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4th Year Medicine 2 > Gastroenterology (Liver) > Flashcards

Gastroenterology (Liver) Flashcards

1
Q

List what is measured in LFTs?

A
  1. ALT
  2. AST
  3. ALP
  4. GGT
  5. Bilirubin
  6. Albumin
  7. PT
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2
Q

ALT and AST are produced by__________
ALP and GGT are produced by _________

A
  • ALT and AST are produced by the liver and ALP and GGT from the hepatobiliary system
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3
Q

What LFTs parameters allow you to assess synthetic function of the liver?

A
  • Bilirubin, albumin and PT allow you to assess liver synthetic function
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4
Q

What are ALT and ALP markers of?

A
  • ALT= marker of hepatocellular injury
  • ALP= marker of cholestasis
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5
Q

LFTs - hepatitis vs cholestasis?

A
  • If there is a higher increase in ALT vs ALP then hepatocellular injury
  • If higher increase in ALP then cholestasis
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6
Q

If ALP is predominantly raised _______

A
  • If ALP is raised review GGT, if both are raised then this suggests cholestasis
  • If ALP raised by GGT is not then there is another cause of raised ALP e.g. bone metastases
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7
Q

If a patient is jaundiced and ALT and ALP are normal?

A

review the bilirubin, an isolated rise in bilirubin is suggestive of pre-hepatic jaundice

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8
Q

Describe how ALT and AST can be used to assess if damage due to alcohol?

A
  • If AST is more than double the ALT this suggests hepatocellular injury related to alcohol
  • If ALT is more than AST this suggests hepatocellular injury related to NAFLD or NASH
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9
Q

If ALT and AST are in the thousands?

A

this suggests ischaemic hepatitis

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10
Q

Explain what PBC is?

A
  • Autoimmune progressive destruction of the small bile ducts in the liver (intrahepatic)
  • This is different from PSC where there is both intra and extrahepatic bile duct destruction
  • The destruction causes obstruction to the outflow of bile and cholestasis
  • There is then back pressure due to this obstruction which causes damage to the liver
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11
Q

Who gets PBC?

A
  • This is condition is most common in middle aged women and is associated with Anti-Mitochondrial antibodies (AMA)
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12
Q

Presentation of PBC?

A
  • Fatigue
  • Itch without rash (due to bile salts in skin)
  • Jaundice
  • Xanthelasma and xanthoma (due to leakage of cholesterol from the bile)
  • May show signs of liver failure late on
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13
Q

Investigations for PBC?

A
  • Diagnosis can generally be made on blood tests and testing for Anti-mitochondrial antibodies
  • ALP is likely to be raised
  • Conjugated bilirubin may be raised
  • ESR may be raised
  • Liver biopsy can be done if required
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14
Q

Management of PBC?

A
  • Ursodeoxycholic acid is given to patients with PBC and is thought to slow disease overall progression
  • Those with liver failure need a transplant however often by the time the disease progresses to liver failure the patient is too old for a transplant
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15
Q

Beaded appearance on MRCP?

A

PSC

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16
Q

Some differences between PBC and PSC?

A

PBC - only intrahepatic ducts - associated with AMA - can treat with ursodeoxycholic acid - middle aged women

PSC - intra and extra hepatic ducts - may have raised ANCA - link with ulcerative colitis - ursodeoxycholic acid less of a role - young men

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17
Q

What is PSC?

A
  • Condition where there is fibrosis of intra and extrahepatic bile ducts
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18
Q

Who gets PSC?

A
  • Thought to be combination of auto-immune, genetic, environmental triggers
  • Strong link with ulcerative colitis
  • Most common in young men with ulcerative colitis
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19
Q

Presentation of PSC?

A
  • May be asymptomatic in early disease
  • Right upper quadrant pain
  • Pruritis
  • Fatigue
  • Jaundice
  • Hepatomegaly
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20
Q

Investigations for PSC?

A
  • LFTs show a cholestatic picture – raised ALP, GGT and conjugated bilirubin
  • ANCA and ANA may be raised
  • MRCP can be used for diagnosis and shows a “beaded appearance”
  • ERCP can also be done to visualise bile ducts instead
  • If necessary biopsy can be done which shows “onion skin fibrosis”
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21
Q

Management of PSC?

A
  • Liver transplant is only curative management
  • ERCP can be used to stent bile ducts and relieve obstruction
  • Ursodeoxycholic acid probably not helpful, neither are steroids are immunosuppressive agents in most cases
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22
Q

Complications of PSC?

A
  • Link with IBD – consider screening
  • Cirrhosis
  • Increased risk of colorectal cancer and cholangiocarcinoma
  • Risk of bacterial cholangitis due to blocked ducts
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23
Q

What is autoimmune hepatitis?

