Colonic polyposis syndrome

Reading File

Finding Sources

Searching PubMed

colonic polyposis syndrome genetics management

Finding Sources

Reading File

Finding Sources

Reading File

Finding Sources

Reading File

Loading Image

Colonic Polyposis Syndromes

Colonic polyposis syndromes are conditions characterized by diffuse polyp formation throughout the colon. Most are inherited and carry significant risk of colorectal cancer (CRC) or other GI/extra-intestinal malignancies. They are classified primarily by the histologic type of the predominant polyp.

Classification (Sleisenger & Fordtran's GI and Liver Disease)

Category	Syndromes
Adenomatous	Classic FAP, Attenuated FAP (AFAP), Gardner syndrome, Turcot syndrome, MUTYH-associated polyposis (MAP), Polymerase proofreading-associated polyposis (PPAP), NTHL1 polyposis
Serrated	Serrated polyposis syndrome
Hamartomatous	Peutz-Jeghers syndrome, Juvenile polyposis, Cowden disease, Bannayan-Ruvalcaba-Riley syndrome
Rare hamartomatous	Hereditary mixed polyposis, Intestinal ganglioneuromatosis, Basal cell nevus syndrome
Non-inherited	Cronkhite-Canada syndrome, Lymphomatous polyposis

I. Adenomatous Polyposis Syndromes

1. Familial Adenomatous Polyposis (FAP)

Gene/Inheritance: APC gene (chromosome 5q21), autosomal dominant; penetrance 80-100%; prevalence 1 in 5,000-7,500. ~20-25% arise from de novo mutations.

Pathogenesis: The APC protein is a key negative regulator of the Wnt signaling pathway. Germline mutation of one APC allele is inherited; adenomas develop when the second allele is also mutated or deleted (two-hit hypothesis).

Colonic features:

Diagnosis requires >100 synchronous colonic adenomas (classic FAP); thousands may be present
Polyps are morphologically indistinguishable from sporadic adenomas
Predominantly in the rectum and left colon; appear in adolescence (present in 15% by age 10, 75% by age 20)
Without prophylactic colectomy, CRC risk approaches 100% by age 35-40 years

Endoscopic/macroscopic appearance:

Colonic adenomas: (A) Pedunculated adenoma (endoscopic view), (B) adenoma with velvety surface, (C) low-magnification photomicrograph of a pedunculated tubular adenoma

Extracolonic intestinal disease:

Duodenal adenomas: >95% of FAP patients; most common around the ampulla of Vater; develop ~15 years after colonic polyps. Duodenal cancer (in 5-10%) is the 2nd leading cause of death in FAP. Staged by the Spiegelman scoring system (Stage IV = 36% cancer risk at 10 years)
Gastric: Fundic gland polyps (30-90%, low malignant potential); gastric adenomas (10-30%, antrum, higher risk in Japanese/Korean patients)

Extraintestinal manifestations:

Feature	Frequency
Osteomas (mandible, skull, long bones)	50-90%
Congenital hypertrophic retinal pigment epithelium (CHRPE)	70-80%
Epidermoid/sebaceous cysts	50%
Desmoid tumors	10-24% (3rd leading cause of death)
Fibromas	25-50%
Thyroid cancer (papillary)	2-3%
Dental abnormalities / supernumerary teeth	Variable
Hepatoblastoma	Rare
Medulloblastoma (Turcot variant)	Rare

Screening:

Annual flexible sigmoidoscopy/colonoscopy from age 10-12 years
Upper endoscopy (EGD) from age 20-25 years
Annual thyroid ultrasound

Surgery (standard of care - prophylactic colectomy):

Operation	Indications
Total abdominal colectomy (TAC) + ileorectal anastomosis (IRA)	Colon cancer; rectum has <20 polyps manageable endoscopically
Total proctocolectomy (TPC) + ileal pouch-anal anastomosis (IPAA)	Profuse polyposis; rectal cancer; rectal polyp burden >20

Surgery is typically deferred to the late teenage years. Indications include cancer, multifocal high-grade dysplasia, or rapidly increasing polyp burden.

2. Attenuated FAP (AFAP)

Gene: APC mutations at the very proximal (5') or distal (3') ends of the gene
Fewer adenomas (typically <100), flat growth pattern, cluster in the proximal colon
Present in adulthood rather than adolescence; CRC risk still high but occurs later (≥55 years)
Surveillance: colonoscopy every 1-2 years from age 25 years
Upper GI surveillance similar to classic FAP

3. Gardner Syndrome

A variant of classic FAP (same APC gene mutation) with the same colonic polyposis but more prominent extracolonic features:

Prominent osteomas, epidermoid cysts, desmoid tumors
Supernumerary teeth, dental abnormalities
Now considered part of the FAP spectrum, not a separate entity

4. Turcot Syndrome (Glioma-Polyposis)

Colonic polyposis + primary CNS tumors
Represents two genetically distinct entities:
- APC mutation → colonic polyposis + medulloblastoma
- DNA mismatch repair (MMR) gene mutation → Lynch syndrome-type polyposis + glioblastoma multiforme
Management of CRC risk differs depending on which gene is mutated

5. MUTYH-Associated Polyposis (MAP)

Gene/Inheritance: MUTYH (MYH) gene (base-excision repair); autosomal recessive - unique among polyposis syndromes. Most common mutations: Y179C and G396D.

Pathogenesis: Defective MUTYH allows G:C → T:A transversions in oxidatively damaged DNA. The APC gene is a major target, so loss of APC function creates an FAP-like adenoma phenotype.

Features:

Usually 5-100 colonic adenomas (florid polyposis can occur)
Phenotype appears later than classic FAP
CRC risk is high (usually microsatellite-stable tumors)
Extra-colonic: gastric cancer, duodenal adenomas, CHRPE, osteomas

Surveillance: Colonoscopy every 1-2 years from age 25; test all patients with >10 adenomas for biallelic MUTYH mutations. Genetic counseling directed to siblings (not parents/children, given recessive inheritance).

