Eduovisual
Gastrointestinal
Nonalcoholic fatty liver disease: workup and management
— Requires hepatic steatosis (≥5% on imaging/biopsy) plus ≥1 cardiometabolic risk factor: BMI ≥25 (≥23 Asian), waist circumference elevated, prediabetes/T2DM, hypertension, hypertriglyceridemia, or low HDL.
— MASH (metabolic dysfunction–associated steatohepatitis) replaces NASH; MetALD describes overlap with moderate alcohol use (women 140–350 g/wk, men 210–420 g/wk).
— Incidental hyperechoic liver on RUQ ultrasound ordered for biliary pain.
— Mildly elevated AST/ALT (typically <5× ULN, ALT > AST) found on routine labs or pre-op screening.
— Metabolic syndrome patient with fatigue, RUQ fullness, or hepatomegaly.
— Incidentally low-density liver on CT done for another reason.
Board pearl: A 52-year-old with BMI 32, A1c 6.4%, ALT 68, AST 42, negative viral and autoimmune workup, and bright liver on US has MASLD — your next move is FIB-4 calculation, not biopsy. Step 3 expects you to know noninvasive fibrosis staging precedes any invasive testing, and that lifestyle plus cardiometabolic optimization is the first prescription written.
— Vague RUQ discomfort or fullness from hepatic capsular stretch.
— Fatigue — common but nonspecific; correlates poorly with histology.
— Pruritus, jaundice, ascites, encephalopathy, variceal bleed → suggest already-cirrhotic MASLD (often previously labeled "cryptogenic cirrhosis").
— Alcohol quantification: Use AUDIT-C; threshold for MASLD is <140 g/wk women, <210 g/wk men (roughly <1 drink/day women, <2 men). Above that → MetALD or ALD.
— Metabolic comorbidities: Diabetes duration, A1c trend, hypertension, dyslipidemia, OSA, PCOS, hypothyroidism, hypopituitarism.
— Medications causing steatosis: Amiodarone, methotrexate, tamoxifen, valproate, corticosteroids, antiretrovirals (older NRTIs), chemotherapy.
— Family history: Cirrhosis, HCC, early CAD, T2DM.
— Risk factors for competing liver disease: IVDU/tattoos/transfusions (HCV), travel/raw shellfish (HEV), autoimmune disease, iron overload family history, COPD/emphysema (A1AT).
— Rapid weight loss, TPN, bariatric history — can drive steatohepatitis.
Step 3 management: When a stem gives ALT 90 in a patient with BMI 34 and A1c 6.8%, do not jump to "fatty liver, reassure." The expected ambulatory sequence is: quantify alcohol, review meds, order viral hepatitis serologies + iron studies + autoimmune panel, calculate FIB-4, and book a 3–6 month follow-up to reassess after lifestyle intervention. Documenting alcohol use precisely is essential because it changes the diagnostic label and counseling plan.
— Central obesity with elevated waist circumference (>102 cm men, >88 cm women; lower thresholds in Asian populations) — the single most useful exam finding.
— Acanthosis nigricans at the nape/axillae → insulin resistance marker, especially in younger patients and children.
— Skin tags, xanthelasma, eruptive xanthomas (severe hypertriglyceridemia).
— Blood pressure — diagnose/confirm hypertension; ≥130/80 in diabetics warrants treatment.
— BMI and waist-to-hip ratio documented at every visit.
— Screen for OSA: STOP-BANG, neck circumference >17" (men)/16" (women), witnessed apneas.
— Hepatomegaly — palpable smooth, nontender liver edge; present in up to 50% but often missed in obese patients.
— Splenomegaly, caput medusae, ascites, spider angiomata, palmar erythema, gynecomastia, asterixis → cirrhosis until proven otherwise; pivot workup toward portal hypertension and HCC surveillance.
— Murphy sign, scleral icterus — point away from uncomplicated MASLD; consider biliary disease or alternative dx.
— Carotid bruits, diminished pedal pulses, retinopathy on funduscopy → cumulative atherosclerotic burden. Because CV death > liver death in MASLD, the exam doubles as cardiovascular risk assessment.
