Papulo-squamous diseases

Dr. lsrael G.M

PSORIASIS

It is a chronic proliferative

skin disease that affects about

1-2% of general population.

Cause: Not known however there

are

Genetic predisposition with triggering factors:

Trauma: can elecit (koebner phenomenon).

Weather: worse in winter.

Endocrinal factors: It may improves with pregnancy and exacerbate with puberty and menopause.

Infection: steptococcal infection may be followed by guttate psoriasis .

Drugs: ß adrenergic blockers, NSAIDs and ACE inhibitors.

Emotional stress.

Alcohol and smoking.

Histopathology

Epidermis:

Parakeratosis (accelerated incomplete keratinization of horny

cells with retention of nuclei) with focal orthokeratosis.

Absent granular cell layer(or hypogranulosis).

Regular acanthosis and elongation of club shaped rete ridges.

Suprapapillary thinning of epidermis.

Munro microabscesses formed of collected neutrophils in

stratum corneum or just beneath it.

Spongiform pustules in malpighian layer.

Dermis:

Elongation and edema of dermal papillae.

Dilated tortuous capillaries in the upper portion

of papillae.

Perivascular mononuclear and neutrophil

inflammatory infiltrate in upper dermis.

Clinical picture:

The primary lesion is a salmon pink papule

covered with silvery scales. Papules may

enlarge or coalesce forming plaques.

Sites: extensor surfaces of limbs, elbows,

knees, scalp, and nails.

Grattage test

Scraping of psoriatic lesion with the edge of

a glass slide results in removal of the scales

layer after layer with accentuation of the

silvery appearance until a smooth glossy red

membrane is finally left. On scratching this

membrane pinpoint hemorrhages appear

(Auspitz's sign).

Morphological patterns

1-Punctate psoriasis (pin point size)

2-Guttate psoriasis (size of drops)

3-Discoid psoriasis (coin shaped)

4-Annular psoriasis (ring shaped lesions produced by involution of center of the lesions)

5-Geographical psoriasis (curved patterns produced on a large area as the back).

6-Linear psoriasis

Clinical varieties- Flexural psoriasis: as in axillae and groins.

- Psoriasis of palms and soles: may be either;

Typical scaly plaques

Or thick, fissured plaques similar to hyperkeratotic eczema

Or pustular type

- Erythrodermic type: generalised erythema and scaling.

- Psoriasis of nails: pitting, yellowish discolouration, circular area ofdiscolouration (oil drop) transverse ridging, onycholysis (distalseparation), thickening, subungual hyperkeratosis.

- Arthropathic psoriasis.

- Psoriasis of scalp: not crossing the hair line (D D from seborrheicdermatitis).

- Pustular psoriasis: localised or generalized, the primary lesionshere is a sterile pustule.

Flexural psoriasis

Psoriasis of palms and soles:

Erythrodermic psoriasis:

Psoriasis of nails:

Psoriasis of scalp:

Pustular psoriasis:

Pathogenesis:

Epidermal keratinocyte hyperproliferation.

The transit time of epidermal cell maturation

from a basal cell to be a horny cell in normal

skin is about 26-28 days whereas in psoriatic

skin it is only 3-4 days.

T-cell mediated inflammatory process

involving mainly Th1 cells.

Koebner phenomenon:

It is development of isomorphic pathologic

lesions in the traumatized uninvolved skin of

patients who have psoriasis.

Psoriasis, warts, lichen planus, vitiligo,

molluscum contagiosum and pityriasis rubra

pilaris (PRP).

Treatment:

A-Topical treatment

1-Tar :crude coal tar 2-5%.

2-Anthralin 0.1-1%.

3-Salicylic acid (3-5%) keratolytic remove scales.

4-Corticosteroids ointment.

5-Intralesional corticosteroid injection oftriamcinolone acetonide in localised resistentplaques but less effective in nail psoriaisis.

6-Calcipotriol ointment (vitamin D analogue). Itinhibits keratinocyte proliferation.

B-Systemic treatment

1-Methotrexate 2.5mg tab (5mg every 12 hour for 3 doses)every week. It is indicated in erythrodermic psoriasis andgeneralized pustular psoriasis. Liver function should bemonitored.

2-Retinoids; etretinate: 1 mg/kg/day and acitretin 0.5-1mg/kg/day in severe cases and erythrodermic psoriasis

3-Photochemotherapy (PUVA): psoralens 0.6 mg/kg 2 hoursbefore the exposure to UVA rays 2-3 times weekly

4- Phototherapy: narrowband UVB rays (NBUVB)

5-Cyclosporin A: immunosuppresive for severe cases 2.5-5mg/kg/day.

LICHEN PLANUS

Lichen planus is an itchy chronic

inflammatory disease which affects

skin and mucous membranes.