6. Polymerase Proofreading-Associated Polyposis (PPAP)

Genes: POLE or POLD1 (DNA polymerase subunits); autosomal dominant
"Ultramutator" phenotype; typically <100 colonic adenomas
High CRC risk; endometrial cancer (especially POLD1 mutations)

7. NTHL1-Associated Polyposis

Gene: NTHL1 (base-excision repair gene, similar to MUTYH); autosomal recessive
~50 colonic adenomas in adulthood; high CRC risk
Broader extra-colonic spectrum: endometrial, breast, and skin cancers
Management similar to MAP

II. Serrated Polyposis Syndrome

Also formerly called hyperplastic polyposis syndrome
Characterized by multiple serrated polyps (hyperplastic, sessile serrated, or traditional serrated adenomas) throughout the colon
Associated with increased CRC risk, particularly through the serrated neoplasia pathway (BRAF mutation, CpG island methylation)
No single gene mutation has been consistently identified

III. Hamartomatous Polyposis Syndromes

These syndromes share hamartomatous polyps as the primary lesion, though adenomas and hyperplastic polyps may co-exist.

Summary Table (Sleisenger & Fordtran):

Syndrome	Gene	Polyp Type	GI Location	Key Extra-intestinal Features
Peutz-Jeghers	STK11/LKB1	Hamartoma (smooth muscle core)	Small intestine, stomach, colon	Mucocutaneous pigmentation; breast, pancreatic, ovarian, GI cancers
Juvenile polyposis	SMAD4, BMPR1A, ENG	Juvenile polyps (dilated crypts)	Colon, small intestine, stomach	Colon cancer; congenital abnormalities; HHT phenotype (SMAD4)
Cowden disease	PTEN	Hamartomas (disorganized muscularis mucosae)	Stomach, colon	Trichilemmomas; breast + thyroid cancer
Bannayan-Ruvalcaba-Riley	PTEN	Juvenile polyps	Colon	Macrocephaly; developmental delay; pigmented penile spots

Peutz-Jeghers Syndrome (PJS)

Gene/Inheritance: STK11/LKB1 (serine-threonine kinase, chromosome 19p); autosomal dominant with variable penetrance. ~80% of affected families have an identifiable STK11 mutation.

Pathogenesis: STK11 regulates AMPK pathways controlling cell polarization and growth. Loss-of-function leads to uncontrolled growth, particularly in epithelium.

Mucocutaneous pigmentation: Melanin deposits on lips, buccal mucosa (pathognomonic), hands, feet, genitalia, perianal region - present in ~95% of patients, appearing in infancy.

Polyp histology: Characteristic arborizing network of connective tissue, smooth muscle, and lamina propria with normal-appearing overlying epithelium. Most common in the small intestine, also stomach and colon. Risk of intussusception (occasionally fatal).

Cancer risks (lifetime ~40%): Colon, gastric, small intestinal, pancreatic (highest relative risk), breast, lung, ovarian, uterine; sex cord tumors of testes; surveillance from birth (testicular) through adulthood.

Juvenile Polyposis Syndrome (JPS)

Gene/Inheritance: SMAD4 (chromosome 18q) or BMPR1A (chromosome 10q22); autosomal dominant. Both genes are TGF-β pathway components. SMAD4 mutations (~20-25% of JPS) carry higher malignancy potential and may cause massive gastric polyposis. BMPR1A mutations account for another ~20%.

Polyp histology: Juvenile polyps - cystically dilated crypts filled with inspissated mucus, inflammatory cells, surrounded by abundant edematous lamina propria (see image below). Surface erosion is common.

Juvenile polyposis histology: (A) Juvenile polyp with surface erosion and cystically dilated crypts; (B) Inspissated mucus, neutrophils, and inflammatory debris within dilated crypts

Features:

Most common hamartomatous syndrome (incidence 1 per 100,000)
Polyps in colon, small intestine, and stomach
Significant CRC risk; upper GI surveillance required for SMAD4 carriers
~30% of patients have congenital abnormalities
SMAD4 carriers: risk of hereditary hemorrhagic telangiectasia (HHT) phenotype

Cowden Syndrome (PTEN Hamartoma Tumor Syndrome)

Gene: PTEN (tumor suppressor, phosphatase and tensin homolog)

GI features: Multiple hamartomatous polyps throughout GI tract (stomach and colon predominant)

Extra-intestinal features:

Trichilemmomas (benign hair follicle tumors) - pathognomonic
Oral papillomas
Increased risk of breast cancer (25-50% lifetime) and thyroid cancer
Macrocephaly

IV. Non-inherited Polyposis

Cronkhite-Canada Syndrome

Acquired (non-inherited), extremely rare
Diffuse GI hamartomatous polyposis with characteristic ectodermal changes: alopecia, nail dystrophy, hyperpigmentation of the skin
Associated with protein-losing enteropathy, diarrhea, and malabsorption

Key Comparisons at a Glance

Feature	FAP	MAP	PJS	JPS
Gene	APC	MUTYH	STK11	SMAD4/BMPR1A
Inheritance	AD	AR	AD	AD
Polyp type	Adenoma	Adenoma	Hamartoma	Hamartoma (juvenile)
No. of polyps	>100 to thousands	5-100 (usually)	Hundreds (small bowel >> colon)	Multiple (usually <100)
CRC risk	~100%	High	~40% (all cancers)	High
Key extra-colonic finding	Osteomas, CHRPE, desmoids	CHRPE, osteomas	Mucocutaneous pigmentation	Congenital anomalies (HHT if SMAD4)
Screening start	Age 10-12	Age 25	Infancy (testicular)	Childhood

Sources: Sleisenger and Fordtran's Gastrointestinal and Liver Disease; Robbins, Cotran & Kumar Pathologic Basis of Disease; Sabiston Textbook of Surgery; Current Surgical Therapy 14e; Emery's Elements of Medical Genetics and Genomics; Yamada's Textbook of Gastroenterology

Make it into a ppt

Reading File

Running Command

ls /home/daytona/workspace/

Running Command

mkdir -p /home/daytona/workspace/colonic-polyposis-ppt

Writing File

~/colonic-polyposis-ppt/make_ppt.js

const pptxgen = require("pptxgenjs");
const { execSync } = require("child_process");

// ─── Fetch images ────────────────────────────────────────────────────────────
const imgUrls = [
  "https://cdn.orris.care/cdss_images/4566501cb12efb4d13ba792e8d3b323765e3f865ccf89212e397314585ec27d6.png",
  "https://cdn.orris.care/cdss_images/a38620b7eb609e06e2c1fb5c2cc5b8702b5f219d4409081cd0f096506b3f427d.png"
];
const imgs = JSON.parse(
  execSync(
    `node /home/daytona/skills/shared/scripts/fetch_images.js ${imgUrls.map(u => `"${u}"`).join(" ")}`
  ).toString()
);
const [adenomaImg, juvenileImg] = imgs;

