Psoriasis, lichen planus, lupus eritematosis, scleroderma Flashcards
Lichen Planus
—Aetiology :inflammatory reaction In a genetically predisposed patient,due to triggers e.g., hepatitis C , stress
—Clinical picture:
classic :
*pruritic flat-topped , polygonal, violaceous papules mostly bilateral symmetrical on
flexors of wrist and forearm .
*The surface of the papule often show a lacy white network (Wickham’s stria)
* The papules may coalesce forming plaques
* New lesions may develop at the site of a scratch or trauma (Koebner phenomen)
—oral mucosa:
- with or without skin lesions.
- buccal mucosa: white streaks.
- tongue :white plaques. Painful erosions (precancerous).
Nail lesions:
-with or without skin lesions.
-Longitudinal ridges, pitting, and splitting.
-Pteryguim (adhesion between of proximal nail fold and nail bed ) is characteristic,
-may produce permanent nail loss.
palms and soles: -non-itchy firm yellowish papules –may ulcers on sole
Follicular lichen : may with typical lichen planus ,may scalp alone (scarring alopecia)
Actinic lichen planus: on the sun-exposed area.
Hypertrophic lichen: Verroucous violaceous papules ,plaques on shins,ankles.
Bullous lichen: Bullae appear on the top of lichen planus
Linear lichen: papules arranged in a linear or zosteriform pattern.
Annular lichen : papules arranged in annular pattern (genitalia mainly)
–Pathology:
1. Hyperkeratosis.
2. Hypergranulosis (increase thickness of granular layer).
3.Acanthosis , Saw-tooth pattern of rete ridges (irregular elongation with pointed ends).
4. Liquefactive degeneration of the basal cell layer
5. Band -like infiltrate of lymphocytes in the upper dermis.
–Course:
* Acute cases clear within few weeks
*If developing gradually subside within 9 - 18 months.
* Hypertrophic and mucous membrane lesions are usually chronic.
*Exacerbation may occur with stress.
*Healing occurs with characteristic hyperpigmentation which may clear in time.
*Atrophy may follow healing of annular or hypertrophic lesions.
—Treatment:
Topical:
* Steroid cream.
*Intralesional steroid injection in hypertrophic skin lesion and erosive oral lesions.
systemic:
* Oral antihistamines.
* Steroids: widespread cases, ulcerative mucosal lesions, scarring nail dystrophy
Psoriasis
—Aetiology :inflammatory reaction In a genetically predisposed patient,due to triggers :
1- Trauma: scratch , wound (Koebner phenomenon). 2- Infection: Streptococcal , AIDS.
3. Endocrine factors: Diabetes, pregnancy 4- Metabolic : Hypocalcemia
5- Sunlight: may worse 6-Climate: cold dry weather may worse
7. stress 8. Drugs: Chloroquine, lithium, B- blockers
—Clinical types:
1. Psoriasis vulgaris: (patterns):
* Plaque psoriasis:
- Well-defined , erythematous papules , plaques covered with silvery white scales.
-common sites are extensor surfaces of elbow’s, knees and lower back.
-Scraping the lesion leads to small bleeding points (Auspitz sign) pathognomonic
- Trauma to normal skin may elicit lesions (koebner phenomenon).
* Scalp psoriasis : discrete or diffuse plaques with firmly adherent asbestos like scales (Pityriasis amiantacia).
* Psoriasis of palms and soles: red patch covered with fine silvery scales.
* Psoriasis of nails:
- pitting, yellowish discoloration of the nail bed
- subungual hyperkeratosis ,onycholysis
* Flexural (Intertriginous) psoriasis:
-Plaques are pink, smooth, and shiny due to lack of scaling,may itching,fissuring
* Mucosal: - Lips : silvery scales - tongue : white plaques, annular or fissuring
2. Guttate psoriasis:
-acute symmetrical eruption of drop-like lesions usually on the trunk and limbs.
-It mostly occurs in children and young adults
-following acute Streptococcal throat infection.
- may subside after about 6 weeks without treatment, or change to plaque psoriasis
3- Erythrodermic psoriasis: > 90% of skin is red and covered with scales
4- Pustular psoriasis:
* Palmoplantar: yellow to brown sterile pustules on the palms or soles.
*Generalized: -serious form of psoriasis
-Sheets of erythema studded with sterile yellowish pustules
-Occur in waves, associated with fever and malaise.
5. Arthropathic psoriasis: Psoriasis associated with arthropathy (5-10% of patients).
–Pathology:
1- Hyperkeratosis, parakeratosis , Munro micro-abscesses: collection of neutrophiles in the horny layer.
2- Absent granular layer(hypogranulosis or agranulosis)
3 - Acanthosis
4- Dermis: -elongated Dermal papillae, thin suprapapillary epidermis.
- dilated and tortuous Capillaries.
-Lymphocytes and neutrophiles infiltrate
—Course: *chronic with remission and relapse.
*the first attack of psoriasis may end without further relapses
*may remain for the rest of the patient’s life,
*usually it improves during summer
—-Treatment:
A- Topical therapy: (The first line treatment in mild and moderate plaque psoriasis).
1. Topical Steroids: -Antimitotic and anti-inflammatory.
- treatment of choice for face, neck, flexures and genitalia.
- applied alone or in combination with salicylic acid .
2. Salicylic acid 3%: Keratolytic to remove scales.
3. calcepotriol (Vitamin D analogue):
- inhtibits cell proliferation
-Hypercalcemia is possible if high dose (systemic absorption)
4. Tar: - Antimitotic by inhibiting DNA synthesis
- Safe but messy.
-( TAR + UVB) called Goeckerman regimen.
5. Anthralin: -has an antimitotic effect:
- Ingram technique: anthralin + UVB.
B- Phototherapy: UVB exposure 3 times weekly in mildly erythemogenic dose
C-Systemic therapy:
Indications: 1) Extensive psoriasis vulgaris 2) Erythrodermic psoriasis.
3) Pustular psoriasis 4) Arthropathic psoriasis.
Drugs used:
Methotrexate (hepatotoxix,myelotoxic)
Cyclosporine (nephrotoxic)
Retinoids(acitretin): teratogenic ,
Biologics: TNF alpha blockers, e.g adalimumabt, I.L 17 inhibitor (seckukinumab)
N.B Oral steroids should be avoided. Cause rebound of psoriasis may even result in
erythrodermic or severe pustular psoriasis.
Lupus Erythematosus
–Range from benign skin only disease(DLE) to severe systemic disease
Discoid Lupus Erythematosus (DLE)
—Clinical picture:
Lesions: Single or multiple well-defined plaques with characteristic features of
1. erythema , telangiectasia. 2. scales. 3. Follicular dilation 4. Atrophy. 5. Dyspigmentation
—Sites: -face especially the butterfly area, scalp, dorsum of hands , retroauricular.
- but, any site may be affected including oral mucosa.
-Lesions on the scalp cause scarring alopecia.
—Course: The prognosis of DLE is good . The cutaneous disease may remit spontaneously or remain
minimally active. DLE may progress to SLE in 6% of cases.
—Treatment:
Topical or intralesional steroid .
Systemic: Chloroquine in cases not responding to topical steroid .
