Disorders of Integument System

epidermal layers deep to superficial

stratum basale, stratum spinosum, stratum granulosum, stratum lucidum, stratum corneum

keratinocytes

keratin

melanocytes

produce melanin

langerhan cells

present processed antigen to T cells

merkel cells

function as slowly adapting mechanoreceptors

fibroblasts

secrete collagen

mast cells

release histamine

macrophages

phagocytic immune cells; includes histiocytes in CT

blood supply in the skin

papillary capillaries

innervation of the skin

sympathetic nervous system regulates vasocontriction/vasodilation through a-adrenergic receptors

*regulated by arteriovenous anastomoses

pressure ulcer

result of unrelieved pressure on skin causing underlying tissue damage

how do pressure ulcers result

shearing forces, friction, moisture, occluded capillary blood flow resulting in ischemia and necrosis

decubitus ulcer

results when an individual lies or sits in one position for too long

stage I pressure ulcer

nonblanchable erythema of intact skin

stage II pressure ulcer

partial-thickness skin loss, including epidermis or dermis

stage III pressure ulcer

full-thickness skin loss, involving damage or loss of subcutaneous tissue

stage IV pressure ulcer

Full-thickness skin loss with damage to bone, muscle, or supporting structures

suspected deep-tissue injury

localized in an area of purple or maroon discolored intact skin or a blood-filled blister caused by underlying soft-tissue damage from pressure and/or shearing

unstageable pressure ulcer

full thicknes tissue loss with the base of the ulcer covered by slough or eschar, or both, in the wound bed

most common sites for pressure ulcers

sacrum, heels, ischia, greater trochanters

how to predict pressure ulcers

braden scale

What does the Braden Scale take into account when predicting risk for pressure sores? (6)

Sensory perception, moisture, activity, mobility, nutrition, friction & shear

keloid

excessive collagen formation/abnormal fibroblast activity; clawlike margins extend beyond original site

Where are keloids common?

darkly pigmented skin types and burns

hypertrophic scar

elevated erythematous fibrous lesions that do not expand beyond injury border

most common symptom of primary skin disorders

pruritus (itching)

what causes itch

specific unmyelinated C-nerve fibers

what can itch cause

scratching- can lead to to skin trauma, infection and scarring

what NS is itch modulated by

CNS

neuropathic itch

Related to any pathologic condition along an afferent pathway

psychogenic itch

Psychologic disorders

most common inflammatory disorders

dermatitis or eczema

what is dermatitis/eczema characterized by

pruritus, lesions with indistinct borders, and epidermal changes

chronic eczema

Thickened, leathery, and hyperpigmented skin from recurrent irritation and scratching

Allergic Contact Dermatitis (ACD)

common form of T-cell mediated or delayed hypersensitivity (type IV)

Cellular process of ACD

allergen comes into contact with skin --> binds to carrier protein to form sensitizing antigen --> langerhan cells process antigen --> carries to T cells --> become sensitized to antigen

clinical manifestations of ACD & ICD

erythema, swelling, pruritus, and vesicular lesions

Irritant Contact Dermatitis (ICD)

nonimmunologic inflammation of the skin caused by chemical irritation or prolonged exposure to irritating substances

atopic dermatitis

aka allergic dermatitis, common in childhood/infancy and can last into adult life

what is atopic derm associated with

fam hx of allergies, hay fever, elevated IgE, increased histamine sensitivity

stasis dermatitis

occurs in legs as a result of venous stasis, edema, and vascular trauma

sequence of events in stasis derm

edema, pruritus, scaling, petechiae, hyperpigmentation, ulcerations

seborrheic dermatitis

chronic skin inflammation involving the scalp, eyebrows, eyelids, nasolabial folds, axillae, chest and back; periods of remissions and exacerbations

what is a common term for seb derm in infants

cradle cap

clinical manifestations of seb derm

greasy, scaly, white, or yellowish plaques

psoriasis

chronic relapsing proliferative skin disorder

what percent of world population has psoriasis

1-8%

does psoriasis have family tendency

yes; complex genetic mechanisms including HLA

psoriasis is a _____ mediated skin disease

T-cell autoimmune

What type of T cells are associated with psoriasis?

helper t cells

What interleukins are associated with psoriasis?