// ─── Palette ─────────────────────────────────────────────────────────────────
const C = {
  navy:    "0D2B45",
  teal:    "1A7A6E",
  mint:    "2FB8A0",
  amber:   "E8A020",
  gold:    "F5C842",
  white:   "FFFFFF",
  offwhite:"F4F7FA",
  ltgray:  "D6E4EF",
  midgray: "7A97B0",
  dark:    "0A1E30",
  red:     "C0392B",
  orange:  "E67E22",
  purple:  "7B3FA0",
  green:   "27AE60"
};

let pres = new pptxgen();
pres.layout = "LAYOUT_16x9";
pres.title = "Colonic Polyposis Syndromes";
pres.author = "Orris Medical";

// ─── Helper: section header bar ──────────────────────────────────────────────
function addHeaderBar(slide, text, barColor) {
  slide.addShape(pres.shapes.RECTANGLE, {
    x: 0, y: 0, w: 10, h: 0.72,
    fill: { color: barColor || C.navy },
    line: { color: barColor || C.navy }
  });
  slide.addText(text, {
    x: 0.3, y: 0, w: 9.4, h: 0.72,
    fontSize: 22, bold: true, color: C.white,
    valign: "middle", margin: 0
  });
}

// ─── Helper: footer ──────────────────────────────────────────────────────────
function addFooter(slide, note) {
  slide.addShape(pres.shapes.RECTANGLE, {
    x: 0, y: 5.35, w: 10, h: 0.275,
    fill: { color: C.navy }, line: { color: C.navy }
  });
  slide.addText(note || "Colonic Polyposis Syndromes  |  Orris Medical", {
    x: 0.2, y: 5.35, w: 9.6, h: 0.275,
    fontSize: 8, color: C.ltgray, valign: "middle", margin: 0
  });
}

// ─── Helper: info card ───────────────────────────────────────────────────────
function addCard(slide, x, y, w, h, title, titleColor, body) {
  slide.addShape(pres.shapes.RECTANGLE, {
    x, y, w, h,
    fill: { color: C.white },
    line: { color: C.ltgray, width: 0.5 },
    shadow: { type: "outer", color: "000000", blur: 4, offset: 2, angle: 135, opacity: 0.08 }
  });
  // title bar
  slide.addShape(pres.shapes.RECTANGLE, {
    x, y, w, h: 0.32,
    fill: { color: titleColor || C.teal },
    line: { color: titleColor || C.teal }
  });
  slide.addText(title, {
    x: x + 0.08, y, w: w - 0.16, h: 0.32,
    fontSize: 9.5, bold: true, color: C.white,
    valign: "middle", margin: 0
  });
  // body bullets
  if (body && body.length) {
    const items = body.map((b, i) => ({
      text: b,
      options: { bullet: { type: "bullet" }, breakLine: i < body.length - 1, fontSize: 8.5, color: C.navy }
    }));
    slide.addText(items, {
      x: x + 0.1, y: y + 0.36, w: w - 0.2, h: h - 0.44,
      valign: "top", margin: 0
    });
  }
}

// ═══════════════════════════════════════════════════════════════════════════════
// SLIDE 1 — Title
// ═══════════════════════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  // Full background
  s.addShape(pres.shapes.RECTANGLE, {
    x: 0, y: 0, w: 10, h: 5.625,
    fill: { color: C.dark }, line: { color: C.dark }
  });
  // Accent stripe
  s.addShape(pres.shapes.RECTANGLE, {
    x: 0, y: 0, w: 0.18, h: 5.625,
    fill: { color: C.mint }, line: { color: C.mint }
  });
  // Bottom bar
  s.addShape(pres.shapes.RECTANGLE, {
    x: 0, y: 4.9, w: 10, h: 0.725,
    fill: { color: C.teal }, line: { color: C.teal }
  });
  s.addText("COLONIC POLYPOSIS SYNDROMES", {
    x: 0.5, y: 1.5, w: 9, h: 1.0,
    fontSize: 36, bold: true, color: C.white,
    align: "center", charSpacing: 2
  });
  s.addText("Classification  •  Genetics  •  Clinical Features  •  Management", {
    x: 0.5, y: 2.65, w: 9, h: 0.5,
    fontSize: 16, color: C.mint, align: "center", italic: true
  });
  s.addShape(pres.shapes.RECTANGLE, {
    x: 3.5, y: 3.3, w: 3, h: 0.03,
    fill: { color: C.gold }, line: { color: C.gold }
  });
  s.addText("Sleisenger & Fordtran  •  Robbins & Kumar  •  Sabiston  •  Yamada", {
    x: 0.5, y: 4.92, w: 9, h: 0.5,
    fontSize: 9, color: C.white, align: "center", italic: true
  });
}

// ═══════════════════════════════════════════════════════════════════════════════
// SLIDE 2 — Overview / Classification
// ═══════════════════════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 0, w: 10, h: 5.625, fill: { color: C.offwhite }, line: { color: C.offwhite } });
  addHeaderBar(s, "Overview: Classification of GI Polyposis Syndromes", C.navy);
  addFooter(s);

  const cats = [
    { label: "ADENOMATOUS", color: C.teal, items: ["Classic FAP", "Attenuated FAP (AFAP)", "Gardner Syndrome", "Turcot Syndrome", "MAP (MUTYH)", "PPAP (POLE/POLD1)", "NTHL1 Polyposis"] },
    { label: "SERRATED", color: C.orange, items: ["Serrated Polyposis Syndrome", "(formerly Hyperplastic\nPolyposis Syndrome)"] },
    { label: "HAMARTOMATOUS", color: C.purple, items: ["Peutz-Jeghers Syndrome", "Juvenile Polyposis", "Cowden Disease (PTEN)", "Bannayan-Ruvalcaba-Riley Syndrome"] },
    { label: "NON-INHERITED", color: C.midgray, items: ["Cronkhite-Canada Syndrome", "Lymphomatous Polyposis", "Nodular Lymphoid Hyperplasia"] }
  ];

