When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

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Ambulatory

Outpatient Diabetes Management

The treatment paradigm has shifted. It's no longer just about A1c -cardiorenal protection drives drug selection. SGLT2 inhibitors and GLP-1 agonists now have organ-protective benefits independent of glucose lowering.

💊 ADA 2026 Treatment Algorithm

What changed in ADA 2026 Standards of Care (released January 2026): (1) GLP-1 RA / dual GIP-GLP-1 (tirzepatide, semaglutide) elevated to first-line after metformin for T2DM with obesity, ahead of SU / TZD (SURMOUNT-1, 2022 · SELECT, 2023). (2) SGLT2i recommended for ALL CKD (eGFR ≥ 20, regardless of A1c) -mirrors KDIGO 2024 (DAPA-CKD, 2020 · EMPA-KIDNEY, 2023 · FIDELIO-DKD, 2020). (3) CGM expanded to T2DM on ANY basal insulin (was intensive-insulin only). (4) Screening starts age 35 for all adults; age 25 if BMI ≥ 25 + risk factors. (5) Lp(a) once per lifetime in DM (parallels 2026 ACC/AHA Dyslipidemia Guideline). (6) GLP-1 RA + SGLT2i preferred over insulin when ASCVD / HF / CKD coexist -insulin is no longer "default escalation" (LEADER, 2016 · EMPA-REG OUTCOME, 2015). (7) Inpatient: glucose target 140-180; basal-bolus over sliding-scale-only; SQ insulin acceptable for mild-moderate DKA.

Step 1 -All Type 2 DM

Metformin (Glucophage) remains first-line for most patients (A1c reduction ~1.5%, weight neutral, cheap, CV benefit UKPDS 34, 1998)
Lifestyle: 150 min/week moderate exercise, 5–7% weight loss target, medical nutrition therapy DPP, 2002
A1c target: < 7% for most DCCT, 1993 (correlates with TIR >70%). < 6.5% if early disease, no hypoglycemia risk ADVANCE, 2008. < 8% if elderly, multiple comorbidities, limited life expectancy ACCORD, 2008. ADA 2026: Older adults with complex health → TIR goal 50% (12 hrs/day); time below 70 <1% (15 min/day).

Step 2 -Add Based on Comorbidities (Not Just A1c)

Default rule: these agents are ADD-ON to metformin, not replacement. Continue metformin (mortality benefit, weight neutral, cheap, synergistic) AND layer the comorbidity-targeted agent on top. Replacement only when metformin is contraindicated -eGFR < 30, severe GI intolerance, or prior lactic acidosis. Rows tagged REPLACE below indicate metformin must come off; rows tagged REPLACE IF INTOLERANT indicate metformin stays if the patient tolerates it. Per ADA 2026, when A1c ≥ 1.5-2% above goal OR CV risk is high, you can start triple therapy on day 1 (metformin + GLP-1 RA + SGLT2i together) rather than wait for stepwise failure.

Comorbidity	Preferred Agent	Key Trial	Notes
ASCVD or high CV risk	GLP-1 RA (semaglutide, liraglutide, dulaglutide) PREFERRED	SUSTAIN-6, 2016 LEADER, 2016	Reduce MACE (MI, stroke, CV death). Weight loss 5–15%. Weekly injection (semaglutide SC) or daily (liraglutide). GI side effects (nausea) limit titration. Also available PO (oral semaglutide).
Heart failure (HFrEF or HFpEF)	SGLT2i (empagliflozin, dapagliflozin) PREFERRED	EMPA-REG, 2015 DAPA-HF, 2019	Reduce HF hospitalization and CV death -even in patients WITHOUT diabetes EMPEROR-Preserved, 2021. Now part of HF guideline-directed therapy. Also renal-protective.
CKD (eGFR 20–60 or albuminuria)	SGLT2i (dapagliflozin, empagliflozin) PREFERRED	DAPA-CKD, 2020 EMPA-KIDNEY, 2022	Slow CKD progression by 30–40%. Can use down to eGFR 20 (initiate) or continue to dialysis. Glucose-lowering effect diminishes at low GFR but renal benefit persists.
Obesity (weight loss priority)	GLP-1 RA (semaglutide > others) or tirzepatide (dual GIP/GLP-1)	SURPASS, 2021 SURMOUNT, 2022	Tirzepatide: most potent A1c reduction (~2.5%) and weight loss (~15–20%). Semaglutide 2.4 mg (Wegovy) FDA-approved for obesity regardless of DM.
MASLD / MASH (liver fibrosis in T2DM)	GLP-1 RA (semaglutide preferred) or tirzepatide ADA 2026 - 1ST LINE	ESSENCE, 2024	First-line for liver fibrosis in T2DM per ADA 2026. Pioglitazone is an alternative (also improves liver histology) but causes weight gain. Semaglutide reverses MASH fibrosis without worsening steatohepatitis. Avoid agents that worsen hepatic disease (sulfonylureas can complicate, methotrexate-like agents).
Stroke history (secondary prevention)	GLP-1 RA (semaglutide, dulaglutide)	REWIND, 2019 SUSTAIN-6, 2016	GLP-1 RA reduces stroke specifically (39% in SUSTAIN-6, 24% in REWIND). Stronger anti-stroke effect than SGLT2i. Add ASA + statin per ASCVD guidelines.
A1c ≥ 10% WITH symptoms (polyuria, polydipsia, weight loss, ketones)	Insulin (often basal + metformin) URGENT	ADA 2026 algorithm	Symptomatic hyperglycemia or evidence of catabolism (DKA, ketosis, >5% weight loss) requires rapid glucose control with insulin. Start basal 0.1-0.2 units/kg, titrate every 3 days. Once stable and asymptomatic, can transition to oral agents based on comorbidities. Rule out T1DM (GAD antibodies, C-peptide).
eGFR < 30	GLP-1 RA preferred (lower hypoglycemia) REPLACE METFORMIN ADA 2026	FDA labeling, ADA 2026	Metformin contraindicated -STOP IT (lactic acidosis risk; some guidelines tolerate down to 30 with reduced dose). SGLT2i loses glucose-lowering effect < 30 but renal/CV benefit persists -continue if already on for renal protection. Sulfonylureas avoid (especially glyburide -prolonged hypoglycemia). DPP-4i (linagliptin only -hepatically cleared, no renal adjustment) and insulin are alternatives.
Older adult / frail (≥ 65, multiple comorbidities, limited life expectancy)	Metformin (if tolerated) or DPP-4i (linagliptin) REPLACE IF INTOLERANT	Geriatric guidelines	Keep metformin if the patient tolerates it; switch to linagliptin if GI side effects, anorexia, or sarcopenia/weight-loss concern. Relax A1c target to < 8% (or 8.5% if frail/dementia). Avoid SU and basal-bolus insulin (hypoglycemia risk = falls, fractures, hospitalization). DPP-4i is well-tolerated, no hypoglycemia. SGLT2i OK if no orthostasis. GLP-1 RA OK if no GI fragility / weight-loss concern.
Cost / simplicity priority	Sulfonylurea (glipizide, glimepiride) or pioglitazone COST-DRIVEN ONLY	UKPDS 1998 (no CV benefit for SU)	Why SUs are NOT first-line in most cases: (1) hypoglycemia risk -severe especially in elderly, CKD, missed meals, alcohol; glyburide is on AGS Beers Criteria. (2) Weight gain 2-3 kg -opposite of what most T2DM patients need. (3) Secondary failure within 5-10 years as β-cell function declines. (4) No CV mortality benefit (unlike metformin, GLP-1 RA, SGLT2i). (5) No renal protection. (6) Possible cardiac harm signal from K-ATP channel effects (mostly historical concern). Genuine indications where SUs ARE preferred: (a) MODY (HNF1A or HNF4A) -first-line on clinical merit, excellent response. (b) Pancreatitis history (precludes GLP-1 RA / DPP-4i). (c) Bridge while awaiting prior auth on a preferred agent. (d) Cost truly is the deciding factor (uninsured patient -SU pennies/day vs SGLT2i $300-500/mo, GLP-1 RA $800-1500/mo). Glipizide preferred over glyburide (shorter half-life, no active renal metabolites). Pioglitazone: useful in MASLD/MASH (improves liver histology), but causes fluid retention (avoid HFrEF), fracture risk in postmenopausal women, weight gain, bladder cancer concern.

