97: Phototoxicity & Photoallergy Flashcards
What is the likely diagnosis for a patient with burning and stinging on sun-exposed areas after taking a new medication?
The likely diagnosis is acute phototoxicity.
What is the mechanism behind acute phototoxicity?
The mechanism involves direct tissue injury caused by the phototoxic agent and radiation, leading to erythema, edema, and in severe cases, vesicles and bullae.
What is the likely explanation for hyperpigmentation lasting for months after PUVA therapy?
PUVA therapy involves psoralen-induced phototoxicity, where the acute response peaks at 48-72 hours and resolves with hyperpigmentation that can last for months.
What condition is indicated by separation of the distal nail from the nail bed after starting doxycycline?
The condition is photoonycholysis.
How does photoonycholysis occur?
It occurs due to the nail plate acting as a lens to focus UV energy on the nail bed. Doxycycline and other tetracyclines are common culprits.
What is the diagnosis for pruritic, eczematous eruptions confined to sun-exposed areas after using a new sunscreen?
The diagnosis is photoallergy.
What is the mechanism behind photoallergy?
The mechanism involves a type IV delayed hypersensitivity response to a photoallergen modified by photon absorption.
What are the two main types of photosensitivity?
Phototoxicity and photoallergy.
What is phototoxicity?
Direct tissue injury caused by the phototoxic agent and radiation, occurring in all individuals exposed to adequate doses of the agent and activating wavelengths of radiation.
What is the difference between exogenous and endogenous photosensitizers?
Exogenous photosensitizers are administered systemically or applied topically, while endogenous photosensitizers are related to cutaneous porphyrias with enzymatic defects in heme biosynthetic pathways.
What is the prevalence range of positive responses in patients who had photopatch testing?
1.5% to 74%.
What are the symptoms of acute phototoxicity?
Burning and stinging on exposed areas, erythema, edema, and in severe cases, vesicles and bullae.
What is photoonycholysis?
Separation of the distal nail from the nail bed, which may be asymptomatic and can manifest as acute phototoxicity.
What factors influence acute phototoxicity?
It is drug-dose and UV-dose dependent, with symptoms appearing within hours of exposure to the phototoxic agent and UV radiation.
What is the role of the nail plate in phototoxicity?
The nail plate can serve as a lens to focus UV energy on the nail bed, potentially leading to phototoxic effects.
What is the clinical significance of the difference between phototoxicity and photoallergy?
Most photosensitivity induced by systemic medications is phototoxicity, while that induced by topical agents is photoallergy.
What are the common drugs associated with slate-gray pigmentation on sun-exposed areas?
Common drugs include Amiodarone, Chlorpromazine, Clozapine, Imipramine, Desipramine (less common), and Minocycline (can also affect non-sun-exposed areas).
What is the most common causative agent of pseudoporphyria?
The most common causative agent of pseudoporphyria is Naproxen.
What are the chronic effects associated with long-term PUVA treatment?
Chronic effects associated with long-term PUVA treatment include premature aging of the skin, lentigines, squamous cell carcinomas, basal cell carcinomas, and melanoma.
What is the relationship between voriconazole use and photosensitivity?
In immunosuppressed patients receiving voriconazole for longer than 12 weeks, the following effects may occur: photosensitivity, pseudoporphyria, photoaging, lentigines, and premature dermatoheliosis.
What are the systemic agents commonly reported to induce photosensitivity?
Common systemic agents that induce photosensitivity include Vemurafenib, Voriconazole, Doxycycline, Hydrochlorothiazide, Amiodarone, and Chlorpromazine.
What is the likely cause of asymptomatic blue-gray pigmentation on sun-exposed areas after prolonged use of a medication?
The condition is slate-gray pigmentation, often caused by drug metabolite-melanin complexes.
What is the underlying mechanism for squamous cell carcinoma development in a patient on voriconazole for over a year?
Voriconazole can cause accelerated photo-induced changes, leading to photosensitivity, pseudoporphyria, photoaging, lentigines, and premature dermatoheliosis.
