Phototherapeutic Agents — MCQs
Replacing alanine by which amino acid, will increase UV absorbance of protein at 280 nm wavelength?
How does narrowband UVB therapy work in psoriasis?
Treatment of choice for Pustular psoriasis is:
Treatment of choice for Nodulocystic Acne is:
Dermatological manifestation of which of the following diseases?
An 8-year-old girl has extreme photosensitivity since birth. She has recently been diagnosed with skin cancer. What is the diagnosis?
A 6-year-old child born to consanguinity has pallor and intolerance to sunlight. His urine was exposed to Wood's light. Probable diagnosis is:
A patient developed fixed drug eruptions after taking certain medications. Which of the following drugs is known to cause these skin lesions?
Which of the following is a topical vitamin D analogue?
Which drug is used for intralesional injection in keloids?
Phototherapeutic Agents Indian Medical PG Practice Questions and MCQs
Question 1: Replacing alanine by which amino acid, will increase UV absorbance of protein at 280 nm wavelength?
- A. Glycine
- B. Tryptophan (Correct Answer)
- C. Arginine
- D. Lysine
Explanation: ***Tryptophan*** - **Tryptophan** contains an **indole ring**, which is a **chromophore** that strongly absorbs UV light at 280 nm. - Increased tryptophan content in a protein directly correlates with a higher **UV absorbance** at this wavelength. *Glycine* - **Glycine** is the simplest amino acid, with only a **hydrogen atom** as its side chain. - It does not contain any aromatic rings or other groups that absorb UV light at 280 nm, so replacing alanine with glycine would not increase UV absorbance. *Arginine* - **Arginine** is a basic amino acid with a **guanidinium group** in its side chain. - While it has a slightly complex side chain, it does not possess any **aromatic rings** that absorb significantly at 280 nm. *Lysine* - **Lysine** is another basic amino acid with a long **aliphatic chain** and an **amino group** at the end. - Similar to arginine, lysine lacks the necessary **aromatic chromophores** to contribute to UV absorbance at 280 nm.
Question 2: How does narrowband UVB therapy work in psoriasis?
- A. Melanin synthesis
- B. Collagen breakdown
- C. Keratinocyte proliferation
- D. T cell apoptosis (Correct Answer)
Explanation: ***T cell apoptosis*** - Narrowband UVB (NB-UVB) therapy primarily works by inducing **apoptosis (programmed cell death)** of activated **T-lymphocytes** in the psoriatic skin lesions. - By reducing the number of these inflammatory cells, NB-UVB helps to suppress the immune response that drives the **excessive keratinocyte proliferation** in psoriasis. *Melanin synthesis* - While UV radiation does stimulate **melanin synthesis**, leading to tanning, this is a secondary effect and not the primary therapeutic mechanism for psoriasis. - Increased melanin helps protect the skin from UV damage but does not directly treat the underlying pathology of psoriasis. *Collagen breakdown* - UV radiation, especially UVA, can contribute to **collagen breakdown** and photodamage over time, but this is an adverse effect, not a therapeutic mechanism for psoriasis. - Psoriasis treatment aims to normalize skin cell growth and reduce inflammation, not degrade collagen. *Keratinocyte proliferation* - Psoriasis is characterized by **accelerated keratinocyte proliferation**; NB-UVB therapy aims to *reduce* this proliferation, not promote it. - The mechanism by which NB-UVB achieves this reduction is primarily through its effects on immune cells, not by directly enhancing keratinocyte growth.
Question 3: Treatment of choice for Pustular psoriasis is:
- A. Methotrexate (Correct Answer)
- B. Psoralen - UV therapy
- C. Systemic steroid
- D. Estrogen
Explanation: ***Methotrexate*** - **Methotrexate** is a systemic immunosuppressant often considered the first-line treatment for severe forms of **pustular psoriasis** due to its efficacy in reducing inflammation and hyperproliferation of skin cells. - It works by inhibiting **dihydrofolate reductase**, thereby interfering with DNA synthesis and cell division, which is crucial in rapidly dividing cells like those found in psoriasis. *Psoralen - UV therapy* - **Psoralen and ultraviolet A (PUVA)** therapy can be used for chronic plaque psoriasis, but it is generally **contraindicated or used with extreme caution** in pustular psoriasis due to the risk of exacerbating the disease or causing irritation. - **UV light therapy** can sometimes trigger or worsen pustular flares, especially in acute generalized pustular psoriasis. *Systemic steroid* - While systemic steroids can provide temporary relief by addressing inflammation, their use in pustular psoriasis is generally **not recommended for long-term management** due to the high risk of severe rebound flares upon withdrawal. - Withdrawal of **systemic corticosteroids** can precipitate or worsen generalized pustular psoriasis, making them a less desirable long-term treatment option. *Estrogen* - **Estrogen** has no direct role in the treatment of psoriasis. Psoriasis is an inflammatory skin condition, and its pathophysiology is not directly influenced by estrogen levels. - Hormonal therapies are not indicated for the management of psoriasis, including its pustular forms.