The key paradigm shift: drug selection is now driven by comorbidities (ASCVD, HF, CKD, obesity), not just A1c. A patient with DM + HF should be on an SGLT2i regardless of their A1c. A patient with DM + ASCVD should be on a GLP-1 RA.

ADA 2026 Updates:
• Initial combo therapy: Start GLP-1 RA + SGLT2i together when A1c is ≥1.5–2% above goal OR high CVD risk, regardless of A1c
• GLP-1 RA in T1DM: Now recommended for adults with T1DM and BMI ≥30 (≥27.5 for Asian Americans), first time ever
• GLP-1 RA for advanced CKD: Preferred for glycemic management when eGFR <30 (lower hypoglycemia risk)
• GLP-1 RA for MASLD/MASH: First-line for liver fibrosis in T2DM
• Dual GIP/GLP-1 (tirzepatide): Added to HFpEF algorithm alongside SGLT2i
• SGLT2i + finerenone: Simultaneous initiation for UACR ≥100 mg/g with eGFR 30–90
• CGM at diagnosis: Recommended at diabetes onset for anyone who may benefit, no longer limited to insulin users
• BP target: Systolic <120 mmHg for high CV or renal risk (lowered from 130)

📋 On Rounds

Why are SGLT2 inhibitors beneficial in HF even without diabetes?

The HF benefit of SGLT2i is independent of glucose lowering. Proposed mechanisms: (1) Osmotic diuresis + natriuresis → reduces preload and congestion without RAAS activation (unlike loop diuretics). (2) Improved cardiac energetics -shifts myocardial fuel from fatty acids to ketone bodies (more efficient substrate). (3) Reduced interstitial fibrosis and inflammation. (4) Improved endothelial function.

Why are SGLT2 inhibitors given even in patients with A1c at goal?

SGLT2 inhibitors have organ-protective benefits independent of glucose lowering. EMPA-REG OUTCOME EMPA-REG, 2015 showed empagliflozin reduced CV death by 38% in T2DM with ASCVD -a benefit too large and too fast to be explained by A1c reduction alone. DAPA-CKD showed dapagliflozin slowed CKD progression even in non-diabetic kidney disease. EMPEROR-Preserved showed benefit in HFpEF.

How do you choose between GLP-1 RA and SGLT2i when a patient has both ASCVD and CKD?

Start both -they work through different mechanisms and benefits are additive. If you must prioritize one: ASCVD-dominant → GLP-1 RA first (semaglutide, liraglutide -proven CV death reduction SUSTAIN-6, LEADER). CKD-dominant → SGLT2i first (empagliflozin, dapagliflozin -proven renal protection CREDENCE, DAPA-CKD, slow eGFR decline, reduce proteinuria).

What is the 'legacy effect' in diabetes and why does early A1c matter?

The legacy effect (metabolic memory) refers to the long-term benefit of early intensive glucose control -even after control is later relaxed. UKPDS, 1998 initially showed modest benefit of intensive control in newly diagnosed T2DM. But the 10-year post-trial follow-up showed the intensively-treated group continued to have lower rates of MI and death even though A1c had equalized between groups.

Clinical Examples

📋 Case 1, T2DM with ASCVD: Adding GLP-1 RA

Patient: 62M with T2DM (A1c 8.2%), prior MI, BMI 31, eGFR 68. Currently on metformin 1000 mg BID. BP 138/82 on lisinopril. LDL 72 on statin.

