Clinician teaching

MASLD: Pathophysiology to FibroScan

A primary-care teaching deck on why steatosis identifies metabolic exposure while fibrosis changes risk and management.

Audience: Primary care physicians and clinicians.

Review status: Source deck adapted locally; Dr. Ayaz final review required before production publication.

Provenance: Byte-identical to the iOS-safe MASLD PowerPoint vendored in this repository on July 16, 2026.

Use: Educational teaching resource only; not individualized medical advice.

Learning objectives

PDF download Presentation handout Original presentation PowerPoint file

Major teaching sequence

  1. Start with the clinical miss: ultrasound finds fat, but the patient who matters is the one whose fibrosis is already advancing.
  2. Return to normal hepatic resilience: the liver can oxidize, export, and store fat before injury becomes persistent.
  3. Follow overload into hepatocyte stress, inflammatory signaling, stellate-cell activation, and collagen deposition in the space of Disse.
  4. Make the invisible measurable: FIB-4 estimates who needs another test; VCTE estimates liver stiffness and fibrosis probability.
  5. Close with risk stratification: steatosis identifies the disease process, while fibrosis identifies the management-changing risk.

Slide viewer

Slide 1: MASLD: when resilience gives way to fibrosis.
Slide 1MASLD: when resilience gives way to fibrosis.
Slide 2: Fat is easy to find. Fibrosis is easy to miss.
Slide 2Fat is easy to find. Fibrosis is easy to miss.
Slide 3: Start with what the disease actually is.
Slide 3Start with what the disease actually is.
Slide 4: MASLD is metabolic syndrome expressed in the liver.
Slide 4MASLD is metabolic syndrome expressed in the liver.
Slide 5: The hepatocyte has four ways to handle excess fatty acid.
Slide 5The hepatocyte has four ways to handle excess fatty acid.
Slide 6: Steatosis is evidence of storage, not proof of fibrosis.
Slide 6Steatosis is evidence of storage, not proof of fibrosis.
Slide 7: When buffering fails, injury becomes persistent.
Slide 7When buffering fails, injury becomes persistent.
Slide 8: Persistent injury turns repair into fibrosis.
Slide 8Persistent injury turns repair into fibrosis.
Slide 9: Fibrosis is laid down in the space of Disse.
Slide 9Fibrosis is laid down in the space of Disse.
Slide 10: Collagen makes the liver less flexible.
Slide 10Collagen makes the liver less flexible.
Slide 11: Steatosis identifies disease. Fibrosis identifies risk.
Slide 11Steatosis identifies disease. Fibrosis identifies risk.
Slide 12: A minority progress. ALT cannot tell us who.
Slide 12A minority progress. ALT cannot tell us who.
Slide 13: Every test answers a different question.
Slide 13Every test answers a different question.
Slide 14: FIB-4 tells you who needs another test.
Slide 14FIB-4 tells you who needs another test.
Slide 15: FibroScan uses one probe to answer two questions.
Slide 15FibroScan uses one probe to answer two questions.
Slide 16: A stiffer liver carries a shear wave faster.
Slide 16A stiffer liver carries a shear wave faster.
Slide 17: Stiffness estimates probability, not an exact stage.
Slide 17Stiffness estimates probability, not an exact stage.
Slide 18: Use FIB-4 first, then VCTE.
Slide 18Use FIB-4 first, then VCTE.
Slide 19: Fibrosis stage changes management.
Slide 19Fibrosis stage changes management.

References