Psoriasis Flashcards

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1
Q

Clinical summary of psoriasis

A

-Rash characterised by scaly red plaques, with a predilection for the extensor surfaces, the nails and scalp
-Runs a waxing and waning course and is associated in around 5-30% of patients with an inflammatory polyarthropathy, and an increased risk of the metabolic syndrome and cardiovascular disease.
-Itch is common but not as severe as in disorders such as eczema or scabies.
-Highly hereditable, cannot be cured, but can be managed with simple emollients through to potent immunosuppressives and ‘biologics’

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2
Q

Histological features of psoriasis

A

-Epidermal hyperproliferation (‘keratinocyte problem’)
-A pronounced inflammatory infiltrate (‘immune system problem’)

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3
Q

Pathogenesis of psoriasis

A

-Epidermal differentiation deranged (time taken shortened= cannot mature properly so rushed in immature state) with hyperproliferation (with lots of mitoses evident)
-Relative absence of the granular layer with retention of nuclei within the stratum corneum (parakeratosis)
-Acanthosis (thickening of the viable cell layers), with elongation of the rete ridges
-Inflammation: oedema in the dermis, a pronounced T-cell rich inflammatory infiltrate in dermis, together with polymorphs in the dermis and in the epidermis.
=In the epidermis polymorphs may form little micro-abscesses (Munro micro-abscesses).
=Collections of polymorphs visible to the naked eye (i.e sterile pustules= pustular psoriasis)
=Capillaries (in the dermis) are increased in number and length

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4
Q

What causes psoriasis?

A

-Hereditable
=If both parents have psoriasis, the risk for each child developing psoriasis is 40-50%.
=If one parent is affected, the risk is ~15%
-Candidate genes involved in:
=Innate immunity
=Adaptive immunity
=The interface between the innate and the adaptive immune system
=Genes involved in skin barrier function and keratinocyte signalling pathways
=Various cytokines (e.g.Il-23) seem causally involved (i.e. if they are blocked, the disease improves)

-Key players involved in the pathogenesis of psoriasis include:
=Antigen presenting cells, T cells,, HLA (particularly HLA-Cw6)
=Tumour necrosis factor (TNF), NF-𝞳B, interferons
-Although psoriasis has been labelled an autoimmune disorder no autoantigen has been identified.

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5
Q

Epidemiology of psoriasis

A

~2% of the European population, ~5% North America.
-Lower in Africans, Norwegian Lapps and some Asians, with rates in the order of 0.5%
-Psoriatic arthritis has been reported to affect between 5% and 30% of patients with psoriasis

-Type 1: starts in the later teenage years/early adulthood and there is more likely to be a family history and positivity for certain HLA groups (HLA-Cw6)
-Type 2: Onset in the 5th or 6th decades

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6
Q

Triggering factors of psoriasis

A

-Streptococcal sore throat (T-cell role?)
=Other infections may also precipitate exacerbations of psoriasis: HIV aggravates psoriasis, and undiagnosed HIV may present with worsening of a known case of psoriasis
-Certain drugs, such as lithium, betablockers, interferon-α and chloroquine
-Bone marrow transplant
-Obesity, smoking and alcohol
-Heavy alcohol consumption= worsening of the disease, and smoking is in particular associated with some types of pustular psoriasis.
-Koebner phenomenon (psoriatic plaque at site of skin insult with 2 week lag)
=sunburn, surgery, viral exanthema, and acupuncture needles
-Psychogenic factors: stress

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7
Q

Types of psoriasis

A

-Stable plaque psoriasis
-Guttate psoriasis
-Erythrodermic psoriasis
-Pustular psoriasis
-Flexural, or inverse, psoriasis
-Palmoplantar psoriasis
-Nail psoriasis

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8
Q

Describe Stable Chronic Plaque Psoriasis

A

-Psoriatic plaque: scaly red well demarcated plaque, most commonly seen on the extensor surfaces, such as the elbows or knees= stable chronic plaque psoriasis (if stable over years)

