Describing, Diagnosing, & Treatment of Skin, Eye, & Ear Disorders
Tiffany22
NUR600Module2-Voiceover.pptx
NUR 600
Module 2
Contact Dermatitis
Contact Dermatitis
Definition: alteration in skin reactivity caused by exposure to an external agent
Causes: combination of genetic and environmental factors
Irritant contact dermatitis (ICD): alteration in skin reactivity caused by exposure to any agent that has a toxic effect on the skin
Allergic contact dermatitis (ACD): alteration in skin reactivity caused by exposure to an antigen that causes an immunologic response
Irritant Contact Dermatitis (ICD)
Not an allergic response; result of damage to the water–protein–lipid matrix of the outer layer of the skin
Appears as erythematous, scaly eruption resulting from friction, exposure to a chemical, or thermal injury
Severity depends on condition of the skin, concentration and toxicity of irritant, and length of exposure
Allergic Contact Dermatitis (ACD)
An immunologically mediated response to an allergen (antigen) occurs.
Initial sensitization phase: the host is immunized to the allergen.
Secondary immune response: T cells are key mediators of the reaction and release cytokines, chemokines, and cytotoxins.
Stimulation of local blood vessels, recruitment of immune cells, and subsequent amplification of the sensitization response occurs.
Allergic Contact Dermatitis (cont.)
Within 5 to 7 days after sensitization, there is visual evidence of the response. On subsequent exposures, however, dermatitis may develop within 6 to 18 hours.
Hypersensitivity can occur after one exposure or after years of repeated exposures. Contact dermatitis may spread extensively beyond the area of contact.
Atopic dermatitis (eczema) is a form of allergic dermatitis characterized as a pruritic, chronic inflammatory condition.
Conditions Occurring in Atopic Dermatitis (Eczema)
High concentrations of serum immunoglobulin (Ig) E
Decreased numbers of immunoregulatory T cells
Defective antibody-dependent cellular cytotoxicity
Decreased cell-mediated immunity
Pathogenesis of Atopic Dermatitis
Genetic factors
Adaptive and innate immune response genes
Skin barrier defects
Deficiency in filaggrin (FLG)
May cause increased transepidermal water loss, infection, and inflammation associated with the exposure of cutaneous immune cells to allergens
Immune dysregulation
Lesions Occurring in Atopic Dermatitis
Papules
Erythema
Excoriations
Lichenification
Treatment for Dermatitis
Prevention is the most effective treatment; patient must be aware of triggers and avoid them.
Mild symptoms are treated with cool compresses; baths with colloidal oatmeal; compresses of Burow solution.
If these fail or dermatitis is more extensive, drug therapy is initiated.
Consideration for Initiating Drug Therapy for Dermatitis
Delivery of the drug to the skin
Protection/barrier function
Cosmetic acceptability
Choosing Drug Therapy for Dermatitis
Ointment and gels offer the best delivery and protection barrier; creams are less greasy but less effective.
Solutions are alcohol-based liquids and are useful for treating the scalp because they do not coat the hair.
Lipid-rich moisturizers both prevent and treat ICD.
Barrier creams containing dimethicone or perfluoropolyethers, cotton liners, and softened fabrics help to prevent ICD.
Choosing Drug Therapy for Dermatitis
Goals of Drug Therapy for Dermatitis
Restoration of a normal epidermal barrier
Treatment of inflammation of the skin
Control of itching
Mainstays of Therapy for Dermatitis
Topical corticosteroids
Topical immunosuppressives
Systemic corticosteroids
Antihistamines
Topical Corticosteroids
Safer than systemic steroidal therapy
Effective for smaller outbreaks
Reduce inflammation and buildup of scale
Least potent topical corticosteroid should be used for the shortest possible time
Should be avoided if there are additional bacterial, viral, or fungal skin infections
Not recommended for prophylaxis
Topical Corticosteroid Therapy
Dosage: initiate treatment with an intermediate- or high-potency topical corticosteroid.
Short-term therapy with more potent topical corticosteroids is preferred to longer-term therapy.
Low-potency corticosteroids should be used in the facial and intertriginous.
Maximum recommended length of treatment with topical corticosteroids is 2 weeks for adults and 1 week for children.
Actions of Systemic Corticosteroids
Inhibit cytokine and mediator release
Attenuate mucus secretion
Upregulate beta-adrenergic receptors
Inhibit IgE synthesis
Decrease microvascular permeability
Suppress the influx of inflammatory cells and the inflammatory process
Dosing Systemic Corticosteroids
Tapering dose schedule is recommended:
Starting dose of 1 mg/kg is decreased by 5 mg every 2 days for 2 to 3 weeks.
