Consequences of portal hypertensionI 3. Ascites(腹水) Theories of ascites formation Underfilling theory(灌注不足假说) Overflow theory(泛溢假说) Arterial vasodilation theory(动脉扩张假说)
Consequences of portal hypertension[II] 3. Ascites (腹水) Theories of ascites formation • Underfilling theory (灌注不足假说） • Overflow theory (泛溢假说) • Arterial vasodilation theory (动脉扩张假说)
CIRRHOSIS Intrahepatic No Albumin vascular resistance Plasma oncotic Arteriolar Portal venous pressure vasodilation Hepatic pressure lymph Splanchnic Cel pooling ASCITES sympathetic outflow t Nat retention -=--4i Effective intravascular ?↓ Renal tubular volumet sensitivit f Resistance to atrial natriuretic Renal perfusion Aldosterone peptide (Intrarenal redistribution of blood flow) Plasma renin activity
Ascites Sodium retention Renin angiotension aldosterone system(RAAST sympathetic nerve system↑, norepinephrine个 Intrarenal factors: Kallikrein-kinin system, Adenosine Water retention ---Antidiuretic hormone(ADHT Impaired renal synthesis of PGs(PGE2l) Renal vasoconstriction RAAS. AngiotensionIIT --SNS ADH个 --ET个
Ascites • Sodium retention ---Renin angiotension aldosterone system(RAAS) ---sympathetic nerve system ,norepinephrine --- Intrarenal factors: Kallikrein-kinin system, Adenosine . • Water retention ---Antidiuretic hormone(ADH) ---Impaired renal synthesis of PGs (PGE2) • Renal vasoconstriction --- RAAS, AngiotensionII ---SNS ---ADH ---ET
Endocrine svstem 米 gynecomastia(男性乳房发育 telangiectases(毛细血管扩张症) spider nevi(蜘蛛痣), palmar erythema(肝掌) testicular atrophy(睾丸萎缩) menstrual irregularities(月经失调)
Endocrine system gynecomastia(男性乳房发育), telangiectases (毛细血管扩张症), spider nevi(蜘蛛痣), palmar erythema(肝掌) testicular atrophy(睾丸萎缩) menstrual irregularities (月经失调)
Pulmonary manifestations Hepatic hydrothorax(肝性胸水) Hepatopulmonary syndrome HPs,肝肺综合征) hrs is characterized clinically by the triad of pulmonary vascular dilatation causing arterial hypoxemia in the setting of advanced liver disease
Pulmonary manifestations Hepatic hydrothorax (肝性胸水) Hepatopulmonary syndrome (HPS, 肝肺综合征) HRS is characterized clinically by the triad of pulmonary vascular dilatation causing arterial hypoxemia in the setting of advanced liver disease