-Erythema can be obscured by an excess of silvery scale
=fraction of a millimetre through to barnacle like lesions that could rarely be up to 1cm thick.
=If the scales removed with keratolytic agents, such as salicylic acid, or the scale rendered less visible with emollients, then the underlying erythema is exposed and is more obvious.
=In darker skin tones, erythema may be less obvious but the clues to the diagnosis lie in the distribution and scale of the plaques

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9
Q

Describe guttate psoriasis

A

-Characterised by up to several hundred small lesions, a centimetre or less, and follows a streptococcal sore throat by 2-3 weeks (multiple teardrop lesions)
-Rash most common on the trunk, and less often as extensive on the face or the limbs.
-Often the first episode of psoriasis an individual develops, and is most commonly seen in children and young adults.
-Prophylactic penicillin to avoid sore throat= no rash BUT few people are treated with tonsillectomy or with continuous antibiotics

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10
Q

Describe erythrodermic psoriasis

A

-Any rash that affects 90% or more of the body surface
-Although it is possible to see patients with plaque psoriasis that is this extensive, you may also see patients who just appear to have widespread erythema with or without apparent oedema of their skin, and without much scale.
-Patients with the former are fairly easy to diagnose, whereas if the patient just has erythema, then the differential is that of any cause of erythroderma (if this is the presenting episode of psoriasis, making a firm diagnosis may be impossible, until later).

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11
Q

Describe pustular psoriasis

A

-Microscopic collections of polymorphs (Munromicro-abscesses) in the epidermis.
=If large: visible to the naked eye.

-2 forms: Palmoplantar pustular psoriasis (PPP) and Generalised pustular psoriasis (Von Zumbusch)

-PPP: pustules are found on the palms and soles (and not elsewhere)- could be distinct disorder
-Generalised: widespread or erythrodermic psoriasis and develop thousands of small white sterile pustules across the body.
=can become systemically very ill, with a pyrexia, rigours and severe malaise.

-Plaques of psoriasis that are continually treated with steroids may become pustular.
-Sudden withdrawal of steroids: pustules may develop

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12
Q

Describe flexural/ inverse psoriasis

A

-Psoriasis seems to predominate in the flexures (natal cleft, inframammary, antecubital fossae, axillae etc).
-The rash will be red and shiny, but scale will generally be lacking= smooth

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13
Q

Describe palmoplantar psoriasis

A

Some patients with psoriasis have chronic hyperkeratotic psoriasis without pustules that is often indistinguishable from chronic hand eczema

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14
Q

Describe nail psoriasis

A

-Nail changes= very common in psoriasis
=Pitting of the nail plate (reflecting the site of foci of parakeratosis) in the dorsal nail matrix. An occasional pit is not uncommon in normal people, but patients with psoriasis often have scores of them
=Onycholysis — separation of the distal nail from the nail bed
=Oily spots — a hazy, slightly yellowy/brown appearance of part of the nail.

-Psoriasis can destroy the normal anatomy of the nails

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15
Q

Describe scalp psoriasis

A

-Scalp very commonly affected
-Discrete lesions, and spread beyond the hair line onto the borders of the scalp
-Scales usually adhere to the hair shafts
-Very rarely alopecia may develop under the plaques.
=Topical treatments are hard to apply.
=Scalp psoriasis is rare in those who have lost their hair.
=Itch can be a major problem in psoriasis of the scalp.

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16
Q

Systemic aspects of psoriasis

A

-Joints
=An inflammatory seronegative arthropathy occurs in between 5 and 30% of patients.
=Nail disease is said to be associated with joint disease
=Patients can present with psoriatic arthritis and develop psoriasis later.

-Cardiovascular
=MI, peripheral vascular disease and emboli are more common in those with severe disease (metabolic syndrome?)
=Hypertension, obesity and diabetes should be managed on their merits.
=retinoids increase lipids; ciclosporin may cause hypertension

17
Q

Diagnosis of psoriasis

A

-Clinical diagnosis
-Psoriasis may be itchy (but not as much as atopic dermatitis or scabies for instance), but patients rarely present with itch as their main concern.
-Skin ‘discomfort’ or ‘irritation’ or pain.

