Orris

Oral hypoglycemic agents, mechanism of action, escalation, considerations, individualization, dosing, monitoring and important clinical caveats

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"oral hypoglycemic agents" AND "type 2 diabetes" AND "guidelines"

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I now have comprehensive data from Lippincott Pharmacology and the Washington Manual. I have enough to write a thorough, well-organized answer. Let me compile the full response now.

Oral Hypoglycemic Agents (OHAs) - Complete Clinical Reference

Overview and Drug Classes

Oral hypoglycemic agents (also called oral antidiabetic agents) are used primarily for type 2 diabetes mellitus (T2DM). They target different pathophysiologic defects: insulin resistance, insulin secretion defects, glucotoxicity, incretin deficiency, and renal glucose reabsorption. Patients with diabetes less than 5 years generally respond best to oral agents; long-standing disease usually requires combination therapy or eventual insulin.
The major classes are:
  • Biguanides (metformin)
  • Sulfonylureas (SUs)
  • Meglitinides (glinides)
  • Thiazolidinediones (TZDs)
  • DPP-4 inhibitors (gliptins)
  • SGLT2 inhibitors (gliflozins)
  • Alpha-glucosidase inhibitors
  • Bile acid sequestrants
  • Dopamine agonists (bromocriptine)

1. Biguanides - Metformin

Mechanism: Metformin activates AMP-activated protein kinase (AMPK) in the liver, which suppresses hepatic glucose production (gluconeogenesis and glycogenolysis). It also improves peripheral insulin sensitivity and reduces intestinal glucose absorption. It does not stimulate insulin secretion.
Dosing:
  • Start: 500 mg once or twice daily with meals, or 850 mg once daily
  • Titrate every 1-2 weeks; max effective dose: 2000-2550 mg/day
  • Extended-release (XR) formulations improve GI tolerability
Key advantages: Weight neutral to modest weight loss, no hypoglycemia risk, low cost, reduces cardiovascular events (UKPDS legacy effect), may reduce cancer risk.
Contraindications/Cautions:
  • eGFR <30 mL/min/1.73m² - contraindicated
  • eGFR 30-45 - use with caution, reduce dose; some guidelines say avoid
  • Iodinated contrast dye - hold metformin on day of procedure and 48 hours after (risk of contrast-induced nephropathy causing metformin accumulation and lactic acidosis)
  • Active hepatic disease, alcohol abuse, heart failure (formerly contraindicated but now acceptable in stable, mild-moderate CHF per current guidelines)
Adverse effects: GI (nausea, diarrhea, abdominal cramping) in up to 30% - dose-related and usually improve with slow titration; lactic acidosis (rare, 0.03 per 1000 patient-years); long-term use depletes vitamin B12 - check B12 annually.
Monitoring: eGFR at baseline and annually (more frequently with declining renal function); B12 levels annually in long-term users; LFTs at baseline.

2. Sulfonylureas (SUs)

Members: Glipizide (Glucotrol), Glyburide (DiaBeta), Glimepiride (Amaryl) - second generation; older: chlorpropamide, tolbutamide.
Mechanism: Bind to sulfonylurea receptors (SUR1) on pancreatic beta-cell ATP-sensitive K⁺ (KATP) channels → channel closure → membrane depolarization → calcium influx → insulin secretion. Work regardless of blood glucose level (hence hypoglycemia risk). Require functional beta cells.
Dosing:
DrugStarting DoseMax DoseDuration
Glipizide5 mg daily40 mg/day12-24 h
Glyburide2.5-5 mg daily20 mg/day16-24 h
Glimepiride1-2 mg daily8 mg/day24 h
Take 30 minutes before meals; glipizide XL taken with breakfast.
Key advantages: Potent HbA1c reduction (1-2%), low cost, extensive clinical history.
Key disadvantages:
  • Hypoglycemia risk (especially glyburide - avoid in elderly and CKD)
  • Weight gain (2-5 kg)
  • Secondary failure (5-10% per year as beta-cell function declines)
  • Glipizide and glimepiride preferred in renal impairment over glyburide (less active metabolite accumulation)
Contraindications: Type 1 diabetes, sulfonamide allergy, severe renal/hepatic impairment (use with extreme caution or avoid).
Monitoring: Fasting blood glucose (FBG) and HbA1c; watch for hypoglycemia especially in elderly, with alcohol use, irregular meals, or concurrent beta-blockers (which mask symptoms).

3. Meglitinides (Glinides)

Members: Repaglinide, Nateglinide.
Mechanism: Same target as sulfonylureas (SUR1/KATP channels) but with a different binding site. Shorter duration of action - specifically designed to cover postprandial glucose spikes. Taken with each meal; skip if meal is skipped.
Dosing: Repaglinide 0.5-4 mg before each meal (up to 3 meals/day, max 16 mg/day); Nateglinide 60-120 mg before meals.
Advantages over SUs: More flexible dosing (meal-by-meal), lower fasting hypoglycemia risk.
Disadvantages: Dosed 3x/day (adherence burden), expensive, modest HbA1c reduction, weight gain.
Renal note: Repaglinide is safer in CKD than SUs (predominantly biliary excretion). Nateglinide - use with caution in renal impairment.

4. Thiazolidinediones (TZDs / Glitazones)

Members: Pioglitazone (Actos), Rosiglitazone (Avandia - restricted use).
Mechanism: Peroxisome proliferator-activated receptor-gamma (PPARγ) agonists. Increase transcription of genes that enhance insulin sensitivity in adipose tissue, muscle, and liver. Reduce hepatic glucose output and improve peripheral glucose uptake. Require weeks to months for full effect.
Dosing: Pioglitazone 15-45 mg once daily; Rosiglitazone 2-8 mg daily.
Key advantages: Durable HbA1c reduction, improves insulin sensitivity, pioglitazone improves lipids (raises HDL, lowers TG), may reduce cardiovascular events (PROactive trial), no hypoglycemia when used alone.
Contraindications / Major concerns:
  • Heart failure (NYHA class III-IV) - absolutely contraindicated; fluid retention causes/worsens HF
  • Bladder cancer risk - pioglitazone; avoid in patients with active or prior bladder cancer
  • Bone fractures - especially in postmenopausal women; TZDs reduce bone density
  • Rosiglitazone - associated with increased myocardial infarction risk; currently restricted (FDA REMS program)
  • Hepatotoxicity risk - check LFTs at baseline
Monitoring: LFTs (baseline, then periodically), weight and edema (fluid retention), signs of HF, bone density in at-risk patients.

5. DPP-4 Inhibitors (Gliptins)

Members: Sitagliptin (Januvia), Saxagliptin (Onglyza), Linagliptin (Tradjenta), Alogliptin (Nesina).
Mechanism: Inhibit dipeptidyl peptidase-4 (DPP-4), the enzyme that rapidly degrades endogenous incretin hormones (GLP-1 and GIP). Elevated incretin levels → glucose-dependent insulin secretion from beta cells + decreased glucagon from alpha cells. Effect is glucose-dependent - minimal hypoglycemia risk when used alone.
Dosing:
DrugDoseRenal Adjustment
Sitagliptin100 mg once dailyReduce to 50 mg if eGFR 30-45; 25 mg if eGFR <30
Saxagliptin5 mg once dailyReduce to 2.5 mg if eGFR ≤45
Linagliptin5 mg once dailyNo renal adjustment (biliary excretion)
Alogliptin25 mg once dailyReduce in renal impairment
Advantages: Weight neutral, low hypoglycemia risk, well tolerated, once-daily oral dosing.
Concerns:
  • Saxagliptin - associated with increased heart failure hospitalization (SAVOR-TIMI trial); use with caution in patients with HF or high HF risk
  • Possible increased risk of pancreatitis and pancreatic cancer (causality not established, remain vigilant)
  • Nasopharyngitis, upper respiratory infections, arthralgia
  • Bullous pemphigoid (rare skin blistering - class warning)
Monitoring: HbA1c, renal function (for dose adjustment), skin for bullous lesions.