— Buffalo hump, striae, moon facies → Cushing-associated steatosis.
— Goiter, bradycardia, delayed reflexes → hypothyroidism (independent MASLD risk).
Key distinction: A patient with MASLD and isolated hepatomegaly with soft edge ≠ a patient with firm nodular liver, splenomegaly, and spider angiomata. The latter triggers immediate fibrosis staging, EGD for varices when indicated, and HCC surveillance with q6-month US ± AFP. Step 3 will reward you for recognizing the cirrhotic phenotype on exam and reorganizing the management plan around portal hypertension and surveillance rather than around lifestyle counseling alone.
— ALT, AST, ALP, GGT, total/direct bilirubin, albumin, INR, platelets, CBC. ALT typically > AST; AST/ALT >1 suggests advanced fibrosis or alcohol contribution.
— Lipid panel, fasting glucose, A1c, TSH.
— Hepatitis B surface antigen, surface antibody, core antibody; Hepatitis C antibody with reflex RNA.
— Iron studies (ferritin, transferrin saturation) — ferritin often mildly elevated in MASLD; TSAT >45% prompts HFE genotyping for hemochromatosis.
— ANA, ASMA, anti-LKM1, total IgG, IgG4 — autoimmune hepatitis screen.
— Ceruloplasmin in patients <40 (Wilson disease).
— Alpha-1 antitrypsin level and phenotype if family history or emphysema.
— Anti-tissue transglutaminase IgA — celiac can cause elevated ALT.
— Right upper quadrant ultrasound — detects steatosis when ≥20–30% hepatic fat; sensitivity drops in BMI >40.
— Findings: increased echogenicity, posterior beam attenuation, blurred vascular margins.
— CT/MRI if already done: liver attenuation <40 HU on noncontrast CT, or liver-to-spleen ratio <0.9, suggests steatosis.
— MRI proton density fat fraction (MRI-PDFF) — gold-standard noninvasive quantification, mainly for trials and ambiguous cases.
— Controlled attenuation parameter (CAP) with FibroScan — bedside steatosis quantification.
— <1.3 (or <2.0 if ≥65): low risk for advanced fibrosis — manage in primary care.
— 1.3–2.67: indeterminate — proceed to vibration-controlled transient elastography (FibroScan) or ELF test.
— >2.67: high risk — refer to hepatology.
Board pearl: Step 3 favors FIB-4 as the first-line risk stratifier because it uses labs you already have. Ordering liver biopsy as the next step after a bright liver on ultrasound is a distractor answer. The correct sequence is rule out competing disease → calculate FIB-4 → elastography if indeterminate → biopsy only when noninvasive testing is conflicting or competing diagnosis is suspected.
— Outpatient, 5-minute test measuring liver stiffness in kPa.
— Stratification: <8 kPa low fibrosis risk; 8–12 kPa indeterminate; >12 kPa suggests advanced fibrosis (F3–F4); >20 kPa suggests clinically significant portal hypertension.
— Limitations: unreliable with ascites, BMI >35 without XL probe, recent meal, acute hepatitis (false elevations).
— Most accurate noninvasive fibrosis test; threshold ≥3.63 kPa for advanced fibrosis. Used when VCTE is unreliable or discordant.
— Serum panel (HA, PIIINP, TIMP-1). ≥9.8 indicates advanced fibrosis; FDA-cleared as a prognostic test in MASH.
— Competing or coexisting disease suspected (e.g., autoimmune hepatitis, hemochromatosis with MASLD).
— Discordant noninvasive results in a patient where staging changes management.
— Pre-treatment for emerging MASH therapies in trials or per resmetirom labeling considerations.
— NAS score ≥4 with stage 2 fibrosis = MASH at risk of progression.
— All MASLD patients with cirrhosis (F4) → abdominal US ± AFP every 6 months.
— Non-cirrhotic MASLD with advanced fibrosis: surveillance individualized; not routinely recommended yet.
— Cirrhotic MASLD with platelets <150k or LSM >20 kPa → EGD for varices (Baveno VII criteria allow deferral if platelets >150k and LSM <20 kPa).
