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Gastroenterology > Liver cirrhosis, ascites > Flashcards

Liver cirrhosis, ascites Flashcards

1
Q

What are the 4 MOST common causes of liver cirrhosis?

A

Alcohol-related liver disease
Non-alcoholic fatty liver disease (NAFLD)
Hepatitis B
Hepatitis C

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2
Q

What are the examination findings you may see in a patient with liver cirrhosis? (List as many, as there are a lot)

A

Cachexia (wasting of the body and muscles)

Jaundice caused by raised bilirubin

Hepatomegaly (enlargement of the liver)

Small nodular liver as it becomes more cirrhotic

Splenomegaly due to portal hypertension

Spider naevi (telangiectasia with a central arteriole and small vessels radiating away)

Palmar erythema caused by elevated oestrogen levels

Gynaecomastia and testicular atrophy in males due to endocrine dysfunction

Bruising due to abnormal clotting

Excoriations (scratches on the skin due to itching)

Ascites (fluid in the peritoneal cavity)

Caput medusae (distended paraumbilical veins due to portal hypertension)

Leukonychia (white fingernails) associated with hypoalbuminaemia

Asterixis (“flapping tremor”) in decompensated liver disease

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3
Q

What is portal hypertension?

A

Elevated pressure in the portal vein due to cirrhosis (scarring of the liver)

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4
Q

How does portal hypertension cause splenomegaly?

A

In portal hypertension, splenic arterial blood flow increases and splenic venous flow into the portal vein is impeded by elevated portal pressure, which cause congestion of intrasplenic blood flow and spleen enlargement.

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5
Q

When the LFT’s for a patient are abnormal, the pt requires a non-invasive liver screen. What does this include?

A

-Ultrasound (to diagnose fatty liver)
-Hep B and C sereology
-Test autoantibodies (autoimmune hepatitis, primary sclerosing cholangitis and primary biliary cholangitis)
-Immunoglobulins (autoimmune hepatitis and primary biliary cholangitis)
-Caeruloplasmin (for Wilsons disease)
-Alpha 1 antitrypsin levels (for alpha 1 -antirypsin deficiency)
-Ferritin and transferrin saturation (for hereditary haemochromatosis)

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6
Q

What imaging do you use to diagnose non-alcoholic fatty liver disease?

A

Ultrasound

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7
Q

What autoantibodies do you see in type 1 autoimmune hepatitis?

A

Anti-nuclear antibodies (ANA)
Anti-smooth muscle antibodies (anti-actin)
Anti-soluble liver antigen (anti-SLA/LP)

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8
Q

What autoantibodies are found in type 2 autoimmune hepatitis?

A

Anti-liver kidney microsomes-1 (anti-LKM1)
Anti-liver cytosol antigen type 1 (anti-LC1)

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9
Q

What autoantibodies are relevant to liver disease?

A

Antinuclear antibodies (ANA)
Smooth muscle antibodies (SMA)
Antimitochondrial antibodies (AMA)
Antibodies to liver kidney microsome type-1 (LKM-1)–> autoimmune hepatitis

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10
Q

What happens to the prothrombin time when you have decompensated liver cirrhosis?

A

Increased prothrombin time due to reduced synthetic function of the liver (reduced production of clotting factors)

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11
Q

What happens to the platelet count in decompensated liver cirrhosis?

A

Low platelets (thrombocytopenia). It indicated more advances disease.

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12
Q

What happens to the albumin level in decompensated cirrhosis?

A

You get low albumin due to reduced synthetic function of the liver

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13
Q

What happens to the sodium levels in decompensated liver cirrhosis?

A

Low Na+ (hyponatraemia).This occurs with fluid retention in severe liver disease

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14
Q

What is the name of the tumour marker seen in hepatocellular carcinoma?

A

Alpha-fetoprotein

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15
Q

What is the FIRST-LINE investigation for assessing fibrosis IN non-alcoholic fatty liver disease?

A

Enhanced liver fibrosis (ELF) blood test

This test is not used in patients with other causes of liver disease.

