Dermatology 2 Flashcards
Psoriasis
General
Chronic, immune-mediated disease with predominantly skin and joint manifestations.
Affects approximately 2% of the US population
Age of onset: 2 peaks
Ages 20-30 and ages 50-60
Strong genetic component with about 30% of patients having a first-degree relative with the disease
Psoriasis
Pathophysiology
Hyperproliferative state resulting in thick skin and excess scale
Skin proliferation is caused by cytokine release from immune cells
Exacerbation by environmental factors
Psoriasis
Psoriasis
Types and signs/phenom
Plaque - well-demarcated scaly, erythematous patches, papules, and plaques with overlying silvery-white scale
Most common form accounting for 80-90% of cases
Auspitz sign - bleeding after scale removal
Koebner phenomenon - lesions are induced by trauma to skin.
Inverse/Flexural
Guttate
Erythrodermic
Pustular
Psoriasis
important Hx questions
4
Are you taking any of these medications: systemic steroids, beta blockers, lithium, NSAIDs, antimalarials, interferons
Joint pain present?
Present in approximately 30% of patients and can lead to joint destruction if not appropriately managed.
Any cardiovascular risk factors?
Patients with psoriasis are at increased risk for cardiovascular disease
Any changes in your nails?
Can see nail pitting, onycholysis, subungual hyperkeratosis, and oil drop sign
Tobacco use? Alcohol consumption?
Both are risk factors and can contribute to symptoms
psoriasis
psoriasis
Topical Tx
Seborrheic dermatitis
general
Chronic, recurrent form of dermatitis occurring in areas rich with sebaceous glands.
Seborrheic dermatitis
Pathophysiology:
unclear
Increase sebaceous gland activity + hypersensitivity reaction to Malassezia furfur
Increase incidence in fall and winter months and with stress.
More pronounced in patients with neurologic diseases and HIV
Seborrheic dermatitis
Clinical Manifestations
Erythematous patches or plaques covered with fine whitish – yellow greasy scales.
Typically found on scalp, eyelids, beard, nasolabial folds, chest
May be associated with burning and pruritis
Seborrheic dermatitis
Dx
Clinical
Seborrheic dermatitis
Tx
Scalp: antifungal shampoo - Ketoconazole 2% or ciclopirox 1% BIW-TIW
+/- topical steroid if inflammation present
Face: topical antifungal agents +/- low potency topical steroid (hydrocortisone 2.5% cream qd-bid x 3-5 days)
Consider topical calcineurin inhibitor tacrolimus/pimecrolimus if needed for long term use.
Severe or refractory: oral antifungals
Pityriasis rosea
General
Etiology unknown - likely associated with viral infections
Common in older children and young adults
Increased incidence in spring and fall
Pityriasis rosea
Pityriasis rosea
Clin Man
Herald patch - solitary, salmon colored macular on the trunk has an initial lesion
Followed by a general exanthem 1 to 2 weeks later: smaller, very pruritic round to oval erythematous papules or thin plaques with a collarette of scale in a Christmas tree pattern
Confined to the trunk and proximal extremities
Pityriasis rosea
Tx
self limited, tends to resolve spontaneously in 4-6 weeks
Symptomatic treatment as needed
Topical corticosteroids – triamcinolone 0.1% cream QD-BID
Emollients
Pityriasis Rosea
Intertrigo
General
Inflammation of large skin folds - Inframammary fold, gluteal cleft, inguinal creases, and folds under pannus
Up to 10% of cases are complicated by Candida yeast colonization
Intertrigo
Clinical Manifestations
Classic symptom: burns more than it itches
Classic sign: satellite macules, papules, or pustules around erythema within the skin fold
Intertrigo
Intertrigo
Tx
Topical antifungals: miconazole, clotrimazole, econazole
Ketoconazole 2% cream bid to AA is most commonly prescribed in practice
Nystatin only works for Candida -typically results in incomplete resolution of symptoms
Topical anti-inflammatory: desonide ointment or hydrocortisone 1% ointment qd-bid for 1-2 weeks
Intertrigo
Prevention
Keep the affected area dry, clean, and cool
Over-the-counter antifungal powders can be used as daily maintenance
KOH exam
This is the easiest and most effective method used to diagnose fungal infection of the hair, skin, and nails
KOH dissolves keratinocytes making it easier to see fungal hyphae
Proper technique interpretation requires training and experience
KOH exam
Procedural steps:
-Clean and moisten in the skin, typically with an alcohol swab
-Collect scale with a 15 blade
-Scrape over the skin, allowing scale to accumulate on the center of a glass slide
-Place coverslip atop scale
-Add one to two drops of KOH
-Microscopy: scan at a low power to locate cells, then study in detail for hyphae at 10X
General :
Tinea Capitis
General
Fungal infection of the scalp, involving the skin and hair.
