{"id":36865,"date":"2026-05-26T12:34:02","date_gmt":"2026-05-26T07:04:02","guid":{"rendered":"https:\/\/atsixty.com\/?p=36865"},"modified":"2026-05-26T13:47:21","modified_gmt":"2026-05-26T08:17:21","slug":"vesiculobullous-disorders","status":"publish","type":"post","link":"https:\/\/atsixty.com\/index.php\/2026\/05\/26\/vesiculobullous-disorders\/","title":{"rendered":"Vesiculobullous 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 #vbul01 -- no bleed into WordPress theme *\/\n#vbul01 *,#vbul01 *::before,#vbul01 *::after{box-sizing:border-box;margin:0;padding:0}\n#vbul01{\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}#vbul01 .mr-opt-text{font-size:0.86rem}}\n<\/style>\n\n<div id=\"vbul01\">\n\n  <div class=\"mr-header\">\n    <div class=\"mr-eyebrow\">Morning Rounds &middot; Daily Clinical Quiz<\/div>\n    <div class=\"mr-title\">\n      Vesiculobullous Disorders<br><em>Immunology, Pathology &amp; Clinical Dermatology<\/em>\n    <\/div>\n    <div class=\"mr-subtitle\">Five cases &middot; Read carefully &middot; Trust your instinct<\/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=\"vbul01-sentinel\"><\/div>\n\n  <div class=\"mr-progress\" id=\"vbul01-progress\">\n    <div class=\"mr-prog-inner\">\n      <div class=\"mr-pips\" id=\"vbul01-pips\"><\/div>\n    <\/div>\n  <\/div>\n\n  <div class=\"mr-body\">\n    <div id=\"vbul01-cases\"><\/div>\n\n    <div class=\"mr-submit-wrap\">\n      <button class=\"mr-btn\" id=\"vbul01-submit\">Submit for Debrief<\/button>\n    <\/div>\n\n    <div class=\"mr-score\" id=\"vbul01-score\">\n      <div class=\"mr-score-in\">\n        <div class=\"mr-score-ey\">Round Complete<\/div>\n        <div class=\"mr-ring\" id=\"vbul01-ring\">\n          <div class=\"mr-ring-in\">\n            <span class=\"mr-ring-pct\" id=\"vbul01-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=\"vbul01-net\"><\/div>\n        <div class=\"mr-verdict\" id=\"vbul01-verdict\"><\/div>\n        <div class=\"mr-bands\">\n          <span class=\"mr-band mr-band-c\" id=\"vbul01-ct-c\"><\/span>\n          <span class=\"mr-band mr-band-w\" id=\"vbul01-ct-w\"><\/span>\n          <span class=\"mr-band mr-band-s\" id=\"vbul01-ct-s\"><\/span>\n        <\/div>\n        <button class=\"mr-retry\" id=\"vbul01-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    = 'vbul01';\n  var TOTAL = 5;\n  var MAX   = 20;\n  var LTRS  = ['A','B','C','D'];\n\n  \/* ================================================================\n     QUESTION BANK -- Vesiculobullous Disorders\n     ================================================================\n\n     Q1  PEMPHIGUS VULGARIS -- SPLIT LEVEL & ANTIGEN (Medium)\n         Suprabasal split; acantholysis; IgG vs desmoglein 3 (mucosa)\n         and desmoglein 1 (skin + mucosa in mucocutaneous type).\n         Nikolsky sign positive. DIF: IgG in chicken-wire\/fish-net\n         pattern around keratinocytes (intercellular).\n         Treatment: systemic corticosteroids + rituximab (now preferred\n         steroid-sparing agent per recent guidelines).\n         Answer: Suprabasal split with acantholysis; IgG against\n                 desmoglein 3\n\n     Q2  BULLOUS PEMPHIGOID -- DISTINGUISHING FEATURES (Medium)\n         Subepidermal split (basement membrane zone); NO acantholysis.\n         Nikolsky sign NEGATIVE. IgG against BP180 (BPAG2, collagen\n         XVII) and BP230 (BPAG1). DIF: linear IgG + C3 at BMZ.\n         Elderly patients; tense (not flaccid) bullae; eosinophilia.\n         Antibody titres correlate with disease activity.\n         Answer: Subepidermal blister; IgG against BP180 and BP230;\n                 Nikolsky sign negative\n\n     Q3  DERMATITIS HERPETIFORMIS -- ASSOCIATIONS (Medium-Hard)\n         Subepidermal split; IgA deposits at TIPS of dermal papillae\n         (pathognomonic on DIF -- not linear like linear IgA disease).\n         Associated with coeliac disease (gluten-sensitive enteropathy)\n         in virtually 100% -- gut biopsy shows subtotal villous atrophy\n         even if GI symptoms absent. HLA-DQ2 \/ DQ8.