  const xs = [0.15, 2.65, 5.15, 7.65];
  const w = 2.3;

  cats.forEach((cat, i) => {
    const x = xs[i];
    s.addShape(pres.shapes.RECTANGLE, {
      x, y: 0.85, w, h: 4.35,
      fill: { color: C.white },
      line: { color: C.ltgray, width: 0.5 },
      shadow: { type: "outer", color: "000000", blur: 5, offset: 2, angle: 135, opacity: 0.1 }
    });
    s.addShape(pres.shapes.RECTANGLE, {
      x, y: 0.85, w, h: 0.4,
      fill: { color: cat.color }, line: { color: cat.color }
    });
    s.addText(cat.label, {
      x: x + 0.08, y: 0.85, w: w - 0.16, h: 0.4,
      fontSize: 10, bold: true, color: C.white,
      valign: "middle", align: "center", margin: 0
    });
    const items = cat.items.map((t, idx) => ({
      text: t,
      options: { bullet: { type: "bullet", characterCode: "25B6" }, breakLine: idx < cat.items.length - 1, fontSize: 9, color: C.navy }
    }));
    s.addText(items, {
      x: x + 0.1, y: 1.3, w: w - 0.2, h: 3.8,
      valign: "top", margin: 0
    });
  });

  s.addText("Most polyposis syndromes are inherited and carry significant CRC or extra-intestinal cancer risk", {
    x: 0.15, y: 5.08, w: 9.7, h: 0.26,
    fontSize: 8, italic: true, color: C.midgray, align: "center"
  });
}

// ═══════════════════════════════════════════════════════════════════════════════
// SLIDE 3 — FAP: Genetics & Pathogenesis
// ═══════════════════════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 0, w: 10, h: 5.625, fill: { color: C.offwhite }, line: { color: C.offwhite } });
  addHeaderBar(s, "Familial Adenomatous Polyposis (FAP): Genetics & Pathogenesis", C.teal);
  addFooter(s);

  // Left panel
  s.addShape(pres.shapes.RECTANGLE, {
    x: 0.15, y: 0.85, w: 4.6, h: 4.35,
    fill: { color: C.white }, line: { color: C.ltgray, width: 0.5 },
    shadow: { type: "outer", color: "000000", blur: 4, offset: 2, angle: 135, opacity: 0.08 }
  });
  s.addShape(pres.shapes.RECTANGLE, {
    x: 0.15, y: 0.85, w: 4.6, h: 0.35,
    fill: { color: C.teal }, line: { color: C.teal }
  });
  s.addText("GENETICS", { x: 0.23, y: 0.85, w: 4.44, h: 0.35, fontSize: 10, bold: true, color: C.white, valign: "middle", margin: 0 });

  const genItems = [
    { text: "Gene: APC (Adenomatous Polyposis Coli) on chromosome 5q21", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "Most mutations between codons 168–1640; key codons: 1061 & 1309", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "Inheritance: Autosomal dominant, penetrance 80–100%", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "Prevalence: 1 in 5,000–7,500", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "20–25% arise from de novo mutations (no family history)", options: { bullet: true, breakLine: true, fontSize: 9, color: C.orange, bold: true } },
    { text: "Pathogenesis: APC is a key negative regulator of Wnt signaling. One mutant allele inherited; second allele lost somatically → adenoma formation (two-hit hypothesis)", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "APC protein: 300 kDa scaffolding protein; promotes β-catenin degradation", options: { bullet: true, fontSize: 9, color: C.navy } }
  ];
  s.addText(genItems, { x: 0.25, y: 1.24, w: 4.4, h: 3.85, valign: "top", margin: 0 });

  // Right panel
  s.addShape(pres.shapes.RECTANGLE, {
    x: 5.0, y: 0.85, w: 4.85, h: 4.35,
    fill: { color: C.white }, line: { color: C.ltgray, width: 0.5 },
    shadow: { type: "outer", color: "000000", blur: 4, offset: 2, angle: 135, opacity: 0.08 }
  });
  s.addShape(pres.shapes.RECTANGLE, {
    x: 5.0, y: 0.85, w: 4.85, h: 0.35,
    fill: { color: C.navy }, line: { color: C.navy }
  });
  s.addText("COLONIC FEATURES", { x: 5.08, y: 0.85, w: 4.68, h: 0.35, fontSize: 10, bold: true, color: C.white, valign: "middle", margin: 0 });

  const colonItems = [
    { text: "Classic FAP: >100 synchronous adenomas (thousands possible)", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "Polyps predominate in rectum and left colon", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "Present by age 10 in ~15% of patients; 75% by age 20", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "Morphologically identical to sporadic adenomas", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "Flat/depressed adenomas and microscopic adenomas also common", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "CRC risk approaches 100% if untreated; typically by age 35–40", options: { bullet: true, breakLine: true, fontSize: 9.5, color: C.red, bold: true } },
    { text: "Symptoms: bleeding, diarrhea, abdominal pain, mucous discharge", options: { bullet: true, fontSize: 9, color: C.navy } }
  ];
  s.addText(colonItems, { x: 5.1, y: 1.24, w: 4.65, h: 3.85, valign: "top", margin: 0 });
}

// ═══════════════════════════════════════════════════════════════════════════════
// SLIDE 4 — FAP Extracolonic Manifestations
// ═══════════════════════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 0, w: 10, h: 5.625, fill: { color: C.offwhite }, line: { color: C.offwhite } });
  addHeaderBar(s, "FAP: Extracolonic Manifestations & Surveillance", C.teal);
  addFooter(s);

  // Left: GI + extra-GI
  addCard(s, 0.15, 0.85, 4.6, 2.3, "EXTRA-INTESTINAL GI DISEASE", C.teal, [
    "Duodenal adenomas: >95% of FAP patients (periampullary region)",
    "Duodenal cancer in 5–10% — 2nd leading cause of FAP death",
    "Gastric fundic gland polyps: 30–90% (low malignant potential)",
    "Gastric adenomas: 10–30% (antrum; higher in Asian populations)",
    "Spiegelman staging guides surveillance intervals"
  ]);
  addCard(s, 0.15, 3.25, 4.6, 1.9, "CAUSE OF DEATH IN FAP", C.red, [
    "1st: Metastatic colorectal carcinoma",
    "2nd: Duodenal / periampullary adenocarcinoma",
    "3rd: Desmoid tumors (locally invasive fibromatoses)"
  ]);

