Cirrhosis Flashcards
What are some common causes of Cirrhosis
- Hepatitis B (D)
- Hepatitis C
- Alcohol
- Hemochromatosis
- Wilson’s Disease
- Non-alcoholic steatohepatitis
- Primary biliary cirrhosis
- Primary sclerosing cholangitis
- Autoimmune hepatitis
- Alpha-1 antitrypsin deficiency
- Budd-Chiari Syndrome
Examination findings of pt with Cirrhosis
- Cachexia
- Jaundice
- Ascites
- Spider angioma
- Dupuytren’s contractures
- Edema
- Breast development
- Testicular atrophy
- Palmar erythema
- Hair loss
- Encephalopathy
Lab findings in pt with cirrhosis
• Elevated bilirubin
• Elevated transaminases
• Elevated alkaline
phosphatase
• Decreased albumin
• Elevated PT/INR
• Thrombocytopenia
• Leukopenia
• Renal insufficiency
• Hyponatremia
What type of muscle wasting do we see in pts with cirrhosis
muscle wasing and temporal wasting
What is specialy about spider angioma’s?
At level of collar and face, when you press on them, middle blanches and the legs fill out with blood
What are two things we see on pts hands with cirrhosis?
palmar erythema and dupuytrens contractures
What does a cirrhotic liver look like on CT?
smaller, nodular with increased fluid levels around it or ascites
spleen will also enlarge
What is the pahtology of hepatic fibrosis?
Stellate cells are activated and lay down collagen in space of Disse, obliterate space
Kupfner cells release cytokines and inflamatory cells
hepatocytes lose vili
***cause of cirrhosis is ongoing activation of stellate cells
What does it mean if pt is given a score of 5-7 for Child Pugh Score
Normal or health cirrhotic liver; no acites, no encephalopathy, normal INR and bilirubin
pts it compensated
Survival is 70-75%
What does it mean if pt is given a score of 7-9 for Child Pugh Score
They are cirrhotic and can control ascites with diuretics and enchephalopty with lactulose, they are decompensated with elevated INR and albumin
Survival is 40-45%
What does it mean if pt is given a score of >9 for Child Pugh Score
Pt has elevated albumin and INR, poorly decompensated, ascites not controlled with diuretics and encephalopty not much better with lactulose
survival 10-15% 5 yrs
New model for End stage liver disease and why its better
MODEL FOR END-STAGE LIVER DISEASE (MELD)
*only uses the INR, bilirubin, creatine
–ascites and encephalopty are subjective
At what MELD score does 3 month survival go down?
starts to go down at 15 then big drop around 25
What happens in pre-hepatic portal hypertension? What vein is involved?
involves the portal vein before entering liver; puts at risk for portal vein thrombosis bc pressure will increase. Liver fnx normally bc still getting blood from hepatic artery
== pre-hepatic portal hypertension
What happens when we have portal hypertension that is Intra-hepatic?
Leads to Cirrhosis; this creates pressure issue across the sinusoids of portal and hepatic veins
What do we worry about with post-hepatic portal hypertension?
- Post-hepatic; blood cant drain out of liver; get big increase in pressure!
- Hepatic vein thrombosis (Budd-Chiari Syndrome) if you have coag issues
- Right heart failure
- Valvular heart disease
COMPLICATIONS OF CIRRHOSIS
- Variceal bleeding
- Ascites
- Spontaneous bacterial peritonitis (SBP)
- Hepatorenal Syndrome
- Hepatopulmonary Syndrome
- Hepatic encephalopathy
What is the reason we see varices in intra-hepatic portal HTN?
Increase pressure in liver may be d/t of scarring of sinusoids from cirrhosis, this creates high pressure for blood. Blood choices low pressure path instead of liver like the esophageal varies or other accessory veins that can rupture with high blood traffic
What happens to spleen in cirrhosis?
Spleen increases in size because of high pressure in the liver and gets redirected to spleen or backed up.
see more sequestering of platelets; thrombocytopenia and leukopenia
What do you use on esophageal varices to prevent bleeding?
• Use non-selective B-blockers (propanolol, nadolol)
Decrease cardiac output by blocking B-1 receptors
Produce splanchnic vasoconstriction by B-2 blockade
Decreases risk of first bleed, rebleeding
and increases survival
• Use non-selective B-blockers (propanolol, nadolol)
Decrease cardiac output by blocking ___receptors
Produce splanchnic vasoconstriction by___ blockade
B-1
B-2
What do you use to treat ACTIVE variceal hemorrhage?
Somatostatin analogues: Octreotide!!!
vasopressin and terlipressin work as well
~ do rubberbanding as well for those that havent ruptured
What causes asictes in cirrhotic pt?
Increases R to portal flow–> portal HTN–> Splanchnic Arterial VasoD
– > Decreases effective circulation volume –>
Activates vasoconstriction and Anti-naturatetic peptide = water +Na retention
Causes volume expansion==> Ascites
What factors are released in response to decreased circulating blood volume?
RAAS, vasopressin, ANaturtetic peptide
Cirrhosis leads to decreased circulating volume causing releases of:
Vasopressin causing:
Renin-angiotensin Aldosterone:
Together both cause:
Vasopressin: water retention
renin-angiotensin/aldosterone: Na retention
Ultimately more Water retention > Na retention = Hyponatremia
Recommended Tx for Ascites
• 2000 mg sodium restricted diet
• Diuretics
spironolactone (aldactone), inhibits aldosterone~~ acts distal convoluted tuble
furosemide (lasix)~~ asceniding tubule
How do patients with Spontaneous Bacterial peritonitis present and what agents cause this?
Mostly with abdominal pain and fever
When gram (-); E.coli, Streptococci, Klebsiella ~ bugs from GI flora
What happens in Hepatorenal Syndrome from cirrhosis?
Over time urine output decreases and serum creatinine increases
kidney biopsy will be normal, the kidney is just underperfused and responding normally.
In Acute tubular necrosis:
Urine sodium:
Urine micro:
CVP:
urine sodium: >20
Urine micro: Cell debris
CVP: Normal
Pre-Renal
Urine Na:
Urine Micro:
CVP:
Urine Na: <10
Urine micro: normal
CVP: Low
Hepatorenal syndrome
Urine Sodium:
Urine Micro:
CVP:
Urine Na: <10
Urine micro: normal
CVP: low
What is going on in hepatopulmonary syndrome?
Dilation of alveoli; have decreased pressure in lung meaning less driving pressure
Pathophysiology of hepatic encephalopathy
Gut derived neurotoxins–> Hepatic insufficiency OR Hepatic bypass –>
Crosses BBB–>
CNS changes
Symptoms of hepatitis encephalopthy
Asterixisis, change consiousness, behavior change
What is used as a Tx for hepatic encephalopthy?
Lactulose: decreases the pH to make bacteria unfavorable environment and increase cathartic effect
Rifaximin also used, Lactulose prescribed 1st and this added if lactulose doesn’t help
***takes up to 2 weeks to get better
What two things result from Fulminant liver failure?
Acute liver fail: hepatocyte necrosis; coagulopathy + encephalopathy
Cerebral edema; liver cant metabolize ammonia
What is the mechanism of cerebral edema seen in fuminant liver failure?
ammonia and glutamate converted by action of
glutamine synthetase into glutamine by brain astrocytes
o astrocyte swelling leads to cerebral edema
o cerebral herniation is leading cause of death
