1. PAPULOSQUAMOUS DISEASES
Psoriasis
Lichen planus
Lichen nitidus
Pityriasis rosea
Pityriasis rubra pilaris
Seborrheic dermatitis
Pityriasis lichenoides et varioliformis acuta
Parapsoriasis

2. PAPULOSQUAMOUS DISEASES (II)
Psoriasis
Seborrheic dermatitis

3. PSORIASIS
Psoriasis is a common, genetically determined, inflammatory and hyperproliferative skin disease. Psoriasis is a hereditary disorder of skin with several clinical expressions. The most frequent type is psoriasis vulgaris, which occurs as chronic, recurring, scaling papules and plaques.

4. CLASSIFICATION Psoriasis vulgaris Psoriatic erythroderma
Acute guttate
Chronic plaque
Inverse
Palmoplantar
Psoriatic erythroderma
Pustular psoriasis
Psoriatic arthritis

6. PSORIASIS VULGARIS

7. Epidemiology
Age of onset: May begin at any age. Uncommon < 10 years. Early: Peak incidence at 22.5 years of age (in children the mean age of onset is 8 years). Late: About age 55.
Sex: Equal incidence.
Race: Low incidence in West Africans, Japanese; very low incidence or absence in North and South American Indians.
Heredity: Polygenic trait. HLA-B13, B17, Bw57, HLA-Cw6 ( aerlier age of onset and with a positive family history)
Triggering Factors: Physical trauma (Koebner’s phenomenon), infections (acute streptococcal), stress, drugs ( glucocorticoids, lithium, antimalarials, interferon, beta-adrenergic blockers), heavy alcohol, smoking
Comorbid disease: Psoriatic arthritis, Crohn’s disease, cancer, depression, non-alcoholic fatty liver disease, metabolic syndrome (or components of it), cardiovascular disorders.

8. Pathogenesis
A chronic inflammatory disorder with polygenic predisposition combined with triggering environmental factors such as trauma,infection, or medication.
Psoriasis is a T-lymphocyte-mediated autoimmune disease (mixed Th1 and Th17 disease). T cells and cytokines play a pivotale role ( overexpression of type 1 cytokines like IL-1, IL-6, IL-8, IL-12, IFN gamma and TNF alpha )
The underlying pathophysiology involves epidermal proliferation and differentiation, angiogenesis and the cellular immune system.
Dysregulated interactions of innate and adaptive components of the immune system with resident cutaneous cell types.
1) Cross-talk between innate (macrophages, mast cells, granulocytes) and adaptive immunity( Tcells)
2) Interleukin-23 / Th 17 axis
3) Effect on resident T cells of the skin (antimicrobial peptides, cytokines and chemokines secreted by keratinocytes act as chemoattractants for infiltrating immune cells)
4)Effect on vascular endothelial cells ( the inflammatory milieu leads to induction and activation of a range of pro-angiogenic factors – VEGF - , TNF alpha-governed pro-inflammatory environment in psoriatic skin induces endothelial adhesion molecules which facilitate the recruitement of circulating leucocytes in psoriatic skin.

