psoriasis + psa Flashcards

1
Q

What is psoriasis?

A

Psoriasis is an autoimmune disease which involves the interaction of T cells with dendritic cells resulting in a papulosquamous skin disorder (red, raised and inflamed fish-scale thick skin).

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2
Q

How is psoriasis presented?

A

It is presented as symmetric, well-demarcated plaques with pruritus. Upon removing the plaques, a pinpoint bleeding can be observed (Auspitz sign).

Common sites include the scalp, elbow and knees followed by hands, feet and trunk.

Nail changes may also occur:
Pitting (tiny holes under nails)
Thickening
Onycholysis (nail elevation)
Subungual hyperkeratosis (chalky build up underneath nails)
trachyonychia (long ridges) and oil spots

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3
Q

List four types of psoriasis.

A

Erythema (red inflammation)
Well demarcated (defined boundary)
Plaques with a silver scale (thick layer of skin)
Papules (small round rash)

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4
Q

How is psoriasis classified?

A

PASI and DLQI scores
(subjective and objective respectively)
- mild/ moderate ≤ 10
- severe > 10

It is severe is DLQI > 10 regardless of PASI
scores

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5
Q

How is psoriasis triggered?

A

Strongly familial and polygenically inherited.
- environmental (trauma, sunburn)
- systemic (bacterial strep infections- pharyngitis and viral - HIV)
- medicine (lithium, ACEI, BB, rapid tapering of systemic corticosteroids, IFN, antimalarials, NSAIDs)
- metabolic endocrine disorder (hypocalcaemia)
- Alcohol consumption, smoking and obesity

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6
Q

List some comorbidities of psoriasis.

A
  • IBD
  • chronic inflammation can affect vascular structure leading to CVD (MI, stroke, hypertension)
  • cancer, diabetes, metabolic syndrome
    psychological aspects: depression, compliance issues
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7
Q

Describe the pathogenesis of psoriasis.

A

Stress or trauma to the skin can release fragments of DNA or RNA which combined is messenger protein LL37. This can then combine with dendritic cells (such as macrophages) and presented to the lymph nodes, activating T cells to differentiate into IL-1, 17, 22). These active T cells can travel from the lymph nodes through the blood vessels to the origin site, causing the release of cytokines such as TNF-a or IL which leads to inflammation and consequently the rapid proliferation of skin cells. However, these skin cells are still immature, so rather than form at an organised fashion, they stack on each other giving its characteristic squamous appearance.

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8
Q

List the treatments for mild/ moderate psoriasis.

A
  • topical corticosteroids and emollients.
  • ant-inflam effects and antiproliferative (used to control but can also treat)
  • try to rotate the corticosteroids to maximise efficacy and reduce SE (i.e. use it on the weekends and emollients during the weekday).
  • Vitamin D analogues (calcipotriol)
  • regulates proliferation and can take up to 6 weeks for adequate clearance.
  • sold in combination with bethamethasone dipropionate as an ointment or spray.
  • topical retinoids (tazarotene)
  • coal tar; can sting
  • for resistant or extensive: phototherapy + psoralen (non-pbs)
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9
Q

List the treatments for severe psoriasis.

A
  • retinoids (acretin)
  • MTX
  • cyclosporine
  • apremilast (PDE4 I)
  • biological DMARDs (targets IL17a, 12, 23 and TNF-a)

Systemic corticosteroids are discouraged as it may exacerbate condition upon withdrawal.

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10
Q

Treatment for psoriasis in pregnancy?

A

psoriasis varies in pregnant women due to changing hormones but are often improved.
- low-medium potency of topical corticosteroids + emollients
- localised phototherapy

  • MTX and retinoids are CI
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11
Q

What is psa?

A

inflammatory arthritis that often occurs in patients with psoriasis.
- affects DIP and PIP joints
(closest to nails and middle joints of fingers).
- stress and injury –> inflammation –> breakdown of bone (osteoclastogenesis) –> formation of new bone structure (petrusion) –> deformity and pain

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12
Q

How can we diagnose it?

A
  • hard to diagnose since lab findings are not definitive (non-specific lab biochemistry such as ESR and CRP are only found in 40% patients).
  • radiographic imaging exhibits coexistence of erosive changes and new bone formation.
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13
Q

Explain the bone alteration process in psa.

A

ongoing inflammation can promote osteoclatogenesis, eroding the bone. However, under the influence of cytokines such as TNF-a and IL, the ligament starts to grow at a rapid rate which triggers the surrounding bones to grow at a rapid rate, forming new petrusions. If left untreated for an extended duration, this can lead to the loss of a joint.

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14
Q

What are the treatments for peripheral psa (mild arthritis)?

A

NSAIDs

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15
Q

What are the treatments for peripheral psa (moderate/ severe arthritis)?

A

conventional DMARDs (MTX >LEF > SSZ)
- For MTX: Prior to Tx: liver function, hepatitis status, chest radiography + folic acid day after MTX administration.

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16
Q

What are the treatments for peripheral psa (severe disease at presentation)?

A

Use biological DMARDS (TNFi), esp if conventional DMARDs aren’t working, use TNFi rather than switching from one conventional DMARD to another.
e.g. of TNFi: etanercept, adalimumab, golimumab, inflixumab.
other biologics:
T-cell targeted: abatacept
B-cell targeted: rituximab

17
Q

What are the treatments for peripheral psa (resistant to non-biologic DMARD)?

A

biological DMARDS (TNFi) or MABs and JAKi if resistant to TNFi as well.
Don’t use JAKi in at-risk patient groups: > 65, CV risk or have CVD, cancer-risk patients and those who smoke