Key findings: Established ASCVD (prior MI), requires cardiorenal protective agent regardless of A1c. Not at A1c goal despite metformin. Overweight.

Management:

Add semaglutide 0.25 mg SQ weekly → titrate to 1 mg (GLP-1 RA with proven CV benefit) SUSTAIN-6, 2016
Continue metformin (complementary mechanism, renal-safe at eGFR > 30)
A1c target < 7% for this patient (established ASCVD, reasonable life expectancy)
Counsel on GI side effects (nausea, improves with slow titration)
Recheck A1c in 3 months; if still above target, consider adding SGLT2i for additive cardiorenal benefit

Teaching point: In T2DM with ASCVD, GLP-1 RA or SGLT2i should be added independent of A1c. The CV benefit is beyond glucose lowering. ADA 2026 recommends these as first-line add-on in ASCVD.

📋 Case 2, T2DM with CKD and HF: SGLT2 Inhibitor

Patient: 58F with T2DM (A1c 7.8%), HFrEF (EF 35%), eGFR 38, UACR 380 mg/g. On metformin 500 BID, lisinopril, carvedilol, spironolactone. BMI 28.

Key findings: Triple indication for SGLT2i: T2DM + HFrEF + CKD with albuminuria. Current A1c near goal but cardiorenal protection is the primary reason to add SGLT2i.

Management:

Add dapagliflozin 10 mg daily (or empagliflozin 10 mg) DAPA-CKD, 2020
Continue metformin (reduce to 500 mg daily if eGFR drops below 30)
Warn: initial eGFR dip of 10-15% is expected and not a reason to stop (hemodynamic, not structural)
Monitor K⁺ closely (on spironolactone + ACEi + SGLT2i)
Counsel on genital mycotic infections (candidiasis risk ~5-8%), maintain hygiene

Teaching point: SGLT2 inhibitors are now pillar therapy for HF and CKD independent of diabetes status. The initial eGFR dip is tubuloglomerular feedback, protective long-term. Do not stop for a 10-15% creatinine rise.

📋 Case 3, Newly Diagnosed T2DM with A1c > 10%

Patient: 47M newly diagnosed T2DM. A1c 11.2%, FBG 310. Polyuria, polydipsia, 15 lb weight loss over 2 months. BMI 36. No ASCVD. eGFR 92. GAD antibodies negative.

Key findings: Symptomatic hyperglycemia with A1c > 10%, indication for initial insulin therapy per ADA guidelines. GAD negative confirms T2DM (not LADA).

Management:

Start basal insulin: glargine 0.2 U/kg/day (or 10 units) at bedtime, titrate by 2 U q3 days to FBG 80-130
Start metformin 500 mg daily → titrate to 1000 mg BID over 4 weeks (GI tolerance)
Plan to add GLP-1 RA once insulin dose stabilizes (weight benefit, potential insulin de-escalation)
DSME referral (diabetes self-management education), nutrition counseling
Recheck A1c in 3 months, once A1c < 9%, may attempt insulin taper with oral/injectable agents

Teaching point: A1c > 10% with symptoms = start insulin (oral agents alone are too slow). This is temporary, once glucose toxicity resolves, beta-cell function often partially recovers and insulin can be weaned.

📣 Sample Presentation

One-Liner

"Mrs. Patel is a 54-year-old with T2DM (A1c 8.6), BMI 34, ASCVD (prior MI), and eGFR 52, currently on metformin 1000 BID only. Here for medication optimization."

Key Points to Cover on Rounds

A1c 8.6 (goal <7). BMI 34. ASCVD + CKD -drug selection driven by comorbidities, not just A1c. Changes: (1) Add semaglutide 0.25 mg SQ weekly, uptitrate to 1 mg (GLP-1 RA -proven CV benefit [SUSTAIN-6, 2016], weight loss, renal protection), (2) Add empagliflozin 10 mg daily (SGLT2i -proven CV + renal benefit [EMPA-REG, 2015, CREDENCE, 2019], even at eGFR 52), (3) Continue metformin 1000 BID. Screening: eye exam (overdue), foot exam done today (monofilament intact), UACR 180 (albuminuria -SGLT2i indicated). Statin confirmed (atorvastatin 80). Plan: recheck A1c in 3 months, titrate semaglutide, UACR in 6 months.

🧪 Workup

Diagnostic Criteria (ADA 2025)

Need TWO abnormal results on different days, OR one abnormal result with classic symptoms (polyuria, polydipsia, unintentional weight loss). Any of the four criteria below qualifies.

Test	Diabetes	Prediabetes	Normal
HbA1c (NGSP-certified, DCCT-aligned)	≥ 6.5%	5.7-6.4%	< 5.7%
Fasting plasma glucose (≥ 8h fast)	≥ 126 mg/dL	100-125 mg/dL (IFG)	< 100 mg/dL
2-hour OGTT (75 g glucose load)	≥ 200 mg/dL	140-199 mg/dL (IGT)	< 140 mg/dL
Random plasma glucose	≥ 200 mg/dL WITH classic symptoms	,	,

HbA1c caveats: falsely low in conditions that shorten RBC lifespan (hemolysis, recent transfusion, hemoglobinopathies like sickle cell, pregnancy 2nd-3rd trimester, EPO therapy). Falsely high in iron deficiency anemia, splenectomy, uremia. Use fasting glucose or fructosamine when A1c is unreliable.

Screening Recommendations

USPSTF 2021: screen adults age 35-70 with overweight/obesity (BMI ≥ 25, or ≥ 23 in Asian Americans). Repeat every 3 years if normal.
ADA 2025: screen all adults age ≥ 35, OR younger if BMI ≥ 25 plus ≥ 1 risk factor. Repeat at least every 3 years.
ADA 2026 update: CGM at diagnosis recommended for anyone who may benefit -no longer limited to insulin users.