\n         Treatment: gluten-free diet (definitive) + dapsone (rapid\n         symptom control; check G6PD before starting).\n         Answer: Granular IgA deposits at tips of dermal papillae;\n                 associated with coeliac disease\n\n     Q4  PEMPHIGUS FOLIACEUS vs VULGARIS -- DESMOGLEIN COMPENSATION\n         (Hard)\n         Pemphigus foliaceus: IgG vs Desmoglein 1 ONLY.\n         Subcorneal\/granular layer split (more superficial than PV).\n         NO mucosal involvement -- because desmoglein 3 (expressed\n         strongly in mucosa) compensates for desmoglein 1 loss there.\n         This is the desmoglein compensation theory.\n         Fogo selvagem = endemic pemphigus foliaceus (Brazil).\n         Answer: Absence of mucosal lesions because desmoglein 3\n                 compensates for desmoglein 1 loss at mucosal surfaces\n\n     Q5  SSSS vs TEN -- SPLIT LEVEL & MECHANISM (Hard)\n         SSSS (Staphylococcal Scalded Skin Syndrome):\n           - Exfoliatin (ET-A, ET-B) toxin cleaves desmoglein 1\n           - Subcorneal split (intraepidermal, superficial)\n           - Nikolsky positive; skin looks scalded\n           - No mucosal involvement (Dsg3 compensates -- same logic)\n           - No full-thickness necrosis; heals without scarring\n           - Children predominantly; staph NOT present in blister fluid\n         TEN (Toxic Epidermal Necrolysis):\n           - Drug-induced (sulfonamides, allopurinol, AEDs, NSAIDs)\n           - Full-thickness epidermal necrosis (subepidermal split)\n           - Mucosal involvement invariable\n           - SCORTEN score for mortality prediction\n           - Biopsy: necrotic keratinocytes throughout entire epidermis\n         Answer: SSSS -- subcorneal split, no mucosal involvement,\n                 heals without scarring; TEN -- full-thickness necrosis,\n                 mucosal involvement, significant mortality\n     ================================================================ *\/\n\n  var QS = [\n\n    \/* ---- Q1 : Pemphigus Vulgaris ---- *\/\n    {\n      id:      1,\n      tag:     'Vesiculobullous &mdash; Pemphigus Vulgaris',\n      stem:    'A <strong>45-year-old woman<\/strong> presents with painful oral erosions for three months, followed by the appearance of <strong>flaccid, easily ruptured bullae<\/strong> on her trunk. Nikolsky sign is <strong>positive<\/strong>. Direct immunofluorescence of perilesional skin shows IgG deposits in a <em>chicken-wire pattern<\/em> around individual keratinocytes. Which of the following correctly identifies the split level, pathological finding, and target antigen?',\n      correct: 'Suprabasal intraepidermal split; acantholysis; IgG against desmoglein 3',\n      opts: [\n        'Suprabasal intraepidermal split; acantholysis; IgG against desmoglein 3',\n        'Subepidermal split; no acantholysis; IgG against BP180 and BP230',\n        'Subcorneal intraepidermal split; acantholysis; IgG against desmoglein 1',\n        'Subepidermal split; no acantholysis; IgA against endomysium'\n      ],\n      exp:     '<strong>Pemphigus vulgaris (PV)<\/strong> is characterised by a <strong>suprabasal intraepidermal split<\/strong> caused by <strong>acantholysis<\/strong> &mdash; loss of cohesion between keratinocytes due to autoantibody-mediated destruction of desmosomes. The target antigen in <em>mucosal-dominant<\/em> PV is <strong>desmoglein 3 (Dsg3)<\/strong>; in <em>mucocutaneous<\/em> PV both <strong>Dsg3 and Dsg1<\/strong> are targeted. The hallmark histology is a <em>row of tombstones<\/em> &mdash; basal keratinocytes remaining attached to the basement membrane while the suprabasal layers separate. DIF shows the pathognomonic <strong>intercellular IgG + C3 in a chicken-wire (fish-net) pattern<\/strong>. Nikolsky sign is positive (lateral pressure on skin produces epidermal sliding). <strong>Extra point:<\/strong> treatment has evolved significantly &mdash; <strong>rituximab<\/strong> (anti-CD20, targeting B cells that produce the pathogenic IgG) is now preferred over high-dose corticosteroids alone per 2023 guidelines, with superior remission rates and fewer steroid side effects. Serum anti-Dsg titres correlate with disease activity and guide treatment decisions.'