Psoriasis

It is a chronic inflammatory skin disorder clinically characterized by erythematous, sharply demarcated papules and rounded plaques, covered by silvery micaceous scale. The skin lesions of psoriasis are variably pruritic. Traumatized areas often develop lesions of psoriasis (Koebner or isomorphic phenomenon). Additionally, other external factors may exacerbate psoriasis including infections, stress, and medications (lithium, beta blockers, and antimalarials
Clinical features
Sharply demarcated, erythematous plaques with mica-like scale; predominantly elbows, knees, and scalp; atypical forms may localize to intertriginous areas; eruptive forms may be associated with infection.
May be aggravated by certain drugs, infection; severe forms seen associated with HIV
he most common variety of psoriasis is called plaque-type. Patients with plaque-type psoriasis will have stable, slowly enlarging plaques, which remain basically unchanged for long periods of time. The most commonly involved areas are the elbows, knees, gluteal cleft, and the scalp. Involvement tends to be symmetric. Plaque psoriasis generally develops slowly and runs an indolent course. It rarely remits spontaneously. Inverse psoriasis affects the intertriginous regions including the axilla, groin, submammary region, and navel; it also tends to affect the scalp, palms, and soleGuttate psoriasis (eruptive psoriasis) is most common in children and young adults. It develops acutely in individuals without psoriasis or in those with chronic plaque psoriasis. Patients present with many small erythematous, scaling papules, frequently after upper respiratory tract infection with -hemolytic streptococci. The differential diagnosis should include pityriasis rosea and secondary syphilis.The other types of psoriasis is pustular psoriasis. About half of all patients with psoriasis have fingernail involvement, appearing as punctate pitting, onycholysis, nail thickening, or subungual hyperkeratosis. About 5–10% of patients with psoriasis have associated arthralgias, and these are most often found in patients with fingernail involvement. Although some have the coincident occurrence of classic rheumatoid arthritis (Chap. 314), many have psoriatic arthritis that falls into one of three types: (1) asymmetric inflammatory arthritis most commonly involving the distal and proximal interphalangeal joints and less commonly the knees, hips, ankles, and wrists; (2) a seronegative rheumatoid arthritis–like disease; a significant portion of these patients go on to develop a severe destructive arthritis; or (3) disease limited to the spine (psoriatic spondylitis).
Treatment:
Treatment of psoriasis depends on the type, location, and extent of disease. All patients should be instructed to avoid excess drying or irritation of their skin and to maintain adequate cutaneous hydration. Most patients with localized, plaque-type psoriasis can be managed with midpotency topical glucocorticoids, although their long-term use is often accompanied by loss of effectiveness (tachyphylaxis) and atrophy of the skin. A topical vitamin D analogue (calcipotriene) and a retinoid (tazarotene) are also efficacious in the treatment of limited psoriasis and have largely replaced other topical agents such as coal tar, salicylic acid, and anthralin.
Ultraviolet light, natural or artificial, is an effective therapy for many patients with widespread psoriasis. Ultraviolet B (UV-B) light, narrowband UV-B, and ultraviolet A (UV-A) spectrum with either oral or topical psoralens (PUVA) are also extremely effective. The long-term use of UV light may be associated with an increased incidence of non-melanoma and melanoma skin cancer. UV light therapy is contraindicated in patients receiving cyclosporine and should be used with great care in all immunocompromised patients due to an increased risk of developing skin cancers.
The FDA approved systemic agents used for psoriasis are methotrexate, Acitretin & Cyclosporine.Etanercept & Infliximab are monoclonal antibodies against TNF alpha which are used in psoriasis

Contact Dermatitis

Contact dermatitis is an inflammatory process in skin caused by an exogenous agent or agents that directly or indirectly injure the skin. This injury may be caused by an inherent characteristic of a compound—irritant contact dermatitis (ICD). An example of ICD would be dermatitis induced by a concentrated acid or base. Agents that cause allergic contact dermatitis (ACD) induce an antigen-specific immune response (poison ivy dermatitis). The clinical lesions of contact dermatitis may be acute (wet and edematous) or chronic (dry, thickened, and scaly), depending on the persistence of the insult
Following types of contact dermatitis is commonly seen in routine practice
Irritant contact dermatitis
Allergic contact dermatitis

Treatment:

If contact dermatitis is suspected and an offending agent is identified and removed, the eruption will resolve. Usually, treatment with high-potency topical glucocorticoids is enough to relieve symptoms while the dermatitis runs its course. For those patients who require systemic therapy, daily oral prednisone beginning at 1 mg/kg, but usually 60 mg/d, is sufficient.
Identification of a contact allergen can be a difficult and time-consuming task. Patients with dermatitis unresponsive to conventional therapy or with an unusual and patterned distribution should be suspected of having ACD. They should be questioned carefully regarding occupational exposures and topical medications. Common sensitizers include preservatives in topical preparations, nickel sulfate, potassium dichromate, thimerosal, neomycin sulfate, fragrances, formaldehyde, and rubber-curing agents. Patch testing is helpful in identifying these agents but should not be attempted on patients with widespread active dermatitis or on those taking systemic glucocorticoids.

