Tropical Dermatology — MCQs

Tropical Dermatology Indian Medical PG Practice Questions and MCQs

Question 31: A 7-year-old child presents with a hypopigmented, anesthetic patch on the face. What is the most probable diagnosis?

A. Intermediate leprosy (Correct Answer)
B. Pityriasis alba
C. Nevus anemicus
D. Nevus achromicus

Explanation: **Explanation:** The diagnosis of **Indeterminate Leprosy** (often referred to in exams as Intermediate leprosy) is based on the classic clinical triad of leprosy: a hypopigmented patch, loss of sensation, and (potentially) nerve involvement. In a pediatric patient, a solitary, ill-defined hypopigmented macule on the face with **definite anesthesia** is pathognomonic for early leprosy. This stage represents the earliest clinical manifestation where the host's cell-mediated immunity is yet to determine the specific polar type (Tuberculoid vs. Lepromatous). **Why the other options are incorrect:** * **Pityriasis alba:** Common in children; presents as scaly, hypopigmented patches on the face. However, **sensation is always intact**, and it is often associated with atopy. * **Nevus anemicus:** A congenital vascular anomaly. The area appears pale due to localized hypersensitivity to catecholamines (vasoconstriction), not a loss of pigment. Sensation is normal, and the patch "disappears" on diascopy (pressure). * **Nevus achromicus (Nevus depigmentosus):** A congenital stable hypopigmented patch present since birth. It has normal sensation and does not change in size relative to body growth. **High-Yield Clinical Pearls for NEET-PG:** * **Cardinal Signs of Leprosy (WHO):** 1. Hypopigmented/reddish patch with definite loss of sensation. 2. Thickened peripheral nerves. 3. Positive skin smear for acid-fast bacilli. * **Face involvement:** In children, the face is the most common site for indeterminate leprosy. * **Sensory Loss Pattern:** Temperature (cold/hot) is lost first, followed by touch, pain, and lastly, deep pressure. * **Histopathology:** Indeterminate leprosy shows non-specific perivascular and periappendageal lymphocytic infiltration; granulomas are not yet formed.

Question 32: All the features of peripheral neuritis in a patient with Hansen's disease EXCEPT?

A. Predominant sensory involvement
B. Decreased tendon reflexes (Correct Answer)
C. Mutilations
D. Peripheral nerve thickening

Explanation: In Hansen’s disease (Leprosy), peripheral neuritis is a hallmark feature caused by the invasion of *Mycobacterium leprae* into Schwann cells. ### **Why "Decreased Tendon Reflexes" is the Correct Answer** In leprosy, the nerve damage is primarily a **mononeuritis multiplex** affecting the **distal, smaller nerve branches** and cutaneous twigs. Deep Tendon Reflexes (DTRs) are mediated by large-diameter fibers and spinal arcs that remain intact until the very late, terminal stages of the disease. Therefore, even in a limb with significant sensory loss or muscle atrophy, the **tendon reflexes are characteristically preserved.** If reflexes are absent early on, one should consider other neuropathies like CIDP or Vitamin B12 deficiency. ### **Explanation of Other Options** * **A. Predominant sensory involvement:** This is a classic feature. Leprosy typically follows a sequence of sensory loss (temperature → pain → touch) before motor involvement occurs. * **C. Mutilations:** These are secondary complications of neuritis. Loss of protective sensation leads to repetitive microtrauma, secondary infections, and resorption of phalanges (auto-amputation). * **D. Peripheral nerve thickening:** This is a cardinal sign of leprosy. The inflammatory response to the bacilli causes palpable enlargement of nerves at sites of predilection (e.g., Ulnar nerve above the elbow, Common Peroneal nerve at the fibular head). ### **NEET-PG High-Yield Pearls** * **Most common nerve involved:** Ulnar nerve. * **Most common nerve involved in the face:** Zygomatic branch of the Facial nerve (leads to lagophthalmos). * **Sequence of sensory loss:** Temperature (cold then hot) → Pain → Light touch. * **Nerve Abscess:** Most commonly seen in the **Ulnar nerve** in BT (Borderline Tuberculoid) leprosy. * **Pure Neuritic Leprosy:** Diagnosed by nerve thickening and sensory loss without any visible skin lesions; usually requires a nerve biopsy for confirmation.

