dermatology PT 2 Flashcards

1
Q

what is psoriasis?

A

Chronic, inflammatory skin disease

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2
Q

what abnormalities does psoriasis cause?

A

– Infiltration of the dermis and epidermis with activated Tlymphocytes & neutrophils
– Stimulation of the cutaneous vasculature leading to new
blood vessel formation in the psoriatic plaques
– Decreased epidermal turnover time (from 28 to ~4 days)-
overproduction of skin cells

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3
Q

what causes psoriasis?

A
  • Cause unknown, genetic aspect may
    predispose some people to the condition
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4
Q

what are the key clinical features of psoriasis?

A
  • A typical psoriatic lesion is red, scaly,
    sharply demarcated plaque
  • May be any size and affect any part of the body
  • Most common sites are extensor surfaces of elbows and knees, sacrum and scalp
  • Hands and feet frequently involved
  • Scale is easily scraped off revealing tiny bleeding points
  • Pruritus
  • Relapsing and remitting condition
  • Often impact on QoL with phsycological/social
    disability
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5
Q

what are the precipitating factors for psoriasis?

A
  • Many people with psoriasis can pinpoint a trigger event or experience that preceded the onset of psoriasis
  • Trauma
  • Infection
  • Hormones
  • Sunlight- usually improves psoriasis but 10% worsen
  • Medication e.g. beta blockers, lithium, antimalarials
  • Alcohol
  • Smoking
  • Profound psychological stress
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6
Q

what is chronic plaque psoriasis?

A

Psoriasis ‘plaques’ are formed by the build up of skin cells
* Red (increased blood supply to area), itchy, sore, white/silvery scales

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7
Q

what is the difference with flexural psoriasis?

A

may have little or no scale due to friction against other skin in these areas e.g. submammary, axillary, ano-genital
folds

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8
Q

what is guttate psoriasis? who does it affect? when does it happen?

A
  • Usually affects children and young adults
  • Can occur as first presentation of psoriasis or as an exacerbation of chronic plaque psoriasis
  • Commonly follows a streptococcal throat infection
  • Usually self-limiting
  • Widespread small, red macules
    which become scaly but clear within a few months
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9
Q

what is erythrodermic psoriasis?

A

Erythromdermic v. rare - a generalised redness of the skin involving all, or nearly all (usually stated as at least 90%) of the skin’s surface.

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10
Q

when does erythrodermic psoriasis occur?

A

Usually occurs in two contexts:
* In the setting of known, progressively worsening chronic plaque psoriasis.
* It may be precipitated by infection, tar, drugs, or withdrawal of corticosteroids

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11
Q

what is generalised pustular psoriasis?

A
  • A v. rare generalised eruptive form of psoriasis accompanied by fever and toxicity
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12
Q

what does generalised pustular psoriasis look like?

A

Acute erythema is seen with a rapid spread of
multiple sterile pustules over the body,
concentrated in the flexures, genital regions
and fingertips.

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13
Q

how common is psoriatic arthritis?

A
  • Affects up to 1 in 5 people with psoriasis
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14
Q

how does psoriatic arthritis affect a patient? how is it treated?

A
  • Most commonly affects hands and feet
  • Swollen, inflamed, painful joints
  • Usually involves referral to rheumatologist
  • NSAIDs/ Steroids/ DMARDs/ Biologics may be
    required
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15
Q

what happens in nail psoriasis?

A
  • Pitting of nails, discolouration (‘oil spots’ ‘salmon patches’), hyperproliferation of nail bed, oncholysis
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16
Q

what/how would you assess the condition?

A

assess disease severity, impact of disease on
physical, psychosocial, social wellbeing, psoriatic arthritis, co-morbidities

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16
Q

what/how would you assess the condition?

A

assess disease severity, impact of disease on
physical, psychosocial, social wellbeing, psoriatic arthritis, co-morbidities

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17
Q

where is psoriasis usually managed?

A

Usually managed in primary care, with specialist referral being needed at
some point for up to 60% of people

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18
Q

what tool do you use to assess the severity of the condition?

A

PASI = psoriasis area severity index

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19
Q

how does PASI work?

A
  • Scoring procedure often used to evaluate psoriasis clinically and to
    measure outcomes in clinical trials.
  • Scores severity of lesions (from 0-4) in terms of redness, thickness and
    scaliness, and the score is weighted according to the area affected.
  • Following treatment or in clinical trials, endpoints such as PASI 75 (a 75%
    reduction in disease activity) are used to measure progress of treatment.
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20
Q

what does the PGA score indicate?

A

Physician Global Assessment
* A scoring system is based on response to treatment as measured by lesion erythema, induration, and scale
* Score assignments that range from clear, almost clear, mild, moderate, to severe

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21
Q

how do emollients work in psoriasis?

A
  • Soften plaques, reduce itching and redness, improve absorption of topical treatments. May have anti-proliferative effect on psoriasis
  • Different products may be needed for different areas
22
Q

what are the first line treatment options for psoriasis?

A
  • topical corticosteroids
  • vitamin D
    analogues
  • dithranol
  • tar preparations
23
Q

what are the first line treatment options for psoriasis?

A
  • topical corticosteroids
  • vitamin D
    analogues
  • dithranol
  • tar preparations
24
Q

what are the second line treatment options?

A
  • phototherapies
  • systemic non-biologic therapies:
  • methotrexate,
  • ciclosporin,
  • acitretin
25
Q

what are the 3rd line treatment options?

A
  • systemic biologic therapies:
  • adalimumab
  • etanercept
  • Infliximab
  • ustekinumab
26
Q

when may salicylic acid be used?