What is the most common cause of pseudoporphyria with skin fragility and vesicles but normal porphyrin levels?
Naproxen is the most common cause.
What drugs are likely responsible for photodistributed telangiectasia in a patient on a calcium channel blocker?
Calcium channel blockers like nifedipine, amlodipine, felodipine, and diltiazem can cause photodistributed telangiectasia.
What is the likely mechanism for a lichenoid photosensitive eruption after starting doxycycline?
The mechanism involves phototoxicity or photoallergy induced by doxycycline.
What drugs are commonly associated with chronic actinic dermatitis?
Drugs like thiazides, quinidine, quinine, and amiodarone are associated with persistent photosensitivity evolving into chronic actinic dermatitis.
What is the diagnosis for exaggerated sunburn reactions after starting vemurafenib?
The diagnosis is phototoxicity.
What is the action spectrum for vemurafenib-induced phototoxicity?
The action spectrum for vemurafenib-induced phototoxicity is in the UVA range.
What are the likely culprits for a burning sensation and erythema on sun-exposed areas after using a topical agent?
Topical agents like fluorouracil, retinoids, and crude coal tar can cause phototoxicity.
What are the most commonly reported phototoxic agents after using a systemic medication?
Common agents include vemurafenib, voriconazole, doxycycline, hydrochlorothiazide, amiodarone, and chlorpromazine.
What is the typical action spectrum for most phototoxic agents?
The action spectrum for most phototoxic agents is in the UVA range.
What is the action spectrum for dyes like porphyrins and fluorescein?
The action spectrum for dyes like porphyrins and fluorescein is in the visible light range.
What are common sources of topical furocoumarins?
Common sources include limes, celery, figs, and parsnips.
What is the likely diagnosis for a burning sensation after exposure to crude coal tar?
The diagnosis is phototoxicity.
What is the mechanism of phototoxic reaction after using systemic fluorouracil?
The mechanism involves direct tissue injury caused by the phototoxic agent and radiation.
What are the most common systemic agents involved in phototoxic reactions?
Common agents include vemurafenib, voriconazole, doxycycline, hydrochlorothiazide, amiodarone, and chlorpromazine.
What skin condition is associated with chronic exposure to diltiazem?
Photodistributed, reticulated, slate-gray pigmentation.
What is the significance of the action spectra in phototoxic agents?
Most action spectra are in the UVA range, except for porphyrins and fluorescein which are in the visible light range.
What are the key steps involved in photodynamic processes leading to tissue injury?
- Absorption of radiation energy by the photosensitizer. 2. Formation of an excited molecule. 3. Generation of reactive oxygen species. 4. Resulting in tissue injury.
What are the histopathological findings associated with acute phototoxicity?
- Individual necrotic keratinocytes; if severe, epidermal damage.
- Epidermal spongiosis and dermal edema with mild infiltrate of neutrophils, lymphocytes, and macrophages.
- Slate-gray pigmentation due to increased dermal melanin and drug deposits.
- Lichenoid eruptions similar to idiopathic lichen planus with more spongiosis and necrotic keratinocytes.
What management strategies are recommended for acute phototoxicity?
- Identification and avoidance of the causative phototoxic agent. 2. Rigorous photoprotection: Seek shade, wear photoprotective clothing, wide-brimmed hats, and sunglasses. 3. Use broad-spectrum sunscreens with high SPF. 4. For acute phototoxicity, apply topical corticosteroids and compresses; consider systemic corticosteroids for severe cases.
What are the clinical features of photoallergy?
- Sensitized individuals experience pruritic, eczematous eruptions within 24 to 48 hours after exposure.
- Clinically indistinguishable from allergic contact dermatitis.
- Predominantly affects sun-exposed areas, but may spread to covered areas.
- Usually resolves without significant postinflammatory hyperpigmentation.
What are the potential long-term effects of UV radiation on photoallergens?
- UV radiation can alter the carrier protein that binds the photoallergen, leading to the formation of a neoantigen.
- This neoantigen can stimulate the immune system over the long term, potentially leading to chronic conditions.