A

condition where there is autoimmune destruction of the liver

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24
Q

Who gets autoimmune hepatitis?

A
  • Often associated with other auto-immune diseases e.g. thyroiditis or coeliacs
  • More common in females than males
  • Associated with anti-nuclear antibodies (ANA) and anti-smooth muscle antibodies (ASMA)
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25
Q

Presentation of autoimmune hepatitis?

A
  • Can be asymptomatic
  • Fever
  • Jaundice
  • Hepatosplenomegaly
  • Fatigue
  • Malaise
  • Lethargy
  • Nausea
  • Abdominal pain
  • Anorexia
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26
Q

Investigations for autoimmune hepatitis?

A
  • Check for ANA and ASMA
  • Raised AST and ALT
  • Liver biopsy is most important diagnostic test – shows “piecemeal necrosis”
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27
Q

Biopsy shows “piecemeal necrosis”

A

autoimmune hepatitis

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28
Q

Management of autoimmune hepatitis?

A
  • Treatment is with prednisolone (induction) and azathioprine (maintenance of remission)
  • In severe cases a transplant may be needed but the disease can actually recur in a transplant
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29
Q

Explain the spectrum of alcoholic liver disease?

A
  • Fatty liver occurs in most heavy drinkers even after one episode of heavy intake, fat accumulates in hepatocytes due to abnormalities in the intermediate metabolism of lipids and carbohydrates
  • Fatty liver is completely reversible on withdrawal of alcohol
  • If alcoholism continues the liver can become inflamed due to the fatty changes, this can be asymptomatic or symptomatic and signs of liver failure may be seen
  • Alcoholic hepatitis is potentially reversible on withdrawal
  • If inflammation continues cirrhosis will occur and this is irreversible
30
Q

List some signs of liver disease?

A

jaundice, hepatomegaly, spider naevi, palmar erythema, gynaecomastia, bruising, ascites, caput medusae, asterxis (in decompensated)

31
Q

What is NAFLD?

A
  • This is fatty liver disease/ steatohepatitis in the absence of another cause
  • Steatosis (abnormal retention of fat in liver cells) occurs
  • This can then progress to steatohepatitis (NASH), fibrosis and then cirrhosis
32
Q

Who gets NAFLD?

A
  • It is associated with metabolic syndrome which includes hypertension, Type 2 diabetes, hyperlipidaemia and insulin resistance
33
Q

Presentation of NAFLD?

A
  • NAFLD may be asymptomatic
  • If progresses to hepatitis could present with symptoms and signs of liver disease
34
Q

Investigations for NAFLD?

A
  • Need to rule out other causes of liver disease e.g. viral hepatitis, auto-antibodies etc
  • Ultrasound can be helpful to confirm diagnosis but does not give an idea of liver function/staging
35
Q

Management of NAFLD?

A
  • Main treatment is lifestyle:
  • Encourage weight loss, exercise, improved diet, BP and blood glucose control, avoid alcohol, control cholesterol
36
Q

What is cirrhosis?

A
  • End stage liver disease
  • Diffuse process affecting the whole liver in which there is fibrosis and conversion of normal liver architecture in abnormal nodules
  • 4 main causes to consider are alcoholic liver disease, NAFLD, hepatitis B and C
  • Other rarer causes e.g. PBC, PSC
37
Q

Diagnosis of liver cirrhosis?

A
  • Transient elastography can be used to diagnose cirrhosis
  • Can also be diagnosed on liver biopsy
38
Q

General management of cirrhosis?

A
  • US and AFP every 6 months to screen for hepatocellular carcinoma
  • Endoscopy every 3 years to check if developed oesophageal varices
  • High protein, low sodium diet
  • MELD score every 6 months
  • Consideration of transplant
  • Manage complications
39
Q

List 6 complications of cirrhosis?

A

malnutrition and muscle wasting
varices
ascites
spontaneous bacterial peritonitis
encephalopathy
hepatorenal syndrome

40
Q

Why do you get malnutrition and muscle wasting in cirrhosis?

A

cirrhosis causes increased use of muscle tissue as fuel due to changes in metabolism of proteins in the liver and disruption to liver ability to store and release glycogen

41
Q

How is ascites in cirrhosis managed?

A

this is managed with sodium restriction and spironolactone, if large ascites may need paracentesis to drain, if refractory ascites BSG suggest considering TIPS

42
Q

Describe spontaneous bacterial peritonitis?

A

this can occur in cirrhosis and ascites and has a high mortality, should have low threshold for suspecting as can be asymptomatic, presents with deranged bloods, fever, abdo pain, ileus and hypotension, ascitic culture and then IV antibiotics

43
Q

Explain hepatic encephalopathy and presentation?

