Papulosquamous and Inflammatory dermatoses Flashcards
etiology and epidemiology
Keratosis Pilaris
Disorder of keratinization of hair follicles of the skin
Exact etiology unclear; genetic link
Sex: F > M
May appear at any age; Affect 50-80% of all adolescents & 40% of adults
Associated with other “dry skin” conditions:
- Ichthyosis vulgaris & xerosis
- Atopic dermatitis
Clinical Features
Keratosis Pilaris
Small (1-2mm), rough folliculocentric keratotic papules (sometimes pustules)
Erythematous papules with light-red halo
Distribution:
Posteriolateral upper arms
Anterior of thighs
Buttocks, face
Can affect any area
Spares palms and soles
ÜAsymptomatic (most) to mild pruritus
Diagnosis
Keratosis Pilaris
Clinical (H&P)
Differential Diagnosis:
- Miliaria rubra
- Acne/ folliculitis
- Drug eruption
Treatment
Keratosis Pilaris
Mild cleansers
Emollients
Keratolytic ,12% ammonium lactate (Lac-Hydrin, AmLactin) or urea cream, topical retinoids (Tazorac or Retin-A cream)
Topical steroids
Patient Education
Xerosis Epidemiology
Dry Skin”
Important feature of the “atopic” state
Affects all ages
Decreased barrier function of skin
Aggravating factors:
-Winter
-Low humidity
-Hot water
-Harsh products (soaps, fragranced lotions…)
Xerosis Clinical Manifestations
Erythema, horizontal linear splits (cracks)
Most common on extensor surfaces; but not limited to these areas
Increased sensitivity, easily irritated
May itch or burn
Xerosis Diagnosis and Treatment
D: Clinical
Treatment:
Avoid triggers
Cotton 100%
Mild or “free” detergent
No bleach or fabric softener
-Use mild → no soap
#Aveeno, Purpose, Dove, Cetaphil, Oil of Olay
Clip nails to ↓ abrasion to skin
Avoid frequent washing and drying
Topical therapies
Wet dressings
Short, cool showers/baths
Emollients IMMEDIATELY after bathing
Frequent “soaking and greasing”
Oils > ointments > creams > lotions
Etiology
Ichthyosis Vulgaris
Disorder of keratinization characterized by the development of dry, rectangular scales.
Ichthys = “fish” in Greek
Onset at birth or later in life?
Various forms: Inherited and acquired
Epidemiology
Ichthyosis Vulgaris
Hereditary (95% of cases) vs Acquired
Autosomal Dominant
Sex: M = F
Often seen in AD patients
-Keratosis pilaris
-Hyperlinear palmar creases
-Atopy
Clinical Features
Ichthyosis Vulgaris
Fine, white, adherent, polygonal scale with central tacking (“pasted on”)
Extensor extremities
(LE>UE)
Flexural folds & diaper = spared
Improves as adult
Diagnosis & Treatment
Ichthyosis Vulgaris
Diagnosis:
Clinical (H & P)
Treatment:
Emollients
Lactic acid, urea, or alpha-hydroxy acids for severe scaling
Patient education about avoiding drying environments
Humidification
Psoriasis General
Common, chronic, inflammatory, papulosquamous disease that affects the skin, nails and joints.
Severity and extent of disease varies widely.
Once expressed, psoriasis is likely to follow a relentless, waxing and waning course.
Proliferation of the outer layers of skin due to abnormal T lymphocyte and dendritic cell function/communication.
reactive increase in growth of epidermal and vascular cells.
8-fold shortening of epidermal cell cycle
Age: onset any age; peaks in 20s and 50s
Heredity: 1/3 have + FHx
Sex: M = F
Triggers:
Trauma (Koebner phenomenon)
Infection (Strep, HIV ,candida, dental)
Stress/ Winter season
Smoking/ Alcohol
Drugs: Beta-blockers, lithium, systemic steroids, antimalarials, NSAIDs, ACE-Inhibitors, terbinafine
Clinical Features
Chronic Plaque Psoriasis
most common form
Red, scaly, round-to-oval plaques.
Symmetrical
Sharply marginated
Loosely adherent “silvery-white” scale
Extensor surfaces, predominantly elbows, knees and scalp gluteal cleft, umbilicus, penis
Usually spares palms, soles and face
Exceptions: based on morphologic variations
The degree of pruritis varies per individual and type
Auspitz sign of Chronic Plaque Psoriasis
pinpoint bleeding when scale removed.