Question 33: What is the treatment for lepra reaction with acute neuritis?

A. Prednisolone (Correct Answer)
B. Thalidomide
C. Clofazimine
D. Dapsone

Explanation: **Explanation:** The management of lepra reactions (Type 1 and Type 2) depends heavily on the presence of nerve involvement. **Acute neuritis** is a medical emergency in leprosy because it can lead to permanent paralysis and deformity within hours or days. **1. Why Prednisolone is Correct:** Systemic corticosteroids, specifically **Prednisolone**, are the gold standard for treating acute neuritis in both Type 1 (Reversal) and Type 2 (ENL) reactions. Corticosteroids act by reducing intraneural edema and suppressing the cell-mediated immune response that causes nerve damage. Prompt initiation of steroids (usually starting at 40–60 mg/day) is essential to prevent irreversible nerve trunk damage. **2. Why the other options are incorrect:** * **Thalidomide:** While highly effective for severe **Type 2 reactions (ENL)**, it is slow to act on nerve inflammation and is **not** the first-line treatment for acute neuritis. It is also contraindicated in Type 1 reactions and pregnancy. * **Clofazimine:** This drug has anti-inflammatory properties and is used as a steroid-sparing agent in chronic ENL, but its onset of action is too slow (weeks) for the management of acute neuritis. * **Dapsone:** This is a bacteriostatic component of Multi-Drug Therapy (MDT). It has no role in managing acute immunological reactions and can occasionally trigger them. **High-Yield Clinical Pearls for NEET-PG:** * **Type 1 Reaction:** Delayed hypersensitivity (Type IV); seen in BT, BB, BL leprosy. * **Type 2 Reaction (ENL):** Immune complex-mediated (Type III); seen in BL and LL leprosy. * **Silent Neuritis:** Nerve damage occurring without pain or tenderness; also treated with Prednisolone. * **MDT Policy:** Never stop MDT during a lepra reaction; continue the standard regimen alongside steroids.

Question 34: All are features of lepromatous leprosy except?

A. Gynaecomastia
B. Madarosis
C. Saddle nose
D. Perforating Ulcer (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Perforating Ulcer**. In Leprosy, **Perforating Ulcers** (trophic ulcers) are a hallmark of **Tuberculoid Leprosy (TT/BT)**. These occur due to anesthesia resulting from early, asymmetric, and severe nerve damage. In contrast, Lepromatous Leprosy (LL) is characterized by high bacterial load but delayed nerve damage; anesthesia occurs much later and is usually symmetrical (glove-and-stocking distribution), making trophic ulcers less characteristic of the early-to-mid clinical presentation of LL. **Analysis of Incorrect Options:** * **Gynaecomastia:** This is a classic feature of LL. It occurs due to testicular atrophy caused by direct *M. leprae* infiltration (orchitis), leading to a hormonal imbalance (decreased testosterone and increased estrogen). * **Madarosis:** This refers to the loss of eyebrows (specifically the lateral one-third). It is a common feature of LL due to the infiltration of lepromas into the hair follicles. * **Saddle nose:** In LL, the bacilli infiltrate the nasal mucosa and cartilage, leading to chronic rhinitis, crusting, and eventually destruction of the nasal septum, causing the bridge of the nose to collapse. **High-Yield Clinical Pearls for NEET-PG:** * **LL Hallmark:** Bilateral symmetrical lesions, Leonine facies, and "Glove and Stocking" anesthesia. * **TT Hallmark:** Asymmetrical, well-defined anesthetic patches with early nerve enlargement. * **Bacteriology:** LL is Multibacillary (BI 3+ to 6+), while TT is Paucibacillary (BI 0 to 1+). * **Internal Organ Involvement:** LL involves the reticuloendothelial system, liver, spleen, and testes; TT is limited to skin and nerves.

