculature

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11
Q

What is the characteristic presentation of morphea (type of scleroderma)?

A

expanding erythematous plaque that progressively becomes indurated, and the central portion becomes hypo pigmented, surrounded by a lilac colored ring; inactive lesions typically hyper pigmented

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12
Q

What symptoms would you expect with limited vs. diffuse scleroderma?

A

limited would affect mostly the face and distal extremities, presenting with tight thickened skin, Raynaud’s phenomenon ***CREST syndrome

diffuse scleroderma involves the trunk and proximal extremities with cutaneous fibrosis, Rynaud’s phenomenon and additional systemic considerations like pulmonary fibrosis, renal insufficiency and cardiac disease

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13
Q

Describe phototaging, what it looks like and what causes these changes.

A

repeated, prolonged ultraviolet radiation causes skin thinning, large freckles, wrinkles, dilated pores and yellow quality to skin because UV light induces thinning of collagen in skin

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14
Q

What are the 3 phases of wound healing?

A

inflammatory, proliferative, and maturation

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15
Q

Why do dermal wounds lead to scarring?

A

depth of wound casuses dermal collagen to be deposited, while the elastin is not well replaced; the strength of a scar is 20% of final strength 3 weeks post injury and final strength is 70-80% of intact skin.

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16
Q

Describe a keloid.

A

a firm scar extending beyond the borders of the wound which may be caused by injury or inflammatory processes, including acne; excision typically causes a larger keloid then first existed

17
Q

Compare erosions and ulcers.

A

erosions affect only the epidermis while ulcers effect the epidermis and dermis; partial thickness wounds is injury to the epidermis and superficial dermis, full thickness involves the deep dermis, resulting loss f adnexal structures that contract during the healing process

18
Q

Name 6 factors that might contribute to delayed wound healing.

A

vascular insufficiency, tissue edema, infection (biofilm) dry wound bed, excessive granulation tissue or chronic radiation injury (destroys skin tissue)

19
Q

Describe panniculitis.

A

an inflammatory disorder of the fibrous septa between fat lobules

20
Q

What are the clinical findings of erythema nodosum?

A

a type of panniculitis, casuses tender, erythematous nodules with ill-defined borders reflecting the deep level of the inflammation which can be triggered by infection (strep common), medications (also sarcoidosis, IBD or idiopathic); treatment involves addressing the trigger, rest, elevation, NSAIDS

drugs that are likely to cause erythema nodosum: contraceptive pills

21
Q

What is a pyrogenic granuloma?

A

rapidly growing, friable vascular lesion that bleeds easily and often arises in sites of trauma which real to reepithelialize unless the lesion is cauterized or surgically removed