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)
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 llar resistance Plasma oncotic Arteriolar Portal veng pressure pressure vasodilation ↑ Hepatic mph/ splanchnic Central pooling ASCITES sympathetic outflow f Na+retention,A- Effective intravascular ?, Renal tubular volumet sensitivity ?↑ Resistance to atrial natriuretic Renal peptide perfusion Aldosterone Intrarenal redistribution of blood flow) Plasma renin activity
Ascites Sodium retention Renin angiotension aldosterone system(RAAST sympathetic nerve system T, norepinephrine 个 Intrarenal factors: Kallikrein-kinin system Adenosine Water retention Antidiuretic hormone(ADHT -Impaired renal synthesis of PGs(PGE2 Renal vasoconstriction RAAS, Angiotension ---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 system 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) a 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