const pptxgen = require("pptxgenjs");

const pres = new pptxgen();
pres.layout = "LAYOUT_16x9";
pres.title = "Genetics — A Medical Overview";
pres.author = "Medical Education";

// ─── THEME ────────────────────────────────────────────────────────────────────
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  orange:  "FF8C42",   // highlight
  red:     "E53935",   // danger/mutation
};

const FONT = "Calibri";

// ─── HELPERS ──────────────────────────────────────────────────────────────────
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// ─── SLIDE 1 — TITLE ──────────────────────────────────────────────────────────
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// ─── SLIDE 2 — WHAT IS GENETICS? ──────────────────────────────────────────────
{
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  addHeader(s, "What Is Genetics?", "The science of heredity and biological variation");

  s.addText([
    bullet("Medical genetics evolved from Mendel's laws (early 20th century) to a specialty central to all of medicine", 0),
    bullet("The Human Genome Project produced a virtually complete sequence of human DNA — ~3 billion base pairs", 0),
    bullet("Modern approach: whole-genome sequencing (genomics) rather than single-gene analysis (genetics)", 0),
    bullet("At least 7,160 phenotypes caused by variants in 4,629 genes are currently catalogued (OMIM, 2022)", 0),
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  addFooter(s);
}

// ─── SLIDE 3 — THE HUMAN GENOME ───────────────────────────────────────────────
{
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  bgDark(s);
  addHeader(s, "The Human Genome", "Structure, size, and organisation");

  // Stat cards
  const cards = [
    { val: "~3 Billion", lbl: "Base pairs" },
    { val: "46",         lbl: "Chromosomes" },
    { val: "~20,000",    lbl: "Protein-coding genes" },
    { val: "~1.5%",      lbl: "Coding DNA" },
  ];
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    bullet("Mitochondrial genome (~16.6 kb, 37 genes) is maternally inherited separately", 0),
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  addFooter(s);
}

// ─── SLIDE 4 — CHROMOSOMES ────────────────────────────────────────────────────
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  addHeader(s, "Chromosomes", "Structure and the karyotype");

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    bullet("Humans: 46 chromosomes (23 pairs) — 22 autosomes + 1 sex chromosome pair (XX or XY)", 0),
    bullet("Each chromosome has: centromere (p/q arms), telomeres at ends, and euchromatin/heterochromatin regions", 0),
    bullet("Banding techniques (G-, Q-, R-banding) allow cytogenetic identification of each chromosome", 0),
    bullet("Histone modifications regulate chromatin accessibility → gene expression", 0),
    bullet("DNA loops (~100 kb each) are attached to a protein scaffold — likely functional units of the genome", 0),
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}

// ─── SLIDE 5 — CATEGORIES OF GENETIC DISEASE ─────────────────────────────────
{
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  bgDark(s);
  addHeader(s, "Categories of Genetic Disease", "Three main groups based on mechanism");

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    {
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      color: CLR.orange,
      pts: [
        "Change in gene dosage (whole chromosomes or segments)",
        "Trisomies, monosomies, copy number variants (CNVs)",
        "Down syndrome (Trisomy 21)",
        "Prevalence: ~3% of liveborn infants",
      ],
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      color: CLR.accent,
      pts: [
        "Single-gene pathogenic variants",
        "Autosomal dominant, recessive, X-linked",
        "CF, Huntington, Marfan syndrome",
        "~1/300 liveborn; 1/50 lifetime prevalence",
      ],
    },
    {
      title: "Multifactorial / Complex",
      color: "#7E57C2",
      pts: [
        "Combined impact of many gene variants",
        "Triggered or modified by environment",
        "Diabetes, heart disease, schizophrenia",
        ">60% of total population burden",
      ],
    },
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  addFooter(s);
}

