Psoriasis Flashcards

Learn what this is

1
Q

What is psoriasis?

A
  • Chronic, immune mediated disease

* Sharply demarcated erythematous plaque with micaceous scale

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2
Q

Why does psoriasis develop?

A
○ Polygenic predisposition + environmental triggers
○ HLA-Cw6 (chromosome 6)
○ PSORS1-9
○ Infection
○ Drugs 
○ Trauma
○ Sunlight
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3
Q

What is the pathogenesis of psoriasis?

A

○ Adaptive immune system
- T cells (epidermal: CD8, dermal CD4&8)
○ Stressed keratinocytes
○ Activation of dermal dendritic cells (dDCs)
- by interleukins, TNF alpha
○ dDCs → lymph nodes, present uncertain antigen to naïve T cells
○ Differentiation into Th (T helper) 1, 17 &22
○ → psoriatic dermis → plaque formation
○ Interleukins & TNF alpha amplify inflammatory cascade, stimulate keratinocyte proliferation
○ VEGF → angiogenesis
○ Neutrophils in acute, active, pustular disease
○ Cell cycle reduced from 28 days to 3-5

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4
Q

Describe the histology of psoriasis

A

○ Hyperkeratosis (thickening of stratum corneum)
○ Neutrophils in stratum corneum (munro’s microabscesses)
○ Psoriasiform hyperplasia: Acanthosis (thickening of squamous cell layer) with elongated rete ridges
○ Dilated dermal capillaries
○ T cell infiltration

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5
Q

Describe chronic plaque psoriasis

A

○ Symmetric

○ Extensor surfaces

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6
Q

Describe palmar plantar psoriasis (pustulosis)

A

○ Studies show that psoriasis of the palms and soles tends to have greater impact on QOL compared to more extensive psoriatic involvement not involving the palms and soles
○ Smoking
○ Sterile inflammatory bone lesions
○ This can be the most resistant to treatment

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7
Q

Describe Guttate psoriasis

A

○ Children, adolescents
○ Can be triggered by viral or bacterial infections. Check ASO titre
○ May resolve, or may trigger chronic psoriasis in susceptible individuals

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8
Q

What can happen in scalp psoriasis?

A

Can lead to alopecia at affected areas

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9
Q

Describe flexural/ inverse psoriasis

A

○ Less scale
○ Can be triggered or superinfected by localised dermatophyte, candidal or bacterial infection – these are also differential diagnoses

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10
Q

Describe pustular psoriasis

A
○ Sterile pustules
○ Sometimes systemic symptoms
○ Causes
	- Pregnancy 
	- Rapid taper/stop steroids 
	- Hypocalcaemia 
	- Infection
○ Overlap with AGEP (pustular drug eruption), however, in AGEP:
	- Patient is more unstable
	- Fever
	- Wide spread eruptions
	- No history of psoriasis
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11
Q

Describe erythrodermic psoriasis

A

○ ‘Red Man’ syndrome

○ >80% body surface area involved

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12
Q

How can psoriasis be managed in primary care?

A
  • Emollients
  • Creams vs Ointments
  • Soap substitutes
  • Vitamin D3 analogues: inhibit epidermal proliferation
  • Coal Tar creams
  • Topical Steroid – with care. Flexures, genitalia
  • Salicylic acid (keratolytic)
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13
Q

How can psoriasis be managed in secondary care?

A
  • Dermatology Referral
  • Crude Coal Tar (inpatient or day treatment)
  • Dithranol: since 1916. Can burn.
  • UVB Phototherapy (not the same as sunbed)
    □ Guttate
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14
Q

What are the systemic treatments of psoriasis?

A
- Retinoid - Acitretin 
	□ Teratogenic, LFTs, lipids
- Immunosuppression
	□ Methotrexate
	□ Can treat Ps Arthritis 
	□ Max improvement 8-12 weeks
	□ Ciclosporin
	□ Renal, cancer risk
- Biologic Therapies
	□ Qualifying criteria, cost
		□ Anti-TNF: Etanercept, infliximab, adalimumab
		□ IL-12,23: Ustekinumab
		□ Patient can form antibodies to biologic
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15
Q

What is the management of erythrodermic psoriasis?

A
  • Recognition
  • Admit
  • FLUID BALANCE
  • Bloods / IV access
  • Thick greasy ointment emollients
  • Systemic or biologic treatment?
  • Trigger?
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16
Q

What are the future treatments of psoriasis?

A
  • Targeted biologics
  • IL-17,20,22
  • Kinase inhibitors
  • Ethical / cost dilemmas
    □ Adalimumab ~£9000 per year (£225000 for 25 years)
    □ Methotrexate ~£12.50 per year
17
Q

How is the progress of psoriasis monitored?

A

○ Psoriasis Area Severity Index (PASI)
- Surface area, plaque colour, thickness, scale
○ Dermatology Life Quality Index (DLQI)
- QOL in last 1 week