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Flashcards in Complications End-Stage Liver Disease Deck (27):

What are main causes of cirrhosis and portal hypertension?

Alcoholism, autoimmune hepatitis, viral hepatitis, hemochromatosis, Wilson's disease, A1AT deficiency, PBC, PSC, toxins, schistosomiasis


What is the difference between compensated and decompensated cirrhosis?

Compensated cirrhosis: asymptomatic; liver functioning well

Decompensated cirrhosis=end-stage liver disease; liver not functioning well and liver transplantation should be considered


What are the important factors in portal hypertension? (2)

Pressure~Vascular Resistance x Blood flow

Increase either venous inflow or resistance to portal flow==>portal hypertension


What is the main site of resistance?
What is the main site of flow control?

Hepatic sinusoids are main site of resistance

Splanchnic capillaries (feed into portal veil) are main site of flow control


What are the major complications of portal hypertension? (5)

Gastroesophageal varices
Spontaneous bacterial peritonitis
Portosystemic encephalopathy


What is the arterial vasodilation theory of ascites pathogenesis?

Arterial vasodilation due to VO leads to effective volume depletion and activation of vasoconstrictors (renin/Angiotensin, ADH)

Impaired Na excretion contributes


How do calculate whether ascites is due to portal hypertension or another cause?

Serum Albumin ascites gradient: Serum albumin-albumin in ascites fluid

SAAG>1.1=portal hypertension (cirrhosis/CHF)


What are the treatment options for ascites?

Low salt diet
Diurects: spironolactone/furosemide
Large volume paracentesis
Transjugular intrehpeatic portosystemic shunting (TIPS): stent to bypass blood around liver


What is the survival for ascites?
General, refractory and in hepatorenal syndrome

Average survival for ascites: 2 years
Refractory ascites: 6 months survival
Hepatorenal syndrome: 6 wk survival


What is hepatorenal syndrome?

Acute renal insufficiency in setting of end-stage liver disease due to dysregulation of vasoactive hormones (vasoconstriction)

No improvement after stopping diuretics and giving IV fluids


What is treatment for hepatorenal syndrome

Dialysis as "bridge" for liver transplant

Liver tx works because the kidney is structurally normal


What is spontaneous bacterial peritonitis?

Infection of ascites


What is presentation of spontaneous bacterial peritonitis?

How is it diagnosed?

Fever, abdominal pain, mental confusion, renal failure

Dx via paracentesis fluid containing more than 250 PMN cells per cc


What are criteria for spontaneous bacterial peritonitis? (2)

1 organism only: most common include E Coli Klebsiella, strep

SAAG>1.1 (must have portal hypertension)


What is treatment for spontaneous bacterial peritonitis?

IV abx
IV albumin to protect kidneys

After episode, give abx to prevent recurrence


Why do varices arise in setting of portal hypertension?

What are common locations

Blood finds "easier route" back to heart

Observe esophageal varices at GEJ and gastric varices


What are predictors for bleeding in esophageal varices? (4)

Size of varies (larger more likely to bleed)
Child class
Pressure gradient
Red signs


Epidemiology of varices: prevalence, bleeding, mortality

Varices in 24-81% of cirrhotics
1/3 of these will bleed in a given year
Mortality from bleed is 40-70%
Risk of dying is 10-15% from bleed within 1 yr of diagnosis of large varices


What is treatment for esophageal varices?

Screen in all cirrhotics by upper endoscopy
Given beta blocker (propanolol) to prevent bleeding


What is treatment for variceal bleeding? (4)

Blood transfusion, ICU

Octreotide: vasoconstrictor to decrease flow
Band ligation: stop bleeding
TIPS for refractory cases


What is mechanical tamponade?

When do you use it?

Inflate balloon to provide mechanical pressure to tamponade bleeding vessel

It is only used for severe, refractory bleeding--it has a high risk of complication: rupture, necrosis of esophageal wall


What is hepatic encephalopathy?

Altered mental status (behavior, insomnia, delirium, seizures, coma) as a result of liver disease


Describe the pathogenesis of hepatic encephalopathy

Bacter catabolize proteins to ammonia-- it is absorbed and bypasses hepatocytes==>it is converted to glutamine in astrocytes and results in increased GABA and decreased glutamate and subsequent cerebral changes


What is treatment for hepatic encephalopathy? (4)

Eliminate underlying cause: treat underlying bleeding, constipation, infection
Lactulose: promotes ammonia trapping
Abx: rifaximin==>eliminates bacteria
Protein restriction: decreases ammonia load but most pts protein wasted


What should be avoided in Hepatic encephalopathy?

No sedatives


What is the MELD score?

Model for End-stage Liver Disease

It provides a 3 month mortality prediction score


What is outcomes for liver transplant patients?

Is this different for Hep C patients?

1 year patient survival: 88%
5 year survival: 75%

~10% lower in HCV due to recurrence