ABD Pigmentary Disorders 2 — Questions and Answers
Question 1: Generalized hyperpigmentation in Addison's disease (primary adrenal insufficiency) is caused by:
- Excess ACTH cross-reacting with MC1R on melanocytes due to loss of cortisol feedback (Correct answer)
- Direct adrenal pigment deposition in the skin
- Secondary hypercortisolism stimulating melanogenesis
- Pineal gland secretion of alpha-MSH
Correct answer: Excess ACTH cross-reacting with MC1R on melanocytes due to loss of cortisol feedback
Loss of cortisol removes negative feedback on the pituitary, causing excess POMC cleavage into ACTH and alpha-MSH; ACTH cross-reacts with the melanocortin-1 receptor (MC1R) on melanocytes, increasing melanin production.
Question 2: Long-term amiodarone therapy produces a distinctive skin discoloration described as:
- Brown-black from direct melanocyte stimulation
- Slate-gray to blue-gray from drug-lipofuscin complexes in dermal macrophages in sun-exposed areas (Correct answer)
- Yellow from lipid-drug complexes in the dermis
- Red-brown from hemosiderin deposition
Correct answer: Slate-gray to blue-gray from drug-lipofuscin complexes in dermal macrophages in sun-exposed areas
Amiodarone's iodine content renders it phototoxic; chronic exposure causes iodine-containing drug-lipofuscin complexes to accumulate in dermal macrophages, producing a characteristic slate-gray or blue-gray pigmentation in photoexposed skin.
Question 3: Which combination of features best differentiates dermal melanocytosis (Mongolian spot) from non-accidental trauma (bruising) in an infant?
- Location on the lumbosacral area only
- Blue-gray color stable over days without color evolution or associated edema
- Presence at birth
- All of the above (Correct answer)
Correct answer: All of the above
Mongolian spots are congenital (present at birth), located characteristically on the lumbosacral region, and show stable blue-gray color without the sequential color change (purple→green→yellow) or swelling that accompanies bruising.
Question 4: A halo nevus with a depigmented ring surrounding a central benign-appearing melanocytic nevus is best explained by:
- Early superficial spreading melanoma replacing nevus cells
- Cytotoxic T-lymphocyte-mediated immune destruction of nevus melanocytes extending to surrounding normal melanocytes (Correct answer)
- Traumatic depigmentation from repeated friction
- Postinflammatory hypopigmentation from prior dermatitis
Correct answer: Cytotoxic T-lymphocyte-mediated immune destruction of nevus melanocytes extending to surrounding normal melanocytes
Halo nevi result from a cytotoxic CD8+ T-cell immune response targeting nevus melanocytes that extends to adjacent normal melanocytes, producing a depigmented halo — a mechanism shared with vitiligo.
Question 5: Progressive macular hypomelanosis is distinguished from pityriasis versicolor by which Wood's lamp finding?
- Brilliant blue-white fluorescence of hypopigmented patches
- Folliculocentric red fluorescence in coalescing hypopigmented trunk macules (Correct answer)
- Yellow-green fluorescence throughout affected areas
- No fluorescence, distinguishing it from pityriasis versicolor's yellow fluorescence
Correct answer: Folliculocentric red fluorescence in coalescing hypopigmented trunk macules
Progressive macular hypomelanosis shows pathognomonic folliculocentric red fluorescence under Wood's lamp, caused by porphyrins produced by Cutibacterium acnes colonizing follicles, unlike pityriasis versicolor's yellow-green fluorescence.
Question 6: Idiopathic guttate hypomelanosis is best described as:
- Autoimmune complete depigmentation in sun-exposed skin of young adults
- Multiple discrete small porcelain-white macules on chronically sun-exposed extremities of middle-aged and older adults due to focal melanocyte loss (Correct answer)
- Congenital hypopigmented macules with central clearing
- Drug-induced melanocyte toxicity presenting on the legs
Correct answer: Multiple discrete small porcelain-white macules on chronically sun-exposed extremities of middle-aged and older adults due to focal melanocyte loss
Idiopathic guttate hypomelanosis presents as multiple small, well-demarcated white macules on chronically sun-damaged extremities (shins and forearms) in older adults, caused by focal loss of melanocytes from cumulative UV exposure.
Question 7: For refractory dermal melasma in a Fitzpatrick skin type IV patient, which laser approach is preferred with the lowest risk of post-inflammatory hyperpigmentation?
- Q-switched Nd:YAG 1064 nm at low fluence (toning protocol) (Correct answer)
- Ablative fractional CO2 laser at high energy
- Pulsed dye laser 595 nm
- KTP 532 nm laser targeting epidermal pigment
Correct answer: Q-switched Nd:YAG 1064 nm at low fluence (toning protocol)
Low-fluence Q-switched Nd:YAG 1064 nm (toning protocol) penetrates to the dermis to target melanophages with minimal epidermal injury, offering the best safety profile for darker skin types with dermal melasma.
ABD Pigmentary Disorders 2
Generalized hyperpigmentation in Addison's disease (primary adrenal insufficiency) is caused by: