PHOTOSENSITIVITY RXNS Flashcards

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1
Q

what is this:

cellular injury following
UVR-induced activation of a phototoxic agent; all are
susceptible to this disorder

or

scattered necrotic keratinocytes with a dermal infiltrate of lymphocytes and
neutrophils

A

Phototoxicity

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2
Q

what is this:

a DTH response with sensitization phase, incubation period (7-10d), and eventual reaction after clinical challenge, just like ACD

or

spongiotic dermatitis with dermal lymphohistiocytic infiltrate indistinguishable from
ACD

A

Photoallergy

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3
Q

phototoxicity requires the generation of?

A

free radicals, superoxide, peroxide, singlet oxygen

also due to tetracycline, chlorpromazine

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4
Q

phytotoxicity manifests as:

A

pseudoporphyria
photonycholysis
slate gray hyperpigmentation
lichenoid eruption

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5
Q

most common cause of photo allergy?

A

organic sunscreens (oxybenzone/benzophenone-3) with no reaction to titanium dioxide or zinc oxide reported

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6
Q

how to treat photo allergy/phototoxicity?

A

identify agent
photoprotection with nighttime dosing
topical, systemic corticosteroids, compress with antihistamines

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7
Q

what are the spectrums used in UV light therapy?

A

narrow band UVB(311-313 nm)
broad band UVB (280-330 nm)
excimer laser (308 nm)
UVA 1/2 (340-400nm), (315-340 nm)

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8
Q

photo chemotherapy equals?

A

UVA with topical or systemic psoralen (photosensitizer)

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9
Q

major effects of UVR?

A
  • Phototoxicity
  • Hyperkeratosis (2-4 fold thickening of stratum corneum)
  • Photo-onycholysis (with very strong exposure)
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10
Q

UV light therapy?

used for many disorders: psoriasis, atopic derm,
vitiligo, primary pruritus, mycosis fungoides, lichen planus. NOT beneficial for deeper disorders (morphea, lichen sclerosis)

the most important chromophore for UVB therapy?

slows cell cycle, induces expression of p53, which arrests cell cycle & → sunburn cells (apoptotic keratinocytes), increases release of prostaglandins and IL-6 & 10 → immunosuppression

Suppresses contact allergy, immune surveillance against UV-induced NMSC, “shocks” Langerhans cells such that they do not present antigen in normal fashion, suppresses Th-type I axis

A

narrow band UVB

Nuclear DNA

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11
Q

side effects of phototherapy?

T/F, UVB has much less carcinogenicity than PUVA

NBUVB is safer or more dangerous than BBUVB?

A

erythema, xerosis, occasional blistering, increased recurrent HSV eruption

T

NBUVB

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12
Q

best treatment for phototherapy and psoriasis?

*vitiligo?

A

PUVA w/ concurrent use of topical steroids

NBUVB approx PUVA, NBUVB has a much lower skin cancer risk

*NBUVB, 2-3x/week, increase dose 10-20%

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13
Q

UV light therapy?

  • 308 nm
  • High multiples of MED can be used to induce longer remissions
  • Fewer treatments
  • Smaller treatment areas
  • Useful for stable vitiligo mgmt, GA, LP, LSC, psoriasis
A

The Excimer Laser

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14
Q

how do Psoralens react with DNA?

effects?

A
  1. Intercalation into DNA
  2. Absorption of photons
  3. Formation of 3’,4’- or 4’,5’-cyclobutane monoadduct with pyrimidine
    bases of native DNA

inhibit DNA replication, cell cycle arrest, free radical damage, increased production and transfer of melanosomes

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15
Q

PUVA is a therapeutical benefit given in what route?

A

topical, oral, bath

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16
Q

starting considerations of PUVA?

maintenance?

what are the combination tx?

A

Tx should not be started until 72 hrs after MPD is determined

2x weekly with final UVA dose used during clearing and indicated in a relapse

PUVA+MTX and PUVA+retinoid

17
Q

tx most effective for psoriasis?

A

RePUVA