A

blood bypasses liver and toxic metabolites go to the brain, presents with disorder of personality, mood and intellect, slurred speech, vomiting or nausea, fetor hepaticus, liver flap, constructional apraxia and decreased mental function

44
Q

Management of hepatic encephalopathy?

A

treat underlying cause by also can manage with lactulose (first line thought to promote excretion of ammonia) and rifaximin (secondary prophylaxis thought to modulate gut flora resulting in decreased ammonia production)

45
Q

Describe hepatorenal syndrome?

A

Hepatorenal syndrome – renal failure caused by cirrhosis – this is fatal within a week unless a liver transplant is done

46
Q

What is alpha 1 antitrypsin deficiency?

A

Alpha-1 antitrypsin is an enzyme inhibitor of proteases produced in the liver
* Proteases are usually released as part of the immune response as they can break down bacteria however, they can also break down lung and liver parenchyma
* AAT works to inhibit the breakdown of connective tissue in the lung and liver by proteases
* In AAT deficiency there is increased damaged as there is less inhibition of proteases

47
Q

Who gets AAT deficiency?

A
  • Autosomal recessive genetic condition
48
Q

Presentation of AAT deficiency?

A
  • Liver cirrhosis – usually after 50 years old
  • Bronchiectasis and emphysema in the lungs after 30 years old
49
Q

Investigations for AAT deficiency?

A
  • Low serum alpha 1 antitrypsin
  • Liver biopsy
  • Genetic testing
  • HR CT diagnoses bronchiectasis and emphysema
50
Q

Management for AAT deficiency?

A
  • Advise not to smoke as this greatly accelerates emphysema
  • Symptomatic management
  • Organ transplant for end stage disease
51
Q

3 types of hepatitis that are parenteral spread?

A

B
C
D

52
Q

2 types of hepatitis that are faeco-oral spread?

A

A
E

53
Q

Hepatitis A
Spread
Severity
Acute or chronic
risk of cancer
vaccine
other information?

A

faeco-oral
usually mild and recover
usually acute and recovers
no risk of cancer
vaccine available
Generally unwell with nausea and anorexia, become jaundiced and then recover

54
Q

Hepatitis B
Spread
Severity
Acute or chronic
risk of cancer
vaccine
other information?

A

parenteral
often severe
can be acute or chronic, about 10% will get chronic
risk of cancer
vaccine available
need follow up to determine if chronic

55
Q

Hepatitis C
Spread
Severity
Acute or chronic
risk of cancer
vaccine
other information?

A

parenteral
usually mild
almost always chronic disease (75%)
risk of cancer
no vaccine
need follow up to determine if chronic

56
Q

Hepatitis D
Spread
Severity
Acute or chronic
risk of cancer
vaccine
other information?

A

parenteral
severe
need infected with hep B to develop - then makes hep B worse
risk of cancer
protected if had hep b vaccine

57
Q

Hepatitis E
Spread
Severity
Acute or chronic
risk of cancer
vaccine
other information?

A

faeco-oral
often mild but severe in pregnancy
acute
no risk of cancer
no vaccine
infection is more common in tropics

58
Q

Management of viral hepatitis?

A
  • If anyone with hepatitis A is severely unwell, admit to hospital, if not can give supportive treatment with pain relief, anti-emetic etc
  • Those with hepatitis B and C need referred to secondary care, get supportive treatment and antivirals e.g. peginterferon, entecavir or tenofovir
  • Important to monitor those who have had a chronic infection for hepatocellular carcinoma
59
Q

HBsAg?

A

acute or chronic infection

60
Q

Anti-HBs?

A

response to HBsAg - past or current infection or have been vaccinated

61
Q

Anti-HBc?

A

previous or current infection

62
Q

HBeAg?

A

active infection - a measure of infectivity

63
Q

HBVDNA?

A

active infection
measure of viral load

64
Q

IgM antibodies?

A

active disease

65
Q

IgG antibodies?

A

recovery or vaccination

66
Q

Person with immunity through vaccination?

A

positive for HbsAB but negative for everything else

67
Q

Person with immunity from infection?

A

positive for Anti-HBs and Anti-HBc but negative for everything else

68
Q

A person with active disease?

A
  • A person with active disease will be positive for HBsAg, Anti-HBc, HbeAG, high HBVDNA but negative for Anti-HBs
69
Q

A person with chronic disease?

A

positive for HBsAG and Anti-HBc but negative for Anti-HBs

70
Q

Effect of COCP on the liver?

A

can cause cholestasis

4th Year Medicine 2 (14 decks)

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