— OGTT or A1c to confirm dysglycemia; ASCVD 10-year risk calculator; consider coronary artery calcium scoring in borderline-risk patients to refine statin decisions.
CCS pearl: In a CCS case with MASLD and platelets 110k, FibroScan 18 kPa, advance the clock 1 week to schedule EGD, order abdominal US with AFP, start a non-selective beta-blocker (carvedilol preferred) if varices or LSM ≥25 kPa, and counsel hepatitis A and B vaccination, pneumococcal, and influenza — these "cirrhosis bundle" orders score consistently.
— Low risk: FIB-4 <1.3 and/or LSM <8 kPa → primary care management, reassess FIB-4 every 2–3 years (annually if diabetes).
— Indeterminate: FIB-4 1.3–2.67 → secondary test (ELF or VCTE); if still indeterminate, refer.
— High risk: FIB-4 >2.67, LSM ≥12 kPa, ELF ≥9.8 → hepatology referral, consider MASH-directed pharmacotherapy, HCC/variceal screening if cirrhotic.
— Weight loss targets: ≥3–5% reduces steatosis; ≥7–10% improves necroinflammation and can regress fibrosis. Document specific goal in chart.
— Mediterranean diet preferred; reduce fructose, sugar-sweetened beverages, ultra-processed foods.
— Physical activity: ≥150 min/week moderate-intensity aerobic + 2 days resistance training.
— Alcohol: Recommend complete abstinence if F2+ fibrosis; minimize otherwise. No safe threshold in advanced fibrosis.
— Coffee: ≥2–3 cups/day associated with reduced fibrosis progression — reasonable to encourage.
— Statin therapy is safe and indicated in MASLD/MASH, including compensated cirrhosis — do not withhold for mildly elevated transaminases. Hold only if ALT >3× ULN with rising trend.
— BP target <130/80; ACEi/ARB preferred in diabetics or proteinuria.
— A1c <7% typical; individualize.
Step 3 management: The single highest-yield outpatient action when MASLD is diagnosed is not ordering more tests — it is calculating ASCVD risk and starting/continuing a statin, because cardiovascular disease is the leading killer in this population. Step 3 stems frequently test whether you will inappropriately stop or withhold statin therapy in MASLD — the answer is continue.
— Thyroid hormone receptor-β agonist; reduces hepatic fat and improves fibrosis on biopsy.
— Indication: Adults with noncirrhotic MASH and moderate-to-advanced fibrosis (F2–F3) confirmed by biopsy or noninvasive surrogates (LSM, MRE, ELF).
— Dosing: 80 mg PO daily (BMI <100 kg) or 100 mg daily (BMI ≥100 kg).
— Monitor: baseline and follow-up LFTs; avoid in decompensated cirrhosis. Drug interactions: strong CYP2C8 inhibitors (gemfibrozil), statins (rosuvastatin/simvastatin dose limits).
— Strong evidence for steatosis resolution and MASH improvement, especially in patients with T2DM or obesity.
— Preferred glucose-lowering agents in MASLD + T2DM along with pioglitazone.
— Bonus: weight loss, CV risk reduction, renal protection.
— Improves MASH histology in biopsy-proven MASH ± T2DM.
— Side effects: weight gain, fluid retention (avoid in HF), bone loss in women, bladder cancer signal (caution prior history).
— Option for biopsy-proven MASH in non-diabetic, non-cirrhotic adults.
— Counsel about possible increased prostate cancer risk and hemorrhagic stroke signal at higher doses.
Board pearl: A non-diabetic MASH patient with F2 fibrosis on biopsy — the Step 3 answer is resmetirom if available, or vitamin E 800 IU/day as the classic second choice. In a diabetic with MASH, the preferred answer is semaglutide or pioglitazone, not vitamin E.
— Strongest durable intervention for MASH with obesity; Roux-en-Y gastric bypass and sleeve gastrectomy produce MASH resolution and fibrosis regression in majority of patients at 5 years.
— Indications (expanded ASMBS 2022): BMI ≥35 regardless of comorbidity; BMI ≥30 with metabolic disease (T2DM, MASH).