6. SGLT2 Inhibitors (Gliflozins)

Members: Empagliflozin (Jardiance), Canagliflozin (Invokana), Dapagliflozin (Farxiga), Ertugliflozin (Steglatro).
Mechanism: Block sodium-glucose cotransporter 2 (SGLT2) in the proximal renal tubule → reduced renal glucose reabsorption → glucosuria (~70-80 g glucose excreted/day) → reduced blood glucose. Mechanism is insulin-independent. Additional benefits: osmotic diuresis reduces preload, hemodynamic benefits in HF; direct cardiorenal protective effects beyond glucose lowering.
Dosing:
DrugDoseNotes
Empagliflozin10-25 mg once dailyCV and renal outcomes proven
Canagliflozin100-300 mg once dailyCV, renal outcomes proven
Dapagliflozin5-10 mg once dailyHFrEF and CKD indications (even without DM)
Ertugliflozin5-15 mg once dailyLess outcomes data
Require eGFR ≥30-45 for glucose-lowering efficacy; cardiorenal benefits may extend to lower eGFR thresholds (per CREDENCE, DAPA-CKD, EMPEROR trials).
Key clinical advantages (beyond glucose):
  • Reduces major adverse cardiovascular events (MACE) - empagliflozin, canagliflozin, dapagliflozin
  • Reduces heart failure hospitalization (all members)
  • Reduces CKD progression
  • Weight loss (1-3 kg)
  • Blood pressure reduction (~3-5 mmHg systolic)
Adverse effects / Major concerns:
  • Genital mycotic infections (candidiasis) - very common, especially in women
  • UTI risk (less well established than genital infections)
  • DKA - can occur at near-normal glucose levels (euglycemic DKA); highest risk with T1DM use (off-label), prolonged fasting, surgery, low-carb diet
  • Amputations - canagliflozin associated with increased risk (Charcot foot, peripheral artery disease patients - caution)
  • Bone fractures - canagliflozin
  • Fournier's gangrene (necrotizing fasciitis of genitalia) - rare class warning
  • Volume depletion/hypotension - especially with diuretics or elderly
  • Hold SGLT2 inhibitors perioperatively (48 hours before surgery) due to DKA risk
Monitoring: eGFR and electrolytes, genital hygiene counseling, signs of DKA, foot/skin inspection (canagliflozin).

7. Alpha-Glucosidase Inhibitors

Members: Acarbose, Miglitol.
Mechanism: Competitively inhibit intestinal brush border alpha-glucosidase enzymes → delayed digestion of complex carbohydrates and disaccharides → blunted postprandial glucose rise. Act locally in the gut; primarily target postprandial hyperglycemia.
Dosing: Acarbose 25-100 mg with each meal (titrate slowly over months); Miglitol 25-100 mg with meals.
Advantages: No systemic absorption (acarbose), no hypoglycemia when used alone, modest weight benefit.
Disadvantages: Significant GI side effects (flatulence, diarrhea, bloating) in ~50-70% - often limits use; modest HbA1c reduction (~0.5-0.8%); three times daily dosing.
Important caveat: If hypoglycemia occurs while on acarbose + another agent (SU or insulin), treat with glucose (dextrose) - NOT sucrose/table sugar (acarbose blocks sucrose digestion).

8. Other Agents

Bile acid sequestrants (Colesevelam): Mechanism in diabetes unclear; modestly reduces HbA1c (~0.5%); additionally lowers LDL-C; useful when lipid and glycemic management needed simultaneously. GI side effects; reduces absorption of fat-soluble vitamins and some drugs.
Bromocriptine (Cycloset): Dopamine D2 agonist; resets hypothalamic circadian rhythms → improves insulin sensitivity; modest HbA1c reduction; may be continued when insulin is added; can cause nausea, orthostatic hypotension, dizziness.

Treatment Escalation Algorithm

First-line:

Metformin remains the recommended first-line agent if tolerated, regardless of HbA1c level at presentation (unless contraindicated).

Individualized early first-line considerations (ADA/EASD consensus):

Clinical ContextPreferred Agent
Established ASCVD or high CV riskGLP-1 RA with proven CV benefit (liraglutide, semaglutide, dulaglutide)
Heart failure (especially HFrEF)SGLT2 inhibitor
CKD (eGFR 25-60, albuminuria)SGLT2 inhibitor (empagliflozin, canagliflozin, dapagliflozin)
Weight loss priorityGLP-1 RA or SGLT2 inhibitor
Minimizing hypoglycemiaDPP-4 inhibitor, GLP-1 RA, SGLT2 inhibitor, TZD
Cost concernMetformin, sulfonylurea, TZD

If HbA1c ≥9% at presentation:

  • Initiate dual therapy from the start, OR
  • Consider insulin directly (especially if symptomatic, A1C >10%, or DKA/HHS risk)

Escalation steps:

  1. Monotherapy (metformin or preferred first-line based on comorbidities)
  2. Dual therapy at 3 months if HbA1c not at goal (add second agent from different class)
  3. Triple therapy at 3 months if still not at goal
  4. Injectable therapy - GLP-1 RA before basal insulin; or both
  5. Basal insulin + bolus insulin (full basal-bolus) if needed
Reassess every 3 months until targets are achieved.

Individualization of Therapy

Patient FactorConsideration
Elderly (>65 years)Avoid glyburide (prolonged hypoglycemia); target HbA1c 7.5-8.5% based on frailty; DPP-4 inhibitors well tolerated
CKD stage 3b-5Avoid metformin (eGFR <30); avoid SUs (except glipizide, small dose glimepiride); SGLT2 inhibitors lose glycemic efficacy at eGFR <45 but retain cardiorenal benefit lower; linagliptin preferred DPP-4 (no dose adjust)
Heart failureAvoid TZDs; prefer SGLT2 inhibitors; avoid saxagliptin
ASCVDGLP-1 RA or SGLT2 inhibitor as early add-on
Liver diseaseAvoid metformin in severe hepatic impairment; avoid TZDs (hepatotoxicity); SUs unpredictable; DPP-4 inhibitors generally safe
PregnancyInsulin is preferred; metformin and glyburide used but cross placenta; all SGLT2/DPP-4/GLP-1 agents - avoid
ObesityGLP-1 RA (most weight loss), SGLT2 inhibitor; avoid TZDs and SUs
Low adherenceLong-acting, once-daily or once-weekly agents (semaglutide weekly, dulaglutide weekly)
Hypoglycemia historyAvoid SUs and meglitinides; prefer GLP-1 RA, SGLT2 inhibitors, DPP-4 inhibitors, TZDs

HbA1c Targets (Individualized)

PopulationHbA1c Target
Most non-elderly adults<7.0%
Short disease duration, no CVD, long life expectancy<6.5%
Elderly, limited life expectancy, hypoglycemia unawareness, multiple comorbidities7.5-8.5% (or even <9%)
Pregnant (during 2nd-3rd trimester)<6.0-6.5%
Intensive therapy (A1C <7%) reduces microvascular complications (retinopathy, nephropathy, neuropathy) but increases hypoglycemia risk. For macrovascular disease, benefit of tight control is less certain and occurs over longer time horizons.

