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Clinical Patterns of Skin Presentation

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PSORIASIS VULGARIS, CHRONIC STATIONARY PSORIASIS, PLAQUE-TYPE PSORIASIS - the most common form of psoriasis ( 90 %) - Red, scaly, symmetrically distributed plaques predilection : extensor aspects of the extremities, particularly the elbows and knees, along with scalp, lower lumbosacral, buttocks, and genital involvement (Other umbilicus & the intergluteal cleft) - psoriasis geographica : single small lesions may become confluent, forming plaques in which the borders resemble a land map. - psoriasis gyrata : lesions may extend laterally & become circinate because of the confluence of several plaques. - annular psoriasis : partial central clearing, resulting in ringlike lesions. - Rupioid psoriasis : lesions in the shape of a cone or limpet. - Ostraceous psoriasis : ring-like, hyperkeratotic concave lesion, resembling an oyster shell. - elephantine psoriasis : uncommon form, thickly scaling, large plaques, usually on the lower extremities.

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GUTTATE (ERUPTIVE) PSORIASIS - Guttate psoriasis (from the Latin gutta, meaning "a drop") is characterized by eruption of small (0.5 to 1.5 cm in diameter) papules over the upper trunk and proximal extremities - It typically manifests at an early age and as such is found frequently in young adults. - strongest association to HLA-Cw6,& streptococcal throat infection frequently precedes or is concomitant with the onset or flare of guttate psoriasis. SMALL PLAQUE PSORIASIS - Small plaque psoriasis resembles guttate psoriasis clinically, but can be distinguished by its onset in older patients, by its chronicity, and by having somewhat larger lesions (typically 1 to 2 cm) that are thicker and scalier than in guttate disease. - common adult-onset presentation of psoriasis in Korea and other Asian countries

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Plaque pattern This is the most common type. Lesions are well demarcated and range from a few millimetres to several centimetres in diameter (Fig. 5.3). The lesions are pink or red with large dry silvery-white polygonal scales (like candle grease). The elbows, knees, lower back and scalp are sites of predilection (Fig. 5.4).

Psoriasis of the submammary, axillary and anogenital folds is not scaly (BERSISIK) although the glistening sharply demarcated (dibatasi)red plaques (Fig. 5.9), often with fissuring in the depth of the fold, are still readily recognizable. Flexural psoriasis is most common in women and in the elderly, and is more common among HIV-infected individuals than uninfected ones

dapat disebabkan oleh pengobatan topikal terlalu kuat atau oleh penyakitnya sendiri yang meluas. Bentuk ini dapat juga ditimbulkan oleh infeksi, hipokalsemia, obat antimalaria, tar dan penghentian kortikosterid, baik topikal maupun sistemik. Biasanya lesi yang khas untuk psoriasis tidak tampak lagi karena terdapat eritema dan skuama tebal universal. Ada kalanya lesi psoriasis masih tampak samar-samar, yakni lebih eritematosa dan kulitnya lebih meninggi. Psoriatic erythroderma represents the generalized form of the disease that affects all body sites, including the face, hands, feet, nails, trunk, and extremities.

Ada dua pendapat mengenai psoriasis pustulosa, pertama dianggap sebagai penyakit tersendiri, kedua dianggap sebagai varian psoriasis. Terdapat dua bentuk psoriasis pustulosa, bentuk lokalisata dan generalisata. Bentuk lokalisata contohnya psoriasis pustulosa palm-plantar (Barber) yang menyerang telapak tangan dan kaki serta ujung jari. Sedangkan bentuk generalisata, contohnya psoriasis pustulosa generalisata akut (von Zumbusch) jika pustula timbul pada lesi psoriasis dan juga kulit di luar lesi, dan disertai gejala sistemik berupa panas / rasa terbakar.

Presents dengan plak eritematosa dengan skala berminyak lokal ke daerah-daerah seboroik (kulit kepala, glabella, lipatan nasolabial, area perioral dan presternal, dan area intertriginosa).

(L40.5) involves joint and connective tissue inflammation. Psoriatic arthritis can affect any joint but is most common in the joints of the fingers and toes. This can result in a sausageshaped swelling of the fingers and toes known as dactylitis. Psoriatic arthritis can also affect the hips, knees and spine (spondylitis). About 10-15% of people who have psoriasis also have psoriatic arthritis.