  // Right: non-GI
  addCard(s, 5.0, 0.85, 4.85, 2.3, "BENIGN EXTRA-INTESTINAL LESIONS", C.navy, [
    "Osteomas (mandible, skull, long bones): 50–90%",
    "CHRPE (detectable at birth): 70–80%",
    "Epidermoid / sebaceous cysts: 50%",
    "Fibromas: 25–50%",
    "Desmoid tumors: 10–24%",
    "Dental abnormalities / supernumerary teeth"
  ]);
  addCard(s, 5.0, 3.25, 4.85, 1.9, "MALIGNANT EXTRA-INTESTINAL", C.orange, [
    "Papillary thyroid carcinoma: 2–3%",
    "Hepatoblastoma (childhood)",
    "Medulloblastoma (Turcot variant)",
    "Adrenal tumors"
  ]);
}

// ═══════════════════════════════════════════════════════════════════════════════
// SLIDE 5 — FAP Endoscopy Image + Histology
// ═══════════════════════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 0, w: 10, h: 5.625, fill: { color: C.offwhite }, line: { color: C.offwhite } });
  addHeaderBar(s, "FAP: Adenoma Morphology", C.teal);
  addFooter(s);

  if (adenomaImg && !adenomaImg.error) {
    s.addImage({ data: adenomaImg.base64, x: 0.3, y: 0.85, w: 9.4, h: 4.05 });
  }
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 4.9, w: 10, h: 0.45, fill: { color: "00000088" }, line: { color: "00000088" } });
  s.addText(
    "(A) Pedunculated adenoma (endoscopy)    |    (B) Adenoma with velvety surface    |    (C) Histology: tubular adenoma (low-power)   —   Robbins & Kumar Pathologic Basis of Disease",
    { x: 0.2, y: 4.9, w: 9.6, h: 0.45, fontSize: 8, color: C.white, align: "center", valign: "middle", italic: true }
  );
}

// ═══════════════════════════════════════════════════════════════════════════════
// SLIDE 6 — FAP Surgery & Screening
// ═══════════════════════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 0, w: 10, h: 5.625, fill: { color: C.offwhite }, line: { color: C.offwhite } });
  addHeaderBar(s, "FAP: Surgical Management & Screening", C.teal);
  addFooter(s);

  // Surgical options table
  s.addShape(pres.shapes.RECTANGLE, {
    x: 0.15, y: 0.85, w: 9.7, h: 0.38,
    fill: { color: C.teal }, line: { color: C.teal }
  });
  ["Procedure", "Indication", "Comment"].forEach((h, i) => {
    s.addText(h, {
      x: [0.2, 3.55, 6.95][i], y: 0.85, w: [3.2, 3.2, 2.85][i], h: 0.38,
      fontSize: 9.5, bold: true, color: C.white, valign: "middle", margin: 4
    });
  });

  const rows = [
    ["Total Abdominal Colectomy + IRA", "Colon cancer; rectum <20 polyps", "Rectum managed endoscopically"],
    ["Total Proctocolectomy + IPAA", "Profuse polyposis; rectal cancer;\nrectal polyps >20", "Stapled anastomosis if anal transition zone clear"],
    ["Pancreas-sparing Duodenectomy", "Spiegelman Stage IV duodenal disease", "Expert centers only"]
  ];
  rows.forEach((row, ri) => {
    const y = 1.23 + ri * 0.72;
    const bg = ri % 2 === 0 ? C.white : "EAF4F1";
    s.addShape(pres.shapes.RECTANGLE, { x: 0.15, y, w: 9.7, h: 0.7, fill: { color: bg }, line: { color: C.ltgray, width: 0.5 } });
    row.forEach((cell, ci) => {
      s.addText(cell, {
        x: [0.2, 3.55, 6.95][ci], y, w: [3.2, 3.2, 2.85][ci], h: 0.7,
        fontSize: 8.5, color: C.navy, valign: "middle", margin: 4
      });
    });
  });

  // Screening panel
  s.addShape(pres.shapes.RECTANGLE, {
    x: 0.15, y: 3.45, w: 9.7, h: 0.35,
    fill: { color: C.navy }, line: { color: C.navy }
  });
  s.addText("SCREENING SCHEDULE", {
    x: 0.25, y: 3.45, w: 9.5, h: 0.35,
    fontSize: 10, bold: true, color: C.white, valign: "middle", margin: 0
  });

  const screenItems = [
    ["Age 10–12 yrs", "Annual colonoscopy (or flexible sigmoidoscopy if known FAP)"],
    ["Age 20–25 yrs", "Upper endoscopy (EGD with side-viewer for periampullary region)"],
    ["Ongoing", "Annual thyroid ultrasound  |  Desmoid awareness  |  Spiegelman duodenal staging"]
  ];
  screenItems.forEach((item, i) => {
    const y = 3.84 + i * 0.36;
    s.addShape(pres.shapes.RECTANGLE, {
      x: 0.15, y, w: 1.6, h: 0.34,
      fill: { color: C.mint }, line: { color: C.mint }
    });
    s.addText(item[0], { x: 0.2, y, w: 1.5, h: 0.34, fontSize: 8.5, bold: true, color: C.dark, valign: "middle", align: "center", margin: 0 });
    s.addText(item[1], { x: 1.85, y, w: 7.9, h: 0.34, fontSize: 8.5, color: C.navy, valign: "middle", margin: 4 });
  });
}

