Post-inflammatory Hypopigmentation Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Post-inflammatory Hypopigmentation. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Post-inflammatory Hypopigmentation Indian Medical PG Question 1: Match the following woods lamp findings: 1. Erythrasma, 2. Pityriasis versicolor, 3. Tinea capitis, 4. Vitiligo || a. Yellow b. Coral red fluorescence c. Pink d. Green e. Milky white
- A. 1-d, 2-a, 3-c, 4-e
- B. 1-b, 2-a, 3-d, 4-e (Correct Answer)
- C. 1-a, 2-c, 3-e, 4-d
- D. 1-b, 2-d, 3-a, 4-c
Post-inflammatory Hypopigmentation Explanation: ***1-b, 2-a, 3-d, 4-e***
- **Erythrasma** is caused by *Corynebacterium minutissimum* and produces **porphyrins** that fluoresce **coral red** under a Wood's lamp [1].
- **Pityriasis versicolor** is caused by *Malassezia furfur* and typically fluoresces **yellow to yellowish-green** [2].
- **Tinea capitis** (especially due to *Microsporum* species) shows **green fluorescence** of infected hairs.
- **Vitiligo** lesions, due to a complete absence of melanin, appear as **milky white** or bright white areas under a Wood's lamp [3].
*1-d, 2-a, 3-c, 4-e*
- This option incorrectly states that Erythrasma fluoresces green. Green fluorescence is characteristic of *Microsporum* species causing **Tinea capitis**.
- Additionally, Tinea capitis is incorrectly associated with pink fluorescence, which is not a typical finding.
*1-a, 2-c, 3-e, 4-d*
- This option incorrectly states that Erythrasma fluoresces yellow. Yellow fluorescence is associated with **Pityriasis versicolor** [2].
- It also incorrectly assigns milky white fluorescence to Tinea capitis and green fluorescence to Vitiligo.
*1-b, 2-d, 3-a, 4-c*
- This option incorrectly associates Pityriasis versicolor with green fluorescence. While some variations exist, **yellow** is the more characteristic finding [2].
- It also incorrectly links Tinea capitis to yellow fluorescence and Vitiligo to pink, which are not typical Wood's lamp findings for these conditions.
Post-inflammatory Hypopigmentation Indian Medical PG Question 2: What is the primary condition for which calcitriol is used as a treatment?
- A. Pemphigus
- B. Secondary hyperparathyroidism (Correct Answer)
- C. Lichen planus
- D. Leprosy
Post-inflammatory Hypopigmentation Explanation: Secondary hyperparathyroidism
- Calcitriol is the active form of vitamin D (1,25-dihydroxyvitamin D₃), and it is crucial for regulating calcium and phosphate levels in the body [1].
- In secondary hyperparathyroidism, often seen in chronic kidney disease (CKD), the kidneys cannot convert vitamin D to its active form, leading to hypocalcemia and increased PTH secretion [1], [2].
- Calcitriol supplementation helps to increase calcium absorption from the gut and suppress the release of parathyroid hormone (PTH), thereby treating the underlying cause of secondary hyperparathyroidism [1], [2].
- This is the primary therapeutic indication for calcitriol in clinical practice.
Lichen planus
- This is a chronic inflammatory condition affecting the skin, hair, nails, and mucous membranes
- Typically treated with corticosteroids or other immunosuppressants
- Calcitriol has no primary role in the treatment of lichen planus; its therapeutic applications are predominantly related to calcium and bone metabolism
Pemphigus
- Pemphigus is a group of rare autoimmune blistering diseases that affect the skin and mucous membranes
- Primary treatment involves immunosuppressants like corticosteroids, often in high doses
- Calcitriol is not indicated for the treatment of pemphigus, as its mechanism of action is unrelated to the autoimmune processes characteristic of this disease
Leprosy
- Leprosy is a chronic infectious disease caused by the bacterium Mycobacterium leprae
- Treated with multi-drug therapy (MDT), which includes antibiotics like rifampicin, dapsone, and clofazimine
- Calcitriol is not an antibiotic and therefore has no role in treating the bacterial infection responsible for leprosy
Post-inflammatory Hypopigmentation Indian Medical PG Question 3: Contraindications for skin traction: a) Dermatitis b) Vascularly compromised status of limb c) Abrasions d) Hypopigmentation (vitiligo) e) Bony deformity
- A. ab
- B. abc (Correct Answer)
- C. acd
- D. bcd
Post-inflammatory Hypopigmentation Explanation: ***abc***
- **Dermatitis**, **vascularly compromised status of limb**, and **abrasions** are all absolute contraindications for skin traction as they compromise skin integrity and circulation.