\n    },\n\n    \/* ---- Q2 : Bullous Pemphigoid ---- *\/\n    {\n      id:      2,\n      tag:     'Vesiculobullous &mdash; Bullous Pemphigoid',\n      stem:    'A <strong>72-year-old man<\/strong> presents with intensely pruritic, <strong>tense bullae<\/strong> on an erythematous base over the flexural surfaces of both thighs and abdomen. There are <em>no oral lesions<\/em>. Nikolsky sign is <strong>negative<\/strong>. Blood count shows peripheral eosinophilia. Direct immunofluorescence shows <strong>linear IgG and C3 deposits at the basement membrane zone<\/strong>. The target antigens are:',\n      correct: 'BP180 (collagen XVII) and BP230, located at the hemidesmosome of the dermoepidermal junction',\n      opts: [\n        'BP180 (collagen XVII) and BP230, located at the hemidesmosome of the dermoepidermal junction',\n        'Desmoglein 1 and desmoglein 3, located at the desmosome between keratinocytes',\n        'Laminin 332 (epiligrin), located in the anchoring filaments of the basement membrane',\n        'Type VII collagen, located in the anchoring fibrils below the lamina densa'\n      ],\n      exp:     '<strong>Bullous pemphigoid (BP)<\/strong> is the most common autoimmune blistering disorder, predominantly affecting the elderly. The split is <strong>subepidermal<\/strong> (below the basement membrane zone) with <em>no acantholysis<\/em> &mdash; explaining why bullae are <em>tense<\/em> rather than flaccid. Target antigens are <strong>BP180 (BPAG2, collagen XVII)<\/strong> &mdash; a transmembrane collagen &mdash; and <strong>BP230 (BPAG1)<\/strong>, both components of the <em>hemidesmosome<\/em>. DIF shows <strong>linear IgG + C3 at the BMZ<\/strong> (n-serrated pattern on salt-split skin: roof of the blister). Nikolsky sign is <strong>negative<\/strong> because the epidermis is intact. <strong>Extra point:<\/strong> BP antibody titres (particularly anti-BP180 NC16A IgG) correlate with disease activity and are used to monitor treatment response. There is a well-documented association of BP with <strong>neurological diseases<\/strong> (dementia, Parkinson disease, stroke) &mdash; BP180 and BP230 are also expressed in neural tissue, and neurological injury may trigger epitope exposure. This association is a favourite exam point. Treatment: potent topical steroids (preferred in elderly to avoid systemic steroid side effects) or doxycycline + nicotinamide in mild disease.'\n    },\n\n    \/* ---- Q3 : Dermatitis Herpetiformis ---- *\/\n    {\n      id:      3,\n      tag:     'Vesiculobullous &mdash; Dermatitis Herpetiformis',\n      stem:    'A <strong>34-year-old man<\/strong> presents with intensely pruritic, grouped vesicles on his <strong>elbows, knees, and buttocks<\/strong> that he has been scratching before they can fully form. He denies diarrhoea but admits to occasional bloating. Direct immunofluorescence of <em>perilesional<\/em> skin reveals <strong>granular IgA deposits at the tips of dermal papillae<\/strong>. The most important associated condition and the definitive treatment are:',\n      correct: 'Coeliac disease (gluten-sensitive enteropathy) in virtually all cases; definitive treatment is a strict lifelong gluten-free diet',\n      opts: [\n        'Coeliac disease (gluten-sensitive enteropathy) in virtually all cases; definitive treatment is a strict lifelong gluten-free diet',\n        'Inflammatory bowel disease in the majority of cases; definitive treatment is systemic corticosteroids',\n        'IgA nephropathy in the majority of cases; definitive treatment is ACE inhibitor therapy',\n        'Thyroid autoimmunity in the majority of cases; definitive treatment is thyroxine replacement'\n      ],\n      exp:     '<strong>Dermatitis