-Psoriasis of the scalp or on the face, chest and head may be confused with seborrhoeic dermatitis
-Palmoplantar hyperkeratotic psoriasis is often impossible to distinguish from chronic hand eczema

18
Q

Assessment of disease severity in psoriasis

A

-PASI (psoriasis area severity index): composite score of area, erythema and scaling
=poor statistical reliability

-Standardised photographs; talk to patients
=psoriasis on the hands and on the face (the latter which is usually relatively spared in psoriasis) clearly may impair quality of life more than on the back or the buttocks.
=scalp: heavy dandruff
=genitals: feelings of guilt and concern about sexual transmission

19
Q

Avoiding precipitants in psoriasis

A

-Recurrent guttate psoriasis following streptococcal sore throats =long-term penicillin may be considered/ tonsillectomy
-Smoking and alcohol: heavy drinkers psoriasis is often severe, and many of us thinks psoriasis improves if alcohol consumption is reduced/ Pustular palmoplantar psoriasis is associated with smoking, and there is some evidence that stopping may improve the skin
-Untreated HIV infection is associated with severe psoriasis
-Drugs: lithium, chloroquine, betablockers, antimalarials

20
Q

Active treatments for psoriasis

A

-Stepwise:

-Topical (i.e. creams and ointments)- safest, lowest efficacy
-Ultraviolet radiation (UVR, whether UVB or PUVA) more effective, risk
-‘Older’ systemic agents (e.g. methotrexate, ciclosporin) most effective and toxic
-‘Newer’ systemic agents (e.g. Biologics) expensive

21
Q

Topical treatments in psoriasis

A

-Emollients
=Bland emollient, with or without salicylic acid (breaks down desmosomes between cells of the stratum corneum so hyperkeratotic scale)
=plaques less visible, less uncomfortable and tend to remove scale

-Corticosteroids
=Reduce the thickness of the plaque, reduce some of the scaling, and make the erythema less apparent
=Cutaneous toxicity (local atrophy with telangiectasia and striae; and systemic absorption),
=may lose efficacy over time. =particularly useful for flexural psoriasis and scalp psoriasis

-Vitamin D
=Normalises epidermal differentiation and inhibits epidermal hyperproliferation.
=Vitamin D receptors are members of the nuclear steroid receptor superfamily
=Topical vitamin D analogues are remarkably safe, unless you use more than 100g per week of the cream (when systemic vitamin D effects can occur), and they are frequently combined with topical corticosteroids.

-Anthralin (dithranol) and Tar (historical)

22
Q

Phototherapy in psoriasis

A

-UVB
=Shorter wavelength UVR (sunburn)
=Out-patient department 2 to 3 times a week and are treated over 10 to 15 weeks
=Narrowband UVB: 75% have substantial therapeutic effect.
=Best for small plaque psoriasis, particularly guttate psoriasis
=Risks: sunburn, increase in the rate of non-melanoma skin cancer (no strong evidence)

-PUVA (Psoralen + UVA)
=Administration of a prodrug (psoralen, natural plant product in parsnips, inert) that is activated by UVA
=When distributed systemically is only active in body areas that UVA can get to — the skin and the eyes
=Inhibit proliferation of both keratinocytes and any inflammatory cells present in the skin (mutations if cells replicate)
=Carcinogenic to skin
=Oral/ bath psoralen
=Several times a week over 10 weeks or more.
=Tanned
=PUVA is no longer used as large increase in the incidence of non-melanoma skin cancer (particularly squamous cell carcinoma), and possibly melanoma

23
Q

Methotrexate in psoriasis

A

-Folic acid antagonist =false substrate for dihydrofolate reductase.
=reduces DNA synthesis
=effects are mediated systemically via the immune system