Koebner phenomenon
Psoriasis developing at sight of trauma (sunburn, scratch, surgery)
Psoriasis Types
- chronic plaque psoriasis
- guttate psoriasis (acute erruptive psoriasis)
- pustular psoriasis
- erythrodermic psoriasis
- inverse psoriasis (intertriginous)
- light sensitive psoriasis
Chronic Plaque Psoriasis
Chronic Plaque Psoriasis
Epidemiology
Guttate Psoriasis
Gutta = “drop” in Latin
>30% of first episodes are before 20 y.o.
+/- preceded 1-2 weeks by Strep pharyngitis or viral infection
Resolves spontaneously in weeks to months
Clinical Features
Guttate Psoriasis
Small , scaly, papules suddenly appear
Trunk and extremities.
Uniform lesions
Spares palms and soles
+/- pruritus
What type
Pustular psoriasis
Localized (palmoplantar pustulosis)
Small sterile pustules on a red base on palms and soles
Generalized (von Zumbusch’s syndrome)
Widespread sterile pustules can coalesce into large areas of pus – life threatening
What type
Inverse psoriasis of armpit
What dermatose
Nail Disease associated with Psorasis
Diagnosis
CLINICAL (H&P)
Biopsy (punch)
Labs (typically un-necessary)
\+ Anti-streptolysin O titer/throat culture (guttate) Potassium hydroxide (KOH) r/o candida (inverse) HIV titer; consider if severe case Autoimmune screens (arthritic symptoms)
-ANA, ESR, RF
What type
Plaque type psoriasis
What type
Erythodermic psoriasis
Entire skin surface is involved
Generalized erythema and scaling
Can be very severe
Differential Diagnosis
Chronic plaque:
Seborrheic dermatitis
Nummular eczema
Tinea corporis
Drug eruption
Guttate:
Pityriasis rosea
Secondary syphilis
Drug eruption
Inverse :
Candida
Contact dermatitis
Bacterial infection
Psoriasis Treatment
Topical
Topical steroids/intralesional
Tar preparations
Salicylic acid (scalp)
Vitamin D analogues
-Calcipotriene (Dovonex)
-Calcipotriol (Vectical)
Retinoid creams
-Tazarotene (Tazorac)
Anthralin (Drithocreme, Micanol cream, Psoriatec)
Phototherapy - UVB
Systemic (refer to dermatology)
Methotrexate
Cyclosporine
Acitretin (Soriatane)
PUVA (psoralen + UVA)
Biologics
**Patient Education/treatment monitoring
Etiology/epidemiology
Pityriasis Rosea
Acute, self-limiting skin eruption
Etiology unclear
-Several theories – Thought to be viral in origin
Age: > 75% between 10-35 years old
-Rare in very young or very old
Sex: M = F (slightly MC in females)
Seasonal predisposition:
-More common in cooler months; Spring/Fall
Clustered in families/close contacts
Higher incidence in immunocompromised
Clinical Features
Pityriasis Rosea
Distinct course
Initial primary plaque (Herald patch)
Generalized secondary rash 1-2 weeks later
Spontaneous resolution 6-8 wk
May be preceded by upper respiratory infections (URI) – 68%
+/- Lymphadenopathy
Mild pruritus in some; and can possibly be severe
Can return to school
Resolves spontaneously; Recurrence 2-3%
Symmetrical eruption
Trunk, extremities
Typically spares palms & soles
Atypical presentations exist; small papules more common in very young, pregnancy
Pityriasis Rosea Primary Lesion Clinical Features
Herald patch
- Solitary lesion; usually annular
- 2-6 cm, round-to-oval lesion
- MC on the trunk, neck, but can occur anywhere
Pityriasis Rosea Secondary Lesion Clinical Features
(1-2 weeks after primary)
Generalized eruption, often trunk and prox. limbs
Salmon-pink, 0.5cm- 1.5cm macules or patches; annular
“Christmas Tree Distribution” = long axis of each lesion follows skin lines
Collarette scale = inward facing, cigarette paper- like in appearance
Pityriasis Rosea Diagnosis
Diagnosis:
Clinical Dx (H&P)
Biopsy
Histology is not pathognomonic
Not typically required
Labs
Not usually necessary
VRDL to R/O syphilis
KOH to R/O tinea
Pityriasis Rosea Diff Dx
Guttate psoriasis
Viral exanthems
Tinea corporis
Nummular eczema
Lichen planus
Drug eruptions
Seborrheic dermatitis
Secondary syphilis
Pityriasis Rosea Treatment
No treatment (self-limiting)
Emollients for scale
Topical corticosteroids (Class V) for itching
Anti-histamines (po), & anti-pruritic lotions
Sarna lotion
NO topical lidocaines or topical benadryls
UVB phototherapy / direct sun
Most helpful if started during 1st week of eruption
Etiology
Lichen Planus
Inflammatory cutaneous & mucous membrane reaction pattern
Sex: F > M
Age: may occur any age; Adults (MC 30-60 y.o.)