The entire dose of steroids can be taken at the same time in the morning to minimize sleep disturbances.
Taking the corticosteroids for less than 2 weeks may cause rebound dermatitis, especially with poison ivy.
If dermatitis flares up during the tapering, the dosage can be increased and tapered again.
Topical Immunosuppressives
Act on T cells by suppressing cytokine transcription.
Used in patients with moderate to severe atopic dermatitis who cannot tolerate topical steroids or are not responsive to other treatments, or where there is a concern for topical steroid–induced atrophy.
Tacrolimus and pimecrolimus are the preparations currently available and are applied twice a day until the lesions clear and then for an additional 7 days.
Antihistamines
Used to relieve pruritus associated with contact dermatitis.
Best time to use them is before bed since side effect is drowsiness.
Selecting the Most Appropriate Agent
First-line therapy: a topical corticosteroid preparation with low to intermediate potency applied twice a day
Second-line therapy: a more potent topical corticosteroid or topical immunosuppressants
Third-line therapy: systemic corticosteroids for treating widespread dermatitis; given on a tapered-dose schedule (1 mg/kg, with the dose decreased every 2 days for at least 2 weeks and up to 3 weeks)
Special Populations
Pediatric
Topical corticosteroids should be used for only 7 days in children younger than age 6 and at the lowest potency.
Geriatric
Topical corticosteroids can cause atrophy of the skin in elderly people.
Patient Education
Teaching to avoid causative substance
1
Using mild soaps without perform
2
Demonstrating how to apply topical preparations and occlusive dressing
3
Hydrating the skin before applying medication
4
Hydrating with bland emollients
5
Taking daily soaking baths for 10 to 20 minutes and using moisturizer afterward
6
Complementary and Alternative Medicine
Vitamin A 50,000 international units daily
Vitamin E 400 international units daily
Zinc 50 mg daily, to be decreased as the condition clears
EPA 540 mg and DHA 360 mg daily or flaxseed oil 10 g daily
Evening primrose oil 3,000 mg daily
Fungal Infections of the Skin
Tinea
Tinea versicolor
Candidiasis
Types of Tinea Infections
Tinea capitis: head
Tinea corporis: body
Tinea pedis: foot
Tinea manus: hand
Tinea unguium (onychomycosis): nails
Tinea cruris: groin
Factors Predisposing People to Fungal Infections
Warm, moist, occluded environments
Family history
Compromised immune system
Five Species of Fungus Causing Most Infections
Trichophyton rubrum
Trichophyton tonsurans
Trichophyton mentagrophytes
Microsporum canis
Epidermophyton floccosum
Diagnostic Criteria for Fungal Infections
Symptoms
Pruritus, burning, and stinging of the scalp or skin, possible erythema and vesicles with inflammatory dermal reactions.
Diagnostic tests
Microscopic evaluation of the stratum corneum with 10% potassium hydroxide (KOH) preparation
Fungal culture
Wood lamp (identifies only Microsporum)
Tinea Capitis Presentation
Inflamed, scaly, alopecic patches, especially in infants
Diffuse scaling with multiple round areas with alopecia secondary to broken hair shafts, leaving residual black stumps
“Gray patch” type with round, scaly plaques of alopecia in which the hair shaft is broken off close to the surface
Tender, pustular nodules
Tinea Corporis
Called “ringworm” when it affects the face, limbs, or trunk but not the groin, hands, or feet
Presentation: ring-shaped lesion with well-demarcated margins, central clearing, and a scaly, erythematous border
Causes: contact with infected animals, human-to-human transmission, and from infected mats in wrestling
Organisms responsible: M. canis, T. rubrum, and T. mentagrophytes
Tinea Cruris
Often referred to a “jock itch.”
A fungal infection of the groin and inguinal folds, tinea cruris spares the scrotum.
Causes are T. rubrum or E. floccosum.
Symptoms: lesions that are large, erythematous, and macular, with a central clearing; a hallmark is pruritus or a burning sensation.
Often fungal infection of the feet is present.
Three Types of Tinea Pedis
Interdigital: scaling, maceration, and fissures between the toes
Plantar: diffuse scaling of the soles, usually on the entire plantar surface
Acute vesicular: vesicles and bullae on the sole of the foot, the great toe, and the instep
Characteristics of Tinea Manus
Dermatophyte infection of the hand
Always associated with tinea pedis and usually unilateral
Lesions marked by mild, diffuse scaling of palmar skin
Vesicles may be grouped on the palms or fingernails involved
Tinea Unguium
Fungal infection of the nail; typically the toenails.
Nails become thick and scaly with subungual debris.