Typically Trichophyton tonsurans or Microsporum canis
Typically affects children and immunocompromised individuals
Increased incidence in African Americans
Spread by contact - either by an infected individual or by fomites
Tinea Capitis
Risk factor
Poor hygiene
Tinea capitis
Clinical Manifestations
Patches of alopecia with black dots or scaly patches of hair loss, commonly with erythema and pruritus.
Kerion: characterized by the development of an inflammatory boggy edematous plaque with pustules, thick crusting, and/or drainage, with suppurative folliculitis. Painful and tender. Can lead to scarring.
Tinea capitis
Dx
clinical, can be confirmed with KOH or Wood’s Lamp
Definitive diagnosis: fungal culture.
Tinea capitis
Tx
1st line: oral griseofulvin
2nd line: oral terbinafine
Additional treatments:
Anti-fungal shampoos at least twice weekly - treat all household members with too
Avoid sharing hats, brushes/combs, hair clippers
Tinea corporis
Tinea corporis
General
Refers to dermatophytosis of the skin, usually affecting the trunk and limbs
Pathogen: Trichophyton rubrum or microsporum
Transmission is due to direct contact
Very common in pre-adolescent age individuals
Tinea corporis
Clinical Manifestations
Solitary or multiple erythematous, scaly, circular or oval plaques or patches with central clearing and well-defined raised borders that spread outward
Often pruritic
Tinea corporis
Dx
KOH prep – best initial test
Fungal culture can be performed for definitive diagnosis
Tinea Corporis
Tx
Topical antifungal – clotrimazole, ketoconazole, butenafine, terbinafine, ciclopirox - typically bid application x 1-3weeks
Oral if refractory: terbinafine
Tinea manuum
General
A dermatophyte infection of one or both hands
Typically Trichophyton species
Results from contact with an infected individual; from another site of infection, particularly the feet or groin; or contact with a fomite
Tinea manuum
Risk Factors
Manual laborers
Hyperhidrosis
Existing hand dermatitis
Tinea manuum
Clinical Manifestations:
Erythematous, scaly patch or plaque with a raised, well-defined border
Slow extending area of peeling, xerosis and mild pruritus
May have increased skin markings or vesicles/bullae
Tinea manuum
Dx and Tx
Best initial test: KOH
Definitive diagnosis: fungal culture
Topical anti-fungal agents
Oral terbinafine if refractory
Tinea cruris
General
Superficial fungal infection of the groin or inner thigh
Typically caused by Trichophyton rubrum
Tinea cruris
Tinea cruris
Risk Factors
Males
Copious sweating
Immunocompromised
Existing fungal infection like tinea pedis
Tinea Cruris
Clinical Manifestations
Hallmark : pruritus, annular, well-demarcated, hyperpigmented patches or plaques with diffuse erythema
May have vesicles
Typically spares the scrotum
Tinea Cruris
Dx
clinical
Best initial test: KOH
Definitive diagnosis: fungal culture
tinea cruris
Tx
Topical anti-fungals - clotrimazole, butenafine, terbinafine, Ketoconazole, ciclopirox
General measures: desiccant powders, avoidance of tight-fitting clothing, put socks on before underwear
Tinea pedis
general
The most common fungal infection seen in developed countries
Most commonly caused by the fungus Trichophyton rubrum
Public showers, gyms are common sources of infection from direct contact and breaks in the skin
tinea pedis
Clinical Manifestations
Most common: Scaling and redness between the toes, maceration may be present
Look for “1 hand, 2 feet” syndrome
Moccasin: Chronic, hyperkeratotic type - sharply marginated scale, distributed along the lateral borders of the feet, heels, souls and is often associated with onychomycosis
Complete KOH prep to confirm diagnosis
tinea pedis
tinea pedis
tinea pedis
Tx
First line: allylamines - terbinafine, naftifine or butenafine cream qd-bid x 1-2 weeks
These are expensive!
Second line: imidazoles - clotrimazole, miconazole, Ketoconazole cream bid x 4-6 weeks
These are more commonly prescribed in practice!
Ciclopirox cream is my personal go-to treatment
Review hygiene practices with patients
Tinea versicolor
general
Not caused by a dermatophyte - actually a colonization of a yeast, typically Malassezia furfur, that is a normal resident of the skin
Tends to onset during summer months
Tinea versicolor
Morphology:
Called “versicolor “because it can be light, dark, or pink to tan
Tinea versicolor
Clinical Manifestations
Diagnostic feature
Characterized by well-demarcated, hypopigmented or hyperpigmented macules, patches, occurring mostly on the trunk and arms
Macules will grow, coalesce and various shapes and sizes are obtained in an asymmetric distribution
Visible scale is often not present but when rubbed scale is readily seen this is a diagnostic feature of tinea versicolor
Tinea versicolor
Tinea versicolor
Dx
clinical, confirmed by KOH
Tinea versicolor-furfur
Tx
3 kinds
Shampoos – apply for at least 5 minutes daily to the affected area
Imidazole creams: Ketoconazole cream, clotrimazole
Oral: fluconazole 300mg 1 dose per week x 2 weeks
Requires liver function studies due to risk of hepatotoxicity
Sudden hair loss can be caused by
Alopecia areata
Telogen effluvium
Tinea capitis
Gradual hair loss can be caused by
Androgenetic Alopecia
Trichotillomania
Focal Hair loss agents
Alopecia areata
Androgenetic alopecia
Tinea capitis
Trichotillomania
Diffuse hair loss agents
Telogen effluvium
Alopecia universalis
Iron deficiency anemia
Drug-induced hair loss
Alopecia
PE
Examine the scalp for inflammation
Compare part width of the top of scalp with the back of scalp
Examine the entire scalp by making small parts in the hair
Note location and extent of hair thinning/loss
Perform a hair pull test and tug test
Cicatrical baldness / Androgenetic Alopecia
General
An extremely common, genetically determined disorder characterized by the gradual conversion of terminal hairs into indeterminate and then finally vellus hairs
Cicatrical baldness / Androgenetic Alopecia
Men vs women
Men: occurs in half of men by age 50
Frontal hairline recede, bitemporal thinning, then thinning on the top and crown
Women: occurs in half of women by their 80s
Unlike men, women tend to retain the shape of their hairline, but tend to go thin on the top and sides
Androgenetic alopecia
Tx
Topical minoxidil 5% foam daily to the affected area
Reassure patients that it will take 6 to 12 months to see improvement or halt progression of hair loss
Oral finasteride or dustasteride daily
Cicatrical baldness / Androgenetic Alopecia
Androgenetic alopecia
Telogen effluvium
general
Telogen effluvium results in faster cycling of the hair and loss of telogen hairs at the root
Often triggered by major stress to the body - think illnesses requiring hospitalization, pregnancy, surgery, significant mental stressors.