Monitoring Schedule

ParameterFrequency
HbA1cEvery 3 months until at goal; then every 6 months
Fasting blood glucose (SMBG)Daily to weekly depending on regimen
eGFR / Serum creatinineBaseline, then annually (or more with declining function)
Urine albumin-to-creatinine ratioAnnually
Lipid panelAnnually
Liver function testsBaseline for TZDs; periodically
Vitamin B12Annually in patients on long-term metformin
Blood pressureEvery visit
Foot examinationAnnually
Retinal screeningAt diagnosis (T2DM), then annually or biannually

Important Clinical Caveats

  1. Metformin and contrast: Hold for 48 hours before and after iodinated contrast in patients with eGFR <60 to prevent metformin-associated lactic acidosis.
  2. Euglycemic DKA with SGLT2 inhibitors: Glucose may be only mildly elevated (150-200 mg/dL). Check beta-hydroxybutyrate/ketones if patient on SGLT2 inhibitor presents with nausea, vomiting, malaise. Hold perioperatively.
  3. Sick-day rules ("SADMAN" - Stop Agents During illness): Stop metformin, ACE inhibitors, diuretics, NSAIDs, and SGLT2 inhibitors during vomiting/diarrhea illness to prevent AKI and drug accumulation.
  4. Beta-blockers mask hypoglycemia symptoms (tachycardia, tremor) in patients on SUs or insulin - sweating is preserved and is the main warning sign.
  5. Hypoglycemia treatment on alpha-glucosidase inhibitors: Must use pure glucose (e.g., dextrose tablets, IV glucose, glucagon) - NOT orange juice or sucrose, because acarbose blocks sucrose hydrolysis.
  6. Sulfonylurea secondary failure: SU efficacy declines over years as beta-cell mass decreases. Do not continue escalating SU dose beyond maximum; switch strategy.
  7. GLP-1 RA and pancreatitis: Contraindicated in patients with history of pancreatitis or medullary thyroid carcinoma (MTC) or MEN2. Advise patients to report persistent abdominal pain.
  8. TZD + insulin combination: Increases fluid retention and HF risk significantly; avoid or use with great caution.
  9. When adding insulin to OHAs: Sulfonylureas and meglitinides are generally discontinued when prandial insulin is added (hypoglycemia risk). Metformin, DPP-4 inhibitors, SGLT2 inhibitors, and GLP-1 RAs can generally be continued.
  10. Cardiovascular outcome trials (CVOTs): DPP-4 inhibitors showed CV safety but no benefit. GLP-1 RAs (liraglutide, semaglutide, dulaglutide) and SGLT2 inhibitors (empagliflozin, canagliflozin, dapagliflozin) showed MACE reduction. SGLT2 inhibitors showed the strongest heart failure hospitalization reduction. These findings should drive drug choice in high-CV-risk and HF/CKD patients, even before glycemic considerations.
  11. Combination of GLP-1 RA + DPP-4 inhibitor: Not recommended - both target the incretin system; the DPP-4 inhibitor has no additive effect when a GLP-1 RA is already present.
  12. Renal function and drug choice summary: As eGFR falls, the pharmacologic armamentarium shrinks. Linagliptin requires no renal dose adjustment. Repaglinide is safer than SUs in CKD. SGLT2 inhibitors lose glycemic efficacy at eGFR <45 but cardiorenal benefit extends lower. Insulin remains effective at all levels of renal function but hypoglycemia risk increases as kidneys clear less insulin.
Sources: Lippincott Illustrated Reviews: Pharmacology, 7th Ed. | Washington Manual of Medical Therapeutics | Textbook of Family Medicine, 9th Ed. | Goldman-Cecil Medicine | Comprehensive Clinical Nephrology, 7th Ed.

give me a python script to generate a stunning presentation for the above information for postgraduate internal medicine students

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don't execute it I just want the script in text

Here is the complete pptxgenjs script. Save it as oha_presentation.js and run with node oha_presentation.js.
// ============================================================
// Oral Hypoglycemic Agents - Postgraduate Internal Medicine
// PptxGenJS v3.x | Run: node oha_presentation.js
// ============================================================

const pptxgen = require("pptxgenjs");

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pres.author = "Internal Medicine Education";

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    { name: "GLP-1 RA",            eg: "Semaglutide, Liraglutide",    color: "5C6BC0" },
    { name: "α-Glucosidase Inh.",  eg: "Acarbose, Miglitol",          color: "7B6FA0" },
    { name: "Other",               eg: "Colesevelam, Bromocriptine",   color: "8D6E63" },
  ];

  const cols = 3, rows = 3;
  const cW = 3.0, cH = 1.18, startX = 0.18, startY = 1.18, gapX = 0.12, gapY = 0.1;

  classes.forEach((cls, i) => {
    const col = i % cols;
    const row = Math.floor(i / cols);
    const x = startX + col * (cW + gapX);
    const y = startY + row * (cH + gapY);

    s.addShape(pres.shapes.ROUNDED_RECTANGLE, {
      x, y, w: cW, h: cH,
      fill: { color: cls.color }, line: { color: cls.color },
      rectRadius: 0.1,
      shadow: { type: "outer", color: "000000", blur: 6, offset: 2, angle: 135, opacity: 0.12 }
    });
    // Number badge
    s.addShape(pres.shapes.OVAL, {
      x: x + cW - 0.38, y: y + 0.08, w: 0.28, h: 0.28,
      fill: { color: C.white, transparency: 70 }, line: { color: C.white, transparency: 50 }
    });
    s.addText(`${i + 1}`, {
      x: x + cW - 0.38, y: y + 0.08, w: 0.28, h: 0.28,
      fontSize: 7, bold: true, color: C.white,
      fontFace: "Calibri", align: "center", valign: "middle", margin: 0
    });
    s.addText(cls.name, {
      x: x + 0.12, y: y + 0.1, w: cW - 0.55, h: 0.42,
      fontSize: 11, bold: true, color: C.white,
      fontFace: "Calibri", valign: "middle", margin: 0
    });
    s.addText(cls.eg, {
      x: x + 0.12, y: y + 0.55, w: cW - 0.22, h: 0.52,
      fontSize: 8.5, color: C.white, fontFace: "Calibri",
      valign: "top", italic: true, margin: 0
    });
  });
}

// ════════════════════════════════════════════════════════════
//  SLIDE 3 — METFORMIN
// ════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.background = { color: C.offWhite };
  addSlideHeader(s, "Metformin — The Cornerstone", "First-line therapy for T2DM unless contraindicated");
  addFooter(s, 3);

  // MOA box
  card(s, 0.18, 1.15, 4.5, 1.55, "MECHANISM OF ACTION", [
    "Activates hepatic AMPK → suppresses gluconeogenesis & glycogenolysis",
    "Improves peripheral insulin sensitivity",
    "Reduces intestinal glucose absorption",
    "Does NOT stimulate insulin secretion → no hypoglycemia risk"
  ], C.teal);

