Liver disease II Flashcards by Nita Gombakomba

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**

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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)

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What are the physical manifestations of cirrhosis?

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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

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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)

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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*

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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

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Which scoring systems are used for grading the severity of cirrhosis? (2)

MELD-Na score

Child-Turcotte-Pugh score

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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

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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

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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

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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

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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

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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)

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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

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Fill in the table of HE classification below

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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