// ─── SLIDE 6 — PATTERNS OF INHERITANCE ───────────────────────────────────────
{
  const s = pres.addSlide();
  bgDark(s);
  addHeader(s, "Patterns of Mendelian Inheritance", "Classic pedigree patterns in monogenic disease");

  const patterns = [
    {
      label: "Autosomal\nDominant",
      color: CLR.orange,
      pts: ["One pathogenic allele sufficient", "Vertical transmission", "50% offspring risk", "E.g. Huntington, Marfan, BRCA1/2"],
    },
    {
      label: "Autosomal\nRecessive",
      color: CLR.accent,
      pts: ["Both alleles must be abnormal", "Horizontal pedigree pattern", "25% risk if both parents carriers", "E.g. CF, PKU, Sickle cell"],
    },
    {
      label: "X-Linked\nRecessive",
      color: "#EF5350",
      pts: ["Gene on X chromosome", "Males primarily affected", "Females are carriers", "E.g. Haemophilia A, DMD"],
    },
    {
      label: "X-Linked\nDominant",
      color: "#AB47BC",
      pts: ["One variant allele = disease", "Affects both sexes", "Often lethal in hemizygous males", "E.g. Fragile X, Rett syndrome"],
    },
  ];

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  addFooter(s);
}

// ─── SLIDE 7 — MITOCHONDRIAL INHERITANCE ────────────────────────────────────
{
  const s = pres.addSlide();
  bgDark(s);
  addHeader(s, "Mitochondrial Genetics", "The 'other' genome — maternal inheritance");

  s.addText([
    bullet("Mitochondrial DNA (mtDNA): circular, ~16,569 bp, 37 genes (13 protein-coding, 22 tRNA, 2 rRNA)", 0),
    bullet("Exclusively maternally inherited — all children of an affected mother are at risk", 0),
    bullet("Heteroplasmy: cells may contain a mixture of normal and mutant mtDNA — explains variable expression", 0),
    bullet("High mutation rate (no introns, limited repair) — susceptibility in energy-demanding tissues", 0),
    bullet("Clinical features: myopathy, encephalopathy, lactic acidosis, stroke-like episodes (MELAS)", 0),
    bullet("Classic syndromes: MELAS, MERRF, Leber hereditary optic neuropathy (LHON), Kearns–Sayre", 0),
  ], {
    x: 0.4, y: 1.3, w: 6.0, h: 4.1, fontFace: FONT, paraSpaceBefore: 7,
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    { text: "✔ ", options: { color: CLR.accent, bold: true, fontSize: 13 } },
    { text: "Maternal-only transmission\n", options: { color: CLR.white, fontSize: 12 } },
    { text: "✔ ", options: { color: CLR.accent, bold: true, fontSize: 13 } },
    { text: "No Mendelian ratio\n", options: { color: CLR.white, fontSize: 12 } },
    { text: "✔ ", options: { color: CLR.accent, bold: true, fontSize: 13 } },
    { text: "Threshold effect\n", options: { color: CLR.white, fontSize: 12 } },
    { text: "✔ ", options: { color: CLR.accent, bold: true, fontSize: 13 } },
    { text: "Replicative segregation\n", options: { color: CLR.white, fontSize: 12 } },
    { text: "✔ ", options: { color: CLR.accent, bold: true, fontSize: 13 } },
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  addFooter(s);
}

// ─── SLIDE 8 — MUTATIONS ──────────────────────────────────────────────────────
{
  const s = pres.addSlide();
  bgDark(s);
  addHeader(s, "Types of Mutations", "Pathogenic variants — from base changes to chromosomal rearrangements");

  const types = [
    { type: "Point Mutations", color: CLR.accent, items: ["Missense — amino acid change", "Nonsense — premature stop codon", "Silent — no amino acid change"] },
    { type: "Frameshift", color: CLR.orange, items: ["Insertion or deletion of non-3x bp", "Alters reading frame downstream", "Usually severe truncating effect"] },
    { type: "Splice Site", color: "#EF5350", items: ["Disrupts donor/acceptor splice sites", "Exon skipping or intron retention", "E.g. some CF CFTR variants"] },
    { type: "Copy Number\nVariants (CNV)", color: "#AB47BC", items: ["Deletions & duplications (kbp–Mbp)", "22q11.2 deletion syndrome", "Detected by array CGH / WGS"] },
  ];

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    bullet("Gain-of-function vs. loss-of-function: determines inheritance pattern and therapeutic approach", 0),
    bullet("Somatic mutations (post-conception) underlie most cancers; germline mutations are heritable", 0),
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  addFooter(s);
}

