{"id":36878,"date":"2026-05-28T09:54:17","date_gmt":"2026-05-28T04:24:17","guid":{"rendered":"https:\/\/atsixty.com\/?p=36878"},"modified":"2026-05-30T07:56:37","modified_gmt":"2026-05-30T02:26:37","slug":"pigmentary-disorders","status":"publish","type":"post","link":"https:\/\/atsixty.com\/index.php\/neet-pg\/pigmentary-disorders\/","title":{"rendered":"Pigmentary Disorders"},"content":{"rendered":"\n\n\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Playfair+Display:ital,wght@0,400;0,600;0,700;1,400;1,600&#038;family=Source+Serif+4:ital,wght@0,300;0,400;0,600;1,400&#038;display=swap\" rel=\"stylesheet\">\n<style>\n\/* All styles namespaced to #pigm01 -- no bleed into WordPress theme *\/\n#pigm01 *,#pigm01 *::before,#pigm01 *::after{box-sizing:border-box;margin:0;padding:0}\n#pigm01{\n  --ter:#8B3D20;--ter-light:#B85A38;--ter-pale:#FDF0EB;--ter-dark:#6B2D14;\n  --correct:#2D6B47;--correct-bg:#EAF6EF;--correct-border:#3A9960;\n  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.mr-stem{font-size:0.9rem}#pigm01 .mr-opt-text{font-size:0.86rem}}\n<\/style>\n\n<div id=\"pigm01\">\n\n  <div class=\"mr-header\">\n    <div class=\"mr-eyebrow\">Morning Rounds &middot; Daily Clinical Quiz<\/div>\n    <div class=\"mr-title\">\n      Pigmentary Disorders<br><em>Hypo- &amp; Hyperpigmentation<\/em>\n    <\/div>\n    <div class=\"mr-subtitle\">Five high-yield clinical cases &middot; +4 \/ &minus;1 scoring &middot; NEET-PG and INI-CET<\/div>\n    <div class=\"mr-chips\">\n      <span class=\"mr-chip\">5 Cases<\/span>\n      <span class=\"mr-chip\">+4 \/ &minus;1 scoring<\/span>\n      <span class=\"mr-chip\">Options reshuffled<\/span>\n    <\/div>\n  <\/div>\n\n  <div class=\"mr-sentinel\" id=\"pigm01-sentinel\"><\/div>\n\n  <div class=\"mr-progress\" id=\"pigm01-progress\">\n    <div class=\"mr-prog-inner\">\n      <div class=\"mr-pips\" id=\"pigm01-pips\"><\/div>\n    <\/div>\n  <\/div>\n\n  <div class=\"mr-body\">\n    <div id=\"pigm01-cases\"><\/div>\n    <div class=\"mr-submit-wrap\">\n      <button class=\"mr-btn\" id=\"pigm01-submit\">Submit for Debrief<\/button>\n    <\/div>\n    <div class=\"mr-score\" id=\"pigm01-score\">\n      <div class=\"mr-score-in\">\n        <div class=\"mr-score-ey\">Round Complete<\/div>\n        <div class=\"mr-ring\" id=\"pigm01-ring\">\n          <div class=\"mr-ring-in\">\n            <span class=\"mr-ring-pct\" id=\"pigm01-pct\">0%<\/span>\n            <span class=\"mr-ring-sub\">net<\/span>\n          <\/div>\n        <\/div>\n        <div class=\"mr-score-title\">Your Debrief<\/div>\n        <div class=\"mr-score-net\" id=\"pigm01-net\"><\/div>\n        <div class=\"mr-verdict\" id=\"pigm01-verdict\"><\/div>\n        <div class=\"mr-bands\">\n          <span class=\"mr-band mr-band-c\" id=\"pigm01-ct-c\"><\/span>\n          <span class=\"mr-band mr-band-w\" id=\"pigm01-ct-w\"><\/span>\n          <span class=\"mr-band mr-band-s\" id=\"pigm01-ct-s\"><\/span>\n        <\/div>\n        <button class=\"mr-retry\" id=\"pigm01-retry\">&#8635; New Round<\/button>\n      <\/div>\n    <\/div>\n  <\/div>\n<\/div>\n\n<script>\n(function () {\n  'use strict';\n\n  var NS    = 'pigm01';\n  var TOTAL = 5;\n  var MAX   = 20;\n  var LTRS  = ['A','B','C','D'];\n\n  \/* ================================================================\n     QUESTION BANK -- Pigmentary Disorders\n     NEET-PG level.\n     ================================================================\n\n     Q1  VITILIGO -- PATHOGENESIS, WOOD LAMP & TREATMENT (Medium)\n         Autoimmune destruction of melanocytes.\n         Complete absence of melanocytes (unlike albinism where\n           melanocytes present but tyrosinase deficient).\n         Wood lamp: chalk-white\/ivory fluorescence (enhanced\n           contrast in dark skin; helps detect early lesions).\n         Koebner phenomenon positive.