A

may be used to remove scale before potent steroid application if initial treatment for 4 weeks is not satisfactory.

27
Q

what guidance is there around corticosteroids?

A

– Useful in acutely inflamed plaques and on face/ flexures
– Not as effective on chronic scaly plaques
– Risk of rebound flare
* BAD guidelines for management of psoriasis with topical steroids
– Do not use regularly for more than 4 weeks without review…..patient may
need follow up appointment
– Do not use potent steroids regularly for more than 7 days
– Review every 3 months
– No more than 100g of a moderately potent or higher potency preparation
should be applied per month
– Attempt to rotate topical steroids with alternative non-steroid preparations

28
Q

what are the vitamin D analogues available?

A
  • Calcipotriol, tacalcitol, calcitriol
29
Q

how long do vitamin D analogues take to work?

A

Useful in mild-moderate chronic plaque psoriasis, can clear psoriasis in 6-8 weeks

30
Q

what are vitamin D analogues MOA?

A

– Inhibit keratinocyte differentiation and proliferation
– May have some anti-inflammatory activity

31
Q

what are the benefits of VIT d analogues?

A
  • Don’t smell/stain like older treatments (tar/dithranol)
  • May be as effective as potent steroid , but with longer duration of remission after treatment has stopped
32
Q

what side effects may vit D analogues have?

A
  • Can cause skin irritation, resulting in transient increased redness/dryness and stinging/burning
    – Calcipotriol should not be used on face/flexures
    – Calcitriol OK, less irritant
33
Q

how should vit D analogues be applied?

A

Adequate quantities should be used – 0.5g (a fingertip unit) for 10cm2 skin (one medium sized adult palm)
* Apply thickly (unlike steroids)
* Maximum weekly dose to avoid risk of hypercalcaemia
– Calcipotriol 100g, calcitriol 210g, tacalcitol 70g

34
Q

what is tazarotene? how does it work?

A
  • Topically active retinoid (vitamin A derivative)
  • Mechanism of action
    – Normalises keratinocyte differentiation
    – antiproliferative and anti-inflammatory effects
35
Q

why is tazarotene generally avoided?

A
  • Use is limited by skin irritation and increased photosensitivity
  • Teratogenic
36
Q

what is the thought MOA o coal tar?

A

thought to be keratolytic with some anti-inflammatory and antiproliferative effects

37
Q

what are the disadvantages of coal tar?

A
  • Stains clothing
  • Smells unpleasant
  • Less effective than vitamin D preparation
    Theoretical risk of carcinogenicity- no epidemiological evidence
38
Q

what are the disadvantages of dithranol?

A
  • Profoundly irritant to skin, causing inflammation and blistering
  • Causes temporary staining of skin, and permanent staining of clothing and bathroom fittings
39
Q

what is used to prevent spreading of dithranol to uninvolved skin areas?

A

lassar’s paste

40
Q

how long does it take dithranol to work?

A
  • Response to treatment can be expected within 3 weeks
41
Q

what is SCDT?

A
  • Short-contact dithranol treatment (SCDT)
    – Application of up to 8% for between 15-30
    minutes with or without UVB
    – Suitable for home use
42
Q

what is phototherapy and how does it work?

A
  • UVB (responsible for sunburn) or PUVA therapy
  • Thought to modulate expression of cellular adhesion molecules and induce T-cell apoptosis
  • UVB Dose adjusted to match the patient’s skin type
    – Usually 80% of minimum erythemogenic dose (MED)
    3 weeks till cleard
43
Q

what is PUVA?

A
  • Combination of 8-methoxypsoralen (MOP) and UVA
44
Q

how is UVA dose determined ?

A

by assessment of skin type
– MOP Tablets: 1-2 hours before irradiation
– Topical (lotion, paint, bath solution)- applied immediately before irradiation
– unlicensed

45
Q

when is the patient not photosensitive?

A
  • Patient remains photosensitive until psoralen cleared from body, therefore advise re sunscreen
46
Q

how does methotrexate work?

A

– Interferes with DNA synthesis by preventing the formation of tetrahydrofolate
– Monitoring in the same way as other indications, purple book etc

47
Q

how does ciclosporin work?

A

– Blocks intracellular components of T-cell activation through a series of interactions
– Results in inhibition of calcineurin phosphatase…….inhibits nuclear factor of activated T-cells
– Doses 2.5-5mg/kg can clear psoriasis in 6-8 weeks
– Sometimes used for maintenance but risks vs benefits.
– Drug interactions, monitoring and side-effects

48
Q

how does the oral retinoid acitretin work?

A
  • Bind to nuclear receptors and regulate gene
    transcription
  • Induce keratinocyte differentiation and reduce epidermal hyperplasia
49
Q

what has to be monitored with acitretin?

A

hepatotoxic so:
* LFTs and lipid profile at start of therapy, then every 2-4 weeks for 2
months then 3 monthly

50
Q

who should oral retaonids not be given in?

A

Contraindications/cautions: concomitant methotrexate or tetracycline,
avoid in children

51
Q

if a woman is of child bearing age what must she agree to with oral retinoids? how long does the prescription last?

A

Oral retinoids contra-indicated in women of child-bearing potential unless used in conjunction with a pregnancy prevention programme (PPP)
– Prescriptions for female patients in a PPP are only valid for 7 days and are limited to 30 days of treatment

52
Q

how do biologics work in psoriasis?

A
  • Monoclonal antibodies and fusion proteins
  • Interfere with T-cell function
53
Q

what are the general psoriasis counselling points?

A
  • Psoriasis cannot be cured, but can be
    controlled
  • Is not infectious
  • Does not develop into skin cancer
  • Cannot be spread to other areas of skin
    through application of topical treatments