- Applying skin traction in these conditions can lead to **skin breakdown**, **infection**, further **ischemic damage**, or failure of adhesive application due to compromised skin surface.
*bcd*
- This option incorrectly includes **hypopigmentation (vitiligo)** as a contraindication, which does not affect skin integrity or prevent safe traction application.
- It omits **dermatitis**, a key contraindication that causes inflamed, compromised skin unsuitable for adhesive traction.
*ab*
- While **dermatitis** and **vascular compromise** are indeed contraindications, this option is incomplete as it omits **abrasions**.
- **Abrasions** represent broken skin integrity that prevents safe adhesive application and increases **infection risk**, making it a clear contraindication.
*acd*
- This option incorrectly includes **hypopigmentation (vitiligo)** as a contraindication, which is merely a cosmetic condition not affecting skin function.
- It omits **vascularly compromised status of limb**, a critical contraindication that can lead to **tissue necrosis** when traction forces are applied.
Post-inflammatory Hypopigmentation Indian Medical PG Question 4: How does narrowband UVB therapy work in psoriasis?
- A. Melanin synthesis
- B. Collagen breakdown
- C. Keratinocyte proliferation
- D. T cell apoptosis (Correct Answer)
Post-inflammatory Hypopigmentation 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.
Post-inflammatory Hypopigmentation Indian Medical PG Question 5: Large unilateral hypopigmented lesions on the right trunk and arm in a female are best explained by which of the following?
- A. Autoimmune theory
- B. Neurogenic theory (Correct Answer)
- C. Genetic predisposition
- D. Lerner's self-destruct theory
Post-inflammatory Hypopigmentation Explanation: ***Neurogenic theory***
- This theory posits that **neural mechanisms** play a role in the development of some hypopigmented disorders. The **unilateral distribution** along a dermatome or nerve pathway strongly supports a neurogenic origin.
- The **large, unilateral hypopigmented lesions on the right trunk and arm** are characteristic of conditions like **segmental vitiligo** or **hypopigmentation following nerve injury**, where neural factors are implicated in melanocyte dysfunction.
*Autoimmune theory*
- The autoimmune theory explains **generalized vitiligo**, where the body's immune system attacks melanocytes, leading to widespread depigmentation.
- It does not account for the **segmental, unilateral distribution** observed in this case, which is typically not seen in autoimmune conditions.
*Genetic predisposition*
- While genetics can increase susceptibility to certain pigmentary disorders, it does not explain the **unilateral, segmental pattern** of hypopigmentation.
- Genetic factors usually lead to more generalized or bilateral presentations rather than a localized, nerve-distribution pattern.
*Lerner's self-destruct theory*
- **Lerner's self-destruct theory** suggests that melanocytes may destroy themselves from within due to metabolic defects or oxidative stress.
- This theory also fails to explain the **unilateral, dermatomal distribution** of the lesions, as self-destruction would likely occur more randomly or symmetrically.
Post-inflammatory Hypopigmentation Indian Medical PG Question 6: A 15cm hyperpigmented macule on an adolescent male undergoes changes such as coarseness, growth of hair & acne. Diagnosis is?
- A. Melanocytic nevus
- B. Becker nevus (Correct Answer)
- C. Sebaceous nevus
- D. Sebaceous adenoma
Post-inflammatory Hypopigmentation Explanation: ***Becker nevus***
- A Becker nevus is a **hyperpigmented patch** that typically appears during adolescence in males, often on the shoulder or upper trunk.