Question 4: Treatment of choice for Nodulocystic Acne is:
- A. Isotretinoin (Correct Answer)
- B. Erythromycin
- C. PUVA
- D. Tetracycline
Explanation: ***Isotretinoin*** - **Isotretinoin** is a systemic retinoid that targets all four major pathogenic factors of acne: **sebum production**, **follicular hyperkeratinization**, **Propionibacterium acnes growth**, and **inflammation**. - It is considered the most effective medication for **severe, nodulocystic acne**, often leading to long-term remission. *Erythromycin* - **Erythromycin** is a topical or oral antibiotic primarily used for its antibacterial and anti-inflammatory properties against *P. acnes*. - While useful for milder inflammatory acne, it is generally **insufficient for severe nodulocystic acne** and carries risks of **antibiotic resistance**. *PUVA* - **PUVA (Psoralen plus ultraviolet A)** therapy is a form of photochemotherapy primarily used for severe **psoriasis**, **eczema**, and **cutaneous T-cell lymphoma**. - It is **not a treatment for acne** and has significant side effects, including increased risk of **skin cancer**. *Tetracycline* - **Tetracycline** is an oral antibiotic often used to treat moderate to severe inflammatory acne due to its anti-inflammatory effects and reduction of *P. acnes*. - While effective for some inflammatory acne, it is typically **less potent than isotretinoin** for severe, **nodulocystic acne** and may not provide a permanent cure.
Question 5: Dermatological manifestation of which of the following diseases?
- A. Photo dermatitis
- B. Pellagra (Correct Answer)
- C. Acrodermatitis enteropathica
- D. Vitamin B deficiency
Explanation: ***Pellagra*** - The image shows a classic "butterfly" rash on the face, specifically a photosensitive dermatitis, which is a hallmark of **pellagra**. - Pellagra is caused by a deficiency of **niacin (vitamin B3)**, characterized by the "3 D's": **dermatitis**, **diarrhea**, and **dementia**. *Photo dermatitis* - While pellagra often presents with photosensitive dermatitis, "photo dermatitis" is a general term for **skin inflammation caused by light exposure** and not a specific disease itself. - It could be caused by various factors, including medication, immune reactions, or other underlying conditions, but the pattern seen here is highly suggestive of pellagra. *Acrodermatitis enteropathica* - This condition is a **hereditary zinc deficiency** that typically presents with a periorificial and acral dermatitis. - The skin lesions are typically **vesicular-pustular or eczematous** and do not usually have the distinct butterfly pattern of photosensitive dermatitis seen in the image. *Vitamin B deficiency* - While pellagra is a vitamin B **(niacin, B3)** deficiency, this option is too broad. - Other vitamin B deficiencies, such as **riboflavin (B2)** or **pyridoxine (B6)** deficiency, have different dermatological manifestations like angular cheilitis, glossitis, or seborrheic dermatitis, but not the characteristic facial rash seen here.
Question 6: An 8-year-old girl has extreme photosensitivity since birth. She has recently been diagnosed with skin cancer. What is the diagnosis?
