[Part 2]Liver-Cirrhosis-Pathophysiology-and-Hepatorenal-Syndrome.pptx

medical analysis 2

1. Liver Cirrhosis: Pathophysiology and Hepatorenal Syndrome Advanced exploration of circulatory dysfunction and renal complications in cirrhotic patients.

2. Circulatory Dysfunction in Cirrhosis Portal Hypertension Primary driver of hemodynamic changes Splanchnic Vasodilation Mediated by NO and endocannabinoids Effective Arterial Hypovolemia Blood pooling in splanchnic circulation RAAS/SNS Activation Compensatory response to perceived hypovolemia

3. Renal Consequences of Circulatory Dysfunction Renal Vasoconstriction Kidneys receive less blood flow Reduced GFR Filtration capacity diminishes HRS-AKI Development Functional kidney failure occurs Treatment Response Vasoconstrictors + albumin reverse HRS-AKI

4. Early Cirrhotic Cardiomyopathy Hyperdynamic Circulation Increased cardiac output (↑ CO) Compensatory Mechanism Response to peripheral vasodilation Clinical Signs Bounding pulse, warm extremities Decreased SVR Systemic vascular resistance falls

5. Advanced Cirrhotic Cardiomyopathy Reduced Cardiac Output Heart fails to meet circulatory demands Impaired Contractility Myocardial dysfunction develops 3 Renal Hypoperfusion Contributes to kidney dysfunction Beta-Blockers Risk May worsen CO and renal blood flow

6. Renal Blood Flow Alterations RAAS/SNS Activation Powerful vasoconstrictors target kidney Impaired Autoregulation Linked to portal pressure Prostaglandin Protection Counteracts vasoconstriction NSAID Risk Blocks protective prostaglandins

7. Systemic Inflammation in Cirrhosis Bacterial Translocation PAMPs enter circulation from intestine Liver Damage DAMPs released from injured hepatocytes Cytokine Storm Elevated IL-6, TNF-α in HRS-AKI Vascular Effects Worsens vasodilation and reduces renal perfusion

8. Integrated Pathophysiology of HRS-AKI 1 Portal Hypertension Initial circulatory disturbance 2 Splanchnic Vasodilation Blood pools in mesenteric circulation 3 Effective Hypovolemia Triggers compensatory systems 4 Renal Vasoconstriction Combined with systemic inflammation 5 HRS-AKI Functional renal failure develops

9. Clinical Features of HRS-AKI Patient Presentation Advanced cirrhosis with ascites Hypotension common Hyponatremia Low urinary sodium (<20 mEq/L) Precipitating Factors Present in 50% of cases Infections (SBP) GI bleeding Large volume paracentesis Diuretic overdose

10. Diagnostic Criteria for HRS-AKI Inclusion Criteria (ICA 2015) Exclusion Criteria Cirrhosis with ascites Shock AKI: sCr ↑ ≥0.3 mg/dL in 48h Nephrotoxic drugs or ≥50% in 7 days Structural kidney injury No response to albumin Proteinuria >500 mg/day No response to diuretic withdrawal Abnormal kidney ultrasound