// ─── SLIDE 9 — EPIGENETICS ─────────────────────────────────────────────────────
{
  const s = pres.addSlide();
  bgDark(s);
  addHeader(s, "Epigenetics", "Gene regulation without DNA sequence changes");

  // Three-column layout
  const cols = [
    {
      title: "DNA Methylation",
      icon: "CH₃",
      color: CLR.accent,
      pts: ["CpG islands at promoters", "Methylation → gene silencing", "Cancer epigenetics", "Imprinting (Prader-Willi, Angelman)"],
    },
    {
      title: "Histone Modification",
      icon: "H3/H4",
      color: CLR.orange,
      pts: ["Acetylation → gene activation", "Methylation → context dependent", "Phosphorylation, ubiquitylation", "Chromatin remodelling complexes"],
    },
    {
      title: "Non-coding RNA",
      icon: "ncRNA",
      color: "#AB47BC",
      pts: ["miRNA — post-transcriptional silencing", "lncRNA — chromatin regulation", "X-inactivation (XIST lncRNA)", "Tissue-specific gene control"],
    },
  ];

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  addFooter(s);
}

// ─── SLIDE 10 — GENOMIC TECHNOLOGIES ─────────────────────────────────────────
{
  const s = pres.addSlide();
  bgDark(s);
  addHeader(s, "Genomic Technologies", "From karyotyping to whole-genome sequencing");

  const techs = [
    { label: "Karyotype / G-banding", era: "1970s–", use: "Gross chromosomal abnormalities, aneuploidies" },
    { label: "FISH", era: "1990s–", use: "Targeted deletion/duplication; interphase cells" },
    { label: "Microarray (aCGH / SNP)", era: "2000s–", use: "Genome-wide CNVs; autism, ID, miscarriage" },
    { label: "Gene Panel Sequencing", era: "2010s–", use: "Targeted NGS for defined disease groups (e.g. cardiomyopathy panel)" },
    { label: "Whole Exome Sequencing", era: "2012–", use: "All ~20,000 protein-coding exons; rare disease diagnosis" },
    { label: "Whole Genome Sequencing", era: "2020s–", use: "First-tier test for heritable disease; structural variants, non-coding regions" },
  ];

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  });

  addFooter(s);
}

// ─── SLIDE 11 — CLINICAL APPLICATIONS ────────────────────────────────────────
{
  const s = pres.addSlide();
  bgDark(s);
  addHeader(s, "Clinical Applications of Genetics", "Where genetics meets patient care");

  s.addText([
    bullet("Genetic counselling: risk estimation, carrier testing, family communication, psychosocial support", 0),
    bullet("Prenatal diagnosis: CVS, amniocentesis, cell-free fetal DNA — chromosomal & monogenic screening", 0),
    bullet("Newborn screening: tandem mass spectrometry identifies treatable IEMs before symptom onset", 0),
    bullet("Pharmacogenomics: CYP2D6, TPMT, HLA-B*5701 — guiding drug selection and dosing", 0),
    bullet("Hereditary cancer: BRCA1/2, Lynch syndrome — prophylactic interventions, surveillance protocols", 0),
    bullet("Rare disease diagnosis: WGS has cut the 'diagnostic odyssey' from years to weeks for many families", 0),
    bullet("Somatic genomics in oncology: tumour mutation burden, driver mutations, targeted therapy selection", 0),
  ], {
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// ─── SLIDE 12 — SUMMARY & KEY TAKEAWAYS ──────────────────────────────────────
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    { n: "01", text: "Genetic disease spans chromosomal, monogenic, and multifactorial categories — each with distinct mechanisms and inheritance patterns." },
    { n: "02", text: "The human genome contains ~20,000 genes within ~3 billion base pairs; non-coding DNA has critical regulatory roles." },
    { n: "03", text: "Classic Mendelian inheritance (AD, AR, XLR, XLD) and mitochondrial inheritance govern different risk calculations in pedigrees." },
    { n: "04", text: "Epigenetic mechanisms — methylation, histone modification, ncRNA — modulate gene expression without altering DNA sequence." },
    { n: "05", text: "Whole-genome sequencing is rapidly becoming the first-tier clinical diagnostic test for heritable disease." },
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