— Caution: Avoid in decompensated cirrhosis; consider in compensated Child A at experienced centers, sometimes combined with transplant evaluation. Rapid weight loss can transiently worsen steatohepatitis — staged approach preferred.
— MASH is now a leading transplant indication in the US, projected to overtake alcohol and HCV.
— Indications: Decompensated cirrhosis (MELD-Na ≥15), HCC within Milan criteria, refractory complications.
— Pre-transplant evaluation in MASH: intensive cardiac workup (stress testing, often coronary angiography) because of high CAD prevalence; OSA screening; nutritional and renal assessment.
— Post-transplant: Recurrent MASLD/MASH common (~30–50% at 5 years); manage weight, glucose, lipids aggressively; tailor immunosuppression (lower-dose steroids, consider mTOR inhibitors).
— EGD with variceal banding for medium/large varices or red wale signs.
— TIPS for refractory ascites or recurrent variceal bleeding; contraindicated in significant encephalopathy or severe heart failure.
— Paracentesis with albumin replacement (6–8 g/L removed if >5 L) for tense ascites.
— HCC management: Resection, ablation, TACE, Y-90, transplant per BCLC staging.
CCS pearl: For a CCS patient with MASH cirrhosis and BMI 42 being considered for transplant, your pre-listing orders should include echocardiogram, dobutamine stress or cardiac cath, carotid duplex if symptomatic, HCC surveillance imaging, MELD-Na labs, hepatology and transplant surgery consults, social work, and nutrition — bundling these scores well in management cases.
— FIB-4 threshold rises to <2.0 for low risk to avoid overestimating fibrosis from age-driven AST elevation.
— Higher prevalence of advanced fibrosis; lower threshold to obtain VCTE.
— Weight loss goals are more conservative — emphasize muscle preservation with resistance training and adequate protein (1.2–1.5 g/kg/day if cirrhotic) to prevent sarcopenia, which worsens outcomes.
— Polypharmacy review: amiodarone, methotrexate, glucocorticoids common offenders.
— Statins remain indicated; avoid stopping for age alone.
— Pioglitazone — caution due to fracture and HF risk; vitamin E safety less established >70.
— MASLD and CKD share metabolic drivers; coexistence common.
— Preferred glucose agents: SGLT2 inhibitors (until eGFR <20) and GLP-1 RAs — both renoprotective and hepatic-fat-reducing.
— Avoid metformin if eGFR <30; reduce dose at eGFR 30–45.
— Contrast imaging: weigh against eGFR; MRI without contrast or non-contrast US for HCC surveillance if eGFR <30 to avoid gadolinium-based agents (use newer macrocyclic if needed).
— Resmetirom contraindicated in decompensated cirrhosis (Child B/C).
— Pioglitazone: avoid in Child B/C and decompensation.
— Metformin: can be continued in compensated cirrhosis (associated with reduced HCC risk); hold in decompensation, sepsis, AKI.
— Statins: safe in compensated cirrhosis; reduce dose or hold in Child C.
— NSAIDs avoided — precipitate AKI, variceal bleed, ascites.
— Acetaminophen ≤2 g/day is preferred analgesic.
— Vaccinate (HAV, HBV, pneumococcal, influenza, COVID, zoster).
— Nutrition: Late-evening snack, branched-chain amino acids if encephalopathy-prone, salt restriction <2 g/day in ascites.
Key distinction: Compensated cirrhosis is not a reason to withhold statins, metformin, or aspirin when otherwise indicated — Step 3 frequently penalizes the reflex to "hold everything because the liver is sick." Decompensation changes the calculus, not compensated disease.
— Most common chronic liver disease in US children, paralleling obesity epidemic.
— Screen with ALT in children with obesity (BMI ≥95th %ile) starting at age 9–11, or earlier if risk factors (T2DM, dyslipidemia, OSA, family history).
— ALT >2× upper limit of normal for age-sex (boys >25.8, girls >22.1 U/L by NASPGHAN) warrants workup.