Rare in kids < 5 y.o.
FHx: 10% +FHx
Unknown etiology
Risk Factors Associated with
may be associated with chronic active hepatitis C
-Hep C antibodies in about 16% with cutaneous lichen planus and approx. 30% with mucosal lesions
Lichen planus – like eruptions (lichenoid) due to:
*medications –thiazide diuretics, gold, chloroquine, methyldopa, penicillamine
*chemical exposure – film processing
*post-bone marrow transplant (graft vs host reaction)
Clinical Features
Location:
Skin, mucous membranes, the genitalia, the nails, scalp,
Most common sites: flexor surfaces of the wrists and forearms, legs just above ankles, lumbar region
The 5 P’s:
Pruritic (20% none)
Planar (flat-topped)
Polyangular
Purple (violaceous)
Papules
Size: 1mm - >1cm
Grouping: random clusters, discrete, linear, annular, or diffusely papular (guttate)
Koebner phenomenon – lesion in response to injury/scratch
Wickham striae: White, lacy reticular pattern of criss-crossed lines
Immersion oil on skin
New lesions appear pink/white and then become purple hue with waxy luster. If persist for months may become thicker and dark red (hypertrophic lichen planus)
Heals with post-inflammatory hyperpigmentation
The 5 P’s of Lichen Planus
Pruritic (20% none)
Planar (flat-topped)
Polyangular
Purple (violaceous)
Papules
Various Patterns of Lichen Planus
Papular (localized) – most common form found on forearms, wrist, ankles and low back typically
Often chronic – average 4 years
Hypertrophic – 2nd most common
- Can be anywhere, but most common on the shins and ankles
- Become confluent, rough red-brown thick
- may have severe itching and last for average 8 yr and develop vesicles/bullae
Follicular (lichen planopilaris) – localized to hair
- follicles and may occur with papular form
- causes hair loss – can be permanent from scarring
Clinical Features
Mucosal Lichen Planus
Mucosal membrane (oral, vulva, glans penis)
Oral – can occur w/out cutaneous lesions
- F>M; mean age onset 60 yo
- seen in greater than 50% with cutaneous lesions
- most common form is non-erosive with white lacy pattern on buccal mucosa
- erosive form more severe and painful; 0.8-3% develop into SCC
Clinical Features
Lichen Planus Nail Disease
Nail changes:
Longitudinal grooving, ridging, splitting, thinning and red streaks/ dots, pterygium
“Tenting” or “pup-tent” = elevation of nail plate +/- longitudinal splitting. Changes are proximal to distal
25% of pts with nail LP have LP at other sites before or after the nail disease is noted
Most common: 50s &60s
Diagnosis and Labs
Lichen Planus
Clinical (H&P)
Biopsy for confirmation if needed.
AST, ALT, & Alk phos
HIV
Hepatitis C
Differential Diagnosis for Lichen Planus
Cutaneous
- Syphilis
- Lichen simplex chronicus
- Guttate vs plaque psoriasis
Mucosal
- Candida
- SCC
- Leukoplakia
Tx for
Lichen Planus
Refer to Dermatology: Generalized or mucosal disease, scarring alopecia, and refractory cases. Unsure of dx.