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16
Q

What is the enhanced liver fibrosis blood test and what do the results of it indicate?

A

It is a blood test that measures 3 molecules in liver metabolism. These are HA, PIIINP and TIMP-1.

It gives a score reflecting the severity of liver fibrosis.

Results:

Under 10.51 = unlikely advanced fibrosis (NICE recommend rechecking every 3 years in NAFLD)

10.51 + = advanced fibrosis

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17
Q

What does NICE recommend for patients with NAFLD for the ELF (enhanced liver fibrosis) blood test?

A

NICE recommend rechecking the results of the ELF blood test every 3 years in patients with NAFLD

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18
Q

In an ultrasound, what would be seen in non-alcoholic fatty liver disease?

A

Nodularity of the liver surface

A “corkscrew” appearance to the hepatic arteries with increased flow as they compensate for the reduced portal flow (due to portal hypertension)

Enlarged portal veins with reduced blood flow

Ascites

Splenomegaly

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19
Q

What screening tool alongside alpha-fetoprotein can be used to diagnose hepatocellular carinoma?

A

Ultrasound

20
Q

What test can CONFIRM the diagnosis of cirrhosis (IMPORTANT TO REMEMBER)?

A

Liver biopsy

21
Q

What scoring system evaluates the severity of liver disease based on bilirubin, creatinine and INR levels?What does it stand for? What does a higher score tell you?

A

The MELD score

Stands for Model for End-Stage Liver Disease

This is given AS A PERCENTAGE

A higher score indicates a greater risk of mortality within a 3 month period.It is used to prioritise pts for liver transplantation

22
Q

When does NICE recommend using the MELD score (to evaluate severity of liver disease)?

A

To use the MELD score every 6 months in patients with compensated cirrhosis

23
Q

What is the Child-pugh score? What are the 5 factors to consider when calculating the score? What is the minimum and maximum score?

A

It is a score used to assess the severity of cirrhosis and the prognosis.

Albumin
Bilirubin
Clotting (prothrombin time)
Dilation (Ascites)
Encephalopathy

5 is the minimum (1 point for each factors) and 15 is the maximum (3 for each)

24
Q

How do you monitor complications in liver cirrhosis? IMPORTANT!!!

A

Use the MELD score EVERY 6 months

Do an ultrasound and alpha-fetoprotein test EVERY 6 months for hepatocellular carcinoma

Do an endoscopy EVERY 3 years for oesophageal varices

25
Q

Liver transplantation is generally considered when there are features of liver disease. What are those 4 KEY features?

A

Ascites
Hepatic encephalopathy
Oesophageal varices bleeding
Jaundice

26
Q

How does cirrhosis affect protein metabolism?

A

It reduces the amount of protein the liver produces.

27
Q

How does cirrhosis affect muscle tissue breakdown? Why?

A

More musccle tissue is broken down to use as a fuel when a pt has cirrhosis as the liver can no longer store glucose as glycogen and can’t release when required so in turn, muscle tissue is broken down to use as fuel. Also less protein is available for maintaining muscle tissue (as the liver cannot produce proteins due to being cirrhotic).

28
Q

Which two veins (when the join) forms the portal vein?

A

The superior mesenteric and splenic vein

29
Q

Why is it important to cross match blood (for example in patients with beeding oesophageal varices)?

A

The purpose of crossmatching blood is to detect the presence of antibodies in the recipient against the red blood cells of the donor. These antibodies attach to the the RBC’s of the donor after the transfusion. An incompatible transfusion can result in a severe haemolytic anaemia and even death.

30
Q

What is refractory ascites and what is it usually a serious complication of?

A

Refractory ascites is ascites that does NOT recede or that recurs shortly after therapeutic paracentesis (DESPITE sodium restriction and diuretic treatment). It is a very serious complication of decompensated liver cirrhosis and requires TIPS procedure.

31
Q

What are the options to control bleeding oesophageal varices if variceal band ligation does not work?