— Always exclude Wilson disease, autoimmune hepatitis, alpha-1 antitrypsin deficiency, celiac, hepatitis B/C, hypothyroidism, drug effect, muscular dystrophy (elevated AST from muscle).
— Treatment: intensive lifestyle modification with family-based behavioral therapy is first line. Vitamin E 800 IU/day has pediatric data (TONIC trial). Pharmacotherapy otherwise limited; bariatric surgery considered for adolescents with severe obesity and comorbidities at specialized centers.
— MASLD does not preclude pregnancy but increases risk of gestational diabetes, preeclampsia, preterm birth.
— Pre-conception counseling: Optimize weight, glycemia, lipids; discontinue statins, ACEi/ARB, SGLT2i, GLP-1 RA, pioglitazone, resmetirom.
— Safe options: lifestyle, metformin (acceptable in pregnancy for GDM), insulin.
— Cirrhotic MASLD pregnancy: High-risk MFM co-management; screen for varices in 2nd trimester (band if needed); avoid NSAIDs; vaginal delivery preferred unless varices contraindicate.
— Distinguish from pregnancy-specific liver diseases: HELLP, acute fatty liver of pregnancy, intrahepatic cholestasis of pregnancy — different acuity and timing.
Board pearl: A 14-year-old boy with BMI 35, A1c 5.9%, ALT 95, AST 50, negative viral and autoimmune workup, normal ceruloplasmin — the Step 3 answer is structured lifestyle intervention with family involvement as first step; vitamin E is the most studied pharmacotherapy in pediatric MASH. Do not order biopsy as the first move.
— MASH → bridging fibrosis (F3) → cirrhosis (F4) in ~20% of MASH patients over 10–15 years; diabetes accelerates progression.
— Hepatocellular carcinoma: Can occur in non-cirrhotic MASLD (uniquely high among chronic liver diseases), though absolute risk is low — surveillance still focused on cirrhotic patients.
— Decompensation events: ascites, variceal bleeding, hepatic encephalopathy, hepatorenal syndrome, spontaneous bacterial peritonitis.
— Acute-on-chronic liver failure can be precipitated by infection, alcohol binge, drug-induced injury, GI bleed.
— Leading cause of death. MASLD is an independent risk factor for MI, stroke, atrial fibrillation, heart failure (especially HFpEF), and CKD progression.
— Aggressive ASCVD risk treatment is required.
— Higher risk of incident T2DM, dyslipidemia, OSA, PCOS.
— Sarcopenic obesity in advanced disease worsens prognosis.
— Increased risk of colorectal, breast, endometrial, and pancreatic cancers — ensure age-appropriate cancer screening.
Step 3 management: When a MASLD patient presents with new ascites or encephalopathy, your management pivots: diagnostic paracentesis with SAAG and cell count to rule out SBP, start empiric ceftriaxone if PMN ≥250/mm³ with albumin 1.5 g/kg day 1 and 1 g/kg day 3, initiate lactulose titrated to 2–3 soft stools/day for encephalopathy, and consider rifaximin for recurrence prevention. These bundles appear repeatedly in CCS cases.
— FIB-4 >2.67, LSM ≥12 kPa, ELF ≥9.8.
— Biopsy-confirmed MASH with F2+ fibrosis being considered for MASH-directed pharmacotherapy.
— Diagnostic uncertainty (overlapping autoimmune features, abnormal iron studies, unexpected progression).
— Any sign of cirrhosis, portal hypertension, or HCC.
— Endocrinology: uncontrolled T2DM, complex obesity care, suspected Cushing or hypopituitarism.
— Bariatric/metabolic surgery: BMI thresholds met, motivated patient.
— Cardiology: Pre-transplant evaluation, established CAD, HFpEF management.
— Nutrition/dietitian: Mandatory member of MASLD care team.
— Behavioral health: weight management, alcohol counseling, depression.
— Variceal hemorrhage, refractory ascites, SBP, severe encephalopathy (grade 3–4), hepatorenal syndrome, acute kidney injury, jaundice with INR rise.
— New decompensation in previously compensated cirrhosis.
— Acute-on-chronic liver failure — admit, calculate CLIF-SOFA, evaluate for transplant.