- It characteristically becomes **hairy (hypertrichosis)**, more coarse, and can develop acne within the lesion, particularly during puberty due to androgen sensitivity.
*Melanocytic nevus*
- While melanocytic nevi are hyperpigmented, they generally do not show the characteristic changes of **coarseness, significant hair growth, or acne** within the lesion during adolescence.
- They are typically stable in size and texture after initial development, with changes raising concern for **melanoma**.
*Sebaceous nevus*
- A sebaceous nevus is a **congenital lesion** often appearing as a yellowish-orange, waxy, or bumpy patch, usually on the scalp or face.
- It does not typically present as a large, flat hyperpigmented macule that develops hair and acne in adolescence; instead, it may become verrucous or develop tumors in adulthood.
*Sebaceous adenoma*
- A sebaceous adenoma is a **benign tumor** of the sebaceous glands, usually appearing as a small, solitary, flesh-colored to yellowish papule or nodule, especially on the face.
- It is not typically seen as a large, hyperpigmented macule that grows hair and acne over a broad area, as described in the question.
Post-inflammatory Hypopigmentation Indian Medical PG Question 7: A 35-year-old obese woman presents with recurrent lesions in both axilla in summer season. Wood lamp examination is shown. The diagnosis is:
- A. Ecthyma
- B. Erythrasma (Correct Answer)
- C. Impetigo contagiosa
- D. Bullous impetigo
Post-inflammatory Hypopigmentation Explanation: ***Erythrasma***
- Erythrasma is a superficial bacterial infection caused by **Corynebacterium minutissimum**, which commonly presents as red-brown patches in intertriginous areas like the axilla, especially in obese individuals and warm, humid conditions (summer season).
- The distinctive **coral-red fluorescence under Wood's lamp** is due to porphyrin production by the bacteria, which is a classic diagnostic feature of erythrasma, as shown in the image.
*Ecthyma*
- Ecthyma is a deeper form of impetigo characterized by **ulcerative lesions with a thick, adherent crust** that extend into the dermis.
- It is typically caused by *Streptococcus pyogenes* and sometimes *Staphylococcus aureus*, and would not exhibit coral-red fluorescence under Wood's lamp.
*Impetigo contagiosa*
- Impetigo contagiosa (non-bullous impetigo) presents with **honey-colored crusted lesions**, usually on the face and extremities.
- While also a bacterial skin infection, it is typically caused by *Staphylococcus aureus* or *Streptococcus pyogenes* and does not show coral-red fluorescence under Wood's lamp.
*Bullous impetigo*
- Bullous impetigo is characterized by **flaccid bullae** (blisters) that rupture to form thin, varnish-like crusts, primarily caused by *Staphylococcus aureus* producing exfoliative toxins.
- Similar to other forms of impetigo, it does not produce the coral-red fluorescence under Wood's lamp.
Post-inflammatory Hypopigmentation Indian Medical PG Question 8: Which of the following is not a part of P. versicolor treatment -
- A. Selenium sulfide
- B. Clotrimazole
- C. Ketoconazole
- D. Griseofulvin (Correct Answer)
Post-inflammatory Hypopigmentation Explanation: **Griseofulvin (Correct - NOT used for P. versicolor)**
- **Griseofulvin** interferes with fungal cell division and is primarily used for dermatophyte infections of the skin, hair, and nails, not superficial yeast infections like *P. versicolor*.
- It is systemically absorbed and incorporated into **keratin precursor cells**, offering protection against dermatophytes in newly formed tissue.
- *Malassezia* species (causing P. versicolor) are **yeasts**, not dermatophytes, making griseofulvin ineffective.
*Selenium sulfide (Incorrect - IS used)*
- **Selenium sulfide** is an effective topical antifungal agent commonly used in shampoos and lotions to treat *P. versicolor* by inhibiting the growth of *Malassezia* species.
- It works by reducing **sebum production** and having a direct fungistatic effect on the yeast.
*Clotrimazole (Incorrect - IS used)*
- **Clotrimazole** is a broad-spectrum azole antifungal that is very effective as a topical treatment for *P. versicolor* by inhibiting ergosterol synthesis in the fungal cell membrane.