// ═══════════════════════════════════════════════════════════════════════════════
// SLIDE 7 — FAP Variants (AFAP, Gardner, Turcot)
// ═══════════════════════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 0, w: 10, h: 5.625, fill: { color: C.offwhite }, line: { color: C.offwhite } });
  addHeaderBar(s, "FAP Variants: AFAP, Gardner Syndrome, Turcot Syndrome", C.navy);
  addFooter(s);

  addCard(s, 0.15, 0.85, 3.1, 4.3, "ATTENUATED FAP (AFAP)", C.teal, [
    "Same APC gene — mutations at 5' or 3' ends",
    "<100 adenomas (usually fewer)",
    "Flat polyp growth pattern",
    "Proximal colon predominance",
    "Presents in adulthood (not adolescence)",
    "CRC risk still high but onset ≥55 years",
    "Colonoscopy every 1–2 years from age 25",
    "Same upper GI surveillance as classic FAP"
  ]);
  addCard(s, 3.45, 0.85, 3.1, 4.3, "GARDNER SYNDROME", C.orange, [
    "APC gene variant — same locus as FAP",
    "Classic FAP + prominent extracolonic features",
    "Prominent osteomas (mandible, skull)",
    "Epidermoid cysts",
    "Desmoid tumors (mesentery, abdominal wall)",
    "Supernumerary teeth / dental anomalies",
    "Now considered a phenotypic variant of FAP, NOT a separate entity"
  ]);
  addCard(s, 6.75, 0.85, 3.1, 4.3, "TURCOT SYNDROME", C.purple, [
    "Colonic polyposis + primary CNS tumors",
    "Two distinct genetic subtypes:",
    "  APC mutation → FAP-like polyposis + medulloblastoma",
    "  MMR gene mutation → Lynch-type colonic lesions + glioblastoma multiforme",
    "CRC management depends on which mutation is present",
    "Brain tumor screening for mutation-positive family members"
  ]);
}

// ═══════════════════════════════════════════════════════════════════════════════
// SLIDE 8 — MAP, PPAP, NTHL1
// ═══════════════════════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 0, w: 10, h: 5.625, fill: { color: C.offwhite }, line: { color: C.offwhite } });
  addHeaderBar(s, "Other Adenomatous Polyposis Syndromes: MAP, PPAP, NTHL1", C.navy);
  addFooter(s);

  // MAP left + center
  s.addShape(pres.shapes.RECTANGLE, { x: 0.15, y: 0.85, w: 6.3, h: 4.3, fill: { color: C.white }, line: { color: C.ltgray, width: 0.5 }, shadow: { type: "outer", color: "000000", blur: 4, offset: 2, angle: 135, opacity: 0.08 } });
  s.addShape(pres.shapes.RECTANGLE, { x: 0.15, y: 0.85, w: 6.3, h: 0.35, fill: { color: C.teal }, line: { color: C.teal } });
  s.addText("MUTYH-ASSOCIATED POLYPOSIS (MAP)", { x: 0.23, y: 0.85, w: 6.12, h: 0.35, fontSize: 10, bold: true, color: C.white, valign: "middle", margin: 0 });

  const mapItems = [
    { text: "Gene: MUTYH (MYH) — base-excision repair gene", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "Inheritance: AUTOSOMAL RECESSIVE — unique among polyposis syndromes", options: { bullet: true, breakLine: true, fontSize: 9, color: C.red, bold: true } },
    { text: "Common mutations: Y179C and G396D", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "Pathogenesis: Defective MUTYH → G:C→T:A transversions → somatic APC loss → adenomas", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "5–100 adenomas (usually); florid polyposis can occur; later onset than FAP", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "Extra-colonic: CHRPE, osteomas, gastric cancer, duodenal adenomas", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "CRC risk: HIGH (MSS tumors); colonoscopy every 1–2 yrs from age 25", options: { bullet: true, breakLine: true, fontSize: 9, color: C.navy } },
    { text: "Test all patients with >10 adenomas for biallelic MUTYH mutations", options: { bullet: true, breakLine: true, fontSize: 9, color: C.orange } },
    { text: "Genetic counseling → directed toward SIBLINGS (not parents/children)", options: { bullet: true, fontSize: 9, color: C.purple, bold: true } }
  ];
  s.addText(mapItems, { x: 0.25, y: 1.24, w: 6.1, h: 3.85, valign: "top", margin: 0 });

  // PPAP + NTHL1 right column
  addCard(s, 6.6, 0.85, 3.25, 2.0, "PPAP (POLE / POLD1)", C.orange, [
    "Autosomal dominant",
    "'Ultramutator' phenotype",
    "<100 colonic adenomas",
    "High CRC + endometrial cancer risk (POLD1)"
  ]);
  addCard(s, 6.6, 3.0, 3.25, 2.15, "NTHL1 POLYPOSIS", C.purple, [
    "Autosomal recessive (like MAP)",
    "~50 adenomas in adulthood",
    "High CRC risk",
    "Broader extra-colonic: endometrial,\nbreast, skin cancers",
    "Management similar to MAP"
  ]);
}

// ═══════════════════════════════════════════════════════════════════════════════
// SLIDE 9 — Peutz-Jeghers Syndrome
// ═══════════════════════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 0, w: 10, h: 5.625, fill: { color: C.offwhite }, line: { color: C.offwhite } });
  addHeaderBar(s, "Peutz-Jeghers Syndrome (PJS)", C.purple);
  addFooter(s);

  addCard(s, 0.15, 0.85, 3.0, 4.3, "GENETICS", C.purple, [
    "Gene: STK11/LKB1 (serine-threonine kinase)",
    "Chromosome 19p",
    "Autosomal dominant, variable penetrance",
    "80% of families have identifiable STK11 mutation",
    "STK11 regulates AMPK — controls cell polarization and growth"
  ]);
  addCard(s, 3.3, 0.85, 3.3, 4.3, "CLINICAL FEATURES", C.navy, [
    "Mucocutaneous pigmentation in 95%:",
    "  Lips, buccal mucosa (pathognomonic), hands, feet, genitalia, perianal",
    "  Dark melanin deposits, appear in infancy",
    "GI polyps: predominantly small intestine, also stomach & colon",
    "Risk of intussusception (can be fatal)",
    "Polyp histology: arborizing smooth muscle network + normal epithelium"
  ]);
  addCard(s, 6.75, 0.85, 3.1, 4.3, "CANCER RISKS (~40% lifetime)", C.red, [
    "Colorectal cancer",
    "Gastric & small intestinal cancer",
    "Pancreatic cancer (highest relative risk)",
    "Breast cancer",
    "Ovarian, uterine, lung cancer",
    "Sex cord tumors (testes)",
    "Surveillance from BIRTH (testicular) through adulthood"
  ]);
}

