psoriasis Flashcards
Psoriasis cause
multifactorial and not yet fully understood
genetic: associated HLA-B13, -B17
immunological: abnormal T cell activity stimulates keratinocyte proliferation. There is increasing evidence this may be mediated by a novel group of T helper cells producing IL-17,
subtypes of psoriasis
plaque psoriasis: the most common sub-type resulting in the typical well-demarcated red, scaly patches affecting the extensor surfaces, sacrum and scalp
flexural psoriasis: in contrast to plaque psoriasis the skin is smooth
guttate psoriasis: transient psoriatic rash frequently triggered by a streptococcal infection. Multiple red, teardrop lesions appear on the body
pustular psoriasis: commonly occurs on the palms and soles
complications of psoriasis
psoriatic arthropathy (around 10%)
increased incidence of metabolic syndrome
increased incidence of cardiovascular disease
increased incidence of venous thromboembolism
psychological distress
what worsens psoriasis ?
psoriasis may be worsened (e.g. Skin trauma, stress),
triggered (e.g. Streptococcal infection)
or improved (e.g. Sunlight) by environmental factors
trauma
alcohol
drugs: beta blockers, lithium, antimalarials (chloroquine and hydroxychloroquine), NSAIDs and ACE inhibitors, infliximab
withdrawal of systemic steroids
Chronic plaque psoriasis management
a potent corticosteroid applied once daily plus vitamin D analogue applied once daily
Calcipotriene/ calcitriol and tacalcitol
should be applied separately, one in the morning and the other in the evening)
for up to 4 weeks as initial treatment
second-line: if no improvement after 8 weeks then offer:
a vitamin D analogue twice daily
third-line: if no improvement after 8-12 weeks then offer either:
a potent corticosteroid applied twice daily for up to 4 weeks,
or
a coal tar preparation applied once or twice daily
Dithranol
inhibits DNA synthesis
wash off after 30 mins
adverse effects include burning, staining
Secondary care management o f chronic plaque psoriasis ?
phototherapy
narrowband ultraviolet B light is now the treatment of choice. If possible this should be given 3 times a week
photochemotherapy is also used - psoralen + ultraviolet A light (PUVA)
adverse effects: skin ageing, squamous cell cancer (not melanoma)
scalp psoriasis managmnet ?
potent topical corticosteroids used once daily for 4 weeks
if no improvement after 4 weeks then either use a different formulation of the potent corticosteroid (for example, a shampoo or mousse) and/or a topical agents to remove adherent scale (for example, agents containing salicylic acid, emollients and oils) before application of the potent corticosteroid
topical steroids in psoriasis
may lead to skin atrophy, striae and rebound symptoms
the scalp, face and flexures are particularly prone to steroid atrophy so topical steroids should not be used for more than 1-2 weeks/month
we aim for a 4-week break before starting another course of topical corticosteroids
they also recommend using potent corticosteroids for no longer than 8 weeks at a time and very potent corticosteroids for no longer than 4 weeks at a time
Face, flexural and genital psoriasis management
offering a mild or moderate potency corticosteroid applied once or twice daily for a maximum of 2 weeks
Psoriatic arthropathy
precedes the development of skin lesions. Around 10-20% of patients with skin lesions develop an arthropathy
pattern of psoriatic arthropathy ?
symmetric polyarthritis
asymmetrical oligoarthritis: typically affects hands and feet (20-30%)
sacroiliitis
DIP joint disease (10%)
arthritis mutilans (severe deformity fingers/hand, ‘telescoping fingers’)
periarticular disease - tenosynovitis and soft tissue inflammation resulting in:
enthesitis: inflammation at the site of tendon and ligament insertion e.g. Achilles tendonitis, plantar fascitis
tenosynovitis: typically of the flexor tendons of the hands
dactylitis: diffuse swelling of a finger or toe
nail changes
pitting
onycholysis
mx of psoriatic arthropathy
mild peripheral arthritis/mild axial disease may be treated with ‘just’ an NSAID, rather than all patients being on disease-modifying therapy as with RA
if more moderate/severe disease then methotrexate is typically used as in RA
use of monoclonal antibodies such as ustekinumab (targets both IL-12 and IL-23) and secukinumab (targets IL-17)
apremilast: phosphodiesterase type-4 (PDE4) inhibitor → suppression of pro-inflammatory mediator synthesis and promotion of anti-inflammatory mediators
has a better prognosis than RA
