Liver disease II Flashcards
What 4 characteristics define liver cirrhosis?
Liver fibrosis
Distortion of architecture + formation of regenerative nodules
Loss of hepatocellular mass + liver function
**irreversible in advanced states**
All causes of liver disease can result in cirrhosis which leads to ___ or ___
The most common causes of cirrhosis in the US are: (3)
All causes of liver disease can result in cirrhosis which leads to chronic hepatic inflammation or cholestasis (bile stasis)
Most common causes of cirrhosis:
Hep C
Alcoholic liver disease
Nonalcoholic fatty liver disease (NAFLD)
What are the physical manifestations of cirrhosis?
What are the cirrhosis features below?
Spider angiomas: dilated blood vessels on the chest
Palmar erythema: due to hormone issues w/ liver function
Caput medusae: dilated vessels that form due to increased abdominal pressure
What are the expected lab values of the following in cirrhosis:
bilirubin
animotransferases
alk phos
platelets
albumin
PTT/INR
sodium
- High bilirubin
- Abnormal aminotransferases
- High alkaline phosphatase – not seen in Wilson’s disease
- Low platelets (thrombocytopenia)
- Low albumin (hypoalbuminemia)
- Prolonged prothrombin time/ high INR (related to the thrombocytopenia/lack of platelet factors)
- Low sodium (hyponatremia) - can’t excrete free water/ascites (increased ADH)
What are two things you woud expect to see on imaging of liver cirrhosis?
Shrunken liver + splenomegaly (results from blood back up from portal HTN)
*Platelets also sequestered by spleen*
Describe the difference between compensated and decompensated cirrhosis. What is the life expectancy in each case?
Compensated Cirrhosis – features of cirrhosis on imaging + labs but no symptoms; Life expectancy greater than 12 years
Decompensated Cirrhosis - complications of cirrhosis: jaundice, ascites, bleeding; life expectancy 1.8 years
Which scoring systems are used for grading the severity of cirrhosis? (2)
MELD-Na score
Child-Turcotte-Pugh score
Describe the MELD-Na score
Score is mathematically derived based on levels of serum bilirubin, creatinine, sodium and INR
**
The higher the meld score, the lower the 3 mth pt survical
Most pts referred for transplant w/ MELD score of 15. Around 30 here at UMMC
Describe the Child-Pugh score
Scoring system based on presence of:
encephalopathy
ascites
bilirubin levels, albumin levels, PTT/INR
Class A is the least severe, Class C is the most severe liver disease
Some complications of cirrhosis include poor liver function, portal HTN, and increased risk of ___
What are the signs of poor liver function (3) - lab values and portal HTN (3) - symptoms?
Some complications of cirrhosis include poor liver function, portal HTN, and increased risk of hepatocellular carcinoma
Poor liver function:
low albumin, high bilirubin, elevated PTT
Portal HTN: bleeding, ascites, hepatic encephalopathy
Define portal HTN
Portal HTN can result from ___ or ___ (hint: both conditions involve an increase in flow)
What is the initial cause of portal HTN in cirrhosis?
Portal HTN: pathologic increase in BP in portal venous system (measured by HVPG - normal <5, portal HTN >5 mmHg)
Portal HTN can result from increased resistance to flow or increased portal VENOUS inflow
The initial cause of portal HTN in cirrhosis is increased intrahepatic resistance to flow
What changes to liver architecture + systemic collaterals do you expect to see with cirrhosis? (5)
Following portal HTN, pts develop dilated sinusoidal architecture (can be seen on biopsy) + scar tissue >> increased resistance + dilated portal systemic collaterals >> varices + splenomegaly
Describe hepatic encephalopathy
How can you tell that a pt may have HE? (hint: they have to put their hands up)
Hepatic encephalopathy is brain dysfunction caused by liver disease (liver insufficiency or portosystemic shunting)
To determine if pt has hepatic encephalopathy: pt exhibits asterixis on exam
Asterixis: pt puts up hands and there is a noticeable flapping. Caused by high ammonia levels (recall that ammonia is metabolized in the liver)
What causes hepatic encephalopathy?
HE is caused by high ammonia levels since the failed liver can’t metabolice ammonia so it shunts to the brain where it acts on GABA-BD receptors and causes brain disease
Fill in the table of HE classification below
Describe the difference between episodic and recurrent hepatic encephalopathy
Episodic HE is when pts who have liver disease + HE have some sort of trigger for the encephalopathy (e.g. not taking meds, infection etc)
Recurrent HE is when pts have HE + liver disease w/o a trigger for the HE (these pts are on medications)
How do you manage HE from a reversible cause vs not from a reversible cause?
*see image below*
Why would limiting protein lead to hepatic encephalopathy? (wouldn’t you need to limit to make sure you don’t get too many NH3’s or whatever from the amino acids?)
Lactulose – laxative that helps pts have bowel mvmts 2-3x daily; binds ammonia and helps w/ clearance
Rifaximin antibiotic that decreases ammonia producing bacteria
What is the mainstay of treatment for hepatic encephalopathy?
Lactulose = mainstay of treatment
Better to use lactulose + rifaximin combo to prevent HE recurrence
Describe the mechanism of action of lactulose
Lactulose works mainly by creating an acidic environment that kills urease-producing bacteria, and the H+ ions convert NH3 to NH4 which excreted in the stool (something about the cathartic effect also being helpful)
A major complication of portal HTN is bleeding from varices.