IL-23, IL-17 loop

manifestations of psoriasis

Scaly, thick, silvery, and elevated lesions, usually on the scalp, elbows, or knees with remissions and exacerbations

what layers of the skin does psoriasis thicken

epidermis and dermis

epidermal turnover with psoriasis

3 to 4 days - cells do not have time to mature or keratinize

how is increase in cell metabolism accommodated for with psoriasis

capillary dilation and increased vascularization, causes erythema

plaque psoriasis

most common type (80-90%) and common on scalp, elbows, and knees as well as sites of trauma

early onset of plaque psoriasis patho

inflammatory lesion with epidermal hyperproliferation and presence of activated T lymphocytes

typical plaque psoriasis looks like

well-demarcated, thick, silvery, scaly, erythematous plaque surrounded by normal skin

inverse psoriasis

rare, involves lesions that develop in skinfolds

inverse psoriasis looks like

large, smooth, dry, and deep red

guttate psoriasis

develops after strep respiratory infection, more common in children, resolves in weeks to months

pustular psoriasis

blisters filled with noninfectious pus, develop over areas of plaque psoriasis

erythrodermic psoriasis

exfoliative dermatitis characterized by widespread red, scaling lesions that are itchy and painful

systemic complications of psoriasis

psoriatic arthritis, ankylosing spondylitis, psoriatic nail disease

Psoriasis is a risk factor for the development of:

IBD, metabolic syndrome (HTN insulin resistence, dyslipidemias, and abdominal obesity), atherosclerosis and CVD

pityriasis rosea

benign self-limiting inflammatory disorder usually occurring in spring and fall

what virus is pityriasis rosea associated with

HHV-6 and HHV-7

manifestations of pityriasis rosea

herald patch (circular, demarcated, salmon-pink)

lichen planus

benign autoinflammatory disorder of skin and mucous membranes

etiology of lichen planus

unknown

autoimmune nature of lichen planus

involves T cells, adhesion molecules, inflammatory cytokines and antigen-presenting cells

clinical manifestations of lichen planus

non-scaling papular violet-colored with pruritis on wrists, ankles, lower legs, and genitailia

acne vulgaris

Inflammatory disease of the pilosebaceous follicles

Pilosebaceous Follicle

the sebaceous glad continuous with a hair follicle

acne vulgaris causes hypertrophy of

sebaceous glands and telangiectasia

when is acne vulgaris most common?

adolescence

acne rosacea

skin inflammation associated with chronic inappropriate vasodilation resulting in flushing and sensitivity to the sun

acne rosacea typically presents in what age group?

middle-aged adults

4 lesions with acne rosacea

erythematotelangiectatic

papulopustular

phymatous (nose enlargement)

ocular

lupus erythematous

inflammatory autoimmune systemic disease with cutaneous manifestations

female:male lupus ratio

10:1

discoid lupus erythematous manifestations

restricted to the skin - photosensitivity, butterfly rash on nose/cheeks

can discoid lupus lead to systemic lupus

yes

patho of discoid lupus

altered immune response w/ development of self-reactive T and B cells

decreased regulatory T cells

increase proinflammatory cytokines

what causes tissue damage with discoid lupus

autoantibodies and immune complexes

Vesiculobullous Disorders

a group of diseases that have different causes and clinical courses but share the common characteristic of vesicle or blister formation

pemphigus

rare, autoimmune, chronic, blister-forming disease of skin and oral mucous membranes

manifestations of pemphigus

blisters in deep and superficial layers of epidermis

what causes pemphigus

circulating IgG autoantibodies --> directed against cell surface adhesion molecules in the epidermis

pemphigus vulgaris

acantholysis at suprabasal layer

patho of pemphigus vulgaris

IgG autoantibodies and C3 complement bind to desmoglein adhesion molecules --> destruction of cell-to-cell adhesion (acantholysis) in epidermis --> fluid accumulation causes blisters

manifestations of pemphigus vulgaris

oral lesions precede skin blisters, prominent on face, scalp, and axilla

pemphigus foliaceus

milder form, acantholysis at subcorneal level

manifestations of pemphigus foliaceus

blistering, erosions, scaling, crusting, and erythema usually on face and chest

NO ORAL INVOLVEMENT

most severe form of pemphigus

paraneoplastic pemphigus

paraneoplastic pemphigus

associated with lymphoproliferative neoplasms

affects internal organs leading to paraneoplastic autoimmine multiorgan syndrome

more benign than pemphigus vulgaris

bullous pemphigoid

bullous pemphigoid

autoimmune disease with bound IgG and IgE, blistering of subepidermal skin

what causes loss of dermal-epidermal adhesion in bullous pemphigoid

inflammatory cytokines

what distinguishes pemphigoid from pemphigus

subepidermal blistering and eosinophils