Topical corticosteroids (Class I – II) initial treatment of localized disease
Intralesional corticosteroids - sometimes used for hypertrophic lesions
Anti-histamines for pruritus
Topical corticosteroids in an orabase for oral lesions (watch for candidiasis with treatment)
Systemic therapies: Generalized or painful disease
Etiology
Granuloma Annulare
Benign inflammatory/reactive dermatosis; self-limited
Pathophysiology : unknown
Several clinical variants
Localized GA is the most common
Sex: 2F : M
Age:
Localized GA: MC in kids & adults < 30 y.o. (70%)
Generalized GA: bimodal < 10 y.o; 30-60 y.o. (rare)
Seasonal: worse in summer; better in winter
Clinical Features
Granuloma Annulare
Primary Lesion: firm, 1-2mm, skin-colored to erythematous papules
Slowly progressing; Grouped lesion expand to arcuate or annular plaques (1-5cm)
Central depression, slightly hypo- or hyperpigmented
Smooth, non-scaling
Location: Dorsal surface of hands, fingers, & feet, Extensor aspects of arms and legs,
Rare on face, scalp, or penis
Symptoms: asymptomatic ; mild pruritus
Duration: variable; Weeks to decades
Spontaneous involution within 2 years in 50%
Hypothesized associations with Granuloma Annulare
Diabetes
Tuberculosis
Insect bites/ trauma
Sun exposure
Thyroid disease
Viral infections:
HIV, Epstein-Barr virus, and herpes zoster virus
Diagnosis and Labs
Granuloma Annulare
Clinical (H&P)
Biopsy +/-
KOH (-)
Consider if indicated:
TSH
Fasting Glucose
Differential Diagnosis
Granuloma Annulare
Tinea
Annular lichen planus
Basal cell carcinoma
Erythema migrans (Lyme disease)
Sarcoidosis
Nummular eczema
Tx
Granuloma Annulare
Asymptomatic localized lesion can be left untreated
Topical corticosteroids - not very effective
Class I or II or lower potency under occlusion (*)
Use in intervals
Intralesional Kenalog
only at the elevated border (*)
Cryotherapy
Other generalized variants may need systemic treatment.
Ü
* Caution: increased risk for atrophy
Etiology
Uticaria
Reactive immunologic/inflammatory process
Also referred to as hives or wheals
Prevalence: May occur at any age – up to 20% of the population will have at least one episode. May be more common in atopic patients.
Cause undetermined in most cases
Classification:
Acute or chronic
Pathophysiology
Uticaria
Major effector cell: Mast cell
Releases histamine – most important mediator of urticaria – in response to immunologic, non-immunologic , physical and chemical stimuli
H1 Receptors:
Triple response of Lewis: Vasodilation (erythema), Axon reflex (pruritus) and wheal
Vasodilation, respiratory and GI smooth muscle contraction, pruritus & sneezing
H2 Receptors:
Vasodilation, increased gastric secretion
Acute versus Chronic Uticaria
Acute: lasts < 6 weeks
majority of cases, lasts from hours to a few weeks. More common in children and young adults. Cause is undetermined in many cases
Chronic: lasts > 6 weeks
more common in young adults and middle-aged women. Cause determined in only 5-20% of cases.
Clinical Features
Uticaria
raised, red, transitory, area of edema
Various sizes and shapes - Papules, plaques, annular, arcuate, polycyclic
Newest lesions = reddest
No scale
Pruritus – varies in severity
\Sudden onset; each lesion lasts< 24 hours
Occur on any skin surface
Common Causes
Uticaria
ÜRecent infection: viral ( hepatitis, mono, coxsackie), bacteria(URI, UTI, gallbladder, dental)
ÜMedications:
ÜACE inhibitors, aspirin, NSAIDs, sulfa-based drugs, penicillins, diuretics, opioids, polymyxin B
ÜFood and food additives:
Ünuts, fish, shellfish, eggs, chocolate, strawberries,tomatoes, cheese, cow’s milk, salicylate, benzoates,dyes
ÜChemical/contact: latex, ammonium persulfate (in hair chemicals),perfumes, plants, cosmetics, textiles, bacitracin
ÜOther misc: parasites, arthropod bites, IV contrast, physical, Sick serum, malignancy, hormones, autoimmune, inhalants (pollens, house dust)
What is Dermatographism?
