Complications End-Stage Liver Disease Flashcards

1
Q

What are main causes of cirrhosis and portal hypertension?

A

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

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2
Q

What is the difference between compensated and decompensated cirrhosis?

A

Compensated cirrhosis: asymptomatic; liver functioning well

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

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3
Q

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

A

Pressure~Vascular Resistance x Blood flow
P~R*Q

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

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4
Q

What is the main site of resistance?

What is the main site of flow control?

A

Hepatic sinusoids are main site of resistance

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

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5
Q

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

A
Ascites
Gastroesophageal varices
Spontaneous bacterial peritonitis
Portosystemic encephalopathy
Hepatorenal
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6
Q

What is the arterial vasodilation theory of ascites pathogenesis?

A

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

Impaired Na excretion contributes

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7
Q

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

A

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

SAAG>1.1=portal hypertension (cirrhosis/CHF)
SAAG

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8
Q

What are the treatment options for ascites?

A

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

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9
Q

What is the survival for ascites?

General, refractory and in hepatorenal syndrome

A

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

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10
Q

What is hepatorenal syndrome?

A

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

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11
Q

What is treatment for hepatorenal syndrome

A

Dialysis as “bridge” for liver transplant

Liver tx works because the kidney is structurally normal

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12
Q

What is spontaneous bacterial peritonitis?

A

Infection of ascites

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13
Q

What is presentation of spontaneous bacterial peritonitis?

How is it diagnosed?

A

Fever, abdominal pain, mental confusion, renal failure

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

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14
Q

What are criteria for spontaneous bacterial peritonitis? (2)

A

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

SAAG>1.1 (must have portal hypertension)

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15
Q

What is treatment for spontaneous bacterial peritonitis?

A

IV abx
IV albumin to protect kidneys

After episode, give abx to prevent recurrence

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16
Q

Why do varices arise in setting of portal hypertension?

What are common locations

A

Blood finds “easier route” back to heart

Observe esophageal varices at GEJ and gastric varices

17
Q

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

A

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

18
Q

Epidemiology of varices: prevalence, bleeding, mortality

A

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

19
Q

What is treatment for esophageal varices?

A

Screen in all cirrhotics by upper endoscopy

Given beta blocker (propanolol) to prevent bleeding

20
Q

What is treatment for variceal bleeding? (4)

A

Blood transfusion, ICU

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

21
Q

What is mechanical tamponade?

When do you use it?

A

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

22
Q

What is hepatic encephalopathy?

A

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

23
Q

Describe the pathogenesis of hepatic encephalopathy

A

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

24
Q

What is treatment for hepatic encephalopathy? (4)

A

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

25
Q

What should be avoided in Hepatic encephalopathy?

A

No sedatives

26
Q

What is the MELD score?

A

Model for End-stage Liver Disease

It provides a 3 month mortality prediction score

27
Q

What is outcomes for liver transplant patients?

Is this different for Hep C patients?

A

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

~10% lower in HCV due to recurrence