Psoriasis

What is psoriasis?
• Psoriasis is a skin disorder that causes skin cells to multiply up to 10
times faster than normal.
• This makes the skin build up into bumpy red patches covered with
white scales.
• Psoriasis is generally thought to be a genetic disease that is triggered
by environmental factors.
• Psoriasis is NOT contagious
Pathogenesis
• NORMAL
• Skin cells rise to the skin surface as they develop where they fall off and
are replaced. This takes about 1 month.
• PSORIASIS
• This process is accelerated and can take just 1 week
• Activation of the immune cells leads inflammation that activates resting
basal keratinocyte stem cells.
 ↑ Activated T-Cells (esp. TH1 and TH17), APCs, and hyperproliferative
keratinocytes.
• The skin cells multiply and accumulate on the surface in silvery scales.
• The pathogenesis of this disease is not completely understood.
• Multiple theories exist regarding triggers of the disease process
including an infectious episode, traumatic insult, and stressful life
event.
• In many patients, no obvious trigger exists at all. However, once
triggered, there appears to be substantial leukocyte recruitment to
the dermis and epidermis resulting in the characteristic psoriatic
plaques.
• Specifically, the epidermis is infiltrated by a large number of activated
T cells, which appear to be capable of inducing keratinocyte
proliferation.
• This is supported by histologic examination and immunohistochemical
staining of psoriatic plaques revealing large populations of T cells
within the psoriasis lesions
• Cells that normally lose their
nuclei in the stratum
granulosum retain their nuclei,
a condition known as
parakeratosis.
• In addition to parakeratosis,
affected epidermal cells fail to
release adequate levels of
lipids, which normally cement
adhesions of corneocytes.
• Subsequently, poorly adherent
stratum corneum is formed
leading to the flaking, scaly
presentation of psoriasis
lesions, the surface of which
often resembles silver scales.
• Well-circumscribed,
erythematous papules
and plaques covered
with silvery scales
 Ocular manifestations
• In addition to skin manifestations, psoriasis may also affect the lid,
conjunctiva, or cornea and give rise to ocular manifestations,
including ectropion and trichiasis, conjunctivitis and conjunctival
hyperemia, and corneal dryness with punctate keratitis and corneal
melt.
• Blepharitis is the most common ocular finding in psoriasis.
• A chronic nonspecific conjunctivitis is fairly common. It usually occurs
in association with eyelid margin involvement.
• Corneal disease is relatively rare. Most often, it is secondary to lid or
conjunctival complications, such as dryness, trichiasis, or exposure.
The most common finding is punctate keratitis.
Histopathological
findings:
• Acanthosis (thickening of epidermis)
• Parakeratotic scaling
• retained nuclei-indicates hyperproliferation
• Stratum spinosum
• increase in size
• Stratum granulosum
• thinned/absent
• Munro micro-abscesses
• neutrophils in stratum corneum
 Psoriasis Triggers
• A number of factors may provoke onset or aggravation of psoriasis.
• Trauma - All types of trauma can lead to the development of plaque psoriasis (eg, physical, chemical, surgical, infective, and
inflammatory). The development of psoriatic lesions at a site of injury is known as the Koebner phenomenon.
• Infection – An acute eruption of guttate psoriasis may be provoked by streptococcal pharyngitis. HIV infection may be
associated with increase in disease severity.
• Drugs . Lithium ,withdrawal of systemic corticosteroids, beta-blockers, antimalarials, and NSAIDs may cause flare of the
disease
• Stress - Many patients report an increase in the psoriasis severity with psychological stress.
• Smoking - Cigarette smoking is associated with an increased risk of chronic plaque psoriasis
• Alcohol - Alcohol is considered a risk factor for psoriasis, particularly in young to middle-aged males.
• Endocrine – the disease state may fluctuate with hormonal changes. Psoriasis may begin during puberty. Pregnancy may
improve the disease. while a flare may occur during post-partum period
 Genetics
• Nine loci identified called Psoriasis Susceptibility 1 through 9 (PSORS).
The major gene is PSORS1, which probably accounts for 35%–50% of
psoriasis heritability.
• It controls genes that affect the major histocompatibility
complex (MHC) and T cells and/or encode skin proteins that are
overabundant in psoriasis.
 Clinical presentation
• Worsening of a long-term erythematous scaly area
• Sudden onset of many small areas of scaly redness
• Recent streptococcal throat infection, viral infection, immunization, use of antimalarial drug, or trauma
• Family history of similar skin condition
• Pain (especially in erythrodermic psoriasis and in some cases of traumatized plaques or in the joints affected
by psoriatic arthritis)
• Pruritus (especially in eruptive, guttate psoriasis)
• Afebrile (except in pustular or erythrodermic psoriasis in which the patient may have high fever)
• Dystrophic nails
• Long-term rash with recent presentation of joint pain
• Joint pain without any visible skin findings
Distribution
• Typically located over the
extensor surfaces and scalp.
• They can grow anywhere, but
most appear on the scalp,
elbows, knees, and lower
back.
Plaque Psoriasis
chronic and recurrent disease characterized by well-circumscribed erythematous
papules/plaques with silvery-white scales often worse in winter (lack of sun and humidity).
Auspitz sign: bleeds from minute points when scale is removed. 85-90% of all psoriatic lesions.
Guttate Psoriasis
Small, drop-shaped salmon colored spots. May be surrounded by a pale halo (halo of
Woronoff). Triggered by bacterial infections such as strep pharyngitis. penicillin V or
erythromycin throat culture (+). UVB phototherapy, sunlight, lubricants, topical steroids.
Inverse Psoriasis
Smooth, red patches in the folds (flexural) of skin near the genitals, breasts, or armpits.
Treatment involves low potency topical corticosteroids, topical vitamin D derivatives such as
calcipotriene (Dovobet = calcipotriene + betamethasone dipropionate), or calcitriol.
Napkin Psoriasis
Begins between the ages of 3 and 6 months and first appears in the Diaper areas red patch
followed by psoriatic papules on the trunk and limbs. The rash responds readily to treatment
and tends to disappear by the age of 1 year
Erythrodermic Psoriasis
Generalized, scaly, red, peeling rash. Related to drugs, infection, and phototoxicity. Associated
with dehydration and electrolyte imbalance. Treat by monitoring fluids and electrolytes, may
require hospitalization. Then give either cyclosporine, acitretin, methotrexate, UV, or biologics.
Pustular Psoriasis
Very rare appears as sudden onset of pus-filled blisters that can be widespread or localized to
the hands or feet. Associated with sudden withdrawal of steroid therapy. Treated with
cyclosporine, methotrexate, acitretin, UV, biologics
Management
• Dependent on severity as determined by Body surface area (BSA)
• Mild (<3% BSA)
 topical steroids, topical vitamin D3 analogues, or a combinations of the two are first line
 topical retinoid ± topical steroid combination, anthralin, and tar are also effective but
tend to be less tolerated than first line therapies
 phototherapy or systemic treatment may be necessary if the lesions are scattered or if it
involves sites that are difficult to treat such as palms, soles, scalp, genitals
• Moderate (3-10% BSA) to Severe (>10% BSA)
 goal is to attain adequate symptom control
 systemic or biological therapy
 Phototherapy
 topical steroid ± topical vitamin D3 analogue as adjunct therapy
Self-Care
• Identify and avoid triggers .
• Limit alcohol consumption and avoid cigarette smoking
• Reduce stress
• Take care of your skin.
• Bathe in warm (not hot) water
• Use fragrance-free Cleansers.
• Do not pick at lesions.
• Choose cotton clothing over synthetic materials