Risk factors warranting earlier / more frequent screening

First-degree family history of DM
High-risk race/ethnicity (African American, Latino, Native American, Asian American, Pacific Islander)
HTN (≥ 140/90 or on antihypertensive)
HDL < 35 or triglycerides > 250
Physical inactivity
PCOS
History of gestational DM, delivery of macrosomic baby (> 9 lb)
Prior CV event or stroke
Acanthosis nigricans, severe obesity
HIV (especially on ART), schizophrenia / on antipsychotics, transplant recipients on calcineurin inhibitors / steroids

Classifying the Diabetes

Type	Mechanism	Clue	Workup
Type 2 (~90-95%)	Insulin resistance + relative β-cell deficiency	Adult onset, overweight/obese, family history, gradual symptoms, often metabolic syndrome features	Antibodies negative. C-peptide normal/high (early). No further classification testing usually needed.
Type 1 (~5-10%)	Autoimmune β-cell destruction	Younger (most < 30, but can occur at any age), lean, rapid onset, DKA at diagnosis common, weight loss	GAD-65 antibodies (most useful), IA-2, ZnT8, ICA, IAA. Low C-peptide. Need lifelong insulin.
LADA (Latent Autoimmune DM in Adults)	Slow-progressing T1 phenotype in adults	Adult onset (≥ 30) appearing as T2, but rapid failure of oral agents, usually leaner than typical T2	GAD-65 positive in adult who looks like T2. Often misdiagnosed for years. Will need insulin sooner than expected.
MODY (Monogenic Diabetes)	Single-gene defects (HNF1A, HNF4A, GCK most common)	Strong family history (autosomal dominant), young onset (< 25), lean, no antibodies, atypical course	Genetic testing. GCK-MODY rarely needs treatment; HNF1A/HNF4A respond well to sulfonylureas.
Secondary DM	Pancreatic disease, drug-induced, endocrinopathy, post-transplant	Pancreatic surgery / chronic pancreatitis / cystic fibrosis / hemochromatosis; on glucocorticoids, antipsychotics, calcineurin inhibitors, thiazides; Cushing's, acromegaly, pheochromocytoma, hyperthyroidism	Workup the underlying cause. Often resolves or improves when the trigger is treated.

When to send antibodies / C-peptide: young (< 30), lean, rapid progression to insulin, atypical course (rapid β-cell failure on oral agents), DKA at presentation, or strong personal/family history of autoimmunity. GAD-65 alone catches ~70-80% of T1/LADA; add IA-2 or ZnT8 for higher sensitivity.

Initial Labs at Diagnosis

Test	Reason We Check	What It Changes
HbA1c	Confirm diagnosis + baseline for treatment response	Drives initial regimen choice. A1c > 9% → consider dual therapy or initial insulin. A1c > 10% with symptoms → likely insulin (especially if T1 not yet excluded).
BMP / eGFR	Baseline kidney function for drug dosing + screen for diabetic nephropathy	eGFR < 30: hold metformin, dose-adjust SGLT2i, avoid sulfonylureas with active metabolites (glyburide). eGFR 30-45: reduce metformin to 1000 mg/day.
UACR	Detect microalbuminuria (earliest sign of diabetic nephropathy)	UACR ≥ 30 mg/g → start ACEi/ARB even if BP is normal. UACR ≥ 100 with eGFR 30-90 → add finerenone (FIDELIO/FIGARO). Add SGLT2i (renal-protective).
Fasting lipid panel	ASCVD risk stratification + statin indication	DM age 40-75 + LDL 70-189 → moderate-intensity statin. ASCVD ≥ 7.5% → high-intensity statin. LDL ≥ 190 → high-intensity regardless.
LFTs (ALT, AST)	Baseline; screen for MASLD/MASH (formerly NAFLD)	ALT elevated → FIB-4 score for fibrosis stratification. ADA 2026: GLP-1 RA is first-line for liver fibrosis in T2DM.
TSH	Higher rate of autoimmune thyroid disease, especially in T1DM	Hypothyroid → levothyroxine; abnormal TSH worsens lipid profile and may complicate weight management.
Vitamin B12	Baseline (or after 4-5 years) for patients on metformin -inhibits B12 absorption	B12 deficiency → switch metformin or supplement; can mimic peripheral neuropathy.
Dilated retinal exam	Detect retinopathy at baseline	T2DM (Type 2): at diagnosis, then q1-2 years if normal. T2DM patients often have ~4-10 years of subclinical hyperglycemia before diagnosis, so 20-30% already have retinopathy at first screen. T1DM (Type 1): within 5 years of diagnosis, then annually. T1DM is diagnosed acutely so retinopathy hasn't had time to develop. Earlier referral if any retinopathy present or pregnancy planned (pregnancy can rapidly worsen retinopathy).
Foot exam (monofilament, vibration, ABI if pulses absent)	Detect peripheral neuropathy + PAD	Neuropathy + foot deformity = high ulcer/amputation risk. Refer podiatry. Document protective sensation, pulses, deformity.

What to send only if T1 is suspected: GAD-65 antibody, IA-2 antibody, ZnT8 antibody, fasting C-peptide. Also screen for celiac disease (TTG IgA + total IgA) and autoimmune thyroid (TSH, TPO antibody) -all are associated with T1DM.

⚡ Management

A1c Targets by Population

Population	Target	Evidence / Rationale
Most adults with T2DM	< 7.0%	UKPDS, 1998 + DCCT, 1993. Below this drives microvascular benefit.
Young, early disease, low hypoglycemia risk	< 6.5%	ADVANCE, 2008. Tighter target acceptable when hypoglycemia risk is low and life expectancy is long.
Established CV disease, advanced complications, or hypoglycemia-prone	< 8.0%	ACCORD, 2008. Avoid < 6.5% in this group -intensive control increased mortality.
Frail elderly, limited life expectancy, dementia	< 8.5% or symptom-driven	Avoid hypoglycemia. ADA 2026: TIR > 50% (12 hr/day) is reasonable goal; time below 70 mg/dL < 1% (15 min/day).
Pregnancy (preexisting or gestational)	A1c < 6.0-6.5% if achievable without hypoglycemia FBG < 95, 1-h PP < 140, 2-h PP < 120	Tight control prevents fetal complications. Insulin is preferred -metformin/glyburide cross placenta with mixed long-term data.

