Pathophysiology.

The pathophysiology of psoriasis is multifactorial and involves

epidermal hyperproliferation, abnormal differentiation of epidermal keratinocytes, and
inflammation with immunologic alterations in the skin. The hyperproliferation is
characterized by increased DNA synthesis and a markedly decreased turnover rate for
the epidermis. Abnormal keratinocyte differentiation involves increased expression of
certain keratins (6 and 16) and a delay in expression of other keratins (1 and 10) that
are expressed in normally differentiating skin. Inflammation results from an infiltrate of
neutrophils in the epidermis and superficial dermis and an infiltrate of T lymphocytes in
the dermis with a predominance of CD8+ cells.
 RISK FACTORS

 Family history. This is one of the most significant risk factors. ...
 Viral and bacterial infections. People with HIV are more likely to develop psoriasis than
people with healthy immune systems
 Stress
 Obesity
 Smoking.

Pharmacotherapy
Medications used in the management of psoriasis include the following:
 Topical corticosteroids (eg, triamcinolone acetonide 0.025-0.1% cream,
betamethasone 0.025-0.1% cream
 Ophthalmic corticosteroids (eg, prednisolone acetate 1% ophthalmic,
dexamethasone ophthalmic)
 Intramuscular corticosteroids (eg, triamcinolone): Requires caution because the
patient may have a significant flare as the medication wears off; 3 months should
elapse between injections
 Intralesional corticosteroids: May be useful for resistant plaques and for the
treatment of psoriatic nails
 Coal tar 0.5-33%
 Keratolytic agents (eg, anthralin, urea): Use of these medications may facilitate
more direct steroid contact with the skin
 Vitamin D analogs (eg, calcitriol ointment, calcipotriene, calcipotriene and
betamethasone topical ointment)
 Topical retinoids (eg, tazarotene aqueous gel and cream 0.05% and 0.1%)
 Antimetabolites (eg, methotrexate)
 Immunomodulators (eg, tacrolimus topical 0.1%, cyclosporine, alefacept,
ustekinumab)
 TNF inhibitors (eg, infliximab, etanercept, adalimumab)
 Phosphodiesterase-4 inhibitors (eg, apremilast)
 Interleukin inhibitors (eg, ustekinumab, secukinumab, tildrakizumab, guselkumab,
risankizumab, ixekizumab, brodalumab) [2, 3, 4, 5]
 Artificial tears
FUNGAL SKIN INFECTIONS

PATHOGENESIS
Compared with bacterial, viral, and parasitic disease, less is known about the
pathogenic mechanisms and virulence factors involved in fungal infections. Analogies to
bacterial diseases come the closest because of the apparent importance of adherence
to mucosal surfaces, invasiveness, extracellular products, and interaction with
phagocytes. Most fungi are opportunists, causing serious disease only in individuals with
impaired host defense systems. Only a few fungi are able to cause disease in previously
healthy persons.

RISK FACTORS:
Immunosuppression and breakdown of anatomical barriers such as the skin are the
major risk factors for fungal infections. Health care workers encounter at-
risk patients in various settings, including AIDS clinics and intensive care,
transplantation and oncology units.

PHARMACOLOGICAL TREATMENT:

Fungal infections are typically treated with antifungal drugs, usually

with antifungal drugs that are applied directly to the affected area (called
topical drugs). Topical drugs may include creams, gels, lotions, solutions, or
shampoos. Antifungal drugs may also be taken by mouth.
Psoriasis pics