// ═══════════════════════════════════════════════════════════════════════════════
// SLIDE 10 — Juvenile Polyposis + Histology Image
// ═══════════════════════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 0, w: 10, h: 5.625, fill: { color: C.offwhite }, line: { color: C.offwhite } });
  addHeaderBar(s, "Juvenile Polyposis Syndrome (JPS)", C.purple);
  addFooter(s);

  addCard(s, 0.15, 0.85, 4.5, 4.3, "GENETICS & FEATURES", C.purple, [
    "Genes: SMAD4 (chr 18q) and BMPR1A (chr 10q22) — both TGF-β pathway",
    "Inheritance: Autosomal dominant",
    "Most common hamartomatous syndrome (1 per 100,000)",
    "Polyp histology: cystically dilated crypts, edematous lamina propria, surface erosion",
    "SMAD4 mutations (~20–25%): higher malignancy potential, massive gastric polyposis",
    "BMPR1A mutations (~20%): similar but less severe gastric involvement",
    "ENG mutations: associated with Hereditary Hemorrhagic Telangiectasia (HHT)",
    "30% of patients have congenital abnormalities",
    "CRC risk: HIGH — colonoscopic surveillance from childhood",
    "Upper GI endoscopy required for SMAD4 mutation carriers"
  ]);

  if (juvenileImg && !juvenileImg.error) {
    s.addImage({ data: juvenileImg.base64, x: 4.85, y: 0.85, w: 4.9, h: 3.25 });
  }
  s.addShape(pres.shapes.RECTANGLE, { x: 4.85, y: 4.1, w: 4.9, h: 0.5, fill: { color: C.dark }, line: { color: C.dark } });
  s.addText("(A) Juvenile polyp: cystically dilated crypts  |  (B) Dilated crypts with inspissated mucus and inflammatory cells   —   Robbins & Kumar", {
    x: 4.95, y: 4.1, w: 4.7, h: 0.5,
    fontSize: 7.5, color: C.white, align: "center", valign: "middle", italic: true
  });
}

// ═══════════════════════════════════════════════════════════════════════════════
// SLIDE 11 — Cowden + Serrated + Cronkhite-Canada
// ═══════════════════════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 0, w: 10, h: 5.625, fill: { color: C.offwhite }, line: { color: C.offwhite } });
  addHeaderBar(s, "Cowden Syndrome, Serrated Polyposis & Cronkhite-Canada", C.navy);
  addFooter(s);

  addCard(s, 0.15, 0.85, 3.1, 4.3, "COWDEN SYNDROME\n(PTEN Hamartoma)", C.purple, [
    "Gene: PTEN (tumor suppressor)",
    "Autosomal dominant",
    "Multiple GI hamartomas (stomach + colon predominant)",
    "Hallmark: Trichilemmomas (benign hair follicle tumors — pathognomonic)",
    "Oral papillomas",
    "Macrocephaly",
    "Breast cancer risk: 25–50% lifetime",
    "Thyroid cancer (follicular)",
    "Bannayan-Riley-Ruvalcaba: PTEN variant with macrocephaly + penile pigmentation"
  ]);
  addCard(s, 3.45, 0.85, 3.1, 4.3, "SERRATED POLYPOSIS\nSYNDROME", C.orange, [
    "Multiple serrated polyps throughout colon",
    "Types: hyperplastic, sessile serrated, traditional serrated adenomas",
    "No single causative gene identified",
    "Pathway: BRAF mutation + CpG island methylator phenotype (CIMP)",
    "Significant CRC risk — through serrated neoplasia pathway",
    "WHO criteria: ≥5 serrated polyps proximal to sigmoid, ≥2 with diameter ≥10 mm",
    "Regular colonoscopic surveillance required"
  ]);
  addCard(s, 6.75, 0.85, 3.1, 4.3, "CRONKHITE-CANADA\nSYNDROME", C.midgray, [
    "NON-inherited (acquired) — extremely rare",
    "Diffuse GI hamartomatous polyposis",
    "Characteristic ECTODERMAL triad:",
    "  Alopecia (hair loss)",
    "  Nail dystrophy (onychodystrophy)",
    "  Skin hyperpigmentation",
    "Protein-losing enteropathy, diarrhea, malabsorption",
    "Not classified as a genetic syndrome"
  ]);
}

// ═══════════════════════════════════════════════════════════════════════════════
// SLIDE 12 — Comparison Table
// ═══════════════════════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 0, w: 10, h: 5.625, fill: { color: C.offwhite }, line: { color: C.offwhite } });
  addHeaderBar(s, "Comparison: Key Polyposis Syndromes at a Glance", C.navy);
  addFooter(s);

  const headers = ["Feature", "FAP", "AFAP", "MAP", "PJS", "JPS", "Cowden"];
  const colW =   [1.35, 1.35, 1.35, 1.35, 1.35, 1.35, 1.35];
  const startX = 0.1;
  const rows = [
    ["Gene", "APC", "APC (5'/3')", "MUTYH", "STK11", "SMAD4/BMPR1A", "PTEN"],
    ["Inheritance", "AD", "AD", "AR ⬅", "AD", "AD", "AD"],
    ["Polyp type", "Adenoma", "Adenoma", "Adenoma", "Hamartoma", "Hamartoma (juvenile)", "Hamartoma"],
    ["Polyp count", ">100–1000s", "<100", "5–100", "Multiple (SI>>colon)", "Multiple", "Multiple"],
    ["CRC risk", "~100%", "High", "High", "~40% (all Ca)", "High", "Moderate"],
    ["Key finding", "Osteomas, CHRPE, desmoids", "Proximal colon, flat polyps", "AR; CHRPE", "Mucocut. pigment", "Congenital anomalies", "Trichilemmomas"],
    ["Screen age", "10–12 yrs", "25 yrs", "25 yrs", "Birth (testicular)", "Childhood", "Adult"]
  ];

  // Header row
  s.addShape(pres.shapes.RECTANGLE, { x: startX, y: 0.82, w: 9.8, h: 0.36, fill: { color: C.navy }, line: { color: C.navy } });
  headers.forEach((h, i) => {
    s.addText(h, {
      x: startX + i * colW[i], y: 0.82, w: colW[i], h: 0.36,
      fontSize: 8.5, bold: true, color: C.white, valign: "middle", align: "center", margin: 2
    });
  });