Question 35: An 8-year-old boy presents with a 6-month history of an ill-defined, hypopigmented, slightly atrophic macule on the face. What is the most likely diagnosis?

A. Pityriasis alba
B. Indeterminate leprosy (Correct Answer)
C. Morphoea
D. Calcium deficiency

Explanation: **Explanation:** The correct diagnosis is **Indeterminate Leprosy**. In the context of the NEET-PG exam, any solitary, ill-defined, hypopigmented macule in a child living in an endemic area should be considered leprosy until proven otherwise. **Why Indeterminate Leprosy is correct:** Indeterminate leprosy is the earliest clinical stage of the disease. It typically presents as a **single, ill-defined, hypopigmented macule** with minimal or no sensory loss (as nerve damage is not yet advanced). While atrophy is more common in late-stage tuberculoid leprosy, early trophic changes or subtle texture alterations can occur. In pediatric cases, the face is a common site of involvement. **Why other options are incorrect:** * **Pityriasis alba:** Presents as multiple, scaly, hypopigmented patches with fuzzy borders, usually associated with atopy. It does **not** cause atrophy. * **Morphoea (Localized Scleroderma):** While it causes atrophy, the initial stage is usually a violaceous or "lilac" patch that progresses to a firm, ivory-white sclerotic plaque. It is not primarily a hypopigmented macule. * **Calcium deficiency:** This is a common **myth**. Nutritional deficiencies (like Vitamin A or Calcium) do not cause localized, atrophic hypopigmented macules on the face. **Clinical Pearls for NEET-PG:** * **Cardinal Signs of Leprosy:** Hypopigmented/reddish patch with (1) definite loss of sensation, (2) thickened nerves, or (3) positive skin smear for AFB. * **Indeterminate Leprosy Histology:** Shows non-specific lymphocytic infiltration around skin appendages and nerves; Lepra bacilli are rarely found. * **Prognosis:** Most cases of indeterminate leprosy in children self-heal, but some progress to the determinate spectrum (TT, BT, BB, BL, or LL).

Question 36: Esthiomene is seen in which of the following conditions?

A. Chancroid
B. Syphilis
C. Lymphogranuloma Venereum (LGV) (Correct Answer)
D. Gonorrhoea

Explanation: **Explanation:** **Esthiomene** is a late-stage chronic manifestation of **Lymphogranuloma Venereum (LGV)**, caused by *Chlamydia trachomatis* (serotypes L1, L2, and L3). The underlying mechanism involves chronic lymphatic obstruction and persistent inflammation. In the tertiary stage of LGV, extensive destruction of the lymphatic vessels leads to chronic lymphedema, resulting in massive, painful, and disfiguring swelling of the external genitalia (vulva in females, scrotum/penis in males), often accompanied by ulceration and fistulae. **Analysis of Options:** * **Chancroid (Option A):** Caused by *Haemophilus ducreyi*, it presents with painful "soft" ulcers and painful inguinal lymphadenopathy (buboes), but does not cause chronic lymphatic obstruction or esthiomene. * **Syphilis (Option B):** Caused by *Treponema pallidum*. Primary syphilis presents with a painless "hard" chancre. While tertiary syphilis can cause gummas, it does not typically result in genital elephantiasis. * **Gonorrhoea (Option C):** Caused by *Neisseria gonorrhoeae*, it primarily presents as urethritis or cervicitis. It does not involve the lymphatic system in a way that leads to esthiomene. **High-Yield Clinical Pearls for NEET-PG:** * **LGV Stages:** 1. Primary: Small, painless transient papule/ulcer. 2. Secondary: **Groove Sign** (inguinal ligament dividing matted lymph nodes). 3. Tertiary: **Esthiomene** (genito-anorectal syndrome). * **Drug of Choice for LGV:** Doxycycline (100 mg BID for 21 days). * **Differential Diagnosis:** Esthiomene must be differentiated from **Donovanosis** (Granuloma Inguinale), which presents with "beefy red" ulcers but lacks significant lymphadenopathy.

