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:
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?
Dapsone is used in which of the following conditions?
Which of the following monoclonal antibodies is used in the treatment of atopic dermatitis?
All of the following statements are true regarding warfarin toxicity (skin necrosis) except?
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: 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 5: 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 6: 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 7: 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 8: Dapsone is used in which of the following conditions?
- A. Dermatitis herpetiformis (Correct Answer)
- B. Pityriasis rosacea
- C. Contact dermatitis
- D. Oculocutaneous albinism
Explanation: **Explanation:** **Dapsone (Diaminodiphenyl sulfone)** is the drug of choice for **Dermatitis Herpetiformis (DH)**. DH is an autoimmune blistering disorder characterized by IgA deposits at the dermal papillae, leading to intense pruritus and neutrophilic infiltration. Dapsone works by inhibiting the enzyme myeloperoxidase and preventing the chemotaxis of neutrophils to the skin, providing rapid symptomatic relief (often within 24–48 hours). **Analysis of Options:** * **A. Dermatitis Herpetiformis:** Correct. It is the primary indication for Dapsone in dermatology. * **B. Pityriasis Rosea:** This is a self-limiting inflammatory condition (likely viral/HHV-6,7). Treatment is supportive (antihistamines, topical steroids); Dapsone has no role. * **C. Contact Dermatitis:** This is a Type IV hypersensitivity reaction. Management involves allergen avoidance and topical or systemic corticosteroids. * **D. Oculocutaneous Albinism:** This is a genetic disorder of melanin synthesis. There is no pharmacological "cure"; management focuses on photoprotection and monitoring for skin cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Antifolate (inhibits dihydropteroate synthase) and anti-inflammatory (inhibits neutrophil recruitment). * **Other Indications:** Leprosy (part of MDT), Pemphigoid, Subcorneal Pustular Dermatosis (Sneddon-Wilkinson disease), and Brown Recluse spider bites. * **Mandatory Pre-screening:** Always check **G6PD levels** before starting Dapsone to prevent severe **hemolytic anemia**. * **Side Effects:** Dose-dependent hemolysis, methemoglobinemia (presents as cyanosis), and the "Dapsone Syndrome" (fever, malaise, exfoliative dermatitis, and hepatitis).
Question 9: Which of the following monoclonal antibodies is used in the treatment of atopic dermatitis?
- A. Ipilimumab
- B. Dupilumab (Correct Answer)
- C. Durvalumab
- D. Reslizumab
Explanation: **Explanation:** **1. Why Dupilumab is Correct:** Dupilumab is a fully human monoclonal antibody that targets the **interleukin-4 receptor alpha (IL-4Rα) subunit**. By binding to this subunit, it inhibits the signaling of both **IL-4 and IL-13**. These cytokines are the key drivers of **Type 2 (Th2) inflammation**, which is the primary pathophysiological mechanism in atopic dermatitis. It is currently the first-line systemic biologic approved for moderate-to-severe atopic dermatitis unresponsive to topical therapies. **2. Why the Other Options are Incorrect:** * **Ipilimumab:** A checkpoint inhibitor that targets **CTLA-4**. It is used in the treatment of advanced melanoma and renal cell carcinoma. * **Durvalumab:** A checkpoint inhibitor that targets **PD-L1**. It is primarily used in the treatment of non-small cell lung cancer (NSCLC) and bladder cancer. * **Reslizumab:** An interleukin-5 (**IL-5**) antagonist. It is used as add-on maintenance treatment for severe eosinophilic asthma, not atopic dermatitis. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Dual inhibitor of IL-4 and IL-13. * **Common Side Effect:** The most characteristic side effect of Dupilumab is **allergic conjunctivitis** and blepharitis. * **Other Indications:** It is also FDA-approved for moderate-to-severe asthma (eosinophilic phenotype) and chronic rhinosinusitis with nasal polyposis. * **Memory Aid:** "Dupi" stops the "D"ermatitis by blocking the "4" and "13" (IL-4/13).
Question 10: All of the following statements are true regarding warfarin toxicity (skin necrosis) except?
- A. Skin necrosis occurs during initiation of therapy.
- B. Most common sites are buttocks and abdomen. (Correct Answer)
- C. Decreased quantity of protein C.
- D. Decreased incidence of adverse effects if therapy with LMWH is started.
Explanation: **Explanation:** Warfarin-induced skin necrosis (WISN) is a rare but severe complication occurring in approximately 0.01% to 0.1% of patients treated with vitamin K antagonists. **Why Option B is the correct answer (The False Statement):** While the buttocks and abdomen are common sites, the **most common sites** for warfarin necrosis are areas with **high subcutaneous fat content**, specifically the **breasts** (in females), followed by the thighs and buttocks. The statement in Option B is considered the "except" because it overlooks the breast as the primary site of predilection. **Analysis of Other Options:** * **Option A:** True. Necrosis typically occurs **3 to 10 days after initiation** of therapy, often due to a large loading dose. * **Option C:** True. Warfarin inhibits Vitamin K-dependent factors (II, VII, IX, X) and anticoagulant proteins (C and S). **Protein C has a shorter half-life** (6 hours) compared to clotting factors. This creates a transient "prothrombotic window" where natural anticoagulants are depleted while procoagulant factors are still active, leading to microvascular thrombosis. * **Option D:** True. Starting **Low Molecular Weight Heparin (LMWH)** as a "bridge" provides immediate anticoagulation, preventing the thrombotic complications during the initial drop in Protein C levels. **Clinical Pearls for NEET-PG:** * **Risk Factor:** Underlying **Protein C deficiency** is the most significant risk factor. * **Clinical Presentation:** Sudden onset of painful, erythematous, or purpuric lesions that rapidly progress to **hemorrhagic bullae and eschar**. * **Management:** Immediate discontinuation of Warfarin, administration of **Vitamin K**, and starting **Heparin** or Protein C concentrates.
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