11. Development of psoriatic lesions
Development of psoriatic lesions. This figure depicts the transition from normal skin to fully developed
lesion described in the text. Normal skin from a healthy individual (panel A) contains epidermal Langerhans cells,
scattered immature dendritic cells (D), and skin-homing memory T cells (T) in the dermis. Normal-appearing skin
from a psoriatic individual (panel B) manifests slight capillary dilatation and curvature, and a slight increase in the
numbers of dermal mononuclear cells and mast cells (M). A slight increase in epidermal thickness is usually present.
In chronic plaque psoriasis, the intensity of these changes may depend on distance from an established lesion. The
transition zone of a developing lesion (panel C) is characterized by progressive increases in capillary dilatation and
tortuosity, numbers of mast cells, macrophages (MP), and T cells, and mast cell degranulation (small arrows). In the
epidermis, there is increasing thickness with increasingly prominent rete pegs, widening of the extracellular spaces,
transient dyskeratosis, spotty loss of the granular layer, and parakeratosis. Langerhans cells (L) begin to exit the epidermis,
and inflammatory dendritic epidermal cells (I) and CD8+ T cells (8) begin to enter the epidermis. The fully developed
lesion (panel D) is characterized by fully developed capillary dilatation and tortuosity with a tenfold increase in blood
flow, numerous macrophages underlying the basement membrane, and increased numbers of dermal T cells (mainly
CD4+) making contact with maturing dermal dendritic cells (D). The epidermis of the mature lesion manifests markedly
increased (approximately tenfold) keratinocyte hyperproliferation extending to the lower suprabasal layers, marked
but not necessarily uniform loss of the granular layer with overlying compaction of the stratum corneum and parakeratosis,
increased numbers of CD8+ T cells, and accumulation of neutrophils in the stratum corneum (Munro’s microabscesses

12. Physical examination
Acute Guttate Type: Eruption of small salmon-pink papules (guttate: Latin gutta, “drop”), with or without scales, disseminated, generalized, mainly on the upper trunk, strongly associated with streptococcal throat infection, frequent in young adults and children
Chronic Stable (plaque) Type: Sharply marginated, dull-red plaques with loosely adherent, lamelar, silvery-white scales. Single lesion or lesions localized to one or more predilection sites: elbows, knees, sacral-gluteal region, scalp, plm/soles. Sometimes only regional involvement(scalp), often generalized.
Special Sites
Palms and Soles
Scalp
Inverse Psoriasis (perianal, genital and body folds)
Nails: pitting, subungual hyperkeratosis, onycholysis, the oil spot (pathognomonic)

13. Laboratory examinations
Dermatopathology
Culture: Throat culture

14. Palmoplantar psoriasis
Chronic, relapsing eruption limited to palms and soles. Numerous very typical sterile, yellow, deep-seated pustules that evolve into dusky-red crusts.
Incidence: Low as compared to psoriasis vulgaris
Age of onset: 50 to 60 years. More common in females (4:1)
Symptoms: Stinging, burning, itching. Eruptions come and go, in waves.
Differential diagnosis: Tinea manus, tinea pedis, dyshidrotic eczema, contact dermatitis, HSV infection.
Course: Persistent for years and characterized by unexplained remissions and exacerbations.

15. Generalized acute pustular psoriasis (Von Zumbusch)
This disorder can be a life-threatening medical problem with an abrupt onset. It starts with a burning fiery-red diffuse erythema that spreads in hours with pinpoint pustules appearing in clusters. Fever, weakness, severe malaise, fast pulse, leukocytosis, shedding of nails, hair loss, skin tenderness
Special types: Impetigo herpetiformis, acrodermatitis continua of Hallopeau

16. Psoriatic arthritis Rare before age 20
Sero(-), “distal”, asymmetric oligoarthritis
Mutilating arthritis (bone erosion, osteolysis or ankylosis.
“Axial” (sacroiliac, hip, cervical)
Dactylitis (sausage fingers)
May be present (in 10% of patients) without any visible psoriasis
Often psoriatic involvement of fingertips and periungual skin
Massive nail involvement by psoriasis is frequent

17. 777

19. Management (1) Factors influencing selection of treatment: Age
Type of psoriasis
Site and extent of involvement
Previous treatment
Associated medical disorders

20. Management (2) Localized psoriasis Topical glucocorticoids
Intralesional triamcinolone acetonide
Topical anthralin
Topical vitamin D analogues( calcipotriene, 0.005%, ointment and cream)
Topical tacrolimus, 0.1%
Tazarotene ( a topical retinoid, 0.05 and 0.1% gel )
Topical dithranol and coal tar
Topical PUVA, UVB
Salicylic acid
Moisturizing

21. Management (3) Generalized psoriasis Narrow-Band UVB Phototherapy
Oral PUVA Photochemotherapy
Oral Retinoids
Methotrexate
Cyclosporine
Diet
Monoclonal Antibodies and Fusion Proteins: Infliximab, Etanercept, Adalimumab, Ustekinumab (IL-12/23)

23. GEOGRAPHIC TONGUE Also known as benign migratory glossitis
The condition usually presents as asymptomatic erythematous patches with serpiginous borders, resembling a map.
These lesions characteristically have a migratory nature.