- A. Xeroderma Pigmentosum (Correct Answer)
- B. Bloom syndrome
- C. Griscelli syndrome
- D. Chediak Higashi syndrome
Explanation: ***Xeroderma Pigmentosum*** - This condition is characterized by an extreme sensitivity to **ultraviolet (UV) light** from birth due to defects in **DNA repair mechanisms**, leading to severe sunburns, pigmentary changes (freckles, hypopigmented macules), and a high risk of developing **skin cancers** at a young age. - The history of extreme photosensitivity since birth and the diagnosis of skin cancer in an 8-year-old girl is highly indicative of Xeroderma Pigmentosum. *Bloom syndrome* - Bloom syndrome is an inherited disorder characterized by **stunted growth**, a **photosensitive facial rash (telangiectatic erythema)**, and a predisposition to **various cancers**, including leukemia and lymphomas. - While photosensitivity and cancer risk are present, the extreme skin damage and early onset of specific skin cancers (as opposed to leukemias/lymphomas often seen in Bloom) make Xeroderma Pigmentosum a more fitting diagnosis. *Griscelli syndrome* - Griscelli syndrome is a rare autosomal recessive disorder characterized by **partial albinism**, immunodeficiency, and neurological impairment. - While it involves pigmentary abnormalities, it does not typically present with the extreme photosensitivity or the very early skin cancer development described in the patient. *Chediak Higashi syndrome* - Chediak-Higashi syndrome is an autosomal recessive disorder characterized by **partial albinism**, recurrent pyogenic infections, and neurological abnormalities, due to defective lysosomal trafficking. - This syndrome is not primarily associated with extreme photosensitivity leading to early skin cancers but rather with immunodeficiency and neurological issues.
Question 7: A 6-year-old child born to consanguinity has pallor and intolerance to sunlight. His urine was exposed to Wood's light. Probable diagnosis is:
- A. SLE
- B. Xeroderma pigmentosum
- C. Gunther disease (Correct Answer)
- D. Bloom syndrome
Explanation: ***Gunther disease*** - The combination of **pallor**, **intolerance to sunlight** (photosensitivity), **consanguinity**, and particularly the **red fluorescence of urine under Wood's light** (due to increased uroporphyrins and coproporphyrins) is highly characteristic of **congenital erythropoietic porphyria (CEP)**, also known as Gunther disease. - This is an **autosomal recessive** disorder of heme synthesis, leading to accumulation of porphyrin precursors. Affected individuals often have **erythrodontia** (reddish-brown discoloration of teeth), severe **anemia**, and **hemolysis**, alongside marked photosensitivity. *SLE* - **Systemic lupus erythematosus (SLE)** can cause **photosensitivity** and **pallor (due to anemia)**, but it is an autoimmune disease, not an inborn error of metabolism. - It does not typically present with red fluorescent urine under Wood's light, which is a specific finding for porphyrias. *Xeroderma pigmentosum* - This is a rare **autosomal recessive** genetic disorder characterized by extreme **photosensitivity** and a high risk of skin cancers due to a defect in DNA repair mechanisms. - While it causes severe photosensitivity, it does not involve abnormalities in porphyrin metabolism or lead to red fluorescent urine. *Bloom syndrome* - **Bloom syndrome** is a rare **autosomal recessive** genetic disorder characterized by **photosensitivity**, **short stature**, a **distinctive facial appearance**, and an increased risk of cancer. - It does not involve porphyrin metabolism or result in red fluorescent urine under Wood's light.
Question 8: A patient developed fixed drug eruptions after taking certain medications. Which of the following drugs is known to cause these skin lesions?
- A. Phenolphthalein
- B. Aspirin
- C. Dapsone
- D. All of the above (Correct Answer)
Explanation: **Explanation:** **Fixed Drug Eruption (FDE)** is a unique type of cutaneous drug reaction characterized by the recurrence of a lesion (usually a dusky red or violaceous macule) at the **exact same anatomical site** every time the offending drug is ingested. This occurs due to the persistence of **CD8+ memory T-cells** in the basal keratinocytes at the site of the lesion. **Why Option D is correct:** All three drugs listed are classic and high-yield triggers for FDE: * **Phenolphthalein:** Historically the most common cause (found in older laxatives). * **Aspirin (NSAIDs):** A very frequent trigger in clinical practice. * **Dapsone (Sulfonamides):** Sulfonamides are among the most common drug classes associated with FDE. **Analysis of Options:** * **Phenolphthalein:** Often presents as "bullous" FDE. * **Aspirin:** Along with other NSAIDs (like Ibuprofen and Naproxen), it is a leading cause of multi-focal FDE. * **Dapsone:** As a sulfone, it shares cross-reactivity patterns and is a well-documented cause. **High-Yield Clinical Pearls for NEET-PG:** 1. **Most Common Site:** The **glans penis** is the most common site for FDE, followed by the lips and palms. 2. **Commonest Causes (Overall):** NSAIDs, Sulfonamides (Cotrimoxazole), Tetracyclines, and Anticonvulsants. 3. **Clinical Feature:** Lesions often leave behind **post-inflammatory hyperpigmentation (PIH)** after healing. 4. **Refractory Period:** After an eruption, there is a brief refractory period where the drug may not cause a reaction. 5. **Diagnosis:** Primarily clinical; however, a **Patch Test** performed at the site of the previous lesion (not on the back) can confirm the offending agent.