A
  1. Sengstaken-blakemore tube (inflatable balloon one for the oesphagus and one for the stomach, and is used to stop bleeding from varices)

2.TIPS (involves creating a bypass/shunt between the hepatic vein and portal vein –>to relieve pressure in portal vein.Is inserted into the internal jugular vein.).It is done under X-ray guidance by an interventional radiologist.

32
Q

What are the indications for TIPS?

A

1.Bleeding oesophageal varices
2.Refractory ascites

33
Q

What is the difference between transudates and exudates?

A

Exudates are fluids, CELLS or OTHER CELLULAR substances that are slowly discharged from BLOOD VESSELS usually from inflammed tissues. Transudates are fluids that pass through a membrane or squueze through tissue/ into the EXTRACELLULAR SPACE of TISSUES.

Exudate (High protein content, may contain some white and red blood cells)

Transudate (low protein content, few cells)

Example of transudate cause is cirrhosis of the liver

34
Q

Does liver cirrhosis cause transudative ascites or exudative ascites?

A

Transudative ascites (where there is low protein content. Transudates —> increase hydrostatic pressure and decrease oncotic pressure.

35
Q

How does increased pressure in the portal system lead to sodium retnetion and fluid re-absroption in the kidneys? (Leading to oedema)

A

Ascites refers to fluid in the peritoneal cavity. The increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and other abdominal organs into the peritoneal cavity. The drop in circulating volume caused by fluid loss into the peritoneal cavity causes reduced blood pressure in the kidneys. The kidneys sense this lower pressure and release renin, which leads to increased aldosterone secretion via the renin-angiotensin-aldosterone system. Increased aldosterone causes the reabsorption of fluid and sodium in the kidneys, leading to fluid and sodium retention

36
Q

How do you manage ascites?

A

Low sodium diet
Aldosterone antagonists (e.g., spironolactone)
Paracentesis (ascitic tap or ascitic drain)
Prophylactic antibiotics (ciprofloxacin or norfloxacin) when there is <15 g/litre of protein in the ascitic fluid
Transjugular intrahepatic portosystemic shunt (TIPS) is considered in refractory ascites
Liver transplantation is considered in refractory ascites

37
Q

What are the most common organisms that cause spontaneous bacterial peritonitis?

A

Esterichia coli
Klebsiella pneumoniae

38
Q

How do you manage spontaneous bacterial peritonitis?

A

Take a sample of the ascitic fluid for culture BEFORE giving antibiotics
Then give IV antibiotics (e.g. piperacillin with tazobactam)

39
Q

How may patients present with spontaneous bacterial peritonitis?

A

Fever
Abdominal pain
Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
Ileus (reduced movement in the intestines)
Hypotension

40
Q

What is hepatorenal syndrome?

A

It involves imparied kidney function caused by changes in the blood flow to the kidneys relating to liver cirrhosis and portal hypertension.It has a poor prognosis unless the patient has a liver transplant.

41
Q

How can ammonia cause hepatic encephalopathy?

A

Ammonia is produced by intestinal bacteria when they break down proteins. Ammonia is absorbed in the intestines.2 reasons for ammonia build up in blood cirrhotic patients: 1.liver cells’ functional impairment.Ammonia can’t be metabolised into harmless products. 2.collaterla vessels between the portal and systemic circulation mean that ammonia bypasses the liver and enters the systemic system directly.

42
Q

What factors can trigger or worsen hepatic encephalopathy?

A

Constipation
Dehydration
Electrolyte disturbance
Infection
Gastrointestinal bleeding
High protein diet
Medications (particularly sedative medications)

43
Q

How do you manage hepatic encephalopathy?

A

Lactulose (aiming for 2-3 soft stools daily)
Antibiotics (e.g., rifaximin) to reduce the number of intestinal bacteria producing ammonia
Nutritional support (nasogastric feeding may be required)

44
Q

Why is rifaximin antibiotics used in hepatic encephalopathy?

A

Rifaximin is the usual choice of antibiotic as it is poorly absorbed and stays in the gastrointestinal tract (so will reduce the intestinal bacteria so less ammonia is produced by them and less ammonia going to the brain).

45
Q
A

Gastroenterology (10 decks)

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