How do you screen for varices?
Suspected cirrhosis >> platelet ct, imaging, elastography >> (elastography >20kPa and platelet ct <150) EGD screening
How often do you conduct variceal screening for at risk pts? (4)
Depends on severity of disease
*see below*
Which beta blockers are used to prevent varices (by controlling portal HTN)? What else could you do to prevent varices?
When would you follow up with pts after treating them w/ the above?
Mainly propanolol and nadolol
Can also do variceal ligation
*see slide below*
Study this slide
Octreotide: decreases pressure in varices
Antibiotics given to prevent infection in fluid (which happens when pt is bleeding)
TIPS (shunting) considered it pt’s bleeding can’t be controlled w/ meds
Describe how the Transjugular intrahepatic portosystemic shunt works
Why woud pts with prior HE not do well or even do worse after undergoing TIPS?
TIPS: shunt that connects hepatic vein and portal vein
TIPs: pts with bad HE prior to TIPS may not do well because since there’s now a shunt, their blood isn’t being detoxified by the liver at all so they might actually be more confused
Gastric varices can also develop in portal HTN. How and when do you treat these?
Gastric varices can also develop and those are treated by cyanoacrylate glue, and only if they are bleeding
What are the pathologies below?
Left: GAVE
**GAVE (aka watermelon stomach) is treated w/ argon plasma coagulation (APC). GAVE cannot be corrected by TIPS**
Right: Portal hypertensive gastropathy
*Portal hypertensive gastropathy is a snake-like appearance in the stomach. Graded from mild-moderate-severe. Severe = affected areas are oozing blood w/o any contact*
What is the mainstay of treatment of ascites?
If that doesn’t work, what other interventions are used before evaluation for transplantation? (3)
Mainstay of treatment is sodium restriction (no need for water restriction
If Na restriction doesn’t work, pts are started on Lasix + Aldactone (literally furosemide + spironolactone) 40:100 (need to monitor electrolyte levels)
If diuretics don’t work, pts can be considered for TIPS because the shunt can relieve the high portal pressure >> decreases ascites
Pts can also undergo therapeutic paracentesis to remove fluid, albumin used to prevent renal disease at > 5L fluid removal
Once pts develop ascites, pts should be considered for transplant
What are (3) complications of ascites and how do you Rx each?
Spontaneous bacterial peritonitis: infected ascitic fluid; if pts are tested and found to be infected, pts will receive antibiotics indefinitely (until they get a liver transplant)
Other complications include umbilical herniation and hydrothorax (treated with thoracentesis)
(note also tense ascites)
SBP is diagnosed at an ascitic neutrophil count of > than ___
In addition to antibiotic prophylaxis (with what antibiotics - 2), patients are also given ___ which mainly helps improve mortality and decreases risk of renal failure
SBP is diagnosed at an ascitic neutrophil count of > than 250
In addition to antibiotic prophylaxis with a fluorouinolone (e.g cipro) or trimethoprim-sulfa, patients are also given albumin which mainly helps improve mortality and decreases risk of renal failure
Any pt w/ cirrhosis should be screened every __ by ultrasound for ___ (type of cancer)
T/F: pts w/ Hep B get screened regardless of presence of cirrhosis because they can develop this cancer w/ underlying cirrhosis
Any pt w/ cirrhosis should be screened every 6 mths by ultrasound for hepatocellular carcinoma
True. Pts w/ Hep can develop hepatocellular carcinoma w/o underlying liver cirrhosis and so will get screened regardless of presence of cirrhosis
(ultrasound >> triphasic CT or contrast MR)
Review the following slide on HCC surveillance.
T/F: You need to do a biopsy in addition to imaging to diagnose HCC
Falsehood. HCC can be diagnosed solely on imaging (no biopsy needed). Most common features on imaging is arterial hyper-enhancement (tumor will light up in the arterial phase)
Review the following slide on HCC transplantation evaluation
Review the following slide on the Milan criteria for HCC
One of the complications of portal HTN is renal failure. How does renal failure develop in portal HTN?
Basically because you have decreased circulating volume resulting from splanchnic vasodilation, that results in the activation of the RAAS, which results in renal vasoconstriction >> decreased renal function (low GFR)
Describe the difference between Type 1 and Type 2 hepatorenal syndrome
Type 1 disease is usually precipitated by some event like infection + rapid doubling of Cr
Typ 2 disease has gradual increase in Cr + no precipitating event
**mainly treated w/ midodrine/octreotide
Describe hepatopulmonary syndrome
HPS is when you have abnormal arterial O2 due to intrapulmonary vascular dilatations
*see below for more info*
____ is pulmonary arterial hypertension ass’d w/ portal HTN
Porto-pulmonary hypertension is pulmonary arterial hypertension ass’d w/ portal HTN
*see below for more info*
Under what conditions would you consider a pt for liver transplantation? (2)
Pts should be considered for liver transplantation if they have severe acute or advanced chronic liver disease (and they’re no longer responding to meds), or if they have a MELD-Na score of 15
Name the complications of cirrhosis (and why each happens) (6)
Encephalopathy
Bleeding (varices)
Ascites
Hepatocellular carcinoma
Hepatopulmonary syndrome
Portopulmonary HTN
Name some systemic diseases that can arise from liver disease
Alpha 1 anti-trypsin -
Familial amyloidosis
Glycogen storage disease
Hemochromatosis
Primary oxaluria
Wilson’s disease