Psoriasis plak Psoriasis arthritis

Up to 10-20% of patients with plaque psoriasis also experience psoriatic arthritis. A population-based study by Wilson et al that spanned more than 30 years reported that less than 10% of psoriasis patients develop clinically recognized psoriatic arthritis. The clinical features that were associated with an increased chance of leading to psoriatic arthritis were reported as being scalp lesions, nail dystrophy, and intergluteal or perianal psoriasis.1

DEFINISI Artritis Proriatik (Psoriatic arthritis) adalah suatu peradangan sendi (artritis) yang terjadi pada orang-orang yang menderita psoriasis pada kulit atau kuku. Penyakit ini mirip dengan artritis rematoid, tetapi tidak menghasilkan antibodi spesifik seperti halnya artritis rematoid.

Psoriatic arthritis (L40.5) involves joint and connective tissue inflammation. Psoriatic arthritis can affect any joint but is most common in the joints of the fingers and toes. This can result in a sausage-shaped swelling of the fingers and toes known as dactylitis. Dactylitis can occur in seronegative arthropathies, such as psoriatic arthritis and ankylosing spondylitis, in sickle-cell disease as result of a vasoocclusive crisis with bone infarcts, and in infectious conditions including tuberculosis and leprosy. Spondyloarthropathies are inflammatory joint diseases of the vertebral column[1] associated with the MHC class I molecule HLA-B27. The term seronegative spondylarthropathy is used by medical practitioners because this set of conditions may mimic rheumatoid diseases such as rheumatoid arthritis, but serological (blood) tests are typically negative for rheumatoid factor (RhF).

Rheumatoid factor (RF or RhF) is an autoantibody (antibody directed against an organism's own tissues) most relevant in rheumatoid arthritis. It is an antibody against the Fc portion of IgG, which is itself an antibody. RF and IgG join to form immune complexes which contribute to the disease process.[citation needed]

Related Physical Findings

a. NAIL CHANGES IN PSORIASIS - Nail pitting : the commonest,fingers > toes, 0.5 - 2.0 mm, single or multiple,results in pitting due to defective keratinization. - deformity of the nail plate (onychodystrophy) include leukonychia,crumbling nail, and red spots in the lunula. - Oil spots and salmon patches are translucent, yellow-red discolorations observed beneath the nail plate often extending distally toward the hyponychium, due to psoriasiform hyperplasia, parakeratosis, microvascular changes, and trapping of neutrophils in the nail bed. - Subungual hyperkeratosis is due to hyperkeratosis of the nail bed and is often accompanied by onycholysis (separation of the nail plate from the nail bed), which usually involves the distal aspect of the nail. - Anonychia is total loss of the nail plate.

Nails are made up of cells that are cornified, which means they have produced large amounts of a PROT, fibrous protein called keratin. In addition, cornified cells no longer undergo any metabolic processes and essentially are dead cells. The nail lies on top of, and is attached to, the nail bed, which is made up of cells that metabolize and divide very slowly. Deformities of the nail are often caused by infection of the nail bed or deformity in underlying bone.

Psoriasis is fundamentally an inflammatory skin condition with reactive abnormal epidermal differentiation and hyperproliferation. Current research suggests that the inflammatory mechanisms are immune based and most likely initiated and maintained primarily by T cells in the dermis.

In this model, antigen-presenting cells in the skin, such as Langerhans cells, are believed to migrate from the skin to regional lymph nodes, where they interact with T cells. Presentation of an as yet unidentified antigen to the T cells, as well as a number of co-stimulatory signals, triggers an immune response, leading to Tcell activation and the release of cytokines. Co-stimulatory signals are initiated via the interaction of adhesion molecules on the antigen-presenting cells, such as lymphocyte functionassociated antigen (LFA)3 and intercellular adhesion molecule-1, with their respective receptors CD2 and LFA-1 on T cells. These T cells are released into the circulation and traffic back into the skin. Reactivation of T cells in the dermis and epidermis and the local effects of cytokines such as tumor necrosis factor lead to the inflammation, cell-mediated immune responses, and epidermal hyperproliferation observed in persons with psoriasis.

The discovery of an interleukin (IL)12-related cytokine, IL-23, was recognized for its involvement in the establishment of chronic inflammation and in the development of a T helper (Th)cell subset producing IL-17, designated Th17. These cells are distinct from Th1 and Th2 populations. Th17 cells are now recognized as a third T-effector cell subset, and the IL-23/IL-17 pathway has been implicated in the induction and progression of a number of inflammatory diseases, including psoriasis.3