Onycholysis (nail separation from bed) may occur.
Under the nail, a hyperkeratotic substance accumulates that lifts the nail up.
Organisms causing onychomycosis: dermatophytes, E. floccosum, T. rubrum, T. mentagrophytes, Candida albicans, Aspergillus, Fusarium, and Scopulariopsis.
Initiating Drug Therapy for Fungal Infections
Prevention: applying powder containing miconazole (Monistat) or tolnaftate (Tinactin) to areas prone to fungal infections after bathing and blow drying on low temperature
Goals of drug therapy: directed against the offending fungus and site of infection; may be topical or systemic depending on location of lesions
Topical Azole Antifungals
Action: work by pairing the synthesis of ergosterol, the main sterol of fungal cell membranes, allowing for increased permeability and leakage of cellular components, resulting in cell death.
Uses: effective against tinea corporis, tinea cruris, and tinea pedis as well as cutaneous candidiasis.
Dosage: applied once or twice a day for 2 to 4 weeks. Therapy should continue for 1 week after the lesions clear.
Topical Allylamine Antifungals
Action: effective against dermatophyte infections but have limited effectiveness against yeast
Dosage: shorter treatment period with less likelihood of relapse; applied twice daily
Adverse events: burning and irritation
Griseofulvin
Action: deposits in keratin precursor cells increasing new keratin resistance to fungal invasion.
Adverse events: nausea, vomiting, diarrhea, headache, or photosensitivity.
Interactions: increases levels of warfarin (Coumadin) and decreases levels of barbiturates and cyclosporine (Sandimmune). It may decrease the efficacy of oral contraceptives and may cause a serious and unpleasant reaction with alcohol.
Systemic Allylamine Antifungals
Action: inhibits squalene epoxidase, a key enzyme in fungal biosynthesis, causing a deficiency of ergosterol causing fungal cell death
Dosage: fingernail onychomycosis: 250 mg/d for 6 weeks; toenail onychomycosis: 250 mg/d for 12 weeks
Adverse events: diarrhea, dyspepsia, rash, increase in liver enzymes, and headache
Interactions: potentiated by cimetidine (Tagamet) and antagonized by rifampin (Rifadin)
Systemic Azole Antifungals
Action: inhibit cytochrome P-450 (CYP) enzymes and fungal 14-a-demethylase, inhibiting synthesis of ergosterol. Systemic therapy is required for tinea capitis and tinea unguium.
Dosage: dosage of itraconazole is 200 mg once daily for 12 weeks for toenail infection. For fingernail infection, the dose is 200 mg twice daily for 1 week, then 3 weeks off, and repeat dosing with 200 mg twice daily for 1 week.
Selecting the Appropriate Agent for Tinea
Tinea capitis
First line: griseofulvin (Grifulvin V) minimum 8 weeks
Second line: terbinafine (Lamisil) or itraconazole (Sporanox) 4 weeks
Tinea corporis, tinea cruris, tinea pedia
First line: topical azole antifungals for 2 to 4 weeks (1 week past clinical cure), 2 weeks even after rash is gone
Second line: systemic therapy: terbinafine (Lamisil) or fluconazole (Diflucan)
Selecting the Appropriate Agent for Tinea (cont.)
Onychomycosis
First line: itraconazole (Sporanox) or terbinafine (Lamisil) 12 weeks with food; not recommended for children
Tinea versicolor
First line: selenium sulfide solution 1% or 2.5% topical azole cream or spray for localized lesions
Second line: itraconazole (Sporanox)
Patient Education for Tinea
Teach hygiene and ways to avoid transferring fungal infection to others.
Complete the full course of treatment and do not stop treatment when symptoms subside.
Inform parents and other caregivers that children can attend school while being treated.
Dry areas susceptible to fungus with a hair dryer after bathing.
Use antifungal powder and sprays for prophylaxis.
Tinea Versicolor (Pityriasis Versicolor)
An opportunistic superficial yeast infection
Causes: overgrowth of the hyphal form of Pityrosporum ovale; occurs mostly in subtropical and tropical areas
Action: an enzyme oxidizes fatty acids in the skin surface lipids, forming dicarboxylic acids, which inhibit tyrosinase in epidermal melanocytes and cause hypomelanosis
Diagnostic criteria: well-defined skin lesions, round or oval macules with an overlay of scales forming on the trunk, upper arms, and neck with mild itching; confirmed by positive KOH test
Candidiasis
Superficial fungal infection of the skin and mucous membranes.
Causes: C. albicans occurs on moist cutaneous sites in people with infection or diabetes, or using systemic and topical corticosteroids, and with immunosuppression.