ECZEMA & DERMATITIS

Eczema is a type of dermatitis and these terms are often used synonymously (atopic eczema or atopic dermatitis). Eczema is a reaction pattern that presents with variable clinical findings and the common histologic finding of spongiosis (intercellular edema of the epidermis)
Atopic dermatitis (AD) is the cutaneous expression of the atopic state, characterized by a family history of asthma, allergic rhinitis, or eczema. The prevalence of AD is increasing worldwide.

Atopic dermatitis (AD) is clinically charecterized by

1. Pruritus and scratching


2. Course marked by exacerbations and remissions


3. 4. Personal or family history of atopy (asthma, allergic rhinitis, food allergies, or eczema)

4. Lesions typical of eczematous dermatitis

5. Clinical course lasting longer than 6 weeks

6. Lichenification of skin

The etiology of AD is only partially defined, but there is a clear genetic predisposition. When both parents are affected by AD, >80% of their children manifest the disease. When only one parent is affected, the prevalence drops to slightly over 50%. Patients with AD may display a variety of immunoregulatory abnormalities including increased IgE synthesis, increased serum IgE, and impaired delayed-type hypersensitivity reactions.

Treatment


Therapy of AD should include avoidance of cutaneous irritants, adequate moisturizing through the application of emollients, judicious use of topical anti-inflammatory agents, and prompt treatment of secondary infection. Patients should be instructed to bathe no more often than daily using warm or cool water, and to use only mild bath soap. Immediately after bathing while the skin is still moist, a topical anti-inflammatory agent in a cream or ointment base should be applied to areas of dermatitis, and all other skin areas should be lubricated with a moisturizer.
Low- to midpotency topical glucocorticoids are employed in most treatment regimens for AD.

Secondary infection of eczematous skin may lead to exacerbation of AD. Crusted and weeping skin lesions may be infected with S. aureus. When secondary infection is suspected, eczematous lesions should be cultured and patients treated with systemic antibiotics active against S. aureus.

Control of pruritus is essential for treatment, since AD often represents "an itch that rashes." Antihistamines are most often used to control pruritus, and mild sedation may be responsible for their antipruritic action. Sedation may also limit their usefulness; however, when used at bedtime, sedating antihistamines may improve the patient's sleep.

Treatment with systemic glucocorticoids should be limited to severe exacerbations unresponsive to topical therapy

Acne treatment

Patients with moderate to severe acne with a prominent inflammatory component will benefit from the addition of systemic therapy, such as tetracycline in doses of 250–500 mg bid, or doxycycline, 100 mg bid. Minocycline may also be useful. Such antibiotics appear to have an anti-inflammatory effect independent of their antibacterial effect
Female patients who do not respond to oral antibiotics may benefit from hormonal therapy. Women placed on oral contraceptives containing ethinyl estradiol and norgestimate have demonstrated improvement in their acne when compared to a placebo control.
Patients with severe nodulocystic acne unresponsive to the therapies discussed above may benefit from treatment with the synthetic retinoid, isotretinoin. Its dose is based on the patient's weight, and it is given once daily for 5 months. Results are excellent in appropriately selected patients. Its use is highly regulated due to its potential for severe adverse events, primarily teratogenicity.

Acne Vulgaris

Acne vulgaris is a self-limited disorder primarily of teenagers and young adults
The permissive factor for the expression of the disease in adolescence is the increase in sebum production by sebaceous glands after puberty. The activity of bacteria (Proprionobacterium acnes) within the comedones releases free fatty acids from sebum, causes inflammation within the cyst, and results in rupture of the cyst wall. An inflammatory foreign-body reaction develops as result of extrusion of oily and keratinous debris from the cyst.The clinical hallmark of acne vulgaris is the comedone, which may be closed (whitehead) or open (blackhead).
The earliest lesions seen in adolescence are generally mildly inflamed or noninflammatory comedones on the forehead. Subsequently, more typical inflammatory lesions develop on the cheeks, nose, and chin The most common location for acne is the face, but involvement of the chest and back is common. Most disease remains mild and does not lead to scarring. A small number of patients develop large inflammatory cysts and nodules, which may drain and result in significant scarring. Regardless of the severity, acne may affect a patient's quality of life. If adequately treated, this may be a transient effect. In the case of severe, scarring acne, the effects can be permanent and profound. Early therapeutic intervention in severe acne is essential.
Treatment of Acne vulgaris
Treatment of acne vulgaris is directed toward elimination of comedones by normalization of follicular keratinization, decreasing sebaceous gland activity, decreasing the population of P. acnes, and decreasing inflammation. Minimal to moderate, pauci-inflammatory disease may respond adequately to local therapy alone. Although areas affected with acne should be kept clean, overly vigorous scrubbing may aggravate acne due to mechanical rupture of comedones. Topical agents such as retinoic acid, benzoyl peroxide, or salicylic acid may alter the pattern of epidermal desquamation, preventing the formation of comedones and aiding in the resolution of preexisting cysts. Topical antibacterial agents such as azelaic acid, topical erythromycin (with or without zinc), or clindamycin are also useful adjuncts to therapy