Both genetic and environmental factors have been implicated in the pathophysiology of psoriasis. Genetic factors: HLA-B13, -B17, and -Cw6 are all associated with plaque psoriasis. Multifactorial inheritance mechanisms and etiologies without any genetic component have not yet been excluded, although many families appear to exhibit autosomal dominant patterns of inheritance with decreased penetrance. Studies of twin siblings have shown concordant disease in 73% of monozygotic twins compared with 20% in dizygotic twins. Several putative genetic susceptibility loci have also been identified, including psoriasis susceptibility 1 (PSOR1) on chromosome 6, which is associated with up to 50% of cases. Six other psoriasis susceptibility loci (PSOR2, PSOR3, PSOR4, PSOR5, PSOR6, PSOR7) have been discovered, as well as the transcription factor RUNX1. While this certainly points to genetic mechanisms, the absence of 100% concordance among monozygotes suggests that environmental factors must play a role in the pathophysiology of this disease. Environmental factors: Infection and a number of physical agents (eg, HIV infection, alcoholism, smoking, UV light) all can affect the course, duration, and clinical appearance of plaque psoriasis. See Causes for more details on the role of environmental factors.

Causes Exacerbating causes of plaque psoriasis can be divided into local and systemic factors. Local factors

Trauma: All types of trauma have been associated with the development of plaque psoriasis (eg, physical, chemical, electrical, surgical, infective, and inflammatory types of injury). Even excessive scratching can aggravate or precipitate localized psoriasis. The development of psoriatic plaques at a site of injury is known as the Koebner reaction. See History for more details on the Koebner reaction. Sunlight: Most patients generally consider sunlight to be beneficial for their psoriasis. Most report a decrease in illness severity during the summer months or periods of increased sun exposure; however, a small minority find that their symptoms are aggravated by strong sunlight, and these individuals actually experience a worsening of their disease in the summer. A severe sunburn can lead to an exacerbation of plaque psoriasis via the Koebner reaction.

Systemic factors Infection: Pharyngeal streptococcal infections have been shown to produce a clinically distinctive disease flare known as guttate psoriasis. Some evidence suggests that subclinical streptococcal colonization or overgrowth could be responsible for refractory plaque psoriasis. HIV infection: An increase in psoriasis activity has been observed in patients who are or become infected with HIV. The extent and severity of skin disease initially appears to parallel the disease stage. Psoriasis often becomes less active in advanced HIV infection. Drugs: A number of medications have been shown to cause an exacerbation of psoriasis. Lithium and withdrawal from systemic corticosteroids are well known to cause flares of disease. Beta-blockers, antimalarials, and nonsteroidal antiinflammatory drugs (NSAIDs) have also been implicated.

Psychogenic/emotional factors: Many patients report an increase in psoriasis severity with psychological stress. A clear cause-and-effect relationship between disease exacerbation and stress unfortunately has not been proven. Patients may show a decreased capacity to cope with their treatment regimen with higher levels of stress. Pruritus in the setting of increased anxiety or depression may promote scratching and a Koebner reaction. Smoking: An increased risk of chronic plaque psoriasis exists in persons who smoke cigarettes. Alcohol consumption: Alcohol consumption is considered a risk factor for psoriasis, particularly in young to middle-aged males. Endocrinological factors: Psoriasis severity has been noted to fluctuate with hormonal changes. Disease incidence peaks at puberty and during menopause. Pregnant patients' symptoms are more likely to improve than worsen, if any changes occur at all. In contrast, the disease is more likely to flare in the postpartum period, again if any changes occur at all.

* Kursus psoriasis plak tidak dapat diprediksi. Memprediksi durasi penyakit aktif, waktu atau frekuensi kambuh, atau durasi remisi adalah mustahil. Penyakit ini jarang mengancam kehidupan tapi sering adalah keras terhadap pengobatan, dengan relaps terjadi pada kebanyakan pasien. * Baik onset awal dan riwayat keluarga penyakit dianggap indikator prognosis yang buruk. * Beberapa menyarankan stres yang juga dikaitkan dengan prognosis yang kurang baik. * Faktor lingkungan (khususnya sinar matahari dan cuaca hangat) membantu meringankan penyakit dan dianggap menguntungkan. * Methotrexate, PUVA, siklosporin, retinoid oral, dan terapi biologis semua telah membantu mendorong dan mempertahankan remisi dalam kasus yang parah psoriasis plak.

* Pasien pendidikan adalah salah satu fondasi untuk mengelola kronis ini dan biasanya kekambuhan gangguan. Tidak hanya psoriasis dikaitkan dengan morbiditas, perawatan perusahaan juga dapat menyebabkan efek buruk yang signifikan. Pasien harus akrab dengan rincian dalam rangka untuk membuat keputusan yang tepat dan informasi tentang terapi. * National Psoriasis Foundation adalah organisasi luar biasa yang memberikan dukungan untuk pasien dengan psoriasis.