— Hemodynamic instability from GI bleed, grade 3–4 encephalopathy needing airway protection, severe sepsis/septic shock, type 1 HRS, multiorgan failure.
— Variceal bleed bundle: IV access ×2, type and cross, octreotide 50 mcg bolus then 50 mcg/h × 3–5 days, ceftriaxone 1 g IV daily × 7 days (reduces rebleeding and mortality), urgent EGD within 12 h, blood transfusion goal Hb 7–8.
— HRS-AKI: Albumin 1 g/kg/day + terlipressin (preferred in US since 2022) or norepinephrine if ICU.
CCS pearl: In a cirrhotic MASH patient admitted with GI bleed, the order set that earns full points is NPO, two large-bore IVs, type & cross, IV PPI, octreotide drip, ceftriaxone, urgent GI consult for EGD, transfuse to Hb 7, and admit to ICU. Forgetting prophylactic antibiotics is the most commonly missed point.
— Same histology as MASH; differentiated by alcohol intake above thresholds (women >140 g/wk, men >210 g/wk).
— Clues: AST/ALT ratio >2, GGT elevation, macrocytosis, elevated CDT, PEth biomarker, social history.
— MetALD: intermediate alcohol use with metabolic risk factors — emerging category.
— Chronic HBV — HBsAg+, HBV DNA detectable; can coexist with MASLD and accelerate fibrosis.
— Chronic HCV — HCV antibody+ with detectable RNA; specifically associated with steatosis (genotype 3).
— Acute HAV/HEV — much higher transaminases (>1000) usually.
— Amiodarone, methotrexate, tamoxifen, valproate, corticosteroids, antiretrovirals, total parenteral nutrition.
— Pattern recognition + temporal relationship key.
— Rapid weight loss, starvation, refeeding.
— Lipodystrophy syndromes (congenital or HIV-associated).
— Endocrine: hypothyroidism, hypopituitarism, Cushing syndrome, PCOS, hypogonadism.
— Celiac disease — can present with isolated transaminitis.
— Wilson disease, alpha-1 antitrypsin deficiency, glycogen storage diseases, Wolman/CESD (LAL deficiency), abetalipoproteinemia.
Key distinction: AST/ALT ratio is the single highest-yield discriminator. ALT > AST (ratio <1) suggests MASLD or viral hepatitis; AST > ALT (>2) suggests alcohol-associated liver disease; AST > ALT with low platelets suggests advanced fibrosis/cirrhosis of any etiology. Step 3 stems exploit this exact pattern.
— Primary biliary cholangitis (PBC): Middle-aged woman, fatigue, pruritus, ALP↑, AMA+, IgM↑. Treat with ursodeoxycholic acid 13–15 mg/kg/day; obeticholic acid second-line (caution with cirrhosis).
— Primary sclerosing cholangitis (PSC): Often with IBD (UC), ALP↑, MRCP shows beaded ducts, p-ANCA+. Higher cholangiocarcinoma risk.
— Choledocholithiasis: RUQ pain, bilirubin↑, dilated CBD on US — distinct from chronic hepatocellular pattern.
— Often young women, ANA/ASMA/anti-LKM1+, elevated IgG, interface hepatitis on biopsy.
— Treat with prednisone ± azathioprine; can overlap with MASLD.
— TSAT >45%, ferritin↑, HFE C282Y homozygosity; phlebotomy is treatment.
— Increased HCC risk; often coexists with MASLD.
— Age <40, neuropsychiatric symptoms, Kayser-Fleischer rings, low ceruloplasmin, high 24-h urine copper.
— Liver disease with COPD/emphysema; PiZZ phenotype.
— Right HF, constrictive pericarditis, severe TR → "nutmeg liver." AST/ALT modest, ALP modest, bilirubin variable.
— Distinguish via JVP, peripheral edema, echo.
— Acute or subacute hepatomegaly, ascites; thrombophilia workup; Doppler US.
— Amyloidosis, sarcoidosis, lymphoma — ALP-predominant, often with extrahepatic findings.