  // Dosing box
  card(s, 4.82, 1.15, 4.98, 1.55, "DOSING", [
    "Start: 500 mg once or twice daily with meals",
    "Titrate every 1–2 weeks to tolerance",
    "Max effective dose: 2000–2550 mg/day",
    "XR formulation improves GI tolerability"
  ], "1A6B8A");

  // Advantages
  card(s, 0.18, 2.85, 3.0, 2.0, "ADVANTAGES", [
    "Weight neutral / modest weight loss",
    "No hypoglycemia monotherapy",
    "Cardioprotective (UKPDS legacy)",
    "Low cost",
    "Possible cancer risk reduction"
  ], "1D6A47");

  // Renal / CI
  card(s, 3.32, 2.85, 3.0, 2.0, "RENAL DOSING", [
    "eGFR 45–60: use with caution",
    "eGFR 30–44: reduce dose, monitor",
    "eGFR <30: CONTRAINDICATED",
    "Hold 48 h before/after iodinated contrast if eGFR <60"
  ], C.red);

  // Monitoring
  card(s, 6.46, 2.85, 3.32, 2.0, "MONITORING & CAVEATS", [
    "eGFR at baseline then annually",
    "Vitamin B12 annually (long-term use depletes B12)",
    "LFTs at baseline",
    "GI side effects in ~30% — dose-dependent, improve with titration"
  ], "7B6FA0");
}

// ════════════════════════════════════════════════════════════
//  SLIDE 4 — SULFONYLUREAS & MEGLITINIDES
// ════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.background = { color: C.offWhite };
  addSlideHeader(s, "Sulfonylureas & Meglitinides", "Insulin secretagogues — require functional beta cells");
  addFooter(s, 4);

  // MOA diagram area
  s.addShape(pres.shapes.ROUNDED_RECTANGLE, {
    x: 0.18, y: 1.15, w: 9.62, h: 0.72,
    fill: { color: C.navy }, line: { color: C.navy }, rectRadius: 0.06
  });
  s.addText([
    { text: "Mechanism: ", options: { bold: true, color: C.gold } },
    { text: "Bind SUR1 on pancreatic β-cell K", options: { color: C.white } },
    { text: "ATP", options: { color: C.white, subscript: true } },
    { text: " channels → channel closure → membrane depolarisation → Ca²⁺ influx → insulin secretion", options: { color: C.white } }
  ], {
    x: 0.32, y: 1.15, w: 9.34, h: 0.72,
    fontSize: 10.5, fontFace: "Calibri", valign: "middle"
  });

  // SU table
  const suHeaders = [
    [{ text: "Drug", options: { bold: true, color: C.white, fill: { color: C.teal } } },
     { text: "Start Dose", options: { bold: true, color: C.white, fill: { color: C.teal } } },
     { text: "Max Dose", options: { bold: true, color: C.white, fill: { color: C.teal } } },
     { text: "Duration", options: { bold: true, color: C.white, fill: { color: C.teal } } },
     { text: "Note", options: { bold: true, color: C.white, fill: { color: C.teal } } }]
  ];
  const suRows = [
    ["Glipizide", "5 mg daily", "40 mg/day", "12–24 h", "Preferred in CKD; take 30 min before meal"],
    ["Glyburide", "2.5–5 mg daily", "20 mg/day", "16–24 h", "AVOID in elderly & CKD — long active metabolite"],
    ["Glimepiride", "1–2 mg daily", "8 mg/day", "24 h", "Once daily; safest in mild CKD of the SUs"],
  ];
  const tableData = [
    ...suHeaders,
    ...suRows.map((r, i) => r.map(cell => ({
      text: cell,
      options: { fill: { color: i % 2 === 0 ? "F0FAFA" : C.white }, color: C.navy, fontSize: 8.5 }
    })))
  ];
  s.addTable(tableData, {
    x: 0.18, y: 1.98, w: 9.62, h: 1.1,
    fontFace: "Calibri",
    border: { type: "solid", pt: 0.5, color: "CCDDDD" },
    colW: [1.5, 1.4, 1.3, 1.1, 4.32]
  });

  // Key concerns
  warningBox(s, 0.18, 3.2, 4.65, 0.58,
    "Hypoglycemia risk (especially glyburide) — weight gain 2–5 kg — secondary failure ~5–10%/yr as β-cell mass declines");

  // Meglitinides card
  card(s, 5.0, 3.2, 4.8, 2.0, "MEGLITINIDES", [
    "Same SUR1 target as SUs — different binding site",
    "Shorter action → cover postprandial spikes only",
    "Repaglinide: 0.5–4 mg before each meal (skip if skipping meal)",
    "Nateglinide: 60–120 mg before meals",
    "Safer in CKD than SUs (biliary excretion of repaglinide)",
    "Hypoglycemia if meal is skipped — adhere to meal timing"
  ], "2E86AB");

  infoBox(s, 0.18, 3.88, 4.65, 0.58,
    "β-blockers mask hypoglycemia symptoms (tachycardia, tremor) — sweating is preserved and is the key warning sign.");
}

// ════════════════════════════════════════════════════════════
//  SLIDE 5 — THIAZOLIDINEDIONES
// ════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.background = { color: C.offWhite };
  addSlideHeader(s, "Thiazolidinediones (TZDs / Glitazones)", "PPARγ agonists — insulin sensitizers with delayed onset");
  addFooter(s, 5);

  card(s, 0.18, 1.15, 4.6, 1.55, "MECHANISM OF ACTION", [
    "PPARγ (nuclear receptor) agonists → transcriptional activation",
    "↑ insulin sensitivity in adipose tissue, muscle & liver",
    "↓ hepatic glucose output, ↑ peripheral glucose uptake",
    "Full effect delayed: weeks to months (not days)"
  ], "457B9D");

  card(s, 4.92, 1.15, 4.88, 1.55, "DOSING", [
    "Pioglitazone: 15–45 mg once daily",
    "Rosiglitazone: 2–8 mg/day (restricted — FDA REMS)",
    "May be combined with metformin, SUs, or insulin (caution with insulin — ↑ fluid retention)",
    "No dose adjustment required for renal impairment"
  ], "457B9D");

  card(s, 0.18, 2.85, 3.1, 2.0, "ADVANTAGES", [
    "Durable HbA1c reduction",
    "No hypoglycemia (monotherapy)",
    "Pioglitazone: ↑ HDL, ↓ TG",
    "PROactive trial: ↓ recurrent CV events (pioglitazone)",
    "Useful in NASH/NAFLD"
  ], "1D6A47");