CGM & SMBG Targets

Time in Range (TIR, 70-180 mg/dL): goal > 70% for most T2DM. > 60% acceptable in older adults / hypoglycemia-prone.
Time below range (< 70 mg/dL): < 4% for most. < 1% in older adults.
Time above range (> 180 mg/dL): < 25% goal.
Glucose variability (CV): < 36% goal.
SMBG frequency: 4× daily (before meals + bedtime) on basal-bolus or pump. 1-2× daily on basal only or oral regimen. Rough rule: 1% A1c reduction needs ≥ 4 daily fingersticks or CGM equivalent.
ADA 2026 expansion: CGM is now recommended at diagnosis for anyone who may benefit (not just insulin users).

Comorbidity Bundle (the non-glycemic management)

A1c is only one number. Most CV deaths in DM come from BP, lipids, and unaddressed CKD -not glucose. Hit all five pillars:

Pillar	Target / Action	Notes
1. BP control	< 130/80 most patients. < 120 SBP if high CV risk (ADA 2026 update from 130).	ACEi or ARB first-line if albuminuria or any compelling indication. Don't combine ACEi+ARB (ONTARGET, 2008). See Outpatient HTN topic.
2. Lipid management	DM age 40-75: moderate-intensity statin. ASCVD ≥ 7.5% or established CVD: high-intensity statin. LDL goal < 70 (ASCVD) / < 100 (no ASCVD).	Atorvastatin 10-20 mg or rosuvastatin 5-10 mg (moderate). Atorva 40-80 / rosuva 20-40 (high). Consider ezetimibe or PCSK9 if not at goal.
3. Renal protection	SGLT2i if eGFR > 20 (regardless of A1c). ACEi/ARB if UACR ≥ 30. Finerenone if UACR ≥ 100 with eGFR 30-90 + on optimized RAAS.	SGLT2i has independent renal benefit (DAPA-CKD, EMPA-KIDNEY). Finerenone reduces CV + renal events (FIDELIO-DKD, FIGARO-DKD).
4. Antiplatelet	ASA for established ASCVD (secondary prevention). Shared decision in primary prevention (ASCEND 2018: small CV benefit, equal bleeding harm in DM without CVD).	Avoid routine primary-prevention ASA in DM > 70 (ASPREE 2018). Clopidogrel if true ASA allergy.
5. Weight management	5-7% weight loss for prediabetes prevention. 10-15% for diabetes remission potential. Bariatric surgery if BMI ≥ 35 + comorbidity.	GLP-1 RA (semaglutide) and tirzepatide are now disease-modifying for obesity-driven T2DM. DiRECT, 2018 showed remission possible with weight loss.

Complication Screening Schedule

Screening	When to start	Frequency	Action on abnormal
Dilated retinal exam	T2DM (Type 2): at diagnosis. T1DM (Type 1): within 5 years of diagnosis. Pregnancy: 1st trimester (or pre-conception).	q1-2 years if normal. Annually if any retinopathy. q3-6 months if proliferative or pregnant.	Refer ophthalmology. Anti-VEGF injections for DME or PDR. Tighter glycemic and BP control.
UACR + serum Cr/eGFR	T2DM: at diagnosis. T1DM: within 5 years of diagnosis. Pregnancy: pre-conception.	Annually. Confirm albuminuria with 2/3 abnormal samples within 6 months before labeling.	UACR ≥ 30: ACEi/ARB. UACR ≥ 100 with eGFR 30-90: add finerenone. Add SGLT2i.
Foot exam (visual + monofilament + vibration + pulses)	At diagnosis	Comprehensive annually. Visual + foot inspection at every visit.	Loss of protective sensation: refer podiatry, prescribe diabetic shoes (Medicare benefit), education on daily foot inspection.
Lipid panel	At diagnosis	Annually if at goal; q3-6 months if titrating.	Statin if criteria met. Recheck 4-12 weeks after dose change.
BP measurement	At diagnosis	Every clinic visit. Encourage home BP monitoring.	≥ 130/80: confirm with home/ABPM. Start or escalate antihypertensive.
Dental exam	At diagnosis	Every 6-12 months	Periodontal disease worsens glycemic control; treat.
Depression screening (PHQ-2 / PHQ-9)	At diagnosis	Annually (more if symptoms)	Higher prevalence in DM. Treat (CBT, SSRI). Worsens self-management.
B12 (if on metformin)	After 4-5 years on metformin	Periodically; sooner if neuropathy or anemia.	Replace if low. Consider switching off metformin if recurrent.

Hypoglycemia Management

Severity	Definition	Treatment
Level 1 (Alert)	BG < 70 mg/dL, patient self-treating	15-15 rule: 15 g fast-acting carbs (4 oz juice, 3-4 glucose tabs, 1 tbsp honey). Recheck in 15 minutes. Repeat if still < 70. Add complex carb + protein after corrected.
Level 2 (Clinically significant)	BG < 54 mg/dL	Same as Level 1, but evaluate regimen. Adjust meds within 24-48 h.
Level 3 (Severe)	Altered mental status / requires assistance, regardless of BG	Glucagon 1 mg IM/SC (or 3 mg intranasal, Baqsimi) at home. D50 25 g IV (1 amp) in clinic/ED. Position in recovery, call EMS. Follow with carbs once awake.

Hypoglycemia unawareness (autonomic failure)

Long-standing T1DM or insulin-treated T2DM lose adrenergic warning symptoms (tremor, sweating, palpitations).
Treatment: 2-3 weeks of strict avoidance of hypoglycemia (relax A1c target temporarily) restores adrenergic awareness.
CGM with predictive low alerts is the single biggest tool for these patients.
Counsel against driving with BG < 100 in a hypo-unaware patient.

