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Acute skin conditions
Bacterial or fungal infection
Contact with offending organism or allergen
Medications
Possible transition to chronic skin conditions
Pain from damage to first layer of skin
Immune system and intact skin protect body
Impaired tissue integrity leads to immune response
Immune response from allergy and inflammation can lead to lack of tissue integrity
Alterations in tissue perfusion can lead to damage or necrosis
Chronic skin conditions
Long term, may or may not resolve
Viral infection
Cellulitis
Diffuse painful inflammation of skin and subcutaneous layers induced by a bacterial infection that enters through a break in the skin (cut, scrap, burn, surgical incision, bug bite)
Damage at dermis
Clinical manifestations
Painful, red, swollen area of skin; hot, tender to touch
Fever and chills
Vesicles, bullae, plaques (with staphylococcus)
Tachycardia, hypotension, confusion, headache
Lymphadenitis and Lymphangitis
Impetigo
Bacterial infection
Superficial acute, highly contagious skin infection
Etiology and pathogenesis
Colonization facilitated by high temperature, humidity, preexisting skin disorders, young age (2-5), recent antibiotic treatment
Furuncle
Bacterial infection
Extension of folliculitis or infection of sebaceous gland
Spreads down hair shaft through follicle and into dermis
a single, painful, pus-filled bump around a hair follicle
Carbuncle
Bacterial infection
Cluster of infected hair follicles
The cluster coalesces to form lesion filled with pus, dead tissue, and fluid
Candidiasis
Fungal infection
Infection of skin or mucous membranes with any species of Candida (C. albicans most common)
Mouth, throat, lungs, vagina, folds of skin, bowel
Usually secondary condition
Etiology and pathogenesis
Candida normal in skin and mucous membranes
Warmth, moisture, breaks in epidermis can cause infection
Life threatening if in bloodstream
Candidiasis- Clinical manifestations
Thrush: white covering of tongue, mouth, throat
Vaginal yeast infection: itching; foul odor; white discharge
Balanitis: flattened pustules, edema, burning, tenderness
Diaper rash: dark red patches in skin folds; fluid-filled spots
Tinea
Contagious infection by different types of fungus
Superficial infections; called dermatophytoses
Named by location on body
Tinea pedis: Athlete’s foot, which affects the feet with symptoms like itching, scaling, and blisters between the toes
Tinea cruris: Jock itch, a rash in the groin area
Tinea capitis: Ringworm of the scalp, cause itchy, red patches and hair loss
Tinea corporis: Ringworm on the body, appearing as a ring-shaped rash
Tinea versicolor: Discolored, scaly, and dry patches on the skin
Necrotizing Fasciitis
Flesh-eating disorder
Rapidly spreading infection caused by aerobic and anaerobic bacteria
Etiology and pathogenesis
Starts from contagious ulcer, wound, untreated skin infection, complication of surgery, abscess
Occlusion of small subcutaneous vessels; tissue ischemia, infarction, necrosis
Stevens-Johnson Syndrome
Rare disorder of skin and mucous membrane
Cell death causes epidermis to separate from dermis
Etiology
Side effect for more than 200 medications
Infectious causes
Delayed hypersensitive reaction
Clinical manifestations
Flulike symptoms
Symmetric burning rash; red, purple target lesions
Toxic Epidermal Necrolysis (TEN)
Inflammation of skin caused by poison
TEN with spots
Widespread with detachment of epidermis, erosion
More than 30% of body surface area
TEN without spots
Widespread with erythema, no lesions
More than 10% of body surface area
Etiology
Reactions to drugs; bacterial infection; malignancy; graft-versus-host disease; vaccinations
Clinical manifestations
Flulike symptoms
Rash; large blisters in center rash; ruptures; skin peels off
Chronic viral skin infections
Examples of common causative organisms
Herpes simplex virus
Varicella-zoster virus
Human papillomavirus
Herpes simplex virus type 1 (HSV-1)
Affected body regions
Herpes labialis: lips; cold sores)
Most common HSV-1 infection
Herpetic keratitis (eye)
Herpetic whitlow (digits or hands)
Herpetic gladiatorum (torso of wrestlers)
Herpetic sycosis (beard follicles)
Usually contracted during childhood
Recurrences persist into old age (adulthood)
Herpes simplex virus type 2 (HSV-2)
Causes most sexually-transmitted anogenital herpes