  // Contraindications — red themed
  s.addShape(pres.shapes.ROUNDED_RECTANGLE, {
    x: 3.42, y: 2.85, w: 6.38, h: 2.0,
    fill: { color: "FFF8F8" }, line: { color: C.red, pt: 1.5 }, rectRadius: 0.08,
    shadow: { type: "outer", color: "000000", blur: 6, offset: 2, angle: 135, opacity: 0.08 }
  });
  s.addShape(pres.shapes.RECTANGLE, {
    x: 3.42, y: 2.85, w: 6.38, h: 0.3,
    fill: { color: C.red }, line: { color: C.red }
  });
  s.addText("⚠  MAJOR CONCERNS & CONTRAINDICATIONS", {
    x: 3.52, y: 2.85, w: 6.18, h: 0.3,
    fontSize: 9, bold: true, color: C.white, fontFace: "Calibri",
    valign: "middle", margin: 0
  });
  const contraItems = [
    { label: "Heart Failure (NYHA III–IV):", detail: "ABSOLUTELY CONTRAINDICATED — causes fluid retention & worsens HF" },
    { label: "Bladder Cancer (Pioglitazone):", detail: "Avoid in active or prior bladder cancer" },
    { label: "Bone Fractures:", detail: "Reduced bone density — especially postmenopausal women" },
    { label: "Rosiglitazone:", detail: "Associated with ↑ MI risk — FDA REMS restricted access" },
    { label: "Hepatotoxicity:", detail: "Check LFTs at baseline; avoid in significant liver disease" },
  ];
  const contraTextArr = contraItems.flatMap((ci, i) => [
    { text: `${ci.label} `, options: { bold: true, color: C.red, fontSize: 8.5 } },
    { text: ci.detail, options: { color: C.navy, fontSize: 8.5 } },
    ...(i < contraItems.length - 1 ? [{ text: "\n", options: { fontSize: 6 } }] : [])
  ]);
  s.addText(contraTextArr, {
    x: 3.55, y: 3.2, w: 6.12, h: 1.55,
    fontFace: "Calibri", valign: "top"
  });
}

// ════════════════════════════════════════════════════════════
//  SLIDE 6 — DPP-4 INHIBITORS
// ════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.background = { color: C.offWhite };
  addSlideHeader(s, "DPP-4 Inhibitors (Gliptins)", "Incretin enhancers — glucose-dependent insulin secretion");
  addFooter(s, 6);

  // Mechanism visual
  s.addShape(pres.shapes.ROUNDED_RECTANGLE, {
    x: 0.18, y: 1.15, w: 9.62, h: 0.62,
    fill: { color: C.darkCard }, line: { color: C.darkCard }, rectRadius: 0.06
  });
  s.addText([
    { text: "DPP-4 inhibition → ↑ endogenous GLP-1 & GIP → ", options: { color: C.white } },
    { text: "glucose-dependent", options: { bold: true, color: C.gold, italic: true } },
    { text: " insulin secretion from β-cells + ↓ glucagon from α-cells", options: { color: C.white } }
  ], {
    x: 0.32, y: 1.15, w: 9.34, h: 0.62,
    fontSize: 10.5, fontFace: "Calibri", valign: "middle"
  });

  // Drug table
  const dppHeaders = [
    [{ text: "Drug", options: { bold: true, color: C.white, fill: { color: "1D6A47" } } },
     { text: "Brand", options: { bold: true, color: C.white, fill: { color: "1D6A47" } } },
     { text: "Standard Dose", options: { bold: true, color: C.white, fill: { color: "1D6A47" } } },
     { text: "Renal Adjustment", options: { bold: true, color: C.white, fill: { color: "1D6A47" } } }]
  ];
  const dppRows = [
    ["Sitagliptin",  "Januvia",   "100 mg once daily",  "50 mg if eGFR 30–45;  25 mg if eGFR <30"],
    ["Saxagliptin",  "Onglyza",   "5 mg once daily",    "2.5 mg if eGFR ≤45"],
    ["Linagliptin",  "Tradjenta", "5 mg once daily",    "NO adjustment needed (biliary excretion) ✓"],
    ["Alogliptin",   "Nesina",    "25 mg once daily",   "Reduce in renal impairment"],
  ];
  const dppData = [
    ...dppHeaders,
    ...dppRows.map((r, i) => r.map(cell => ({
      text: cell,
      options: { fill: { color: i % 2 === 0 ? "EBF8F0" : C.white }, color: C.navy, fontSize: 8.5 }
    })))
  ];
  s.addTable(dppData, {
    x: 0.18, y: 1.88, w: 9.62, h: 1.3,
    fontFace: "Calibri",
    border: { type: "solid", pt: 0.5, color: "BDD8CC" },
    colW: [1.6, 1.4, 2.2, 4.42]
  });

  card(s, 0.18, 3.3, 4.6, 1.55, "ADVANTAGES", [
    "Weight neutral",
    "Low hypoglycemia risk (monotherapy)",
    "Well tolerated — once daily",
    "Safe in elderly patients",
    "Suitable in mild–moderate CKD with dose adjustment"
  ], "1D6A47");

  card(s, 4.92, 3.3, 4.88, 1.55, "CLINICAL CAVEATS", [
    "Saxagliptin: ↑ heart failure hospitalisation (SAVOR-TIMI) — avoid in HF",
    "Do NOT combine with GLP-1 RA (same incretin pathway — no additive benefit)",
    "Pancreatitis risk — not definitively proven; monitor",
    "Bullous pemphigoid — rare class-wide skin reaction",
    "Nasopharyngitis, URTI common"
  ], C.red);
}

// ════════════════════════════════════════════════════════════
//  SLIDE 7 — SGLT2 INHIBITORS
// ════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.background = { color: C.offWhite };
  addSlideHeader(s, "SGLT2 Inhibitors (Gliflozins)", "Insulin-independent glucosuria + compelling cardiorenal outcomes");
  addFooter(s, 7);

  s.addShape(pres.shapes.ROUNDED_RECTANGLE, {
    x: 0.18, y: 1.15, w: 9.62, h: 0.58,
    fill: { color: C.navy }, line: { color: C.navy }, rectRadius: 0.06
  });
  s.addText([
    { text: "Block SGLT2 in proximal renal tubule → glucosuria (~70–80 g/day) → ↓ blood glucose.  ", options: { color: C.white } },
    { text: "Mechanism is insulin-independent.", options: { bold: true, color: C.gold } }
  ], {
    x: 0.32, y: 1.15, w: 9.34, h: 0.58,
    fontSize: 10, fontFace: "Calibri", valign: "middle"
  });

  // Drug table
  const sgltHeaders = [
    [{ text: "Drug", options: { bold: true, color: C.white, fill: { color: C.teal } } },
     { text: "Brand", options: { bold: true, color: C.white, fill: { color: C.teal } } },
     { text: "Dose", options: { bold: true, color: C.white, fill: { color: C.teal } } },
     { text: "Key Outcomes Evidence", options: { bold: true, color: C.white, fill: { color: C.teal } } }]
  ];
  const sgltRows = [
    ["Empagliflozin",  "Jardiance",  "10–25 mg od",   "EMPA-REG: ↓ MACE, ↓ CV death, ↓ HF hospitalisation, ↓ CKD progression"],
    ["Canagliflozin",  "Invokana",   "100–300 mg od", "CANVAS: ↓ MACE; CREDENCE: ↓ renal progression (caution: ↑ amputation)"],
    ["Dapagliflozin",  "Farxiga",    "5–10 mg od",    "DAPA-HF: ↓ HF events regardless of DM; DAPA-CKD: ↓ CKD progression"],
    ["Ertugliflozin",  "Steglatro",  "5–15 mg od",    "Less outcomes data than above three"],
  ];
  const sgltData = [
    ...sgltHeaders,
    ...sgltRows.map((r, i) => r.map(cell => ({
      text: cell,
      options: { fill: { color: i % 2 === 0 ? "EBF6F6" : C.white }, color: C.navy, fontSize: 8 }
    })))
  ];
  s.addTable(sgltData, {
    x: 0.18, y: 1.83, w: 9.62, h: 1.2,
    fontFace: "Calibri",
    border: { type: "solid", pt: 0.5, color: "BBDDDD" },
    colW: [1.6, 1.3, 1.3, 5.42]
  });

  card(s, 0.18, 3.15, 4.55, 2.1, "ADVERSE EFFECTS", [
    "Genital mycotic infections (candidiasis) — very common, especially ♀",
    "Euglycemic DKA — occurs at near-normal glucose; highest risk with fasting, surgery, T1DM use",
    "Volume depletion / hypotension — especially with diuretics",
    "Canagliflozin: ↑ amputations (peripheral artery disease), bone fractures",
    "Fournier's gangrene — rare but class-wide serious warning",
    "UTI — modest increased risk"
  ], C.red);

  card(s, 4.87, 3.15, 4.93, 2.1, "CRITICAL CAVEATS", [
    "Glycaemic efficacy requires eGFR ≥45; cardiorenal benefit extends to lower eGFR",
    "HOLD perioperatively (≥48 h before surgery) — euglycemic DKA risk",
    "HOLD during sick-day illness (vomiting/diarrhoea) — 'SADMAN' rule",
    "Check ketones (not just glucose) if patient presents unwell on SGLT2i",
    "Do NOT use in T1DM without specialist supervision"
  ], C.teal);
}

