UV therapy Flashcards

1
Q

What are the wavelength ranges for UVA and UVB?

A

UVA = 320-400nm UVB= 280-320nm

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2
Q

How is the dose of UV determined for UV therapy?

A

Varies by skin type, usually 70% of minimum erythema dose (minimal dose needed to induce erythema) and increased as tolerated with each visit to maximum dose

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3
Q

Why are psoralen’s used with UVA (mechanism of PUVA)?

A

DNA doesn’t absorb UVA much. Psoralens are absorbed and intercalated into the DNA prior to the UV exposure. Photoactivated psoralen molecules –> 3,4 or 4’,5’ cyclobutane monofunctional adducts to pyrimidines in DNA–> interstrand DNA cross-link and decreased DNA synthesis/cell cycle arrest –> selective immunosuppression, selective cytotoxicity (via the production of ROS and free radicals) and melanocyte stimulation

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4
Q

Uses in dermatology for PUVA?

A

Psoriasis, vitiligo, CTCL, dermatitis, photodermatoses (desensitization protocols), GVHD, and LP

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5
Q

Where are psoralens metabolized?

A

By the liver

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6
Q

How should psoralens be taken?

A

Ideally fasting, if there is nausea/upset stomach can try taking with food

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7
Q

Side effects of PUVA?

A

Nausea/vomiting, phototoxic reactions (symptomatic erythema, if widespread hold treatment), pruritus, hepatic toxicity, bronchoconstriction, HSV recurrences, cardiovascular stress CNS disturbances, photoaging melanoma NMSC (usually if >250 tx; skin exam q 6-12 months), ocular issues (cataracts)

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8
Q

Contraindications to PUVA?

A

Lactation, lupus erythematosus, pemphigus/pemphigoid, albinism, porphyria, and XP

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9
Q

Dosing strategy of PUVA?

A

Usually 2-3x per week until the dz is mostly clear, then maintenance schedule where radiation dose is kept the same and visit frequency is decreased and then stopped

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10
Q

What wavelengths of UV light are used for UVA-1 therapy?

A

340-400 (UVA1)

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11
Q

How does dosing work for UVA-1 therapy?

A

Can be low, medium, or high dosing –> sensitivity to UVA can vary significantly, so dose is based on minimum erythema dose

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12
Q

What disorders can be treated with UVA-1?

A

Not many centers have this, so not often used and not superior to PUVA or NB-UVB

  • Can be used for SLE (low dose), scleroderma/other sclerodermoid skin conditions (at least 30 tx’s), AD, MF
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13
Q

What is the mechanism of action for UVB therapies?

A

Decrease DNA synthesis (important in psoriatic epidermis), increase p53 leading to cell cycle arrest and keratinocyte apoptosis, decrease pro-inflammatory cytokines, decrease Langerhans cells in the skin

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14
Q

What wavelength is used for narrowband UVB?

A

311-313

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15
Q

How is dosing controlled for NB-UVB?

A

Based on skin type or 70% minimal erythema dose. Treatments start at 3x/week and then the dose is increased by 10-15% with each visit (with adjustments depending on reaction).

UV opaque goggles and protection on genitals are warn

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16
Q

What are some important side effects of NB-UVB?

A

Erythema/pruritis and other skin reactions, recurrent HSV (damage from the sun is a risk, if they are at risk consider tx), worsening of SLE or blistering dz, and NMSC (lower than PUVA or broadband UVB)

17
Q

What is narrowband UVB used for?

A

Psoriasis (most common indication), vitiligo (tx of choice), MF (patch/plaque), AD, photodermatoses for desensitization, pruritus

18
Q

What are the wavelengths used for broadband UVB?

A

280-320 nm

19
Q

What are some advantages of broadband UVB?

A

More convenient in darker-skinned patients (takes less time to treat) but most centers are using narrowband

20
Q

What wavelength does the excimer laser use?

A

308nm

21
Q

What is the excimer laser used for?