25. RELATED PHYSICAL FINDINGS
NAIL CHANGES IN PSORIASIS.

28. Generalized Pustular Psoriasis
is a distinctive characterized by acute variant of psoriasis. Attacks are fever that lasts several days and a sudden generalized eruption of sterile pustules 2–3 mm in diameter.
The pustules are disseminated over the trunk and extremities, including the nail beds, palms, and soles.
The pustules usually arise on highly erythematous skin, first as patches and then becoming confluent as the disease becomes more severe.

29. ERYTHRODERMIC PSORIASIS
generalized form of the disease that affects all body sites, including the face, hands, feet, nails, trunk, and extremities
Erythema is the most prominent feature, and scaling is different
Instead of thick, adherent, white scale there is superficial scaling.
Psoriatic skin is often hypohidrotic due to occlusion of the sweat ducts

31. INVERSE (FLEXURAL) PSORIASIS
lesions may be localized in the major skin folds, such as the axillae, the genito-crural region, and the neck.
Scaling is usually minimal or absent, and the lesions show a glossy sharply demarcated erythema, which is often localized to areas of skin-to-skin contact.
Sweating is impaired in affected areas.

59. SEBORRHEİC DERMATİTİS
SD is a very common chronic dermatosis characterized by redness and scaling and occuring in regions where the sebaceous glands are most active, such as the face and scalp, the presternal area, and the body folds.

60. EPIDEMIOLOGY AND ETIOLOGY
Age of Onset: Infancy (within the first months), puberty, most between 20 and 50 years or older
Infantile SD: Usually begins about one week after birth and may persist for several months
Adult SD: Chronic relapsing course; dandruff ( pityriasis capitis simplex), non-purulent otitis externa, intertrigo
Sex: More common in males
Predisposing and Exacerbating Factors: Hereditary diathesis, parkinson’s disease, some neuroleptic drugs, emotional stress, HIV disease

61. PATHOGENESİS
1) Immune responses to Malassezia furfur (P.ovale): Part of the normal resident skin flora. Studies on the cellular immunity have yielded contradictory results. The inflammation may be irritant ? caused by toxic metabolites, lipase and reactive oxygen species.
2) Active sebaceous glands: Often associated with sebum overproduction.
3) Abnormal composition of the skin surface lipids ( increased triglycerides and cholesterol, decreased squalene and FFA ) and imbalance of the microbial flora

62. HİSTORY AND SKİN LESİONS
Gradual onset
Seasonal variations: Worse in winter, sunlight ( dual effect)
Pruritus is variable, often increased by perspiration
Hairy areas of head, face, trunk, body folds, genitalia

63. COURSE AND PROGNOSIS
The condition improves in the summer and flares in the fall.
Recurrences and remissions
Infantile and adolescent SD disappears with age.
Differential diagnosis: Atopic dermatitis, irritant diaper dermatitis, psoriasis, langerhans-cell hystiocytosis, Leiners’ disease, Wiskott Aldrich syndrome

64. MANAGEMENT
This chronic disorder requires initial therapy followed by chronic maintenance therapy
Initial topical therapy: Glucocorticoid cream or lotion, ketoconazole cream, pimecrolimus cream, tacrolimus ointment, medicated shampoos (selenium sulfide, zinc pyrithione, ketoconazole, tar)
Systemic therapy: Itraconazole, fluconazole
Maintenance therapy