// ════════════════════════════════════════════════════════════
//  SLIDE 8 — GLP-1 RA & OTHER AGENTS
// ════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.background = { color: C.offWhite };
  addSlideHeader(s, "GLP-1 Receptor Agonists & Other Agents", "Incretin mimetics + alpha-glucosidase inhibitors + miscellaneous");
  addFooter(s, 8);

  card(s, 0.18, 1.15, 6.0, 2.35, "GLP-1 RECEPTOR AGONISTS", [
    "Mechanism: Mimic endogenous GLP-1 → glucose-dependent insulin secretion, ↓ glucagon, ↓ gastric emptying, ↑ satiety → weight loss",
    "Agents: Semaglutide (once-weekly SC or daily oral), Dulaglutide (weekly SC), Liraglutide (daily SC), Exenatide (BD or weekly)",
    "HbA1c reduction 1.0–2.0% + weight loss 2–5 kg (higher doses approved for obesity management)",
    "CVOT evidence: Liraglutide (LEADER), Semaglutide (SUSTAIN-6), Dulaglutide (REWIND) — all ↓ MACE",
    "Contraindicated: Personal/family history of MTC or MEN2 syndrome",
    "Adverse: GI (nausea, vomiting, diarrhoea) — worst on initiation; pancreatitis risk (avoid in chronic pancreatitis)"
  ], "5C6BC0");

  card(s, 6.32, 1.15, 3.48, 2.35, "INCRETIN INTERACTION NOTE", [
    "GLP-1 RA + DPP-4 inhibitor: NO additive benefit — same pathway; avoid combination",
    "GLP-1 RA + SGLT2 inhibitor: ADDITIVE benefits — complementary mechanisms",
    "Oral semaglutide: must be taken fasting with small sip of water; no food/drug for 30 min after"
  ], "5C6BC0");

  card(s, 0.18, 3.62, 3.1, 1.68, "α-GLUCOSIDASE INHIBITORS", [
    "Acarbose, Miglitol",
    "Competitively inhibit intestinal brush-border enzymes → delayed carbohydrate digestion → blunt postprandial glucose",
    "No systemic absorption (acarbose) — no hypoglycaemia alone",
    "CRITICAL: Hypoglycaemia on acarbose + SU/insulin → treat with pure GLUCOSE (not sucrose — acarbose blocks sucrose hydrolysis!)",
    "GI side effects (flatulence, bloating) limit use — 50–70%"
  ], "7B6FA0");

  card(s, 3.42, 3.62, 3.0, 1.68, "COLESEVELAM", [
    "Bile acid sequestrant",
    "Mechanism in DM: unclear — modestly ↓ HbA1c ~0.5%",
    "Bonus: ↓ LDL-C (dual glycaemic + lipid benefit)",
    "GI side effects; reduces absorption of fat-soluble vitamins & co-prescribed drugs",
    "Take other medications ≥4 h before colesevelam"
  ], "8D6E63");

  card(s, 6.56, 3.62, 3.22, 1.68, "BROMOCRIPTINE (CYCLOSET)", [
    "Dopamine D2 agonist",
    "Resets hypothalamic circadian rhythm → improves insulin sensitivity",
    "Modest HbA1c ↓ ~0.5–0.7%",
    "Can be continued when insulin is initiated",
    "Adverse: nausea, orthostatic hypotension, dizziness",
    "Take within 2 h of waking in the morning"
  ], "8D6E63");
}

// ════════════════════════════════════════════════════════════
//  SLIDE 9 — TREATMENT ESCALATION ALGORITHM
// ════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.background = { color: C.offWhite };
  addSlideHeader(s, "Treatment Escalation Algorithm", "ADA/EASD consensus approach — reassess every 3 months");
  addFooter(s, 9);

  // Step boxes with arrows
  const steps = [
    { label: "STEP 1", title: "Lifestyle + Metformin", detail: "All patients unless contraindicated\nA1C ≥9% or symptomatic → consider dual therapy at start", color: C.teal },
    { label: "STEP 2", title: "Add 2nd Agent (3 months)", detail: "Choose based on comorbidities:\n• CVD/ASCVD → GLP-1 RA\n• HFrEF/CKD → SGLT2 inhibitor\n• Weight → GLP-1 RA or SGLT2i\n• Cost → SU or TZD", color: "1A6B8A" },
    { label: "STEP 3", title: "Add 3rd Agent (3 months)", detail: "Triple therapy with complementary mechanisms\nConsider injectable GLP-1 RA if not already used", color: "2E86AB" },
    { label: "STEP 4", title: "Basal Insulin ± GLP-1 RA", detail: "Start basal insulin 10 U/night\nContinue: metformin, SGLT2i, DPP-4i\nDiscontinue: SU/meglitinide when prandial insulin added", color: "457B9D" },
    { label: "STEP 5", title: "Full Basal-Bolus Insulin", detail: "A1C >10% or DKA/HHS:\nconsider insulin from the start\nCombine with insulin sensitisers as tolerated", color: C.navy },
  ];

  steps.forEach((step, i) => {
    const x = 0.18 + i * 1.94;
    const y = 1.15;
    const w = 1.84;
    const h = 4.1;

    s.addShape(pres.shapes.ROUNDED_RECTANGLE, {
      x, y, w, h,
      fill: { color: step.color }, line: { color: step.color },
      rectRadius: 0.1,
      shadow: { type: "outer", color: "000000", blur: 6, offset: 2, angle: 135, opacity: 0.15 }
    });
    s.addShape(pres.shapes.OVAL, {
      x: x + w / 2 - 0.35, y: y + 0.12, w: 0.7, h: 0.7,
      fill: { color: C.white, transparency: 15 }, line: { color: C.white, transparency: 15 }
    });
    s.addText(step.label.replace("STEP ", ""), {
      x: x + w / 2 - 0.35, y: y + 0.12, w: 0.7, h: 0.7,
      fontSize: 18, bold: true, color: step.color,
      fontFace: "Calibri", align: "center", valign: "middle", margin: 0
    });
    s.addText(step.title, {
      x: x + 0.1, y: y + 0.92, w: w - 0.2, h: 0.55,
      fontSize: 9, bold: true, color: C.white,
      fontFace: "Calibri", align: "center", valign: "middle"
    });
    s.addShape(pres.shapes.RECTANGLE, {
      x: x + 0.15, y: y + 1.52, w: w - 0.3, h: 0.02,
      fill: { color: C.white, transparency: 60 }, line: { color: C.white, transparency: 60 }
    });
    s.addText(step.detail, {
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      valign: "top"
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    }
  });
}