Question 37: What is the drug of choice for Erythema Nodosum Leprosum?

A. Steroids (Correct Answer)
B. Thalidomide
C. Clofazimine
D. Aspirin

Explanation: **Explanation:** **Erythema Nodosum Leprosum (ENL)**, also known as a **Type 2 Lepra Reaction**, is a Type III hypersensitivity reaction (immune-complex mediated) occurring primarily in Lepromatous (LL) and Borderline Lepromatous (BL) leprosy. **Why Steroids are the Correct Answer:** Systemic **Corticosteroids (Prednisolone)** are the **first-line drug of choice** for managing ENL. They are preferred because they provide rapid control of acute inflammation, stabilize lysosomal membranes, and prevent nerve damage. In the context of NEET-PG, unless the question specifically asks for the "most effective" or "drug for recurrent/chronic ENL," steroids remain the standard initial treatment. **Analysis of Incorrect Options:** * **B. Thalidomide:** While Thalidomide is the **most effective** drug for ENL and the treatment of choice for chronic/recurrent cases, it is not the first-line choice due to its severe **teratogenicity** (phocomelia) and restricted availability. * **C. Clofazimine:** This drug has anti-inflammatory properties and is used as a **steroid-sparing agent** in chronic ENL. However, it has a slow onset of action (takes 4–6 weeks) and is not suitable for acute management. * **D. Aspirin:** Used only for very **mild** cases of ENL to manage pain and fever; it cannot control the systemic immune response in moderate to severe reactions. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Type 2 reaction involves Arthus-type phenomenon with deposition of Ag-Ab complexes and TNF-α release. * **Clinical Feature:** Characterized by tender, evanescent, erythematous nodules, fever, and systemic involvement (neuritis, orchitis, iridocyclitis). * **Thalidomide Contraindication:** Strictly contraindicated in women of childbearing age. * **MDT Status:** During a lepra reaction, **never stop** the Multi-Drug Therapy (MDT).

Question 38: All of the following are true regarding erythrocyanosis frigida, EXCEPT:

A. Seen exclusively in alcoholic males (Correct Answer)
B. Occurs in the lower third of leg on leg or ankle
C. Causes Bazin's ulcer
D. Sympathectomy may be beneficial in some patients

Explanation: **Explanation:** **Erythrocyanosis frigida** (also known as *erythrocyanosis crurum puellarum frigida*) is a localized vascular disorder caused by an abnormal response to cold. **1. Why Option A is the Correct Answer (The Exception):** The statement is false because the condition is seen **almost exclusively in young women**, particularly those with "heavy" or fat legs. It is not associated with alcoholic males. The pathogenesis involves cold-induced vasospasm of the arterioles followed by secondary dilatation of the capillaries and venules in areas with thick subcutaneous fat. **2. Analysis of Other Options:** * **Option B:** It characteristically involves the **lower third of the leg**, the ankles, and sometimes the posterior aspect of the calves. The affected skin appears dusky, cyanotic, and cold to the touch. * **Option C:** Severe cases can lead to the formation of painful, chronic ulcers known as **Bazin’s ulcers** (Erythema Induratum). While Bazin's disease is traditionally associated with tuberculosis, the term is also used for the ulcerative stage of erythrocyanosis. * **Option D:** Treatment focuses on keeping the limbs warm. However, in severe or refractory cases, **lumbar sympathectomy** may be beneficial to improve peripheral blood flow and promote healing of ulcers. **Clinical Pearls for NEET-PG:** * **Triad of Erythrocyanosis:** Coldness, cyanosis (bluish-red discoloration), and swelling. * **Differential Diagnosis:** Must be distinguished from **Chilblains** (Pernio), which presents as itchy/burning papules on fingers/toes, and **Livedo Reticularis**. * **Key Demographic:** Think "Young females with thick legs in cold climates."