Board pearl: When an MASLD-appearing patient has ALP-predominant elevation and pruritus, pivot toward PBC and check AMA. When the patient is a young man with IBD, check MRCP for PSC. Step 3 loves these "looks like fatty liver but isn't" pivots.
— Statin therapy per ASCVD risk; do not withhold for transaminase elevation <3× ULN.
— BP goal <130/80; ACEi/ARB preferred in diabetes or albuminuria.
— A1c individualized, typically <7%; prefer GLP-1 RA, SGLT2i, pioglitazone in T2DM + MASLD.
— Aspirin for established ASCVD; primary prevention selectively (ages 40–59 with elevated risk, low bleed risk).
— Smoking cessation — independent fibrosis driver.
— Lifestyle reinforcement every visit; document weight, BP, A1c, lipids.
— Resmetirom continuation with periodic LFT monitoring in F2–F3 MASH.
— Reassess fibrosis with FIB-4 every 1–2 years (annually in diabetes) and VCTE every 2–3 years in indeterminate/high risk.
— Alcohol minimization — abstinence in F2+.
— HCC surveillance: RUQ ultrasound ± AFP every 6 months.
— EGD surveillance per Baveno VII (q1–3 years depending on prior findings).
— Vaccinations: HAV, HBV, pneumococcal (PCV20 or PCV15→PPSV23), annual flu, COVID, zoster ≥50, RSV per age.
— Bone health: DEXA every 2 years.
— Nutrition counseling: adequate protein, salt restriction if ascites, late-evening snack.
Step 3 management: The discharge medication list for a newly diagnosed MASH patient with cirrhosis typically includes a statin, an antihypertensive (often ACEi), a GLP-1 RA or SGLT2i for T2DM, a non-selective beta-blocker if varices/LSM ≥25 kPa, lactulose ± rifaximin if encephalopathy history, and a multivitamin/vitamin D. Documenting alcohol abstinence counseling and vaccination status is expected on exam.
— Low-risk MASLD (FIB-4 <1.3, no diabetes): Every 12 months for weight, BP, A1c, lipids; recheck FIB-4 every 2–3 years.
— Diabetic MASLD: Every 3–6 months — A1c, lipids, BP, weight, FIB-4 annually.
— Indeterminate/high-risk MASLD: Every 3–6 months with hepatology co-management.
— Compensated cirrhosis: Every 6 months — HCC surveillance US/AFP, labs (CBC, CMP, INR, AFP), MELD-Na calculation.
— Decompensated: Every 1–3 months; transplant team co-management.
— Resmetirom: LFTs at baseline, 3 and 6 months, then periodically; assess T3/T4 if clinical signs.
— Pioglitazone: weight, edema, HF symptoms, A1c, fracture risk; LFTs.
— Vitamin E: annual review; no specific labs but counsel on risk-benefit.
— GLP-1 RA: A1c, weight, GI tolerance, lipase if symptomatic; thyroid history.
— Statin: LFTs only if symptomatic; baseline then as clinically indicated.
— Specific weight loss goal in pounds/kg; written prescription.
— Mediterranean-style diet with cut-back on sugar-sweetened beverages and ultra-processed food.
— Exercise prescription: 150 min/week moderate aerobic + 2 days resistance.
— Alcohol counseling at every visit; use motivational interviewing; offer SBIRT and referral.
— Sleep apnea screening (STOP-BANG); refer for polysomnography if positive.
— Behavioral support: registered dietitian, structured weight loss program, group support.
— Documenting FIB-4 calculation in EHR is increasingly a quality metric.
— Population health screening for at-risk T2DM patients with annual FIB-4 calculation is recommended.
Board pearl: Coffee 2–3 cups/day is associated with reduced fibrosis progression in MASLD — a frequent "which lifestyle item to recommend" distractor item that is actually the right answer.
— Patients commonly underreport alcohol use, fearing transplant ineligibility or judgment. Build rapport, use validated screening (AUDIT-C), and biomarkers (PEth, CDT) when stakes are high (transplant evaluation).
— Document quantitatively; the diagnostic label (MASLD vs MetALD vs ALD) shapes prognosis and therapy.