\n         Types: non-segmental (bilateral, symmetric, commonest)\n                segmental (unilateral, dermatomal, stable).\n         Associations: thyroid disease (Hashimoto, Graves),\n           DM type 1, Addison disease, pernicious anaemia,\n           alopecia areata.\n         Treatment: topical calcineurin inhibitors (tacrolimus) --\n           safe on face; topical corticosteroids; narrowband UVB\n           (NB-UVB) -- treatment of choice for widespread vitiligo.\n         Leukotrichia (white hair in vitiligo patch) = poor\n           prognosis for repigmentation (melanocyte stem cells\n           in hair follicle destroyed).\n         Answer: autoimmune melanocyte destruction; chalk-white\n                 fluorescence on Wood lamp; NB-UVB for widespread\n                 disease\n\n     Q2  ALBINISM -- OCULOCUTANEOUS vs OCULAR (Medium)\n         Oculocutaneous albinism (OCA): autosomal recessive.\n           OCA1: tyrosinase gene mutation; most severe;\n                 white hair, pink skin, blue\/pink irides.\n           OCA2: P gene mutation; most common worldwide;\n                 some pigment may be present.\n         Features: photophobia, nystagmus, reduced visual acuity,\n           strabismus (due to abnormal optic nerve decussation).\n         Risk: squamous cell carcinoma in sun-exposed skin\n           (major cause of mortality in Africa).\n         Melanocytes are PRESENT but non-functional (contrast\n           with vitiligo where melanocytes are absent).\n         Hermansky-Pudlak: OCA + platelet dysfunction + pulm\n           fibrosis -- NOT required at NEET-PG level.\n         Answer: melanocytes present but non-functional due to\n                 tyrosinase deficiency; risk of SCC in sun-exposed\n                 skin; nystagmus and photophobia\n\n     Q3  MELASMA -- PATTERNS & TREATMENT (Easy-Medium)\n         Acquired hyperpigmentation; women > men; reproductive age.\n         Triggers: sun exposure, pregnancy (chloasma\/mask of\n           pregnancy), OCP, thyroid disease.\n         Distribution: centrofacial (most common), malar, mandibular.\n         Wood lamp: epidermal type accentuated (superficial);\n                    dermal type not accentuated (deep, harder to\n                    treat).\n         Treatment: strict photoprotection (sunscreen) -- mandatory\n           and lifelong; triple combination cream (hydroquinone +\n           tretinoin + mild steroid -- Kligman formula) is the most\n           effective single agent; azelaic acid; chemical peels.\n           Hydroquinone: inhibits tyrosinase; most used depigmenting\n           agent; prolonged use can cause ochronosis (paradoxical\n           darkening).\n         Answer: centrofacial pattern most common; Wood lamp\n                 differentiates epidermal vs dermal; triple\n                 combination (Kligman) most effective\n\n     Q4  FRECKLES (EPHELIDES) vs LENTIGINES (Easy)\n         Ephelides (freckles):\n           - Increased melanin in basal layer; melanocyte COUNT\n             normal.\n           - Appear in childhood; sun-exposed areas (face).\n           - Darken in summer, fade in winter.\n           - Associated with fair skin, red hair, MC1R gene.\n           - Benign, no malignant potential.\n         Lentigines (lentigo simplex \/ solar lentigo):\n           - INCREASED melanocyte count (not just melanin).\n           - Do not fade in winter (unlike freckles).\n           - Solar lentigo (liver spots): elderly, sun-exposed.\n           - PUVA lentigo: after PUVA therapy.\n           - Lentigo maligna: premalignant; elderly; large\n             irregular pigmented macule on sun-damaged skin;\n             can progress to lentigo maligna melanoma.\n         LEOPARD syndrome: multiple lentigines + ECG abnormalities\n           + Ocular hypertelorism + Pulmonary stenosis + Abnormal\n           genitalia + Retardation of growth + Deafness.