Reverse the regimen, not just the episode. Recurrent hypoglycemia signals over-medication. Common culprits: sulfonylureas (especially glyburide -has long-acting renal metabolites; avoid in CKD), insulin doses out of proportion to current weight/A1c, missed meals, alcohol on a sulfonylurea / insulin, recent renal decline (drugs accumulate). Switch off SU to a DPP-4i, GLP-1 RA, or SGLT2i if hypoglycemia is recurrent.

Sick-Day Rules (counsel every patient on insulin)

Tell every insulin-treated patient: "Don't stop your insulin even if you can't eat." Stopping insulin during illness in T1DM is the #1 outpatient cause of DKA admissions.

Continue insulin (especially basal). Adjust bolus to carbs eaten -reduce by 25-50% if eating less, but don't stop.
Check BG q3-4 h while ill. Check ketones (urine or blood β-hydroxybutyrate) if BG > 250 in T1DM.
Hydration: sip clear fluids; alternate sugar-free and sugar-containing if BG dropping.
Hold metformin if vomiting, dehydrated, or hospitalized. Resume when eating and stable.
Hold SGLT2i if NPO, severe illness, surgery within 3 days, or any GI illness with poor PO intake (euglycemic DKA risk). Resume when eating normally.
When to call provider / go to ED: persistent vomiting, BG > 300 despite correction, ketones moderate-large, AMS, RR > 24, abdominal pain, can't keep fluids down for 4+ hours.

Vaccinations Specific to DM

Influenza -annually. Higher mortality in DM with flu.
Pneumococcal -PCV20 alone, OR PCV15 followed by PPSV23 ≥ 1 year later. ACIP 2022 algorithm.
Hepatitis B -3-dose series for adults age 19-59 with DM (and shared decision ≥ 60). Higher HBV exposure risk via fingerstick equipment in shared settings.
Tdap -once, then Td or Tdap booster q10 years.
Shingrix (zoster) -2 doses for adults ≥ 50.
RSV -single dose for adults ≥ 60 with DM (CDC 2024 expanded).
COVID-19 -keep current per CDC.

Referral / DSME (Diabetes Self-Management Education)

DSMES referral at 4 critical times: at diagnosis, annually, when complications develop, when transitions in care occur (insulin start, pump start, pregnancy, transplant).
Medical Nutrition Therapy (MNT) with a registered dietitian -Medicare covers.
Endocrinology referral: T1DM, complex T2DM, recurrent severe hypoglycemia, hypoglycemia unawareness, considering pump or advanced CGM, A1c not at goal despite triple therapy.
Bariatric surgery referral: BMI ≥ 35 with T2DM (or BMI ≥ 30 with poor glycemic control on multiple agents). Roux-en-Y and sleeve gastrectomy both produce diabetes remission rates of 60-80% at 1 year.
Mental health referral: depression, eating disorder, diabetes distress.

💊 Medications

Metformin (still first-line)

Drug	Starting → Target Dose	Key Notes
Metformin (Glucophage) 1ST LINE	500 mg PO daily/BID with meals → titrate q1-2 weeks to 1000 mg BID (max 2000-2550 mg/day)	A1c reduction ~1-1.5%. Weight neutral, very cheap, mortality benefit (UKPDS 34, 1998). GI side effects (diarrhea, nausea) -titrate slowly, take with food, ER form better tolerated. B12 deficiency after 4-5 years -check B12 periodically. Lactic acidosis rare; hold at eGFR < 30, dose-reduce 30-45 to 1000 mg/day max. Hold 48 h around iodinated contrast if eGFR < 60 or AKI.

SGLT2 Inhibitors (cardiorenal protective)

Drug	Dose	Key Notes
Dapagliflozin (Farxiga) HF + CKD	10 mg PO daily (no titration)	HFrEF/HFpEF benefit (DAPA-HF, DELIVER). CKD benefit (DAPA-CKD). Initiate down to eGFR 20; continue to dialysis. A1c ~0.5-0.7%.
Empagliflozin (Jardiance) HF + CKD + ASCVD	10 mg PO daily (T2DM); titrate to 25 mg if needed for glycemia. 10 mg only for HF/CKD indication.	EMPA-REG, 2015 first to show CV benefit. EMPEROR-Reduced/Preserved/EMPA-KIDNEY all positive. Initiate to eGFR 20.
Canagliflozin (Invokana)	100 mg PO daily → 300 mg if eGFR ≥ 60	CREDENCE, 2019 showed renal protection. Black-box warning for amputation (mostly toe) and bone fracture from CANVAS -less seen with newer agents but still on label.
Ertugliflozin (Steglatro) LESS USED	5 mg PO daily → 15 mg	VERTIS-CV was non-inferior but didn't show same CV/renal benefits as the others. Reserve if cost dictates.

SGLT2i class warnings: genitourinary mycotic infections (~5-8%, candidiasis -hygiene counseling), euglycemic DKA (especially T1DM, NPO, surgery, severe illness -hold 3 days pre-op, pause during acute illness), volume depletion (especially with diuretics -reduce loop dose ~25% when starting), Fournier's gangrene (very rare but mortality > 20%, urgent surgical), initial 0.2-0.3 Cr bump (hemodynamic, reverses, do NOT stop), UTI risk modestly increased. Avoid in T1DM unless under endocrinologist guidance.