A

It is good for smaller lesions that would need narrowband UVB (<2cm2)

  • Small lesions of psoriasis or vitiligo are potential candidates
22
Q

What is the mechanism of extracorporeal photochemotherapy?

A

Blood is drawn via a venous catheter in the arm, then the RBC’s are separated into the leukocytes into a buffy coat (WBC layer), The RBC’s go back to the patient and then the WBC’s are exposed to 8-methoxypsoralen. UVA radiation is given to the cells and then this is reinfused back into the patients. There is a net gain of about 500mL (there are 200-400mL that are originally taken out).

  • This serves to cause apoptosis of activated T-cells, cytokine alterations (favors immunoregulatory cytokines, and decreases dendritic cells
23
Q

Dosing of extracorporeal photochemotherapy?

A

Usually done on a two day cycle every 4 weeks and then you slowly wean after than

24
Q

What is extracorporeal photochemotherapy useful for?

A

CTCL (can be used with other treatments), scleroderma, chronic GVHD, nephrogenic systemic fibrosis, pemphigus

25
Q

What is extracorporeal photochemotherapy used for?

A

CTCL (selectively targets lymphoma cells), can be used with other treatments for this,

26
Q

What are the contraindications to extracorporeal photochemotherapy?

A

Severe cardiac disease (because of the added volume), caution in patients w/ low BP, hematocrit and CHF

27
Q

Side effects of extracorporeal photochemotherapy?

A

Nausea, hypotension, photosensitivity, CHF exacerbation and tachycardia

28
Q

What is the principle of photodynamic therapy (PDT)?

A

This is the use of a light source (blue light, red light, etc) to activate a photosensitizer (methyl aminolevulinate for red light and aminolevulinic acid for blue light).

29
Q

Which photosensitizers should be used with blue light vs red light? which one requires occlusion?

A

Aminolevulinic acid: This is activated by blue light and does not require occlusion

Methyl aminolevulinate: This is activated by red light and this should be under occlusion

30
Q

What is the mechanism of action of photodynamic therapy?

A

The photosensitizers (ALA or MAL) are converted into protoporphyrin IX within the cells which leads to the cells being activated to a higher energy state, the production of reactive oxygen species (singlet O2), localize by mitochondria and you get necrosis and apoptosis of cells.

  • This targets neoplastic cells because they accumulate more porphyrins than normal cells.
31
Q

What condition is protoporphyrin IX also seen in?

A

Protoporphyria

32
Q

What are the wavelengths that activate ALA and MAL for photodynamic therapy?

A

Blue: 410nm (Soret band, blue)

Red: 635 nm

33
Q

What is the mechanism of photodynamic therapy in acne?

A

Sebaceous glands and p. acnes accumulate porphyrins (photosensitizer is not required but can be used for this condition, light source alone can be effective)

34
Q

What is photodynamic therapy used for?

A

Only FDA approved use is for actinic keratoses (90% response) but has also been used for BCC, SCCis, photoaging, hidradenitis, and MF

35
Q

How is photodynamic therapy performed?

A
  1. skin is cleansed (acetone if using ALA, gentle curettage/debridement of crusts for MAL)
  2. photosensitizer is put on
  3. incubation (3-4 hrs for MAL, 1-4 hrs for ALA)
  4. light exposure = 37 j/cm2 for MAL, 7-9 minutes; 10 J/cm2, 16 minutes for ALA
  5. Retreatment needed in 7 days for MAL, and 1-2 months for ALA, if needed
36
Q

Precations for patients after photodynamic therapy?

A

They should wear protective eyewear during the procedure and avoid sunlight for 48 hrs

Pregnancy class C

37
Q

What are the potential side effects of photodynamic therapy?

A

Phototoxic reactions and photosensitivity, post-inflammatory hyper/hypopigmentation, hypersensitivity to photosensitizer, pain, systemic absorption, and inflammation (edema, blistering and crusting)