Action: C. albicans invades the epidermis when warm, moist conditions prevail.
Diagnostic criteria: red, moist papules, or pustules found in the axillae, inframammary areas, groin, and between the fingers and toes.
Order of Treatment for Candidiasis
First line: cool soaks with Burow solution, topical azole for 10 days, oral nystatin
Second line: itraconazole (Sporanox) or fluconazole (Diflucan)
Complementary and Alternative Medicine
Apple cider vinegar
Palin yogurt
Tea tree oil
Tea
Three Groups of Viruses Producing Skin Lesions
Herpes viruses: replicate their own polymerase, along with several of their own enzymes
Papilloma viruses: contribute to the initiation of DNA replication
Pox viruses: replicate entirely in the cytoplasm
Viruses
Viruses are obligate intracellular parasites consisting of a nucleic acid core surrounded by one or more proteins.
A host cell is required for viral replication.
Several mechanisms exist for viral replication, and different DNA viruses replicate by their own specific mechanism.
Seven Types of Herpes Virus Infections
Herpes simplex type 1 (HSV-1): involves the face and skin above the waist
Herpes simplex type 2 (HSV-2): involves genitals and skin below the waist
Varicella-zoster virus (VZV): causes varicella (chickenpox) and herpes zoster (shingles)
Epstein-Barr virus: associated with infectious mononucleosis
Seven Types of Herpes Virus Infections (cont.)
Cytomegalovirus: causes mononucleosis and pneumonia
Human herpesvirus type 6 (HHV-6): associated with roseola
Human herpesvirus type 8 (HHV-8): associated with Kaposi sarcoma, especially in patients with HIV infections
Herpes Viruses
Action:
Herpes viruses replicate their own polymerase along with several of their own enzymes.
After primary infection, the virus becomes dormant until reactivated by triggers.
The virus is highly contagious and spread by direct contact with skin or mucous membrane.
Diagnostic criteria: vesicular eruptions that are painful and often recurrent.
Drug Therapy for Herpes Virus
Primarily treated with topical agents
Soaks with Burow solution
Viscous lidocaine (Xylocaine) 2%
Diphenhydramine (Benadryl) elixir and aluminum hydroxide/magnesium hydroxide (Maalox)
Systemic drug therapy in case of severe infection in immunocompromised patient
Antiviral treatment for herpes zoster
Topical Antiviral Agents
Types: acyclovir 5%, penciclovir (Denavir)
Action: inhibiting viral DNA synthesis; decrease healing time
Dosage: apply topical acyclovir every 3 hours, six times per day, for 7 days; apply penciclovir every 2 hours, during waking hours, for 4 days
Adverse effects: mild skin irritation and pruritus
Systemic Antiviral Agents
Types: acyclovir (Zovirax), famciclovir (Famvir), valacyclovir (Valtrex)
Contraindications: patients with renal disease
Adverse events: headache vertigo depression, tremors
Interactions: effect increase in patients taking probenecid; patients taking zidovudine (Retrovir) may experience drowsiness
Dosing Acylovir
Immunocompetent host: initial episode: 200 mg orally five times per day for 7 to 10 days; recurrent episodes: 200 mg five times per day for 5 days
Immunocompromised host: 400 mg five times per day for 7 to 10 days: suppression therapy, 400 mg twice a day is the dosage
Children: 5 mg/kg/d in five divided doses for 7 days
VZV infections: children 20 mg/kg four times per day for 5 days; adults: 800 mg five times per day for 7 to 10 days
Famciclovir
Action: diacetyl ester prodrug of penciclovir that is an acyclic guanosine analog; oral bioavailability ranges from 5% to 75%
Dosage: initial episode: 250 mg three times per day for 7 to 10 days; recurrent episodes: 1,000 mg twice daily for 1 day and 250 mg twice a day for suppression therapy
Valacyclovir
Action: prodrug of acyclovir that is converted rapidly with 50% bioavailability
Dosage: initial infection: 1,000 mg three times a day for 7 to 10 days; recurrent infection: 2,000 mg two times a day for 1 day; suppression therapy: 1,000 mg daily
Recommended Order of Treatment for HSV-1 Infection
First line
Topical therapy with acyclovir 5% (Zovirax) or penciclovir 1% (Denavir); treating at earliest signs of outbreak
Second line
Systemic therapy with acyclovir (Zovirax), famciclovir (Famvir), or valacyclovir (Valtrex)
First-Line Therapy: Varicella-Zoster Virus
First-Line Therapy: Herpes Zoster
Patient Education
Hygiene
Precipitating factors
Prevention methods
Zostavax vaccine for herpes zoster
Safe sex practices for patients with HSV-2 infection
Wearing gloves when applying medication and careful hand washing
Avoiding skin-to-skin contact
Types of Warts (Verrucae)
Verruca vulgaris—common warts: infection with HPV-2; occur on the fingers or toes at sites of trauma
Plantar warts—HPV-1: occur on the soles of the feet and the palms of the hands; flesh-colored to brown, hyperkeratotic papules
Flat warts—HPV-3: located on the face, neck, and chest or flexor regions of the forearms and legs
Factors Predisposing to HPV
Infection with HIV
Intake of drugs that decrease cell-mediated immunity (prednisone, cyclosporin)
Chemotherapeutic agents
Pregnancy (may cause proliferation)
Handling raw meat, fish, or other animal matter
Warts
Action: HPV proteins contribute to the initiation of DNA replication; incubation period is usually 4 to 6 months with transmission by direct contact or by fomite
Diagnostic criteria:
Papillomatous, corrugated, hyperkeratotic growths found only on the epidermis, especially in areas subjected to repeated trauma
Can be solitary, multiple, or clustered
Named for clinical appearance, location, or both
Initiating Drug Therapy for Warts
Choice of medication depends on age of the patient, whether pain is involved, and the location of the wart.