GLP-1 Receptor Agonists (CV protective + weight loss)

Drug	Dose	Key Notes
Semaglutide SC (Ozempic) PREFERRED GLP-1	0.25 mg SC weekly × 4 wk → 0.5 → 1.0 → 2.0 mg weekly	SUSTAIN-6, 2016. Strongest A1c reduction in class (~1.5-2%). Weight loss 5-10 kg.
Semaglutide PO (Rybelsus)	3 mg daily × 30 d → 7 → 14 mg daily	Take fasting with ≤ 4 oz water, then wait 30 min. Same class CV benefit (PIONEER trials). Lower bioavailability than SC.
Semaglutide for obesity (Wegovy) OBESITY INDICATION	0.25 → 0.5 → 1.0 → 1.7 → 2.4 mg weekly	FDA-approved for obesity (BMI ≥ 30, or ≥ 27 with comorbidity). STEP 1, 2021: ~15% weight loss. SELECT, 2023: 20% MACE reduction in obesity without DM.
Liraglutide (Victoza / Saxenda)	0.6 mg SC daily × 1 wk → 1.2 → 1.8 mg daily (Victoza, T2DM); up to 3.0 mg (Saxenda, obesity)	LEADER, 2016. Daily injection. Largely replaced by once-weekly options.
Dulaglutide (Trulicity)	0.75 mg SC weekly → 1.5 → 3.0 → 4.5 mg	REWIND, 2019. Easier injection device than semaglutide.
Tirzepatide (Mounjaro / Zepbound) DUAL GIP/GLP-1	2.5 mg SC weekly × 4 wk → titrate by 2.5 mg q4 wk → max 15 mg	SURPASS, 2021: A1c ~2-2.5%, weight loss 12-15 kg. SURMOUNT-1, 2022: 20% weight loss in obesity. CV outcomes pending (SURPASS-CVOT).
Exenatide ER (Bydureon BCise) LESS USED	2 mg SC weekly	Older agent. Modest A1c. Largely replaced by semaglutide/dulaglutide.

GLP-1 RA / dual agonist warnings: GI side effects are rate-limiting (nausea, vomiting, diarrhea, constipation -slow titration helps; ~15-20% discontinue), pancreatitis (rare; hold for severe abdominal pain), gallbladder disease (~1-2% incidence with rapid weight loss), retinopathy progression with rapid A1c drop (counsel + retinal exam pre-initiation in patients with known retinopathy), thyroid C-cell tumor concern (animal data only -avoid with personal/family hx of MTC or MEN2), delayed gastric emptying (pre-anesthesia hold per ASA 2023: 1 week for weekly agents, 1 day for daily). Combine with caution if insulin or sulfonylurea -reduce those doses to avoid hypoglycemia.

DPP-4 Inhibitors (modest A1c, weight neutral)

Drug	Dose	Key Notes
Sitagliptin (Januvia)	100 mg PO daily (50 if eGFR 30-45; 25 if < 30)	Most-used DPP-4i. A1c ~0.5-0.7%. Weight neutral.
Linagliptin (Tradjenta) CKD-FRIENDLY	5 mg PO daily (no renal adjustment)	Hepatically cleared. Useful when eGFR fluctuates or CKD limits other choices.
Saxagliptin (Onglyza) HF SIGNAL	5 mg PO daily (2.5 if eGFR < 45)	SAVOR-TIMI 53, 2013 showed increased HF hospitalization. Avoid if HFrEF; switch to sitagliptin or linagliptin.
Alogliptin (Nesina)	25 mg PO daily (12.5 if eGFR 30-60; 6.25 if < 30)	Less commonly used; similar profile to sitagliptin.

DPP-4i warnings: pancreatitis (rare), severe joint pain (FDA warning 2015 -reversible on discontinuation), bullous pemphigoid (rare). Don't combine DPP-4i with GLP-1 RA (overlapping mechanism, no added benefit, more nausea).

Sulfonylureas (cheap, but hypoglycemia risk)

Drug	Dose	Key Notes
Glipizide (Glucotrol) PREFERRED SU	2.5-5 mg PO daily → max 20 mg/day (split BID if > 15)	Shorter half-life and no active renal metabolites -preferred SU in CKD or elderly. A1c ~1-1.5%. Cheap. Weight gain ~2 kg.
Glimepiride (Amaryl)	1-2 mg PO daily → max 8 mg	Once-daily, modest hypoglycemia risk. OK in mild CKD; cautious if eGFR < 30.
Glyburide (Diabeta) AVOID IN CKD / ELDERLY	2.5-5 mg PO daily → max 20 mg	Avoid: long half-life and active metabolites cleared renally → severe prolonged hypoglycemia in CKD or elderly. AGS Beers Criteria flags it explicitly.

SU pearls: rapid A1c drop (1-1.5%) but secondary failure within 5-10 years as β-cell function declines. Hypoglycemia is the limiting toxicity -especially in patients on insulin, with skipped meals, alcohol, or declining renal function. Hold or reduce dose if patient becomes NPO. Largely replaced by SGLT2i and GLP-1 RA in modern algorithms.

Insulin (when oral agents aren't enough or for T1DM)

Insulin	Onset / Peak / Duration	Role
Glargine U-100 (Lantus, Basaglar) BASAL	1-2 h / no peak / 20-24 h	Once-daily basal. Most commonly used. Less hypoglycemia than NPH.
Glargine U-300 (Toujeo)	6 h / no peak / 30-36 h	Flatter profile than U-100. Less nocturnal hypoglycemia.
Detemir (Levemir)	1-2 h / mild peak 6-8 h / 12-24 h	Often needs BID dosing. Less popular than glargine.
Degludec (Tresiba)	1-2 h / no peak / > 42 h	Ultra-long. Lowest hypoglycemia rate. Flexible dosing time. DEVOTE, 2017.
NPH (Humulin N, Novolin N) CHEAP	1-2 h / 4-10 h / 12-18 h	OTC, cheap. More hypoglycemia (peak), variable absorption. Budget option only.
Rapid-acting (bolus / mealtime)
Lispro (Humalog), Aspart (Novolog), Glulisine (Apidra)	10-15 min / 1 h / 3-5 h	Take 15 min before meal. Standard mealtime insulins. Lispro U-200 / Aspart fast-acting (Fiasp) are concentrated/faster variants.
Inhaled insulin (Afrezza)	~5 min / 30 min / 1.5-3 h	Niche use. Required PFTs (avoid in COPD/asthma). Bronchospasm risk.
Pre-mixed (rarely used in modern practice)
70/30, 75/25, 50/50	Combined	Two daily injections. Less flexible than basal-bolus. Used for adherence-limited patients.