Question 39: Which of the following statements about Yaws is not true?

A. Spread by sexual transmission (Correct Answer)
B. Caused by Treponema pallidum pertenue
C. Has cross immunity with syphilis
D. Cannot be differentiated serologically from T. pallidum

Explanation: **Explanation:** **Yaws** is a chronic, non-venereal treponematosis caused by the bacterium *Treponema pallidum pertenue*. 1. **Why Option A is correct:** Unlike Syphilis, Yaws is **not** a sexually transmitted infection. It is primarily a disease of childhood (usually under 15 years) and is transmitted through **direct skin-to-skin contact** with infectious lesions. It thrives in warm, humid, tropical environments where poor hygiene and overcrowding are prevalent. 2. **Why the other options are wrong:** * **Option B:** This is a true statement. The causative agent is *T. pallidum pertenue*, which is morphologically identical to the agent of syphilis. * **Option C:** This is true. Infection with Yaws provides a degree of **cross-immunity** against syphilis, which is why venereal syphilis was historically less common in areas where Yaws was endemic. * **Option D:** This is true. Because the organisms are so closely related, standard serological tests (both non-treponemal like **VDRL/RPR** and treponemal like **TPHA/FTA-ABS**) cannot distinguish between Yaws and Syphilis. Diagnosis relies on clinical presentation and epidemiological history. **High-Yield Clinical Pearls for NEET-PG:** * **Stages:** Primary (Mother Yaw/Frambesioma), Secondary (Daughter Yaws), and Tertiary (Goundou – swelling of nasal bones; Gangosa – destructive rhinopharyngitis). * **Bone Involvement:** Saber shin (periostitis) is a common late feature. * **Treatment:** A single dose of **Oral Azithromycin** is now the preferred treatment (WHO Morges Strategy), replacing injectable Penicillin G Benzathine. * **Target:** Yaws is targeted by the WHO for global eradication.

Question 40: All of the following are characteristic features of lepromatous leprosy except?

A. Presence of globi
B. Subepidermal free zone
C. Decreased cell-mediated immunity
D. Presence of granulomas subdermally (Correct Answer)

Explanation: In Lepromatous Leprosy (LL), the immune system fails to mount an effective response against *Mycobacterium leprae*, leading to specific histopathological and immunological findings. **Why Option D is the Correct Answer:** In LL, the characteristic finding is a **diffuse dermal infiltration** of foamy macrophages (Virchow cells) laden with bacilli. True **granulomas** (organized collections of epithelioid cells, lymphocytes, and giant cells) are a hallmark of **Tuberculoid Leprosy (TT)**, where cell-mediated immunity (CMI) is strong. In LL, the lack of CMI prevents the formation of organized granulomas. **Explanation of Incorrect Options:** * **A. Presence of globi:** Due to high bacterial load (multibacillary), acid-fast bacilli (AFB) aggregate in large clumps within macrophages; these are called globi. * **B. Subepidermal free zone (Grenz zone):** This is a classic histopathological feature of LL. It is a thin layer of normal collagen separating the epidermis from the underlying dermal infiltrate, caused by the lack of a delayed-type hypersensitivity reaction. * **C. Decreased cell-mediated immunity:** LL represents the Th2-dominant pole of the spectrum. There is a specific anergy to *M. leprae* antigens, resulting in a negative Lepromin test. **NEET-PG High-Yield Pearls:** * **Leonine Facies:** Caused by diffuse infiltration of the face in LL. * **Lepromin Test:** Strongly positive in TT (strong CMI) and **negative** in LL (absent CMI). * **Nerve Involvement:** In LL, nerve involvement is **symmetrical** and occurs late, whereas in TT, it is **asymmetrical** and occurs early. * **Foamy Macrophages:** Also known as Lepra cells or Virchow cells.

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