Filiform and flat warts are removed by a dermatologist.
Topical treatment with salicylic acid (DuoFilm) is usually the starting point for all other warts.
The goal of therapy is eradication of the virus and lesion, although there is no way to actually kill HPV.
First-Line Therapy for Warts
Common Primary Bacterial Skin Infections
Impetigo
Bullous impetigo
Folliculitis
Felons
Paronychias
Cellulitis
Causes of Bacterial Skin Infections
Staphylococcus aureus
Beta-hemolytic forms of streptococci such as Streptococcus pyogenes (group A Streptococcus, or GAS)
Streptococcus agalactiae (group B Streptococcus)
Impetigo and Ecthyma
Cause: due primarily to S. aureus
Diagnostic criteria: scattered, discrete macules that itch and spread and develop into vesicles and pustules on an erythematous base; honey-colored crust occurs
Ecthyma: chronic form of impetigo affecting deeper layers of the skin; vesicles form that then develop into shallow ulcerations often causing scarring
Contributing factors: person-to-person contact in schools or day care centers; poor hygiene, crowded living conditions
Cellulitis
Infection involving the skin and subcutaneous layers, with the potential to spread systemically and cause serious illness
Causes: GAS or S. aureus; insect bite or wound
Methicillin-resistant S. aureus (CA-MRSA):
S. aureus organisms that are resistant to commonly used antibiotics; major cause of community-acquired skin infections; furuncle with necrotic center
Erysipelas
Superficial form of cellulitis; most common in children, especially infants and the elderly, but it can occur in healthy individuals who have sustained only minor wounds.
Most commonly found on the lower extremities but can also be present on the face and scalp.
Begins as an area of sharply demarcated erythema that spreads rapidly in minutes to hours. The affected area is slightly raised, firm, warm, and tender to the touch (classic orange peel appearance).
Pustular Infections
Folliculitis
Superficial infection of the hair follicle commonly caused by S. aureus
Furunculosis and carbunculosis
Pustular infections usually caused by S. aureus. Both conditions involve deeper areas of the skin and can develop from unresolved cases of folliculitis.
Manifests as pus-filled nodule that encircles a hair follicle found in hairy areas.
Paronychia and Felon
Paronychia
Infection of tissue surrounding a nail bed
Associated with nail biting, hangnails, or finger sucking
Felon
Fingertip wound of the pulp space in the tip of a digit, which is erythematous, edematous, and tender
If left untreated, abscess/tissue necrosis can occur
Necrotizing Fasciitis
An extremely serious infection of the subcutaneous tissues that can be life threatening if not diagnosed early and treated appropriately
Management: often requires emergent surgical interventions to remove infected tissue in combination with antibiotic therapy
Occurrence: middle-aged, elderly, or seriously debilitated patients
Treatment: IV antibiotic, surgical debridement
Necrotizing Fasciitis/Diagnostic Criteria
Initial lesion is often minor.
Infection may initially appear similar to cellulitis, although severe pain, erythema, and edema are commonly present.
May be differentiated from cellulitis by its rapid spread, tissue destruction, and lack of response to usual antibiotic therapy.
Symptoms: high fever (102°F to 105°F [38.9°C to 40.6°C]), intense pain and tenderness at the site, swelling of the affected extremity.
Risk Factors for Skin Infections
Diabetes
Immune system disorders
Malnutrition from alcoholism
Circulatory compromise of arterial, venous, or lymphatic system