Usually resolves within 6 to 12 months of onset
Lasts longer for some people especially those with subtle changes in hormone levels, use of retinoids, cortisol, ferritin, vitamin D3, beta blockers, and general anesthetics as these are involved in hair cycle regulation
Telogen effluvium
lab work up
Labs: TSH, T4, CBC, iron studies, vitamin D, possibly RPR
what is the most common cause of female Telogen effluvium
Iron deficiency
Telogen effluvium
Tx
Reassurance is the mainstay of treatment if there is no underlying cause as determined by labs
Tips for practice: most dermatology providers will recommend multivitamin supplementation and topical minoxidil to help stabilize hair loss if onset is relatively recent
Alopecia areata
general
An autoimmune attack on hair follicles by lymphocytes - the hairs will fall out in well-defined patches
Associated with other autoimmune disorders, most commonly thyroid disease
Unpredictable course, but usually results without treatment in about six months
Regrowth can start with thin or white hairs
Focal and rapid
Alopecia areata
lab work up
consider Thyroid panel
bc often associated with other autoimmune disorders like thyroid
Alopecia areata
Tx
Intralesional triamcinolone injections 2.5 - 10 mg/mL every 4 to 6 weeks
ILK5 is most commonly used in practice
Topical steroids - start with potent or ultra-potent steroids
I recommend betamethasone valerate 0.01% foam or betamethasone dipropionate 0.05% lotion daily
Topical minoxidil 5% foam
If extensive - refer to dermatology
Trichotillomania
Trichotillomania
general and ClinMan
Caused by forceful pulling and removal of the hair
Clinical Manifestations
Different lengths of hair present within the patch
May also have black dots from short hairs
Lack scale or inflammation
Trichotillomania
Tx
Screen for anxiety and depression
Behavioral interventions including habit reversal, self monitoring, competing reaction training, relaxation training, psychotherapy, hypnosis
Medical therapy: SSRIs - fluoxetine, sertraline, fluvoxamine
Cherry angioma
general
A benign lesion formed due to abnormal mature capillary proliferation
Most commonly seen in middle-aged and older adults
Cherry angioma
Clinical Manifestations
Cherry red to purple papules that may be flat topped or dome shaped
Blanch with pressure
Most commonly seen on the trunk
Tend to bleed profusely if they are traumatized
Cherry angioma
DX and Tx
Diagnosis : clinical
Treatment: observation
Can be removed for cosmetic reasons with electrocauterization or laser therapy
cherry angioma
Pyogenic granuloma
Pyogenic granuloma
General
Benign vascular tumor of the skin or mucous membranes, characterized by rapid growth and friable surface
Most common in children and young adults
Seen after hormonal changes, such as pregnancy, or after the initiation of new medication or chemotherapy
Pyogenic granuloma
Clinical Manifestations
Solitary glistening, friable, bright red rapidly-growing nodule or papule that often bleeds after minor trauma or ulcerates
Found in arms, hands, legs or at sites of skin trauma
Pyogenic granuloma
Dx and Tx
Diagnosis: biopsy
Treatment:
Excision with wound closure or curettage followed by electrocautery
Kaposi Sarcoma
Kaposi Sarcoma
general
Vascular cancer associated with Herpes virus 8 infection
Most commonly seen in immunosuppressed patients - HIV
Cutaneous KS typically seen on lower extremities, face, oral mucosa, genitalia
Kaposi Sarcoma
Clin Man
Painless, non-pruritic pink, brown, erythematous or violaceous macules, papules or plaque-like nodules
Kaposi Sarcoma
Dx and Tx
Diagnosis: biopsy
Management: refer to oncology
Chemotherapy, radiation
HIV- Antiretroviral therapy
Stasis dermatitis
general
Inflammatory skin changes associated with chronic venous insufficiency
Stasis dermatitis
Clin Man
Erythematous to brownish or dark purple hyperpigmented patches or plaques with eczematous features (scale, pruritis, weeping erosions and crusting)
Leg edema, increased leg circumference, variscosities are common - pulses are maintained
Stasis dermatitis
Tx
management of underlying venous insufficiency
General measures: leg elevation, compression stockings, exercise
Gentle cleansing
Acute lesions: topical corticosteroids
Severe or refractory: oral prednisone
Stasis dermatitis
Stasis dermatitis
Decubitus Ulcer
general
Pressure ulcer
Ulcers resulting from vertical pressure.
