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acute/chronic skin

patho exam 3

QuestionAnswer
acute skin conditions bacterial or fungal infection, contact with offending organism or allergen, medications
acute skin conditions have a possible transition to... chronic skin conditions
acute skin disorders 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
cellulitis diffuse painful inflammation of skin and subcutaneous layers induced by a bacterial infection that enters through a break in the skin
what population does cellulitis occur in? adult population
cellulitis clinical manifestations painful, red, swollen area of skin; hot, tender to touch. fever and chills. vesicles, bullae, plaques (with Staphylococcus). tachycardia, hypotension, confusion, headaches, lymphadenitis, and lymphangitis
impetigo superficial acute, highly contagious skin infection
impetigo etiology and pathogenesis colonization facilitated by high temperature, humidity, preexisting skin disorders, ages 2-5, recent antibiotic treatment
furuncle extension of folliculitis or infection of sebaceous gland. spreads down hair shaft through follicle and into dermis
carbuncle cluster of infected hair follicles. the cluster coalesces to form lesion filled with pus, dead tissue, fluid
candidiasis infection of skin or mucous membranes with any species of Candida (c. albicans most common); usually secondary condition
where does candidiasis occur mouth, throat, lungs, vagina, folds of skin, bowel
candidiasis etiology and pathogenesis 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
candidiasis clinical manifestations: vaginal yeast infection itching, foul odor, white discharge
candidiasis clinical manifestations: balanitis flattened pustules, edema, burning, tenderness
candidiasis clinical manifestations: diaper rash dark red patches in skin folds, fluid filled spots
tinea contagious infection by different types of fungus; superficial infections called dermatophytoses
how is tinea 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
necrotizing fasciitis 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 membranes- cell death causes epidermis to separate from dermis
stevens-johnson syndrome etiology more than 200 medications, infectious causes, delayed hypersensitive reaction
stevens-johnson syndrome clinical manifestations flulike symptoms, symmetric burning rash; red; purple
toxic epidermal necrolysis (TEN) inflammation of skin caused by poison
TEN with spots widespread with detachment of epidermis, erosion
what percent of body surface area is TEN with spots? 30%
TEN without spots widespread with erythema, no lesions
what percent of body surface area is TEN without spots? 10%
toxic epidermal necrolysis etiology reactions to drugs; bacterial infection; malignancy; graft-versus-host disease; vaccinations
toxic epidermal necrolysis (TEN) clinical manifestations flulike symptoms, rash; large blisters in center rash; ruptures; skin peels off
examples of common causative organisms of chronic viral skin infections herpes simplex virus, varicella-zoster virus, human papillomavirus
herpes simplex virus type 1 (HSV-1) affected body regions herpes labialis, herpes keratitis, herpetic whitlow, herpes gladiatorum, herpetic sycosis
most common HSV-1 infection herpes labialis
where is herpes labialis? lips, cold sores
where is herpes keratitis? eye
where is herpes whitlow? digits or hands
where is herpes gladiatorum? torso of wrestlers
where is herpes sycosis? beard follicles
why does HSV-1 occur? because of stress and weakened immune system
when is HSV-1 usually contracted? during childhood
Recurrences of HSV-1 persist into? old age
Herpes simplex virus type 2 (HSV-2) causes? most sexually transmitted angiogenital herpes; lesions on genitals, perineum, or anus
HSV-2 may cause? cold sores (less common cause than HSV-1)
HSV-2 is likely to be contracted via? sexual contact, typically in adolescence or young adulthood
fifth most common U.S. sexually transmitted infection HSV-2
1 in _ adolescents and adults of both genders have HSV-2 6
How does HSV enter skin or mucous membrane? (HSV etiology and pathogenesis) via microscopic tear
Once HSV enters skin or mucous membrane where does it travel to? (etiology and pathogenesis) sensory root ganglion
HSV 1 and 2 etiology and pathogenesis virus become dormant and permanent resident of sensory root ganglion, cell-mediated immune system triggered, viral activation, travels from neuron to skin innervated by neuron, enters dermal and epidermal cells, replication causes recurrent rash outbreak