Pathogenesis:

1-Genetic predisposition

2-Autoimmune

3- Strong association with hepatitis C infection

4- Emotional stress

Clinical picture

The primary lesion is a pruritic shiny violaceous flat toppedpolygonal papule which retains the skin lines and showswhite streaks (wickham’s striae). These striae can be seenwell with a magnifying lens.

It is commonly seen on wrist, back of hands, shin and anklesin hypertrophic type, lumbar region, glans penis in annulartype and palms and soles.

Mucous membrane lesions are very common (in 30-70% ofcases) and may occur alone without skin involvement.

After disappearance of the lesions deep pigmentation is leftfor several months

Clinical varieties: 1- Atrophic lichen planus; fading annualr or hypertrophic type.

2- Hypertrophic Lichen planus: deep violet rough papules over shin of tibiaand ankles.

3- Linear lichen planus.

4- Annular lichen planus (on glans penis).

5- Lichen planus bullosus.

6- Lichen planus circinatus.

7- Lichen plano-pilaris: follicular papules which result in cicatricial alopecia.

8- Lichen planus actinicus: on sun exposed areas in the form of annularlesions with violet brown centre and well defined hypopigmented margin.

9- Lichen planus of mucous membrane: (White streaks or network on thebuccal mucosa, fixed white plaques on the tongue or ulcerative lesions).

10- Lichen planus of palms and soles: firm rough non itchy deep yellowishpapules.

11- Lichen planus of the nails: thinning of nail plate, linear ridges andgrooves, adhesions between dorsal nail fold and nail bed may cause partialdestruction of nail (pterygium).

Histopathology:

1-Compact hyperkeratosis.

2-Focal hypergranulosis.

3-Irregular acanthosis and irregular elongation of rete

ridges giving a (saw toothed appearance).

4-Liquefactive degeneration of basal layer.

5-Band like inflammatory infiltrate.

Treatment:

1-Assurance and avoidance of stress

2-Topical therapy:

a- Fluorinated topical steroid ointment

b- Topical tacrolimus

c- Intralesional steroids

(Hypertrophic LP and lichen planus of nail)

3-Systemic therapy:

a-Antihistamines

b-Systemic steroids (15-20mg/day for 6 weeks) indicated in:

1-severs pruritic or generalized cases

2-ulcerative mucous membrane lesions

3-progressive nail destruction

4-extensive lichenplanopilaris to prevent cicatricial alopecia

c- Retinoids d- Cyclosporin A

e- Antimalarials for actinic L.P

f- NBUVB and PUVA

PITYRIASIS ROSEA

It is an acute self limited disorder

characterized by superficial, scaly

lesions on the trunk.

It is more common in spring and

autumn.

Clinical picture:

1- The primary lesion is the herald patch.

2- It is followed after 5-15 days by multiple similarmacules or patches.

3- The long axes of lesions follow lines of cleavageparallel to the ribs in a Christmas tree pattern on theupper chest and back.

4- The eruption fades within 4-8 weeks.

Types:

1- Classical type.

2- Inverted type.

3- Abortive type.

4- Localised type.

Etiology:

a- Infective agent: virus (HHV6-7).

b-Drug induced (pityriasiform drug eruption) as

captopril, metronidazole, ketotifen and

barbiturates.

c- Autoimmune disease.

Treatment:

1-Reassurance

2-Antihistaminics

3-Calamine lotion

4-Narrow band UVB

PITYRIASIS RUBRA

PILARIS

This is a chronic disease characterized

by follicular hyperkeratosis, branny

scales, orange red erythema and

palmoplanter keratoderma.

Etiology:

Unknown.

It may be dominantly inherited.

Vitamin A deficiency is also reported.

Clinical signs:

1-Diffuse scaliness of scalp.

2- Patches showing keratotic follicular papules.

3- Dry scaly erythematous areas simulating psoriasis.

4- Hyperkeratosis of palms and soles.

5- Follicular hyperkeratosis of proximal phalanges of

fingers and toes.

6- Nails: dull, thickened rough dystrophic.

7-Erythroderma with islands of normal skin.

Types:

1. Classical adult type (most common

55%)

2. Atypical adult type (5%)

3. Classical juvenile type (10%)

4. Circumscribed juvenile type (25%)

5. Atypical juvenile type (5%)

Treatment:

1-Emollients in cases of erythroderma to reduce scaling

and restore skin barrier

2-Topical steroids and salicylic acid ointment

3-Topical vitamin D analogues (calcipotriol)

4-Oral Vit A: 150,000-300,000 IU/day

5-Isotretinoin and acitretin

6-Methotrexate 10-25mg/week

7-Narrow band UVB

8-PUVA alone or/and oral retinoid

THANKS FOR LISTENING