“skin writing”
Minor trauma/scratch = hive
Lasts < 30 minutes
Diagnosis and Labs
Uticaria
Detailed H&P
Evaluate for the 5 “I”s
- Infections (bacterial, viral, fungal, parasitic)
- Ingestants (meds, foods, additives)
- Inhalants (dust, pollen)
- Injectants (drugs, stings, bites)
- Internal disease (SLE, hyperthyroid, cancer, JRA)
Contact/Chemical
LABS
No routine labs for mild acute or pressure urticaria
Chronic: Based on HX
CBC, ESR, BMP, LFTs, UA
Allergen testing
Stool cultures/sinus xray/dental exam
Autoimmune/CT work-up
Malignancy work-up
Thyroid disease (TSH)
**Biopsy if indicated
5 I’s to Evaluate Uticaria
Infection
Ingestants
Inhalants
Injectants
Internal Disease
Differential Diagnosis of Acute and Chronic Uticaria
Acute: drug eruption, viral exanthem, insect bites, angioedema, urticaria vasculitis, pityriasis rosea
Chronic: Erythema multiforme, Bullous pemphigoid, Lyme disease, Mastocytosis, urticarial vasculitis
Tx
Uticaria
Refer to Dermatology; if recurrent or chronic
Treat underlying condition
Antihistamines preferred initial treatment
(will control the majority of acute and chronic urticaria)
1st generation (sedating): hydroxyzine (Atarax)
diphenhydramine (Benadryl)
2nd generation(low sedating): fexofenadine (Allegra)
cetirizine (Zyrtec)
loratadine (claritin)
Topicals:
Tepid baths, oatmeal baths
Avoid:
Aspirin, NSAIDS, tight clothing, alcohol, wool
For difficult cases:
H2-receptor antagonists (added to H1 antagonists):
Ranitidine (zantac) , Famotidine (pepcid), cimetidine (Tagamet)
Corticosteroids
Oral (for refractory cases): Various tapering doses possible. Prednisone or methylprednisolone
tricyclic; H1 and H2: Doxepin
Etiology
Angioedema
Definition: abrupt and evanescent swelling of the skin, mucous membranes, Resp/GI tracts
Deeper rxn – more diffuse swelling than hives
Histologically deeper form of urticaria - deep dermis & subcutaneous tissue
Caused by increased vascular permeability
Potentially life-threatening
Sex: F > M
+/- FHx
+/- Urticaria
+/- systemic symptoms
Clinical Features
Angioedema
3 Prominent sites:
- Subcutaneous tissue:
Face including lips, hands, arms, legs, genitals
- GI Organs: (MC in inherited types)
Stomach, intestines, bladder
Nausea, vomiting, colicky pain, diarrhea
- Upper airway/larynx:
Dyspnea, dysphagia
Non-pitting swelling
+/- pain & burning
Pruritus typically absent
Marked periorbital/ perioral swelling
- +/- throat, tongue, hands, feet and/or genitals
Diagnosis and Labs
Angioedema
Detailed H&P
+/- Biopsy
Labs
Immunologic studies to be deferred to Allergy or Dermatology
Some recommend CBC/diff; basic metabolic panel, LFTs, thyroid
If HAE is suspected: C1 esterase inhibitor and C4
Differential Diagnosis
Angioedema
Anaphylaxis
Urticaria
Cellulitis
Erysipelas
Contact dermatitis
Tx
Angioedema
Acute severe attacks: epinephrine and antihistamines +/- steriods
IV vs po antihistamines
IV vs po corticosteriods
Refer to Dermatology/Allergist
ID bracelets with Dx
Epi-pen; Epi-pen Jr.
HAE – replacement with C1 inhibitor concentrate; fresh frozen plasma
Intense support may be necessary, depending on symptoms
intravenous fluids, hospitalization.
