Astavalence

PathoSchema® by Astavalence · Cirrhosis Architecture Simulator

PathoSchema® by Astavalence

Cirrhosis Architecture Simulator

Advanced fibrosis state

1 Architecture Lobules collapse into scar bands and regenerative nodules.

2 Portal pressure Portal blood backs up against a high resistance liver.

3 to 6 Complications Varices, spleen, ascites and encephalopathy.

7 System stress Renal dysfunction and falling reserve.

Cirrhosis architecture

The key transformation is architectural: organised lobules become bridged by scar, trapped into nodules and converted into a high resistance vascular organ.

Disease state

F3 model

Current mechanism

Architecture transformation

Healthy liver is organised into lobules with structured inflow, outflow and bile drainage. Cirrhosis replaces that order with bridging fibrosis, regenerative nodules, surface distortion and high intrahepatic resistance.

Severity controls

Ongoing injury46%

Fibrosis and nodules58%

Portal pressure50%

Functional reserve62%

Selected structure

Architecture readout

Live clinical snapshot

Core rule

Cirrhosis is not just scar. It is scar plus nodules plus vascular distortion plus reserve failure. The architecture change is why portal pressure rises and why blood tests can deteriorate later than the structural damage.

Exam pearls

Bridging fibrosisScar links vascular territories and disrupts normal lobular flow.

Regenerative nodulesSurviving hepatocytes grow inside scarred compartments.

Portal hypertensionArchitectural resistance causes pressure to rise upstream.

PlateletsMay fall before dramatic jaundice because splenic sequestration starts early.

DecompensationAscites, bleed, encephalopathy, jaundice or renal dysfunction.

HCC riskChronic regeneration within damaged tissue creates cancer risk.

Reset

Advanced fibrosis. High priority for cause removal.

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