// ════════════════════════════════════════════════════════════
//  SLIDE 10 — INDIVIDUALIZATION OF THERAPY
// ════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.background = { color: C.offWhite };
  addSlideHeader(s, "Individualization of Therapy", "Match drug to patient — comorbidities, eGFR, age, weight, cost");
  addFooter(s, 10);

  const rows = [
    ["Clinical Context", "Preferred Agent(s)", "Agents to Avoid"],
    ["Established ASCVD / High CV risk", "GLP-1 RA (liraglutide, semaglutide, dulaglutide)", "—"],
    ["Heart Failure (HFrEF)", "SGLT2 inhibitor (empagliflozin, dapagliflozin)", "TZDs; saxagliptin"],
    ["CKD (eGFR 25–60, albuminuria)", "SGLT2 inhibitor; linagliptin (no renal dose adjust)", "Metformin <30; glyburide; exenatide"],
    ["Obesity / weight loss priority", "GLP-1 RA (most weight loss), SGLT2 inhibitor", "TZDs, SUs (weight gain)"],
    ["Hypoglycaemia risk / elderly", "DPP-4i, GLP-1 RA, SGLT2i, TZD — all low hypo risk", "Glyburide (longest action = worst hypo)"],
    ["Liver disease", "DPP-4 inhibitors generally safe; metformin in mild disease only", "TZDs, metformin (severe hepatic disease)"],
    ["Cost-sensitive patient", "Metformin, generic SU, pioglitazone", "SGLT2i, GLP-1 RA (expensive)"],
    ["Pregnancy", "Insulin is preferred agent", "SGLT2i, DPP-4i, GLP-1 RA (avoid all)"],
  ];

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    colW: [2.4, 4.1, 3.12]
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}

// ════════════════════════════════════════════════════════════
//  SLIDE 11 — HbA1c TARGETS & MONITORING
// ════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.background = { color: C.offWhite };
  addSlideHeader(s, "HbA1c Targets & Monitoring", "Individualised targets — benefits of tight control vs. hypoglycaemia risk");
  addFooter(s, 11);

  // HbA1c target cards
  const targets = [
    { pop: "Most non-elderly adults", target: "<7.0%", color: C.teal },
    { pop: "Short disease duration, no CVD, long life expectancy", target: "<6.5%", color: "1D6A47" },
    { pop: "Elderly, frail, limited life expectancy, multiple comorbidities", target: "7.5–8.5%", color: "8D6E63" },
    { pop: "Pregnancy (2nd–3rd trimester)", target: "<6.0–6.5%", color: "5C6BC0" },
    { pop: "Hypoglycaemia unawareness / advanced CKD", target: "<8.0–9.0%", color: C.red },
  ];

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    s.addText(t.pop, {
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      fontSize: 7.5, color: C.white, fontFace: "Calibri",
      align: "center", italic: true
    });
  });

  // Monitoring table
  const monRows = [
    [{ text: "Parameter", options: { bold: true, color: C.white, fill: { color: C.navy } } },
     { text: "Frequency", options: { bold: true, color: C.white, fill: { color: C.navy } } },
     { text: "Notes", options: { bold: true, color: C.white, fill: { color: C.navy } } }],
    [{ text: "HbA1c", options: { color: C.navy, fill: { color: "F0FAFA" } } },
     { text: "Every 3 months until at goal; then 6-monthly", options: { color: C.navy, fill: { color: "F0FAFA" } } },
     { text: "Reflects ~3-month average glucose", options: { color: C.navy, fill: { color: "F0FAFA" } } }],
    [{ text: "eGFR / Creatinine", options: { color: C.navy, fill: { color: C.white } } },
     { text: "Baseline, then annually (more if declining)", options: { color: C.navy, fill: { color: C.white } } },
     { text: "Drives dose adjustment of multiple agents", options: { color: C.navy, fill: { color: C.white } } }],
    [{ text: "Urine ACR", options: { color: C.navy, fill: { color: "F0FAFA" } } },
     { text: "Annually", options: { color: C.navy, fill: { color: "F0FAFA" } } },
     { text: "Albuminuria triggers SGLT2i / ACEi consideration", options: { color: C.navy, fill: { color: "F0FAFA" } } }],
    [{ text: "Vitamin B12", options: { color: C.navy, fill: { color: C.white } } },
     { text: "Annually (if on metformin)", options: { color: C.navy, fill: { color: C.white } } },
     { text: "Long-term metformin depletes B12 → peripheral neuropathy", options: { color: C.navy, fill: { color: C.white } } }],
    [{ text: "Foot examination", options: { color: C.navy, fill: { color: "F0FAFA" } } },
     { text: "Annually", options: { color: C.navy, fill: { color: "F0FAFA" } } },
     { text: "Monofilament + pulse assessment", options: { color: C.navy, fill: { color: "F0FAFA" } } }],
  ];
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    colW: [1.8, 3.0, 4.82]
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}

// ════════════════════════════════════════════════════════════
//  SLIDE 12 — KEY CLINICAL CAVEATS
// ════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.background = { color: C.offWhite };
  addSlideHeader(s, "Key Clinical Caveats", "High-yield pearls for the wards, clinics & examinations");
  addFooter(s, 12);

  const caveats = [
    {
      n: "1", title: "Contrast + Metformin",
      text: "Hold metformin 48 h before and after iodinated contrast if eGFR <60. Risk: contrast nephropathy → metformin accumulation → lactic acidosis.",
      color: C.teal
    },
    {
      n: "2", title: "Euglycaemic DKA (SGLT2i)",
      text: "Glucose may be only mildly elevated (150–200 mg/dL). Check beta-hydroxybutyrate if patient on SGLT2i presents unwell. Hold perioperatively ≥48 h before surgery.",
      color: C.red
    },
    {
      n: "3", title: "SADMAN Sick-Day Rule",
      text: "Stop Sulfonylureas, ACEi/ARB, Diuretics, Metformin, And NSAIDs during vomiting/diarrhoea illness. Add SGLT2 inhibitors to this list.",
      color: C.red
    },
    {
      n: "4", title: "Acarbose Hypoglycaemia",
      text: "If hypoglycaemia occurs while on acarbose + SU/insulin, treat with PURE GLUCOSE (dextrose tablets/IV). Sucrose and fruit juice will not work — acarbose blocks sucrose hydrolysis.",
      color: "7B6FA0"
    },
    {
      n: "5", title: "GLP-1 RA + DPP-4i",
      text: "Never combine — both target the incretin axis. DPP-4i has no additive benefit when a GLP-1 RA is present.",
      color: "5C6BC0"
    },
    {
      n: "6", title: "CV Outcomes Summary",
      text: "DPP-4i = CV safe (no benefit). GLP-1 RA = ↓ MACE (atherosclerosis-driven). SGLT2i = ↓ HF hospitalisation + ↓ CKD progression (haemodynamic + renal tubular mechanism).",
      color: C.navy
    },
  ];

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    const col = i % 2;
    const row = Math.floor(i / 2);
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    });
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    });
  });
}