HSV-1 and HSV-2 usually begins with? prodrome- fever or flu-like symptoms
clinical manifestations of HSV-1 and HSV-2 may have asymptomatic herpes or mild fever; 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 clinical manifestations may cause dysuria and urinary retention, especially in women
herpes zoster chronic viral skin condition
how many people does herpes zoster affect? about 1 million
what is herpes zoster also known as? shingles
What is herpes zoster caused by? varicella zoster virus
Varicella zoster virus (VSV) also causes? chicken pox
first VZV infection causes? chicken pox
First VZV infection 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 herpes zoster prevents virus reactivation in the form of HZ, decreases with aging
cell mediated immunity decreasing with aging causes increased risk for? reactivation of VZV as HZ
potential complications of HZ postherpetic neuralgia (PHN), TIA and stroke, encephalitis and aseptic meningitis, chronic eye disorders and retinal necrosis, bacterial superinfection of lesions, cranial or peripheral nerve palsies, pneumonitis, hepatitis
most common complication of herpes zoster postherpetic neuralgia (PHN)
diagnosis of HZ history and physical examination, laboratory testing
diagnosis of HZ history and physical examination usually sufficient for? diagnosis after rash appears
diagnosis of HZ: atypical or recurrent rashes (more than episodes) may require? laboratory testing to identify cause
diagnosis of HZ laboratory testing direct immunofluorescent assay, PCR assay
warts cause various types of Human papillomavirus (HPV)
sites of occurrence of warts anywhere on skin or mucous membranes
warts malignancy: most lesions caused by HPV are? benign
warts malignancy: some HPV types are linked to? dysplasia and cancer
What is an example of HPV linked to dysplasia and cancer? genital HPV
most frequently occurring sexually transmitted infection in U.S. genital HPV
pathogenesis of warts HPV, viral replication occurs in cell nuclei, HPV causes nuclear atypia, nuclear atypia triggers epidermal cell changes, wart develops
Pathogenesis of warts: HPV enters skin via small openings, infects epidermal basal layer
pathogenesis of warts: HPV causes nuclear atypia structural abnormality in a cell
pathogenesis of warts: nuclear atypia triggers epidermal cell changes replication and hyper proliferation of keratinocytes
most important risk factor for certain chronic skin diseases family history
examples of chronic skin disorders with a genetic component atopic dermatitis, psoriasis, hidradenitis suppurativa
eczema general term, describes inflammatory skin disorders
eczema includes? atopic dermatitis
most severe form of eczema atopic dermatitis
atopic dermatitis chronic, recurring, itchy, inflammatory disorder
atopic dermatitis is associated with? increased serum IgE
affected individuals with atopic dermatitis often have? other atopic disorders (ex. asthma, allergic rhinitis)
atopic dermatitis most often affects? children
atopic dermatitis may persist into? adulthood
AD and susceptibility to infection? dysfunctional epidermal barrier
clinical manifestations of AD exacerbation and remission of dry, itchy, red skin; constant pruritis; skin excoriations and lichenification, negative impact on overall quality of life
AD begins in? infancy
clinical manifestations of AD: constant pruritis prevailing symptom, precedes eczematous rash
clinical manifestations of AD: negative impact on overall quality of life sleep disturbances, depression
psoriasis etiology immune-mediated disease, genetic and environmental causation
psoriasis pathogenesis hyperproliferation of keratinocytes, decreased epidermal cell turnover rate, inflammation, proliferation of keratinocytes, thickening of dermis and epidermis
psoriasis manifestations plaque psoriasis- skin lesions usually round or oval, well-demarcated plaques
hidradenitis suppurativa etiology genetic, immunologic, hormonal, and environmental factors
hidradenitis suppurativa pathogenesis occlusion of hair follicle via infundibular kyperkeratosis, hyperplasia follicular epithelium, collection cell wastes, cyst form apocrine sweat gland next to follicle, nodule under skin, spreads laterally, abscess/ sinus tract forms, keloid-like scarring
hidradenitis suppurativa manifestations painful nodules, abscesses, and sinus tract formations; lesions develop in skinfold areas
Created by: camrynfoster
 

 



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