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Flashcards in Cirrhosis Deck (23)
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1
Q

Common causes of cirrhosis

A
Hep B
Hep C
Alcohol
Hemochromatosis 
Wilson's disease
Non-alcoholic steatohepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
Autoimmune hepatitis 
Alpha-1 antitrypsin deficiency 
Budd Chiari syndrome
2
Q

Examination findings of cirrhosis

A
Cachexia
Jaundice
Ascites
Spider angiomas
Dupuytren's contractures
Edema
Breast development 
Testicular atrophy 
Palmar erythema
Hair loss
Encephalopathy
3
Q

Lab findings in cirrhosis

A
Elevated bilirubin
Elevated transaminases
Elevated alk phos
Decreased albumin
Elevated PT/INR
Thrombocytopenia
Leukopenia
Renal insufficiency 
Hyponatremia
4
Q

What cell is responsible for cirrhosis?

A

Stellate cell!

Lays down collagen, obliterates Space of Disse, fenestrations go away, lose villi

5
Q

What criteria does the Child-Pugh Scoring Criteria look at?

A
Albumin
Bilirubin
INR
Ascites
Encephalopathy
6
Q

What are the 5 year survivals for class A, B and C Child-Pugh Scores?

A

A- 50-75% (liver transplant)
B- 40-45%
C- 10-15%

7
Q

What is the current method for identifying liver transplant needs?

A

Model for End-Stage Liver Disease (MELD)
Looks at INR
Bilirubin
Creatinine +/- dialysis
*At 15, the risk of transplant outweighs the mortality of liver disease

8
Q

What are some causes of portal hypertension?

A

Pre-hepatic: portal vein thrombosis

Intra-hepatic: cirrhosis

Post-hepatic: hepatic vein thrombosis (Budd-Chiari syndrome), Right heart failure, Valvular heart disease

9
Q

What are some complications of cirrhosis?

A
Variceal bleeding
Ascites
Spontaneous bacterial peritonitis (SBP)
Hepatorenal syndrome
Hepatopulmonary syndrome
Hepatic encephalopathy
10
Q

What is used to prevent esophageal varicose?

A

Non-selective B-blockers (propranolol, nadolol)
-Decrease CO by blocking B-1 receptors
-Produce splanchnic vasoconstriction by B-2 blockade
Decreases risk of first bleed, rebelling and increases survival

11
Q

What is used to treat active esophageal bleeds?

A

Octreotide – decreases blood flow into portal vein
Somatostatin
Vasopressin
Terlipressin

12
Q

What is the pathophysiology of ascites?

A

Cirrhosis –> Increased resistance to portal flow –> portal hypertension –> Splanchnic arterial vasodilation –> Decreased effective circulating volume –> Activation of vasoconstrictor and antinatriuretic factors (RAAS) –> Na and H20 retention –> Plasma volume expansion –> Ascites

13
Q

What is the pathophysiology of hyponatremia in ascites?

A

Water retention is greater than sodium retention

14
Q

What is used to treat ascites?

A

2000 mg Na restricted diet

Diuretics: spironolactone (inhibits aldosterone), furosemide (lasix)

15
Q

What are some common signs and symptoms of someone with spontaneous bacterial peritonitis (SBP)??

A

Abdominal pain and fever

Also encephalopathy, hypoperistalsis, diarrhea, septic shock, GI bleed, vomit, asymptomatic

16
Q

What pathogens are responsible for SBP?

A
E. coli 
Streptococci 
Klebsiella
Other gram negatives
Anaerobes
17
Q

What is hepatorenal syndrome?

A

Complication of ascites

Progressive renal failure associated with advanced cirrhosis and ascites

18
Q

What are some differentials of renal failure in cirrhosis?

A

Acute tubular necrosis
Pre-renal
Hepatorenal syndrome

19
Q

What is hepatopulmonary syndrome?

A

Complication of ascites

Vasodilation syndrome in the lungs – no treatment besides liver transplant

20
Q

What is the pathophysiology of hepatic encephalopathy?

A

Gut derived neurotoxins –> hepatic insufficiency and hepatic bypass –> cross BBB –> CNS changes

21
Q

What is the treatment for hepatic encephalopathy?

A

Lactulose –> lactic acid and decreases pH and allows NH4+ to be protonated and excreted

If lactulose doesn’t work Rifaximin

22
Q

What is the most common cause of acute liver failure in the USA?

A

Acetominophen

23
Q

What is fulminant liver failure?

A

Acute liver failure – hepatocyte necrosis –> coagulopathy, encephalopathy

Cerebral edema: inability of liver to metabolize ammonia, ammonia and glutamate are converted by action of glutamine synthetase into glutamine by brain astrocytes –> astrocyte swelling leads to cerebral edema, cerebral herniation is leading cause of death