Question 9: Which of the following is a topical vitamin D analogue?
- A. Cholecalciferol
- B. Doxercalciferol
- C. Calcipotriol (Correct Answer)
- D. Paricalcitol
Explanation: **Explanation:** **Calcipotriol** is a synthetic analog of **1,25-dihydroxyvitamin D3 (Calcitriol)**. In dermatology, it is primarily used as a first-line topical treatment for **Psoriasis vulgaris**. Its mechanism of action involves binding to intracellular vitamin D receptors (VDR), leading to the inhibition of keratinocyte proliferation and the induction of keratinocyte differentiation. It also possesses anti-inflammatory properties by inhibiting T-cell activation. **Analysis of Options:** * **Calcipotriol (Correct):** It is specifically designed for topical use. It is as effective as potent topical corticosteroids but has a better safety profile for long-term maintenance, as it does not cause skin atrophy. * **Cholecalciferol (Option A):** This is Vitamin D3, typically administered orally as a nutritional supplement to treat Vitamin D deficiency. * **Doxercalciferol (Option B) & Paricalcitol (Option D):** These are synthetic Vitamin D analogs administered **systemically** (oral or IV). They are primarily used in the management of secondary hyperparathyroidism in patients with chronic kidney disease (CKD). **High-Yield Clinical Pearls for NEET-PG:** * **Combination Therapy:** Calcipotriol is frequently combined with **Betamethasone dipropionate** (e.g., Daivobet) for synergistic effects in psoriasis. * **Side Effects:** The most common side effect is local skin irritation. Systemic hypercalcemia is rare unless the dose exceeds **100g per week**. * **Contraindication:** It should not be applied to the face (due to irritation) and is generally avoided in patients with pre-existing hypercalcemia. * **Other Topical Analogs:** Tacalcitol and Maxacalcitol are other topical analogs used globally.
Question 10: Which drug is used for intralesional injection in keloids?
- A. Prednisolone
- B. Triamcinolone (Correct Answer)
- C. Androgen
- D. Hydrocortisone
Explanation: **Explanation:** **Triamcinolone acetonide (TAC)** is the gold standard and most commonly used drug for the intralesional treatment of keloids and hypertrophic scars. **Why Triamcinolone is the Correct Answer:** Triamcinolone is a potent, intermediate-acting synthetic corticosteroid. It works by: 1. **Inhibiting Fibroblasts:** It reduces the proliferation of fibroblasts and the synthesis of collagen. 2. **Anti-inflammatory Action:** It decreases the release of inflammatory mediators (like TGF-β) that drive excessive scarring. 3. **Increasing Collagenase:** It reduces levels of alpha-2-macroglobulin, which normally inhibits collagenase, thereby promoting the breakdown of existing collagen. The concentration typically used is **10–40 mg/mL**, injected directly into the mid-dermis of the lesion. **Analysis of Incorrect Options:** * **A & D (Prednisolone & Hydrocortisone):** These are shorter-acting corticosteroids with lower potency. They are highly soluble and rapidly absorbed into the systemic circulation, making them ineffective for maintaining the sustained local concentration required to break down dense keloidal tissue. * **C (Androgen):** Androgens have no role in the treatment of keloids; in fact, hormonal fluctuations (like puberty or pregnancy) are sometimes associated with keloid exacerbation. **High-Yield Clinical Pearls for NEET-PG:** * **Side Effects:** The most common side effects of intralesional TAC include **dermal atrophy, telangiectasia, and hypopigmentation** at the injection site. * **Combination Therapy:** For resistant keloids, TAC is often combined with **5-Fluorouracil (5-FU)** to improve efficacy and reduce atrophy. * **Cryosurgery:** Performing cryotherapy immediately before injection (the "cryo-insult" technique) softens the keloid, making the injection easier and more effective.
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