liver cirrhosis Flashcards
cirrhosis definition
fibrosis(progressive scarring) of hepatic parenchyma forming nodules, which disrupt the hepatic function, restriced venous ouflow and portal hypertention
Scarring is accompanied by loss of viable hepatocytes (the functional cells of the liver).
Complications of cirrhosis and the associated portal hypertension include:
Cirrhosis is irreversible and leads to portal hypertension
* esophageal varices
* gastric varices
* ascites
* spontaneous bacterial peritonitis
* hepatic encephalopathy
* hepatorenal syndrome
Most common causes of Cirrhosis:
- Alcohol ingestion: decades of heavy driking more quickly develope in woemn thn men
- Viral hepatitis B & C infection: acute reversible hepatic inflammation chronic B OR C cause cirrhosis
both b and c transmitted through iv drugs and sexual route more common in B
normal portal vein pressure and portal hypertention
Normal portal vein pressure is 5 - 10 mm Hg
portal hypertension, which is a consequence of increased resistance to hepatic blood flow, occurs when portal pressure exceeds 10 - 12 mm Hg
Portal hypertension can result from
pre-hepatic, intrahepatic, or post-hepatic damage. The most common cause is intrahepatic damage.
symtoms of cirrhosis
The liver processes metabolic waste products for excretion; in cirrhosis, bilirubin (from the enzymatic breakdown of heme) can accumulate, causing jaundice (yellowing of the skin), scleral icterus (yellowing of the sclera), and tea-colored urine (urinary bilirubin excreted as urobilinogen).
Pathophysiology of portal HTN
Portal hypertension results from fibrotic changes within the hepatic sinusoids, changes in the levels of vasodilatory and vasoconstrictor mediators, and an increase in blood flow to the splanchnic vasculature.
Ascites
Ascites is the accumulation of fluid in the peritonium.
It is the most common condition associated with cirrhosis and indicates a poor prognosis
ascites pathophysiology
- cirrohtic changes and decrease in synthetic function lead to hypoalbumin
- low albumin, increase hydrostatic pressure and capillary permialbility allow fluid to leak from the vascular space into body tissues
- Lowered effective intravascular volume kidney perfusion cause activation of aldoestron, RAAS system which retain water and salt
varices definition
and caused by?
- varices are weak superficial vessels that product into gastric lumen and may rupture and bleed due to increase in pressure
- varices are most imp result of increase portal hypertention
- they are caused by devleopment of another route to blood flow to overcome resistance to drainage from the originating organ.
- Patients with cirrhosis are at risk for varices?
- varices location
- hemmorage and death rate in varices
- when portal pressure exceed the vena cava pressure by ≥ 12 mm Hg
- Varices may develop in the esophagus, stomach, and rectum to compensate for the increased blood volume.
- Hemorrhage from varices occurs in 25% to 40% of patients with cirrhosis
- Each episode of variceal bleeding carries a 25% to 30% risk of death.
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hepatorenal syndrome
decrease in renal function due to cirrhosis that is not caused by intrusic renal disease
* if not treated fetal with mortility rate 50 % in 14 days
kidney compensation to HRS
The kidneys attempt to counteract the drop in renal perfusion by: RAAS activation which causes fluid retention and renal vasoconstriction in an attempt to increase renal blood flow.
Spontaneous Bacterial Peritonitis (SBP)
SBP is an acute bacterial infection of peritoneal (ascitic) fluid in the absence of intra-abdominal infection or intestinal perforation
Up to 30% of patients with ascites develop SBP
The most common bacteria isolated from patients with SBP are:
Gram-negative aerobes e.g. Escherichia coli, Klebsiella pneumoniae
Gram-positive pathogen e.g. Streptococcus pneumoniae.