Cirrhosis development of Tetralogy

Cirrhosis of the liver is a common chronic liver disease, may be one or more causes liver damage, liver showed progressive, diffuse, fibrous lesions.

 (A) pre-ascites

 At this point in patients with cirrhosis without ascites, it does not appear circulation artery expansion and filling enough, but it will cause excessive sodium intake of salt and water retention, that is, at this time of renal sodium handling obstacles that have taken place. This is due to liver dysfunction and portal pressure increase directly affected by reflex renal handling of sodium caused by sodium retention, but this water is self-limited in nature.

 (2) reaction ascites Issue

 This period a marked increase in renal sodium and water retention, to a total blood volume expansion, followed by expansion of peripheral arteries in order to reduce vascular resistance. The expansion of peripheral arteries is due to the release of a large variety of visceral vasodilator substances, which led to visceral circulation and systemic circulation followed by expansion. Followed, according to the hypothesis of peripheral arterial formed ascites.

 (C) The period of refractory ascites

 This period in patients with severe liver disease, obviously sodium and water retention, is not sensitive to the diuretic therapy, hemodynamic instability. Plasma renin – angiotensin – aldosterone system and the sympathetic nervous system activity in hyperthyroidism, peripheral vascular reactivity to the vasoactive substances reduced. However, renal blood vessels are very sensitive to the vasoconstrictor, and renal reabsorption of sodium excretion increased further reduction in resistance to diuretic and natriuretic factor effect.

 (D) The period of hepatorenal syndrome

 This mostly occurs in a period of refractory ascites in patients with decompensated cirrhosis. As a further expansion of peripheral arterial hypotension, machine as to maintain effective circulating volume, resulting in increased synthesis of vasoconstrictor substances, in particular the increase in plasma endothelin levels. Because at this time of renal blood vessels to the contraction of the high sensitivity of the material, leading to selective renal hypoperfusion, severe sodium and water retention and renal failure.

This entry was posted on Thursday, October 1st, 2009 at 8:02 am and is filed under Cirrhosis. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.

 

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