- It works well for localized patches of the infection.
*Ketoconazole (Incorrect - IS used)*
- **Ketoconazole**, another azole antifungal, is highly effective for *P. versicolor* and can be used topically (shampoos, creams) or orally in more extensive or recalcitrant cases.
- It disrupts the fungal cell membrane by inhibiting the synthesis of **ergosterol**.
Post-inflammatory Hypopigmentation Indian Medical PG Question 9: Match the following scale types with their lesions.
| Scales | Lesions |
| :-- | :-- |
| 1. Collarette scales | a. Pityriasis versicolour |
| 2. Silvery scales | b. Pityriasis rosea |
| 3. Mica-like scales | c. Psoriasis |
| 4. Branny scales | d. Pityriasis lichenoides |
- A. 1-d, 2-c, 3-a, 4-b
- B. 1-c, 2-b, 3-d, 4-a
- C. 1-a, 2-b, 3-d, 4-c
- D. 1-b, 2-c, 3-d, 4-a (Correct Answer)
Post-inflammatory Hypopigmentation Explanation: ***1-b, 2-c, 3-d, 4-a***
- **Collarette scales** are pathognomonic of **Pityriasis rosea**, appearing as fine, trailing scales around the periphery of oval lesions in a "Christmas tree" distribution.
- **Silvery scales** are the classic hallmark of **Psoriasis**, presenting as thick, adherent, silvery-white scales overlying well-demarcated erythematous plaques.
- **Mica-like scales** are characteristic of **Pityriasis lichenoides**, appearing as thick, shiny, adherent scales that can be peeled off like mica sheets.
- **Branny scales** are typical of **Pityriasis versicolor**, presenting as fine, powdery scales caused by **Malassezia** yeast overgrowth.
*1-d, 2-c, 3-a, 4-b*
- Incorrectly matches **collarette scales with Pityriasis lichenoides**, which typically presents with mica-like scales, not collarette scales.
- Misassociates **mica-like scales with Pityriasis versicolor**, which characteristically has branny (fine, powdery) scales.
*1-c, 2-b, 3-d, 4-a*
- Wrongly pairs **collarette scales with Psoriasis**, which is known for thick silvery scales, not peripheral collarette scales.
- Incorrectly matches **silvery scales with Pityriasis rosea**, which has collarette scales at lesion periphery, not silvery scales.
*1-a, 2-b, 3-d, 4-c*
- Falsely associates **collarette scales with Pityriasis versicolor**, which has branny scales from yeast infection, not collarette scales.
- Mismatches **branny scales with Psoriasis**, which has characteristic thick silvery scales, not fine powdery scales.
Post-inflammatory Hypopigmentation Indian Medical PG Question 10: A patient presents with the skin finding shown in the image. Identify the most likely diagnosis for this lesion.
- A. Vitiligo
- B. Contact leukoderma
- C. Piebaldism (Correct Answer)
- D. Albinism
Post-inflammatory Hypopigmentation Explanation: ***Piebaldism***
- The image shows a **localized patch of depigmentation** on the forehead, characteristic of **piebaldism**.
- **Piebaldism** is a rare, congenital autosomal dominant disorder caused by a defect in melanocyte development and migration, resulting in stable, well-demarcated depigmented areas, often with a **white forelock**.
*Vitiligo*
- **Vitiligo** typically presents as **progressive, acquired macules and patches of depigmentation** that often enlarge over time.
- While it can appear on the face, the sharply demarcated, congenital appearance seen here is more consistent with piebaldism.
*Contact leukoderma*
- **Contact leukoderma** is an **acquired depigmentation** resulting from exposure to chemicals (e.g., rubber, phenols).
- It would usually present in areas of direct contact, and the congenital nature of the lesion in the image rules this out.
*Albinism*
- **Albinism** is a **generalized hypopigmentation** affecting the skin, hair, and eyes due to a defect in melanin production.
- The image shows a localized patch of depigmentation, not a widespread lack of pigment characteristic of albinism.
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