-Administered once weekly (not daily) with a dose of up to 25mg per patient per week
-Side effects: Hepatic fibrosis and cirrhosis (synergistic with alcohol, chronic use)/ Bone marrow inhibition (acute effect)/ Teratogenicity (folate antagonism)/ mutagenic (causes mutations in sperm, and so men wishing to father children should wait 3 months after stopping methotrexate)-
-Immunosuppressive= response to live vaccines may be impaired, the risk of malignancy may be increased, and patients are at increased risk of some infections
-Nausea: this may limit use. It is said that IM weekly injection causes less nausea than weekly oral dosing.
-Monitored with a full blood count, assessment of liver function tests, U+Es (MTX is excreted via the kidney) routinely
-Patients are often treated over many years, and monitoring can be stabilised after 3 to 6 months, often at 3-month intervals.
=Beware of drugs that may interfere with methotrexate metabolism and action (particularly NSAIDs which will displace methotrexate from binding in the blood, and hence increase its toxicity to the bone marrow); and renal disease that impairs methotrexate excretion

24
Q

Describe ciclosporin in psoriasis

A

-Calcineurin inhibitor that blocks T-cell activation.
-Short-term treatment, where it will result in clearing of the disease in over 60% of patients when administered over 3-4months.
=Repeated short courses of ciclosporin (~ 1 per year)

=Toxicities: Nephrotoxicity/ Hypertension/ Increases in the risk of some virally associated cancers (EBV associated lymphoma, HPV associated cervical and anal cancer); and non-melanoma skin cancer
=Common side effects: hypertrichosis and gingival hyperplasia
=Immunosuppressive

25
Q

Describe retinoids in psoriasis

A

-Vitamin A like actions
-Potent morphogens (and are therefore highly teratogenic).
-Acitretin mainly used, long-term

-Side-effects: Teratogenicity/Elevation of triglycerides (and therefore potentially precipitating pancreatitis)/ increase in cardiovascular morbidity/ Mucosal and cutaneous dryness/ hair loss/ Musculoskeletal pain, especially in athletes
-Accumulate in fat, and are eliminated slowly, so women of childbearing potential should not be allowed to conceive for 3 years following acitretin

26
Q

Biologics in psoriasis

A

-Highly effective and expensive
-All parenteral only

-Group 1: including etanercept, infliximab, and adalimumab
=act so as to inhibit the action of tumour necrosis factor (TNFα)
-Group 2: block other cytokine pathways in psoriasis

-Risks: immunosuppression and development of infection
=TNFα inhibitors increase the risk of TB
=some increase the risk of reactivation of rare and potentially fatal viral infections such as that of the JC polyomavirus.
=Some of these agents act so as to worsen other inflammatory disorders (LE, Crohn’s)

27
Q

Other systemic agents in psoriasis

A

-Older agents= fumarates, mycophenolate, and hydroxyurea
-Newer: phosphodiesterase-4 inhibitor, Apremilast.

28
Q

The approach to management of patients with psoriasis

A

-Start with topicals, but unless the disease is very mild, topicals are of very limited efficacy — they are however very safe
=Clearance treatment is generally impossible in primary care because topical agents are of limited efficacy

-If topicals are not enough, consider phototherapy. But will the patient be able to attend 2-3 times per week for an extended period? Do they have transport and will their employer release them? If these options do not work or are impractical, then consider systemics.

-You also have to decide whether a drug is for the short term or the long term.

29
Q

Differentials of psoriasis

A

-Eczema: less well-defined than plaque, dry scaly red skin with scratch marks, skin biopsy
-Pityriasis rosea: Christmas tree distribution
-Seborrheic dermatitis: limited to scalp, eyebrows, chest, fine scales not lamellar
-Tinea corporis: annular scaly patches
-Actinic keratosis: forehand and dorsal aspect of hands, older age
-Lichen planus: violaceous papules, oral mucosa more likely involved (skin biopsy shows lichenoid lymphocyte infiltrates under epidermis)

30
Q

Investigation of associated conditions of psoriasis

A

-Arthritis: joint swelling or pain (PEST tool: psoriasis epidemiological screening tool)
-Cardiovascular risk
-Metabolic syndrome