— Listing requires multidisciplinary assessment; obesity alone is not an absolute contraindication but very high BMI may require pre-transplant weight loss.
— Equity considerations: MASLD disproportionately affects Hispanic/Latino patients and certain Asian populations; ensure equitable access to advanced therapies and surveillance.
— Discuss risks: bleeding (~1%), pneumothorax, infection, mortality (~1/10,000).
— Confirm coagulopathy (INR <1.5, platelets >50k typical) and hold antithrombotics per protocol.
— Verify statin continuation at hospital discharge — frequently dropped erroneously when LFTs are mildly elevated.
— Reconcile diabetes medications: hold metformin if AKI, sepsis, contrast; resume at discharge.
— At discharge from a variceal bleed admission, ensure non-selective beta-blocker, antibiotic course completion, scheduled EGD follow-up within 2–4 weeks, and outpatient hepatology appointment — gaps here cause readmissions.
— MASLD/MASH is not reportable; HIV/HBV/HCV co-infections have specific public health reporting rules.
— Driving safety: hepatic encephalopathy can impair driving — counsel and document; jurisdiction-specific reporting requirements may apply.
— Resmetirom is expensive; engage prior authorization early and discuss access in shared decision-making.
Step 3 management: A patient discharged after variceal bleed without prophylactic ceftriaxone, beta-blocker, or follow-up EGD is the most common transition-of-care safety failure tested — your job is to close every loop in the discharge summary.
Board pearl: If the stem mentions bright liver, BMI 32, A1c 6.5%, ALT 70, AST 45, normal viral/autoimmune workup, your single best next step is almost always calculate FIB-4 and initiate lifestyle + statin, not biopsy or MRI.
— RUQ ultrasound for biliary symptoms shows bright echogenic liver in an obese, diabetic patient with mild ALT elevation. Best next step: Rule out competing disease (viral, autoimmune, iron, ceruloplasmin if young) + calculate FIB-4. Not biopsy.
— Patient with MASLD and FIB-4 of 2.1. Best next step: Vibration-controlled transient elastography (or ELF). Not immediate referral, not biopsy.
— Biopsy-proven MASH with F2 fibrosis, no diabetes. Answer: Resmetirom (or vitamin E classically). With diabetes, prefer GLP-1 RA or pioglitazone.
— Patient with MASLD and ALT 80, LDL 145, ASCVD risk 12%. Answer: Start statin — do not withhold.
— Stem describes splenomegaly, platelets 95k, LSM 22 kPa. Answer: Initiate HCC surveillance with US/AFP every 6 months and arrange EGD for varices.
— Order set: octreotide + ceftriaxone + EGD within 12 h + transfusion to Hb 7. Most missed: antibiotics.
— Obese adolescent with elevated ALT. First step: intensive lifestyle intervention with family involvement; rule out Wilson disease.
— MASLD patient on statin + GLP-1 + ACEi planning pregnancy. Answer: Discontinue all three; continue metformin if needed; counsel on weight optimization.
— Ratio >2 with macrocytosis — pivot toward alcohol-associated liver disease even if patient minimizes alcohol; consider biomarker testing.
— Compensated cirrhosis: Continue statin, aspirin, metformin as indicated. Decompensated: hold case-by-case.
Step 3 management: Recognize that the test rewards action sequences (calculate, stratify, treat the metabolic disease, statin, follow up) and penalizes both over-testing (jumping to biopsy) and under-treating (withholding statins).
MASLD/MASH is the hepatic expression of cardiometabolic disease — risk-stratify everyone with FIB-4 (then VCTE/ELF if indeterminate), treat the metabolic syndrome aggressively because cardiovascular disease (not the liver) kills most patients, and reserve MASH-directed pharmacotherapy (resmetirom, GLP-1 RA, pioglitazone, vitamin E) plus bariatric surgery and transplant for those with significant fibrosis.
Board pearl: When in doubt on a MASLD stem, the right answer almost always involves calculating FIB-4, optimizing the cardiometabolic profile, and starting/continuing a statin — three actions that together capture the modern Step 3 approach to this disease.