\n         Answer: freckles -- normal melanocyte count, increased\n                 melanin, fade in winter; lentigines -- increased\n                 melanocyte count, do not fade in winter\n\n     Q5  CAFE-AU-LAIT SPOTS & NEUROFIBROMATOSIS (Medium)\n         Cafe-au-lait macules (CALMs): well-defined, uniformly\n           hyperpigmented, light-brown macules.\n         NF-1 (von Recklinghausen): autosomal dominant; NF1 gene\n           (chr 17); neurofibromin (tumour suppressor).\n           Diagnostic criteria include >= 6 CALMs (>5mm prepubertal,\n           >15mm postpubertal).\n           Lisch nodules: iris hamartomas -- pathognomonic of NF-1.\n           Axillary\/inguinal freckling (Crowe sign).\n           Cutaneous neurofibromas.\n         NF-2: bilateral acoustic neuromas; fewer CALMs; chr 22;\n           merlin protein.\n         McCune-Albright syndrome: large CALMs with irregular\n           (coast of Maine) borders + polyostotic fibrous dysplasia\n           + precocious puberty.\n         NF-1 CALMs: smooth (coast of California) borders.\n         Answer: >=6 CALMs >15mm in adults diagnostic of NF-1;\n                 Lisch nodules pathognomonic; coast of Maine\n                 border = McCune-Albright\n     ================================================================ *\/\n\n  var QS = [\n\n    \/* ---- Q1 : Vitiligo ---- *\/\n    {\n      id:      1,\n      tag:     'Pigmentary Disorders &mdash; Vitiligo',\n      stem:    'A <strong>28-year-old woman<\/strong> presents with depigmented patches on her hands, around her mouth, and on her elbows. A few patches contain <strong>white hairs<\/strong>. Wood lamp examination shows <strong>chalk-white fluorescence<\/strong>. She has a history of hypothyroidism. Regarding this condition, which statement is most accurate?',\n      correct: 'Melanocytes are absent from the depigmented patches due to autoimmune destruction; white hairs within a patch (leukotrichia) indicate a poor prognosis for repigmentation',\n      opts: [\n        'Melanocytes are absent from the depigmented patches due to autoimmune destruction; white hairs within a patch (leukotrichia) indicate a poor prognosis for repigmentation',\n        'Melanocytes are present but non-functional due to tyrosinase deficiency; the condition is inherited as autosomal recessive',\n        'Melanocytes are present but produce reduced melanin due to iron deficiency; treatment with iron supplementation reverses depigmentation',\n        'Melanocytes are destroyed by Staphylococcus aureus exotoxin; the association with hypothyroidism is coincidental'\n      ],\n      exp:     '<strong>Vitiligo<\/strong> results from <strong>autoimmune destruction of melanocytes<\/strong> &mdash; the patches are completely devoid of melanocytes, which distinguishes it from albinism (where melanocytes are present but non-functional). Wood lamp reveals <strong>chalk-white (ivory) fluorescence<\/strong>, enhancing contrast especially in dark skin types and helping detect early or subtle lesions. <strong>Leukotrichia<\/strong> (white hairs within a vitiligo patch) indicates destruction of melanocyte stem cells in the hair follicle bulge &mdash; these stem cells are the source of repigmenting melanocytes, so leukotrichia is a <strong>poor prognostic sign<\/strong>. <strong>Associations:<\/strong> thyroid disease (Hashimoto, Graves), type 1 diabetes, Addison disease, pernicious anaemia, alopecia areata &mdash; all organ-specific autoimmune conditions. Koebner phenomenon is positive. <strong>Treatment:<\/strong> topical tacrolimus (safe on face and flexures); topical corticosteroids; <strong>narrowband UVB (NB-UVB)<\/strong> is the treatment of choice for widespread vitiligo. <strong>Extra point:<\/strong> repigmentation in vitiligo begins perifollicularly &mdash; small pigmented dots around hair follicles at the margin of lesions &mdash; because residual follicular melanocyte stem cells migrate out to repopulate the epidermis. This perifollicular pattern on examination indicates a favourable response to treatment.'