Etiology
Erythema Multiforme
Common, acute, +/- recurrent, inflammatory, hypersensitivity disease
EM minor: localized skin eruption with no mucosal involvement
EM major: more severe mucosal and skin
Steven-Johnson Syndrome, Toxic Epidermal Necrolysis
potentially life-threatening disorders
Dermatologic Emergencies
Sex: M>F, slightly
Age: 20-40 y.o.; 20% in adolescents
Causes
Erythema Multiforme
MC = HSV, Mycoplasma pneumoniae, acute upper respiratory infection
Medications
Other Infection:
Bacterial, viral, fungal, parasitic
Contact allergens
Flavoring, preservative, food
Immunologic disorders; connective tissue diseases
Mechanical (tattoos)
Other – cancers, pregnancy, xray therapy
Clinical Features
Erythema Multiforme
(Prodromal sxs, morphology, intensity varies)
Prodrome: malaise, fever, itching, burning, cough
Numerous lesions: target lesions, erythematous macules & papules, urticarial-like, vesicles, bullae
Primary lesion: small dull red macule or urticarial papule with central papule/vesicle that may flatten and clear
Hallmark = Targetoid lesion – spreads Centripetally up to 1-3 cm in size
Symmetrical on palms, soles, hands, feet, extensor surfaces of forearms and legs
+/- itch, burn; asymptomatic
+/- Koebner phenomenon
- Nikolsky sign
Mucosal lesions: ( up to 70%)
Lips, the palate, and gingiva
Painful
Ocular involvement mild
ÜHeal without scarring
Ü+/- post-inflammatory hyper/hypo-pigmentation
Diagnosis and Labs
Erythema Multiforme
Detailed H&P
Biopsy – helpful if dx uncertain
Labs
HSV PCR if lesions suggestive
More systemic work-up in severe cases
Differential Diagnosis
Erythema Multiforme:
Urticaria
Steven-Johnson Syndrome
Toxic Epidermal Necrolysis
Drug eruption
Bullous pemphigoid
Tx
Erythema Multiforme
Most mild cases don’t require tx
Antiviral therapy
If associated with reactivated HSV
– used for prevention of Recurrent episodes
Antihistamines for pruritis
Systemic steroids for more wide-spread disease
Soothing mouthwashes
Symptomatic for wounds – topical antibiotics
Supportive care
IV fluids with electrolytes if severe
Refer to Dermatology
Etiology
Erythema Nodosum
Hypersensitivity reaction to various triggers
Inflammatory reaction in the panniculus
Self-limiting
55% cases = idiopathic
Age: mean 18-34 y.o.
Sex: 5 F:1 M adults: children affected equally
Triggers
Erythema Nodosum
Bacterial
- Streptococcal infections (MC), TB, Yersinia, Mycoplasma pnemoniae, Salmonella, Campylobacter, Shigella
Fungal
- Coccidiomycosis (San Joaquin Valley fever); Histoplasmosis
Viruses
- Hepatitis B, Herpes simplex, Epstein-Barr
Parasitic
- Amebiasis, Giardiasis, Ascariasis
Drugs
- Sulfonamides, OCPs, Minocycline, PCN, Salicylates
Inflammatory conditions
Sarcoidosis, Inflammatory bowel disease
Malignancy
Lymphoma, leukemia, renal cell CA, post-radiation therapy
Pregnancy
Idiopathic
Clinical Features/Manifestations
Erythema Nodosum
Lesions start as poorly defined, red, firm, tender subcutaneous nodules, 2-6cm in size that fade over 1-3 weeks similar to a bruise and do not scar
Extensor surfaces; bilateral but not symmetrical, most common on pretibial surfaces. Can see on head, neck, torso , arms and thighs.
New lesions appear for 3-6 weeks
Ankle edema and leg pain are common.
May have prodrome of flulike symptoms, fever, myaligias, and polyarthralgias a few weeks prior or with onset of lesionsÜArthralgias > 50%
Erythema, swelling, tenderness, +/- effusion, morning stiffness
MC in knees, ankles, wrists
Synovial fluid is acellular
May last for 6 months
Resolves without adverse reactions
Diagnosis and Labs
Erythema Nodosum
Detailed H&P
Biopsy, if atypical, include fat
Labs
Throat culture/rapid strep/Antistreptolysin titer
Complete CBC
CXR
PPD
ESR
Stool culture with GI sxs
Rheumatoid Factor (-)
Differential Diagnosis
Erythema Nodosum:
Erysipelas
Cellulitis/Thrombophelbitis
Infected Insect Bites
Acute urticaria
Physical abuse
Henoch-Schonlein purpura
Tx
Erythema Nodosum
Treat underlying conditions; stop offending medication
NSAIDs
Rest
Cool wet compresses
Potassium iodide (only if severe or recurrent)
Corticosteroids (only if severe or recurrent)