herpetiformis (DH)<\/strong> is the cutaneous manifestation of <strong>coeliac disease<\/strong>, present in virtually 100% of patients even when GI symptoms are absent. Jejunal biopsy shows subtotal villous atrophy. The pathognomonic DIF finding is <strong>granular IgA deposits at the <em>tips<\/em> of dermal papillae<\/strong> &mdash; this distinguishes DH from Linear IgA disease, where deposits are linear at the BMZ. The antigen in DH is <strong>epidermal transglutaminase (eTG, TG3)<\/strong>; gliadin peptides cross-react with TG3 via molecular mimicry. HLA association: <strong>HLA-DQ2 (90%) and HLA-DQ8 (10%)<\/strong>. <strong>Treatment:<\/strong> a strict <strong>gluten-free diet<\/strong> is the only definitive treatment &mdash; it resolves both the skin and gut disease over months to years. <strong>Dapsone<\/strong> provides rapid symptom relief (within 24&ndash;48 hours) but does not treat the underlying enteropathy. <strong>Check G6PD before starting dapsone<\/strong> &mdash; it causes haemolysis in G6PD-deficient patients. <strong>Extra point:<\/strong> patients with DH have a significantly reduced risk of GI lymphoma compared to coeliac disease alone, possibly because the skin manifestation prompts earlier dietary adherence.'\n    },\n\n    \/* ---- Q4 : Pemphigus Foliaceus & Desmoglein Compensation ---- *\/\n    {\n      id:      4,\n      tag:     'Vesiculobullous &mdash; Pemphigus Foliaceus',\n      stem:    'A <strong>38-year-old woman<\/strong> presents with superficial, easily ruptured bullae and crusted erosions predominantly over the <strong>seborrhoeic areas<\/strong> of the scalp, face, and trunk. There are <strong>no mucosal lesions<\/strong>. Histology shows a <em>subcorneal split<\/em> with acantholysis in the granular layer. Serology is positive for IgG against <strong>desmoglein 1 only<\/strong>. Why are mucosal surfaces spared in this condition?',\n      correct: 'Desmoglein 3, expressed abundantly in mucosal epithelium, compensates for desmoglein 1 loss and maintains mucosal adhesion',\n      opts: [\n        'Desmoglein 3, expressed abundantly in mucosal epithelium, compensates for desmoglein 1 loss and maintains mucosal adhesion',\n        'Mucosal epithelium does not express desmoglein 1, so the autoantibody has no target there',\n        'IgG antibodies cannot penetrate the thick mucus layer overlying mucosal surfaces',\n        'The subcorneal split level is too superficial to affect the deeper mucosal epithelial layers'\n      ],\n      exp:     '<strong>Pemphigus foliaceus (PF)<\/strong> targets <strong>desmoglein 1 (Dsg1) only<\/strong>. The <strong>desmoglein compensation theory<\/strong> explains the clinical distribution: in <em>mucosal epithelium<\/em>, <strong>Dsg3 is expressed abundantly<\/strong> and can compensate for Dsg1 loss, maintaining adhesion &mdash; hence <em>no mucosal lesions<\/em>. In <em>superficial skin<\/em> (granular\/subcorneal layer), Dsg3 expression is low and Dsg1 dominates &mdash; hence blistering occurs there. Conversely, in <strong>pemphigus vulgaris<\/strong> (anti-Dsg3 &plusmn; Dsg1), mucosal lesions appear because Dsg1 cannot compensate for Dsg3 loss in the mucosa. This elegantly explains why PV <em>always<\/em> has mucosal lesions and PF <em>never<\/em> does. <strong>Fogo selvagem<\/strong> (&ldquo;wild fire&rdquo;) is endemic PF in rural Brazil and Colombia, triggered by an environmental factor (possibly black fly bite) in genetically predisposed individuals &mdash; same Dsg1 antibody, same clinical picture. <strong>Extra point:<\/strong> the same desmoglein compensation logic explains SSSS &mdash; staphylococcal exfoliatin cleaves Dsg1 selectively, producing a superficial split with <em>no mucosal involvement<\/em>, mirroring PF.'