\n    },\n\n    \/* ---- Q2 : Albinism ---- *\/\n    {\n      id:      2,\n      tag:     'Pigmentary Disorders &mdash; Albinism',\n      stem:    'A <strong>5-year-old child<\/strong> is brought with white hair, pale pink skin, and <strong>pink irides<\/strong> since birth. He has <strong>nystagmus, photophobia<\/strong>, and reduced visual acuity. His parents are consanguineous. The fundamental defect, the key distinction from vitiligo, and the most important long-term risk are:',\n      correct: 'Tyrosinase deficiency (OCA1): melanocytes are present but cannot synthesise melanin; unlike vitiligo, melanocytes are not absent; major long-term risk is squamous cell carcinoma in sun-exposed skin',\n      opts: [\n        'Tyrosinase deficiency (OCA1): melanocytes are present but cannot synthesise melanin; unlike vitiligo, melanocytes are not absent; major long-term risk is squamous cell carcinoma in sun-exposed skin',\n        'Melanocyte absence due to autoimmune destruction: identical mechanism to vitiligo; major long-term risk is basal cell carcinoma',\n        'Defective melanocyte migration from neural crest: melanocytes absent from skin and eyes; major risk is malignant melanoma',\n        'Iron deficiency causing reduced melanin synthesis: melanocytes present and structurally normal; responds to iron supplementation'\n      ],\n      exp:     '<strong>Oculocutaneous albinism type 1 (OCA1)<\/strong> is caused by mutations in the <strong>tyrosinase gene<\/strong> (chromosome 11), inherited as autosomal recessive. <strong>Melanocytes are present in normal numbers<\/strong> but cannot produce melanin because tyrosinase &mdash; the rate-limiting enzyme of melanogenesis &mdash; is absent or deficient. This is the critical distinction from vitiligo, where melanocytes are destroyed and absent. The ocular features &mdash; nystagmus, photophobia, reduced visual acuity, and strabismus &mdash; arise from abnormal decussation of optic nerve fibres at the chiasm (melanin is required for normal optic pathway development). <strong>Major long-term risk: squamous cell carcinoma (SCC)<\/strong> of sun-exposed skin, due to complete absence of photoprotective melanin. In sub-Saharan Africa, SCC is the leading cause of death in people with albinism. <strong>Management:<\/strong> strict photoprotection (sunscreen, protective clothing, sun avoidance), regular skin surveillance, and low-vision aids. <strong>Extra point:<\/strong> OCA2 (P gene mutation, chromosome 15) is the most common type worldwide and in Africa; some residual pigment may be present. OCA1 (tyrosinase mutation) is the most severe form with complete absence of melanin in OCA1A.'\n    },\n\n    \/* ---- Q3 : Melasma ---- *\/\n    {\n      id:      3,\n      tag:     'Pigmentary Disorders &mdash; Melasma',\n      stem:    'A <strong>32-year-old woman<\/strong> develops symmetrical, irregular <strong>brown patches over her cheeks, forehead, and upper lip<\/strong> during her second pregnancy. Wood lamp examination <strong>accentuates<\/strong> the hyperpigmentation. She asks about treatment options. The Wood lamp finding, the most effective topical treatment, and an important side effect of long-term use of the primary depigmenting agent are:',\n      correct: 'Wood lamp accentuation indicates epidermal (superficial) melasma, which responds better to treatment; triple combination cream (hydroquinone + tretinoin + mild steroid) is most effective; prolonged hydroquinone use can cause ochronosis',\n      opts: [\n        'Wood lamp accentuation indicates epidermal (superficial) melasma, which responds better to treatment; triple combination cream (hydroquinone + tretinoin + mild steroid) is most effective; prolonged hydroquinone use can cause ochronosis',\n        'Wood lamp accentuation indicates dermal (deep) melasma, which is the most treatment-resistant type; topical corticosteroids alone are sufficient; long-term use causes no pigment side effects',\n        'Wood lamp accentuation confirms malignant transformation; excision biopsy is the next step; hydroquinone is contraindicated',\n        'Wood lamp accentuation indicates mixed-type melasma; oral tranexamic acid is the only evidence-based treatment; sunscreen is not required'\n      ],\n      exp:     'Melasma is acquired hyperpigmentation predominantly affecting women of reproductive age, driven by UV exposure, hormonal factors (pregnancy, OCP), and genetic predisposition. <strong>Wood lamp examination:<\/strong> <em>epidermal melasma<\/em> (melanin in basal\/suprabasal epidermis) is <strong>accentuated<\/strong> &mdash; the contrast increases, indicating superficial pigment that responds better to treatment. <em>Dermal melasma<\/em> (melanophages in the dermis) is <strong>not accentuated<\/strong> &mdash; harder to treat. <strong>Treatment:<\/strong> <em>strict daily photoprotection is mandatory and lifelong<\/em> &mdash; without sunscreen, all other treatments fail. The <strong>Kligman formula<\/strong> (triple combination: hydroquinone 4% + tretinoin 0.05% + fluocinolone acetonide 0.01%) is the most effective single topical regimen. <strong>Hydroquinone<\/strong> inhibits tyrosinase; prolonged use can cause <strong>exogenous ochronosis<\/strong> (paradoxical blue-black darkening of treated skin from polymerisation of homogentisic acid) &mdash; a feared complication, especially in darker skin types. <strong>Extra point:<\/strong> <em>oral tranexamic acid<\/em> (an antifibrinolytic that reduces UV-induced plasminogen activator activity in keratinocytes, thereby reducing melanin stimulation) is increasingly used for treatment-resistant melasma &mdash; a relatively new addition to the evidence base that has appeared in recent NEET-PG papers.'\n    },\n\n    \/* ---- Q4 : Freckles vs Lentigines ---- *\/\n    {\n      id:      4,\n      tag:     'Pigmentary Disorders &mdash; Freckles vs Lentigines',\n      stem:    'A <strong>45-year-old fair-skinned woman<\/strong> has multiple small pigmented macules on her face. Some have been present since childhood and <em>fade noticeably in winter<\/em>. Others appeared in her 40s and are present on the back of her hands; these <em>do not fade in winter<\/em>. A third type, noted by her dermatologist, is a large, irregular, variably pigmented macule on her cheek that has been slowly enlarging. Which of the following correctly classifies all three lesions?',\n      correct: 'Childhood lesions fading in winter = ephelides (freckles, normal melanocyte count); non-fading lesions on hands = solar lentigines (increased melanocyte count); enlarging irregular macule = lentigo maligna (premalignant)',\n      opts: [\n        'Childhood lesions fading in winter = ephelides (freckles, normal melanocyte count); non-fading lesions on hands = solar lentigines (increased melanocyte count); enlarging irregular macule = lentigo maligna (premalignant)',\n        'All three lesions are ephelides with varying degrees of sun exposure; none carry malignant potential; reassurance only required',\n        'Non-fading hand lesions = ephelides; childhood lesions = solar lentigines; enlarging macule = seborrhoeic keratosis with no malignant potential',\n        'All three lesions are solar lentigines at different stages; the enlarging macule represents benign regression and requires no further investigation'\n      ],\n      exp:     'The two most tested facts about ephelides vs lentigines: <strong>Ephelides (freckles)<\/strong> have a <em>normal melanocyte count<\/em> &mdash; only the melanin content per cell is