// ════════════════════════════════════════════════════════════
//  SLIDE 13 — RENAL DOSING QUICK REFERENCE
// ════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
  s.background = { color: C.offWhite };
  addSlideHeader(s, "Renal Dosing Quick Reference", "As eGFR declines, the pharmacological toolkit narrows");
  addFooter(s, 13);

  const renalData = [
    [
      { text: "Drug Class", options: { bold: true, color: C.white, fill: { color: C.navy } } },
      { text: "eGFR ≥60", options: { bold: true, color: C.white, fill: { color: C.navy } } },
      { text: "eGFR 45–59", options: { bold: true, color: C.white, fill: { color: C.navy } } },
      { text: "eGFR 30–44", options: { bold: true, color: C.white, fill: { color: C.navy } } },
      { text: "eGFR 15–29", options: { bold: true, color: C.white, fill: { color: C.navy } } },
      { text: "eGFR <15 / ESRD", options: { bold: true, color: C.white, fill: { color: C.navy } } },
    ],
    ["Metformin",
      { text: "✓ Full dose", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "✓ Full dose", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "⚠ Reduce / caution", options: { fill: { color: "FFF8E6" }, color: "C07000" } },
      { text: "✗ Avoid", options: { fill: { color: "FFE8E8" }, color: C.red } },
      { text: "✗ Avoid", options: { fill: { color: "FFE8E8" }, color: C.red } },
    ],
    ["Sulfonylureas (Glipizide, Glimepiride)",
      { text: "✓ Full dose", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "✓ Low dose, caution", options: { fill: { color: "FFF8E6" }, color: "C07000" } },
      { text: "⚠ Low dose only", options: { fill: { color: "FFF8E6" }, color: "C07000" } },
      { text: "✗ Avoid glyburide; glipizide low dose only", options: { fill: { color: "FFE8E8" }, color: C.red } },
      { text: "✗ Avoid all SUs", options: { fill: { color: "FFE8E8" }, color: C.red } },
    ],
    ["DPP-4i — Linagliptin",
      { text: "✓ 5 mg od", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "✓ 5 mg od", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "✓ 5 mg od", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "✓ 5 mg od", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "✓ 5 mg od (no adjustment)", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
    ],
    ["DPP-4i — Sitagliptin",
      { text: "✓ 100 mg od", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "✓ 100 mg od", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "⚠ 50 mg od", options: { fill: { color: "FFF8E6" }, color: "C07000" } },
      { text: "⚠ 25 mg od", options: { fill: { color: "FFF8E6" }, color: "C07000" } },
      { text: "⚠ 25 mg od", options: { fill: { color: "FFF8E6" }, color: "C07000" } },
    ],
    ["SGLT2 Inhibitors",
      { text: "✓ Full dose", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "✓ Full dose (glycaemic + CV benefit)", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "⚠ Glycaemic efficacy ↓; CV/renal benefit continues", options: { fill: { color: "FFF8E6" }, color: "C07000" } },
      { text: "⚠ No glycaemic effect; CV/renal benefit (empagliflozin, dapagliflozin)", options: { fill: { color: "FFF8E6" }, color: "C07000" } },
      { text: "✗ No use at ESRD for glycaemia; discontinue", options: { fill: { color: "FFE8E8" }, color: C.red } },
    ],
    ["GLP-1 RA",
      { text: "✓ Full dose", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "✓ Full dose", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "✓ Most — full dose (avoid exenatide)", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "⚠ Semaglutide, dulaglutide — use with caution; avoid exenatide", options: { fill: { color: "FFF8E6" }, color: "C07000" } },
      { text: "✗ Limited data; generally avoid", options: { fill: { color: "FFE8E8" }, color: C.red } },
    ],
    ["Insulin",
      { text: "✓ Standard dosing", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "✓ Standard dosing", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "✓ Monitor — ↑ hypoglycaemia risk", options: { fill: { color: "E6F9EE" }, color: "1D6A47" } },
      { text: "✓ Reduce dose — kidneys clear less insulin", options: { fill: { color: "FFF8E6" }, color: "C07000" } },
      { text: "✓ Use but reduce dose; highest hypo risk", options: { fill: { color: "FFF8E6" }, color: "C07000" } },
    ],
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    x: 0.18, y: 1.15, w: 9.62, h: 4.15,
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    border: { type: "solid", pt: 0.5, color: "BBCCDD" },
    colW: [2.0, 1.2, 1.3, 1.6, 1.9, 1.62]
  });
}

// ════════════════════════════════════════════════════════════
//  SLIDE 14 — SUMMARY / TAKE-HOME
// ════════════════════════════════════════════════════════════
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  const s = pres.addSlide();
  s.background = { color: C.navy };

  // Background decorative shapes
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  const points = [
    { icon: "▶", text: "Metformin remains first-line unless eGFR <30, contrast exposure, or significant hepatic disease." },
    { icon: "▶", text: "For ASCVD/high CV risk → add GLP-1 RA with proven CVOT benefit early (liraglutide, semaglutide, dulaglutide)." },
    { icon: "▶", text: "For Heart Failure or CKD with albuminuria → SGLT2 inhibitor is the priority second agent (benefits are insulin-independent)." },
    { icon: "▶", text: "DPP-4 inhibitors are CV safe but offer no CV benefit; avoid saxagliptin in HF." },
    { icon: "▶", text: "Euglycaemic DKA on SGLT2i: check ketones, not just glucose. HOLD perioperatively." },
    { icon: "▶", text: "Individualize HbA1c targets — tight control prevents microvascular disease; lax targets acceptable in elderly/frail." },
    { icon: "▶", text: "Never combine GLP-1 RA + DPP-4i. Always re-evaluate every 3 months and escalate without delay." },
  ];

  points.forEach((p, i) => {
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    italic: true, valign: "middle"
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}

// ════════════════════════════════════════════════════════════
//  WRITE FILE
// ════════════════════════════════════════════════════════════
pres.writeFile({ fileName: "Oral_Hypoglycemic_Agents_PG_IM.pptx" })
  .then(() => console.log("✅  Oral_Hypoglycemic_Agents_PG_IM.pptx created successfully"))
  .catch(err => console.error("❌  Error:", err));

How to run

# 1. Install dependency (only needed once)
npm install pptxgenjs

# 2. Run the script
node oha_presentation.js

# Output: Oral_Hypoglycemic_Agents_PG_IM.pptx

What's inside (14 slides)

#Slide
1Title slide — dark navy with geometric teal/gold accents
2Drug class overview — 9 colour-coded class tiles
3Metformin — MOA, dosing, renal thresholds, monitoring
4Sulfonylureas + Meglitinides — mechanism banner, drug table, warnings
5Thiazolidinediones — PPARγ mechanism, pioglitazone vs rosiglitazone, full contraindications
6DPP-4 inhibitors — drug/dose/renal table, saxagliptin HF warning
7SGLT2 inhibitors — CVOT outcomes table, euglycaemic DKA, periop hold
8GLP-1 RAs, alpha-glucosidase inhibitors, colesevelam, bromocriptine
9Treatment escalation algorithm — 5-step colour-coded vertical columns
10Individualization table — context vs. preferred vs. avoid
11HbA1c targets (big number cards) + monitoring schedule table
126 clinical caveat cards — contrast, euglycaemic DKA, SADMAN, acarbose glucose rule, GLP-1+DPP-4, CVOT summary
13Renal dosing quick reference — full eGFR band table across all classes
14Summary / take-home — dark closing slide with 7 key bullet points
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