\n    },\n\n    \/* ---- Q5 : SSSS vs TEN ---- *\/\n    {\n      id:      5,\n      tag:     'Vesiculobullous &mdash; SSSS vs TEN',\n      stem:    'A <strong>3-year-old boy<\/strong> develops widespread skin tenderness, erythema, and superficial peeling starting around the mouth and eyes, with a <em>positive Nikolsky sign<\/em>. He is febrile. There are <strong>no mucosal erosions<\/strong>. Skin biopsy shows a <strong>subcorneal split<\/strong> with no inflammatory cells in the blister fluid. Cultures from the blister fluid are <strong>sterile<\/strong>. The most likely diagnosis, causative toxin, and key distinguishing feature from Toxic Epidermal Necrolysis are:',\n      correct: 'Staphylococcal Scalded Skin Syndrome; exfoliatin toxin cleaving desmoglein 1; subcorneal split and absence of mucosal involvement distinguish it from TEN',\n      opts: [\n        'Staphylococcal Scalded Skin Syndrome; exfoliatin toxin cleaving desmoglein 1; subcorneal split and absence of mucosal involvement distinguish it from TEN',\n        'Toxic Epidermal Necrolysis; drug-induced full-thickness epidermal necrosis; mucosal involvement and full-thickness split distinguish it from SSSS',\n        'Pemphigus vulgaris; IgG against desmoglein 3; intercellular IgG on DIF distinguishes it from TEN',\n        'Bullous impetigo; localised exfoliatin production; presence of staphylococci in blister fluid distinguishes it from SSSS'\n      ],\n      exp:     '<strong>Staphylococcal Scalded Skin Syndrome (SSSS)<\/strong> is caused by <em>Staphylococcus aureus<\/em> phage group II producing <strong>exfoliatin toxins (ET-A and ET-B)<\/strong>, serine proteases that <strong>specifically cleave desmoglein 1<\/strong> at the extracellular EC1-EC2 domain &mdash; the same target as pemphigus foliaceus. This produces a <strong>subcorneal (intraepidermal) split<\/strong>. Key features: predominantly <strong>children under 5<\/strong> (adults lack protective antibodies and have reduced renal excretion of toxin); <strong>no mucosal involvement<\/strong> (Dsg3 compensates, as in PF); <strong>sterile blister fluid<\/strong> (toxin is haematogenously disseminated from a remote focus &mdash; conjunctivitis, ear, umbilicus &mdash; not from the skin itself); <strong>heals without scarring<\/strong> (split is superficial). <strong>TEN<\/strong>, by contrast, shows <strong>full-thickness epidermal necrosis<\/strong> (subepidermal split), invariable <strong>mucosal involvement<\/strong>, drug aetiology (sulfonamides, allopurinol, aromatic antiepileptics, NSAIDs), and carries <strong>significant mortality<\/strong> (predicted by the <strong>SCORTEN score<\/strong>). <strong>Extra point:<\/strong> the Nikolsky sign is positive in <em>both<\/em> SSSS and TEN &mdash; it does not distinguish them. Biopsy level does. In SSSS: subcorneal. In TEN: subepidermal, full-thickness necrosis. Frozen section of the blister roof is the rapid intraoperative test used to distinguish the two emergently.'\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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'correct' : 'wrong');\n    if (qid > 1) { var pl = gid('pl' + qid); if (pl) pl.className = 'mr-pip-line done'; }\n  }\n\n  function showScore() {\n    var c, w, s, net, pct, disp, vlist, vi, sc;\n    if (done) return;\n    done = true;\n    c = countVal('c'); w = countVal('w'); s = TOTAL - answered;\n    net  = c * 4 - w;\n    pct  = Math.max(0, Math.round((net \/ MAX) * 100));\n    disp = Math.min(100, Math.max(0, pct));\n    var rg = gid('ring');\n    if (rg) rg.style.background = 'conic-gradient(#8B3D20 ' + disp + '%, #E8DDD8 0%)';\n    var pe = gid('pct'); if (pe) pe.textContent = pct + '%';\n    var ne = gid('net'); if (ne) ne.textContent = 'Net Score: ' + net + ' \/ ' + MAX;\n    vlist = [\n      [5, 'Perfect round. The desmoglein map is yours.'],\n      [4, 'Strong \\u2014 one split level to revisit before exam day.'],\n      [3, 'Solid base \\u2014 the compensation theory rewards a second read.'],\n      [2, 'Halfway there \\u2014 the debrief panels have everything you need.'],\n      [0, 'These disorders reward persistence. 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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