increased. They appear in childhood on sun-exposed areas, are associated with fair skin and red hair (MC1R gene variants), and characteristically <strong>fade in winter<\/strong> (sun-dependent). <strong>Lentigines<\/strong> have an <em>increased melanocyte count<\/em> &mdash; this is the fundamental histological distinction. <strong>Solar lentigines<\/strong> (liver spots) appear on sun-exposed skin of older adults and <strong>do not fade in winter<\/strong>. <strong>Lentigo maligna<\/strong> is a slow-growing, irregularly pigmented macule on chronically sun-damaged skin of elderly patients; it is the <em>in situ<\/em> form of lentigo maligna melanoma and is premalignant. <strong>Extra point:<\/strong> <strong>LEOPARD syndrome<\/strong> (Noonan syndrome with multiple lentigines) involves multiple lentigines + <strong>L<\/strong>entigos + <strong>E<\/strong>CG abnormalities + <strong>O<\/strong>cular hypertelorism + <strong>P<\/strong>ulmonary stenosis + <strong>A<\/strong>bnormal genitalia + <strong>R<\/strong>etardation of growth + <strong>D<\/strong>eafness. Caused by PTPN11 gene mutations (same gene as Noonan syndrome). The lentigines here are unrelated to sun exposure and appear early in life.'\n    },\n\n    \/* ---- Q5 : Cafe-au-lait Spots & NF-1 ---- *\/\n    {\n      id:      5,\n      tag:     'Pigmentary Disorders &mdash; Caf&eacute;-au-lait Spots',\n      stem:    'A <strong>10-year-old boy<\/strong> is referred for evaluation of multiple light-brown skin patches. Examination reveals <strong>8 uniformly pigmented macules<\/strong> with smooth, well-defined borders, the largest measuring <strong>18&nbsp;mm<\/strong>. There is also freckling in the <strong>axillae<\/strong>, and small tan-coloured nodules on the iris bilaterally. His mother has similar skin findings. The diagnosis, the pathognomonic ocular finding, and how the border of these macules differs from those in McCune-Albright syndrome are:',\n      correct: 'Neurofibromatosis type 1; Lisch nodules (iris hamartomas) are pathognomonic; NF-1 macules have smooth (coast of California) borders vs irregular (coast of Maine) borders in McCune-Albright',\n      opts: [\n        'Neurofibromatosis type 1; Lisch nodules (iris hamartomas) are pathognomonic; NF-1 macules have smooth (coast of California) borders vs irregular (coast of Maine) borders in McCune-Albright',\n        'McCune-Albright syndrome; Brushfield spots on the iris are pathognomonic; macules have irregular borders and are associated with precocious puberty',\n        'Neurofibromatosis type 2; bilateral acoustic neuromas are the pathognomonic finding; skin lesions are identical to NF-1',\n        'LEOPARD syndrome; multiple lentigines are the primary finding; Lisch nodules confirm the diagnosis'\n      ],\n      exp:     '<strong>Neurofibromatosis type 1 (NF-1)<\/strong> is the most common neurocutaneous syndrome (autosomal dominant; <strong>NF1 gene on chromosome 17<\/strong>; encodes neurofibromin, a tumour suppressor). <strong>Diagnostic criteria<\/strong> require &ge;2 of: <em>&ge;6 CALMs<\/em> (&gt;5&nbsp;mm prepubertal, <strong>&gt;15&nbsp;mm postpubertal<\/strong>); axillary\/inguinal freckling (<strong>Crowe sign<\/strong>); &ge;2 neurofibromas; <strong>Lisch nodules<\/strong> (&ge;2); optic glioma; &ge;2 osseous lesions; first-degree relative with NF-1. <strong>Lisch nodules<\/strong> (iris hamartomas) are <em>pathognomonic of NF-1<\/em> &mdash; they appear as small tan\/brown dome-shaped nodules on the iris, visible on slit-lamp examination, and increase in number with age. <strong>Border distinction:<\/strong> NF-1 CALMs have smooth, regular borders &mdash; <em>coast of California<\/em>. McCune-Albright CALMs have large, irregular, jagged borders &mdash; <em>coast of Maine<\/em> &mdash; associated with polyostotic fibrous dysplasia and precocious puberty. <strong>Extra point:<\/strong> NF-2 (chromosome 22; merlin protein) features bilateral vestibular schwannomas (acoustic neuromas), meningiomas, fewer CALMs, and no Lisch nodules &mdash; the skin findings are far less prominent than in NF-1. The exam always tests this NF-1 vs NF-2 distinction.'