Lesions on genitals, perineum, or anus, any opening at genitals
May cause cold sores
Less common cause than HSV-1
Likely to be contracted via sexually contact
Typically in adolescence or young adulthood
5th most common U.S sexually transmitted infection
1 in 6 adolescents and adults of both genders
HSV-1 and HSV-2: Etiology and Pathogenesis
Virus enters skin or mucous membrane via microscopic tear
Virus travels to sensory root ganglion
Virus becomes dormant and permanent resident of ganglion
Cell-mediated immune system is triggered
Viral activation occurs
Virus travels from neuron to skin innervated by neuron
Virus enters dermal and epidermal cells
Viral replication causes recurrent rash outbreak
HSV-1 and HSV-2: clinical manifestations
May have asymptomatic herpes or mild fever
Usually begins with prodrome- fever or flu-like symptoms
Red, swollen area of skin or mucous membrane develops
Eruption of painful vesicles
Regional lymph nodes swell
Lesions open and form painful ulcers that crust and begin healing
Primary genital herpes
May cause dysuria and urinary retention, especially in women
Herpes Zoster
First VZV infection causes chickenpox
Each skin lesion contains viral particles
Viral particles travel to other structures
Sensory dorsal-root ganglia or a cranial nerve
Viral particles become dormant for life
Cell-mediated immunity
Prevents virus reactivation in the form of HZ
Decreases with aging
Increased risk for reactivation of VZV as HZ
Herpes Zoster- Potential Complications
Postherpetic neuralgia (PHN)- most common complication
Transient ischemic attack (TIA) and stroke
Encephalitis and aseptic meningitis
Chronic eye disorders and retinal necrosis
Bacterial superinfection of lesions
Cranial or peripheral nerve palsies
Pneumonitis
Hepatitis
Herpes Zoster- Diagnosis
History and physical examination
Usually sufficient for diagnosis after rash appears
Atypical or recurrent rashes (more than episodes)
May require laboratory testing to identify cause
Laboratory testing
Direct immunofluorescent assay
PCR assay
Warts
Cause: Various types of human papillomavirus (HPV)
Sties of occurrence
Anywhere on skin or mucous membranes
Malignancy
Most lesions caused by HPV are benign
Some HPV types linked to dysplasia and cancer
Genital HPV
Most frequently occurring sexually transmitted infection in US
Warts- Pathogenesis
HPV
Enters skin via small openings
Infects epidermal basal layer
Viral replication occurs in cell nuclei
HPV causes nuclear atypia
Structural abnormality in a cell
Nuclear atypia triggers epidermal cell changes
Replication and hyperproliferation of keratinocytes
Wart develops
Skin Disorders with a Genetic Basis
Family history
Most important risk factor for certain chronic skin diseases
Several chronic skin disorders have genetic component
Examples
Atopic dermatitis
Psoriasis
Hidradenitis suppurativa
Eczema- Atopic Dermatitis
Eczema- general term
Describes inflammatory skin disorders
Includes atopic dermatitis
Most sever form of eczema
Atopic Dermatitis
Chronic, recurring, itchy, inflammatory disorder
Associated with increased serum IgE
Affected individuals often have other atopic disorders
Ex: asthma, allergic rhinitis
Most often affects children
May persist into adulthood
AD and susceptibility to infection: Dysfunctional epidermal barrier
Clinical manifestations
Exacerbation and remission of dry, itchy, red skin
Begins in infancy
Constant pruritus
Prevailing symptoms
Precedes eczematous rash
Skin excoriations and lichenification
Negative impact on overall quality of life: sleep disturbances, depression
Psoriasis
Etiology
Immune-mediated disease
Genetic and environmental causation
Pathogenesis
Hyperproliferation of keratinocytes
Decreased epidermal cell turnover rate
Inflammation
Thickening of dermis and epidermis
Manifestations
Plaque psoriasis- skin lesion usually round or oval, well-demarcated plaques
Hidradenitis Suppurativa
Etiology
Genetic, immunologic, hormonal, and environmental factors
Pathogenesis
Occlusion of hair follicle via infundibular hyperkeratosis
Hyperplasia of follicular epithelium
Collection of cellular wastes
Cyst forms in apocrine sweat gland adjacent to hair follicle
Nodule opens beneath the skin and spreads laterally
May lead to abscess formation and sinus tract formation
Keloid-like scarring may occur
Manifestations
Painful nodules, abscesses and sinus tract formations
Lesions develop in skinfold area