  // Data rows
  rows.forEach((row, ri) => {
    const y = 1.18 + ri * 0.59;
    const bg = ri % 2 === 0 ? C.white : "EEF4F9";
    s.addShape(pres.shapes.RECTANGLE, { x: startX, y, w: 9.8, h: 0.57, fill: { color: bg }, line: { color: C.ltgray, width: 0.5 } });
    row.forEach((cell, ci) => {
      const bold = ci === 0;
      const color = (cell.includes("AR") || cell === "~100%") ? C.red : C.navy;
      s.addText(cell, {
        x: startX + ci * colW[ci], y, w: colW[ci], h: 0.57,
        fontSize: ci === 0 ? 8 : 7.8, bold, color,
        valign: "middle", align: ci === 0 ? "left" : "center", margin: 3
      });
    });
  });
}

// ═══════════════════════════════════════════════════════════════════════════════
// SLIDE 13 — Key Take-Aways
// ═══════════════════════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 0, w: 10, h: 5.625, fill: { color: C.dark }, line: { color: C.dark } });
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 0, w: 0.18, h: 5.625, fill: { color: C.mint }, line: { color: C.mint } });
  s.addShape(pres.shapes.RECTANGLE, { x: 0, y: 4.9, w: 10, h: 0.725, fill: { color: C.teal }, line: { color: C.teal } });

  s.addText("KEY TAKE-AWAYS", {
    x: 0.5, y: 0.25, w: 9, h: 0.55,
    fontSize: 26, bold: true, color: C.gold, align: "center", charSpacing: 3
  });

  const points = [
    { icon: "▶", text: "FAP (APC gene, chr 5q21) carries near-100% lifetime CRC risk if untreated; prophylactic colectomy is standard of care" },
    { icon: "▶", text: "De novo mutations account for 20–25% of FAP — absence of family history does NOT exclude the diagnosis" },
    { icon: "▶", text: "MUTYH-Associated Polyposis is the only AUTOSOMAL RECESSIVE adenomatous polyposis syndrome; test siblings, not parents/children" },
    { icon: "▶", text: "Turcot syndrome has two distinct subtypes: APC mutation → medulloblastoma; MMR mutation → glioblastoma" },
    { icon: "▶", text: "Peutz-Jeghers (STK11) = hamartomatous polyps + mucocutaneous melanin pigmentation (95%) + ~40% lifetime cancer risk including pancreatic" },
    { icon: "▶", text: "SMAD4 mutations in JPS carry higher gastric polyposis burden and are linked to HHT phenotype; require upper GI surveillance" },
    { icon: "▶", text: "Cowden syndrome (PTEN) = trichilemmomas + high breast/thyroid cancer risk; Cronkhite-Canada is the only non-inherited polyposis" }
  ];

  points.forEach((pt, i) => {
    s.addText([
      { text: pt.icon + "  ", options: { color: C.gold, bold: true, fontSize: 9.5 } },
      { text: pt.text, options: { color: C.white, fontSize: 9.5 } }
    ], {
      x: 0.4, y: 0.95 + i * 0.52, w: 9.4, h: 0.5,
      valign: "middle", margin: 0
    });
  });

  s.addText("Sources: Sleisenger & Fordtran  |  Robbins & Kumar  |  Sabiston  |  Current Surgical Therapy  |  Yamada's Gastroenterology  |  Emery's Medical Genetics", {
    x: 0.5, y: 4.92, w: 9, h: 0.32,
    fontSize: 7.5, color: C.white, align: "center", italic: true
  });
}

// ─── Write file ───────────────────────────────────────────────────────────────
pres.writeFile({ fileName: "/home/daytona/workspace/colonic-polyposis-ppt/Colonic_Polyposis_Syndromes.pptx" })
  .then(() => console.log("✅ Done: Colonic_Polyposis_Syndromes.pptx"))
  .catch(e => { console.error("Error:", e); process.exit(1); });

Running Command

cd /home/daytona/workspace/colonic-polyposis-ppt && node make_ppt.js 2>&1

Running Command

cd /home/daytona/workspace/colonic-polyposis-ppt && node /home/daytona/skills/shared/scripts/fetch_images.js "https://cdn.orris.care/cdss_images/4566501cb12efb4d13ba792e8d3b323765e3f865ccf89212e397314585ec27d6.png" > /tmp/img1.json 2>&1; echo "exit: $?"

Running Command

node /home/daytona/skills/shared/scripts/fetch_images.js "https://cdn.orris.care/cdss_images/a38620b7eb609e06e2c1fb5c2cc5b8702b5f219d4409081cd0f096506b3f427d.png" > /tmp/img2.json 2>&1; echo "exit: $?"

Running Command

node -e "const d=JSON.parse(require('fs').readFileSync('/tmp/img1.json')); console.log(d[0].error, d[0].base64 ? d[0].base64.substring(0,60) : 'null')"

Editing File

~/colonic-polyposis-ppt/make_ppt.js

Successfully replaced 1 instance(s) of the string in '/home/daytona/workspace/colonic-polyposis-ppt/make_ppt.js'

Editing File

~/colonic-polyposis-ppt/make_ppt.js

Successfully replaced 1 instance(s) of the string in '/home/daytona/workspace/colonic-polyposis-ppt/make_ppt.js'

Running Command

cd /home/daytona/workspace/colonic-polyposis-ppt && node make_ppt.js 2>&1

Running Command

ls -lh /home/daytona/workspace/colonic-polyposis-ppt/Colonic_Polyposis_Syndromes.pptx

Your presentation is ready (11 MB, 13 slides):

Colonic Polyposis Syndromes

Presentation · PPTX

What's inside (13 slides):

Slide	Content
1	Title slide (dark navy + teal)
2	Full classification overview - 4 category cards
3	FAP: Genetics & Pathogenesis
4	FAP: Extracolonic manifestations (GI + non-GI cards)
5	FAP: Adenoma morphology - real textbook histology image
6	FAP: Surgical management table + screening schedule
7	FAP Variants: AFAP, Gardner, Turcot
8	MAP, PPAP, NTHL1 polyposis
9	Peutz-Jeghers Syndrome
10	Juvenile Polyposis - with real histology image of juvenile polyps
11	Cowden Syndrome, Serrated Polyposis, Cronkhite-Canada
12	Comparison table (all 6 major syndromes side-by-side)
13	Key take-aways (dark slide)

Design: Navy/teal/mint palette, color-coded category cards, info panels with title bars, real pathology images from Robbins & Kumar, footer on every slide, and a clean comparison table for exam/revision use.

This is a shared conversation. Sign in to Orris to start your own chat.