\n    }\n\n  ];\n  \/* ================================================================\n     END OF CONTENT -- engine logic below, do not edit\n     ================================================================ *\/\n\n  var answers  = {};\n  var answered = 0;\n  var shuffled = {};\n  var done     = false;\n\n  function byId(id) { return document.getElementById(id); }\n  function gid(sfx) { return byId(NS + '-' + sfx); }\n\n  function shuffleArr(arr) {\n    var a = arr.slice(), i, j, t;\n    for (i = a.length - 1; i > 0; i--) {\n      j = Math.floor(Math.random() * (i + 1));\n      t = a[i]; a[i] = a[j]; a[j] = t;\n    }\n    return a;\n  }\n\n  function countVal(val) {\n    var k, n = 0;\n    for (k in answers) {\n      if (answers.hasOwnProperty(k) && answers[k] === val) n++;\n    }\n    return n;\n  }\n\n  function buildPips() {\n    var cont = gid('pips'), i, q, wl, wp, line, pip;\n    if (!cont) return;\n    cont.innerHTML = '';\n    for (i = 0; i < QS.length; i++) {\n      q = QS[i];\n      if (i > 0) {\n        wl = document.createElement('div'); wl.className = 'mr-pip-wrap';\n        line = document.createElement('div'); line.className = 'mr-pip-line';\n        line.id = NS + '-pl' + q.id;\n        wl.appendChild(line); cont.appendChild(wl);\n      }\n      wp = document.createElement('div'); wp.className = 'mr-pip-wrap';\n      pip = document.createElement('div'); pip.className = 'mr-pip';\n      pip.id = NS + '-pip' + q.id; pip.textContent = String(q.id);\n      wp.appendChild(pip); cont.appendChild(wp);\n    }\n  }\n\n  function build() {\n    var cont, i, q, opts, card, top, nd, meta, tg, st,\n        rule, od, ed, lb, tx, j, oe, ls, ts;\n    cont = gid('cases');\n    if (!cont) return;\n    cont.innerHTML = '';\n    answers = {}; answered = 0; shuffled = {}; done = false;\n    if (gid('score')) gid('score').style.display = 'none';\n    buildPips();\n    for (i = 0; i < QS.length; i++) {\n      q    = QS[i];\n      opts = shuffleArr(q.opts);\n      shuffled[q.id] = opts;\n      card = document.createElement('div'); card.className = 'mr-case';\n      top  = document.createElement('div'); top.className  = 'mr-case-top';\n      nd   = document.createElement('div'); nd.className   = 'mr-num';\n      nd.textContent = q.id < 10 ? 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Every spot, patch, and macule identified.'],\n      [4, 'Strong \\u2014 one pigment disorder to revisit before exam day.'],\n      [3, 'Solid base \\u2014 the coast of California vs Maine border trick rewards a second read.'],\n      [2, 'Halfway there \\u2014 the debrief panels have everything you need.'],\n      [0, 'Pigmentary disorders reward careful reading. Come back tomorrow.']\n    ];\n    var ve = gid('verdict');\n    if (ve) {\n      ve.textContent = vlist[4][1];\n      for (vi = 0; vi < vlist.length; vi++) {\n        if (c >= vlist[vi][0]) { ve.textContent = vlist[vi][1]; break; }\n      }\n    }\n    var cc = gid('ct-c'); if (cc) cc.textContent = '\\u2705 ' + c + ' Correct';\n    var cw = gid('ct-w'); if (cw) cw.textContent = '\\u274C ' + w + ' Wrong';\n    var cs = gid('ct-s'); if (cs) cs.textContent = '\\u23ED ' + s + ' Skipped';\n    sc = gid('score');\n    if (sc) { sc.style.display = 'block'; sc.scrollIntoView({ behavior: 'smooth', block: 'center' }); }\n  }\n\n  function initObserver() {\n    var sn = gid('sentinel'), bar = gid('progress');\n    if (!sn || !bar || !window.IntersectionObserver) return;\n    new IntersectionObserver(function (en) {\n      bar.className = en[0].isIntersecting ? 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