Insulin initiation in T2DM (when to start)

A1c ≥ 10% with symptoms at diagnosis -consider insulin initially (often with metformin).
BG ≥ 300 with ketones or DKA features -start insulin urgently.
A1c not at goal on triple therapy (metformin + SGLT2i/GLP-1 + third agent).
Pregnancy -insulin is the agent of choice.
Hospitalized / acute illness -insulin (basal-bolus or sliding scale).

Starting basal insulin (the simplest first step)

Start 10 units bedtime OR 0.1-0.2 units/kg daily (glargine, degludec, or detemir).
Titrate by 2 units q3 days until fasting BG < 130 (or per regimen).
Continue metformin and other oral agents (especially SGLT2i and GLP-1 RA -synergistic with insulin).
Hypoglycemia < 70 once → reduce by 10-20%. Severe hypoglycemia → reduce by 20-30% and reassess.

Adding bolus insulin (basal-bolus regimen)

Start when basal alone insufficient and PP glucose elevated.
Total daily dose (TDD): 0.4-0.6 units/kg in T2DM (less in T1DM, more in steroid-induced DM).
50/50 rule: half TDD as basal (once-daily long-acting), half divided across 3 meals as bolus.
Carb counting: insulin-to-carb ratio (ICR) starts at 1 unit per 10-15 g carbs; correction factor (CF / ISF) starts at 1 unit per 50 mg/dL above target.
Refer to endocrinology / CDE for pump or hybrid closed-loop systems if multiple injections aren't controlling.

Less Common / Niche Agents

Drug	Dose	When Used
Pioglitazone (Actos)	15-45 mg PO daily	A1c ~1-1.5%. Useful in NAFLD/MASH and insulin resistance. Avoid: HFrEF (fluid retention), bladder cancer history (PROactive signal), high fracture risk (postmenopausal women). Causes weight gain ~3-5 kg.
Acarbose (Precose) / Miglitol (Glyset) RARELY USED	25-100 mg PO TID with first bite of meal	α-glucosidase inhibitors -delay carb absorption. Modest A1c (~0.5%). Severe flatulence/diarrhea limits use. Cheap but rarely tolerated.
Bromocriptine quick-release (Cycloset) RARELY USED	0.8-4.8 mg PO each morning	Dopamine agonist, modest A1c (~0.3-0.5%). Takes advantage of morning dopaminergic signaling. Largely abandoned.
Colesevelam (Welchol) RARELY USED	3.75 g (6 tabs) PO daily	Bile acid sequestrant. Modest A1c (~0.5%). Bonus LDL reduction. Constipation. Can interfere with absorption of other drugs (separate by 4 h).
Pramlintide (Symlin) NICHE	15-60 mcg SC pre-meals (T1) / 60-120 mcg (T2)	Amylin analog, used as adjunct to insulin to control PP glucose and weight. Severe hypoglycemia if not paired with reduced bolus insulin.
Finerenone (Kerendia) CKD ADJUNCT	10 mg PO daily (eGFR 25-60); 20 mg if K⁺ stable	Non-steroidal MRA. Not a glycemic agent but reduces CV + renal events in DM with CKD on top of ACEi/ARB + SGLT2i. FIDELIO-DKD, 2020 + FIGARO-DKD, 2021. Watch K⁺ and eGFR.

Drugs to AVOID or use with caution in DM

Glucocorticoids -drive hyperglycemia (especially PP). Adjust insulin and BBG monitoring during courses.
Atypical antipsychotics (olanzapine, clozapine, quetiapine) -metabolic syndrome, weight gain, can precipitate DM. Use aripiprazole or lurasidone if equivalent.
Calcineurin inhibitors (tacrolimus > cyclosporine) -post-transplant DM common.
Thiazides at high dose -worsen glycemic control (modestly). Low dose (12.5-25 mg HCTZ or chlorthalidone) is fine.
Statins -small absolute increase in DM diagnosis (~9% relative; ~1 case per 1000 patient-years), but CV benefit far outweighs. Continue.
β-blockers -mask hypoglycemia symptoms (especially atenolol). Use with caution in insulin-treated patients with hypoglycemia unawareness.
Niacin at high doses -worsens glycemia, often discontinued in DM.
Saxagliptin (DPP-4i) -avoid in HFrEF (SAVOR-TIMI 53 HF signal).
Glyburide -avoid in CKD and elderly (renal active metabolites, prolonged hypoglycemia).

⚡ Summary

Summary

Drug Selection

ASCVD → GLP-1 RA first [SUSTAIN-6, 2016, LEADER, 2016]. CKD → SGLT2i [CREDENCE, 2019, DAPA-CKD, 2020]. HF → SGLT2i [DAPA-HF, 2019]. Obesity → GLP-1 RA. Continue metformin in most.

A1c Targets

< 7% for most DCCT, 1993. < 6.5% for newly diagnosed, young, no complications. < 8% for elderly, limited life expectancy, hypoglycemia risk, long-standing disease ACCORD, 2008.

Screening

Eye exam annually. Foot exam annually (monofilament). UACR annually if ≥ 5 years T1DM or at diagnosis T2DM. Lipid panel. BP every visit.

SGLT2i Caveats

Monitor for euglycemic DKA (especially in T1DM, surgery, fasting). Mycotic genital infections. AKI risk with dehydration. Avoid if eGFR < 20.

GLP-1 RA Caveats

GI side effects (titrate slowly). Pancreatitis risk (debated). Thyroid C-cell tumors (rodent data). Contraindicated in MEN2 or medullary thyroid cancer.

Legacy Effect

Early intensive control has lasting benefits decades later UKPDS 34, 1998 DCCT/EDIC, 1993. Treat early and aggressively. Relax targets as disease advances.