Commonly seen on bony prominences – sacrum, calcaneus, ischium
Decubitus Ulcer
Risk Factors
Elderly, immobilization, incontinence
Decubitus ulcer
Decubitus ulcer
stage 1 manifestation and tx
superficial, nonblanchable erythematous macule
preventive measures, wound protection
Decubitus ulcer
stage 2 manifestation and tx
epidermal damage extending into the dermis. Resembles a bulla or abrasion
maintain a moist wound environment – hydrocolloids or hydrogels
Decubitus ulcer
stage 3 manifestation and tx
Full thickness loss of the skin.
May extend into the subcutaneous layer
Wound cleansing, maintain a moist wound environment, debridement of necrotic tissue, and treatment of wound infection if necessary
Decubitus ulcer
stage 4 manifestation and tx
Deepest. Extends beyond the fascia, into the muscle, tendon, or bone
Wound cleansing, maintain a moist wound environment, debridement of necrotic tissue, and treatment of wound infection if necessary
Pyoderma gangrenosum
Pyoderma gangrenosum
general
An auto-inflammatory ulcerative process mediated by an influx of neutrophils into the dermis
Typically triggered by trauma, surgical debridement, or attempts to graft an area
Pyoderma gangrenosum
often misdiagnosed as
misdiagnosed as a spider bite or an infection and debridement occurs it will worsen the condition
Pyoderma gangrenosum
associated with
Can be associated with inflammatory bowel disease, rheumatoid arthritis, hematologic conditions, arthritis, and malignancy
Pyoderma gangrenosum
Clin Man
Begins as a small pustules that breaks down and rapidly expands forming an ulcer with an undermined violaceous border - tends to have a rapid progression
Satellite alterations may merge with the central larger ulcer
Can occur anywhere on the body
Can be very painful
Pyoderma gangrenosum
Tx
refer to Dermatology - this is a DERMATOLOGIC EMERGENCY
Topical: Superpotent steroids, tacrolimus
Systemic: steroids, cyclosporine, tacrolimus, cellcept, thalidomide, TNF-inhibitors
Drug eruptions
general
Acute or subacute adverse cutaneous reactions to a medicine
Most are hypersensitivity reactions
Majority or self-limited the offending drug is discontinued.
drug eruptions
triggers
Antigen from foods, insect bites, environmental, exercise induced, and infections
type 1 drug eruption
IgE-mediated
e.g. Urticaria, angioedema
slide 57 ppt2
drug eruption
Morbilliform Drug Eruption
Most commonly occurs 5 to 14 days after initiation of a new medication or within one to two days in previously sensitized individuals
Type 4 T-cell mediated hypersensitivity reaction
Common medication: penicillin, sulfas, NSAIDs, allopurinol, anticonvulsants
(SAPAN)
Morbilliform Drug Eruption
Clinical Manifestations
Characterized by erythematous macules or small papules after initiation of a medication
Generalized distribution that typically coalesce to form plaques, primarily involving the trunk and proximal extremities
May have mild systemic symptoms including low-grade fever, pruritus
Morbilliform Drug Eruption
Tx
Stop attending medication
Oral antihistamines, +/- short course oral corticosteroids
Morbilliform Drug Eruption
Vitiligo
Vitiligo
General
An acquired, chronic, depigmenting disorder of the skin, in which melanocytes are progressively lost
It is widely accepted that vitiligo is a result of autoimmune destruction of melanocytes
Appears in all races, all ages with ages 20-25 years most commonly affected, and both men and women appear to be equally affected
A familial component is present as more than 20 to 30% of affected individuals report vitiligo in a first or second-degree relative
vitiligo
is associated with
Associated with several other disease states
Rheumatoid arthritis, insulin-dependent diabetes, B12 deficiency, SLE, alopecia areata, Addison disease, and other autoimmune dermatological conditions
Vitiligo
Clin Man
Most common: complete loss of pigment in a single or multiple macules or patches of the skin with characteristic chalky or milky white coloration
Typically asymptomatic, but can be pruritic
Well defined with convex borders
Small patches may coalesce together merging into more complex shapes
Typically found in the sun exposed areas or in areas prone to repetitive trauma
vitiligo
Tx
Topical potent corticosteroids have mixed results
New Janus Kinase inhibitor: Ruxolitinib (Opzelura) just FDA approved!
