Liver & Biliary Disease Flashcards

1
Q

What is the management for the prophylaxis of spontaneous bacterial peritonitis in patients with ascites and a protein concentration of <= 15 g/L?

A

Oral ciprofloxacin or norfloxacin.

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2
Q

What is spontaneous bacterial peritonitis?

A

Form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis.

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3
Q

What are the features of spontaneous bacterial peritonitis?

A

Ascites, abdominal pain and fever.

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4
Q

How is spontaneous bacterial peritonitis diagnosed?

A

Paracentesis - neutrophil count > 250 cells/ul

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5
Q

What is the most common organism found on ascitic culture of spontaneous bacterial peritonitis?

A

E.coli

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6
Q

What is the management of spontaneous bacterial peritonitis?

A

IV cefotaxime

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7
Q

What is the treatment for acute cholecystitis?

A

IV antibiotics and laparoscopic cholecystectomy within 1 week of diagnosis.

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8
Q

Pigmented gallstones are associated with which condition?

A

Sickle cell anaemia

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9
Q

Does blockage of the cystic duct/gallbladder cause jaundice?

A

No

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10
Q

Where does the pain radiate to with biliary colic?

A

Interscapular region (referred pain from diaphragmatic irritation).

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11
Q

Which antibiotic can cause cholestasis?

A

Co-amoxiclav

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12
Q

What is the most common causative agent for ascending cholangitis?

A

E.coli

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13
Q

What is Reynolds’ pentad?

A

Charcot’s triad (RUQ pain, fever and jaundice) + hypotension and confusion. Indicates severe case of ascending cholangitis.

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14
Q

Subcutaneous (surgical) emphysema is a known complication of what type of surgery?

A

Laparoscopic - surgical emphysema is the presence of gas in subcutaneous soft tissues. Crepitus on palpation.

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15
Q

What is the treatment for biliary colic?

A

Elective laparoscopic cholecystectomy.

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16
Q

What test is useful in determining the cause of isolated hyperbilirubinaemia?

A

FBC - to determine haemolysis or Gilbert’s syndrome.

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17
Q

Obesity and abnormal LFTs suggest what diagnosis?

A

Non-alcoholic fatty liver disease.

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18
Q

What is the treatment for asymptomatic gallstones?

A

Reassurance

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19
Q

What would you expect the LFTs and CRP levels to be in biliary colic?

A

Normal

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20
Q

A 22-year-old man returns to the UK from holiday in India. He presents with painless jaundice. On examination he is not deeply jaundiced and there is no organomegaly.

A

Hepatitis A

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21
Q

A 56-year-old man presents with jaundice. He has a long history of alcohol misuse. On examination he is jaundiced and ultrasound shows multiple echo dense lesions in both lobes of the liver. His alpha feto protein is elevated 6 times the normal range

A

Hepatocellular carcinoma

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22
Q

A 32-year-old man who has suffered from Crohns disease for many years presents with intermittent jaundice. When it occurs it is obstructive in nature. It then usually resolves spontaneously.

A

Bile duct stones - impaired bile salt absorption in terminal ileum to gallstones develop.

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23
Q

What is the first line investigation for acute cholecystitis?

A

Abdominal ultrasound

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24
Q

Where is bile produced and stored?

A

Produced in liver and stored in gallbladder.

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25
Q

Which hormone stimulates bile release into duodenum via contraction of gallbladder?

A

CCK

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26
Q

Where is bile reabsorbed?

A

Terminal ileum

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27
Q

List the components of bile

A

Bile salts, cholesterol, phospholipids, bilirubin, electrolytes and water.

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28
Q

What is the function of bile?

A

Emulsifies fat and eliminates waste e.g. bilirubin.

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29
Q

What is bilirubin?

A

Breakdown product of rbc.

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30
Q

Where is bilirubin conjugated?

A

Liver

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31
Q

As most of the bilirubin in reabsorbed by the terminal ileum and returned to the liver, what happens to the bilirubin that is excreted?

A

Excreted by kidney as urobilin or excreted by bowel as stercobilinogen.

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32
Q

Name the pre-hepatic (unconjugated), hepatic (mixed) and post-hepatic (conjugated) causes of jaundice

A

Pre-hepatic: haemolytic anaemia, Gilbert’s syndrome, Criggler-Najjar syndrome.
Hepatic: viral hepatitis, alcoholic liver disease, medication, autoimmune hepatitis, hereditary haemochromatosis, hepatocellular carcinoma, primary sclerosing cholangitis, primary biliary sclerosis.
Post-hepatic: ascending cholangitis (intra-luminal), pancreatic cancer (extra-mural), cholangiocarcinoma (mural), primary sclerosing cholangitis (mural), strictures (mural), lymphoma (extra-mural).

33
Q

Where does the ampulla of Vater open into?

A

Duodenum

34
Q

What is the sphincter of Oddi?

A

Ring of muscle surrounding the ampulla of Vater that controls the flow of bile and pancreatic secretions into the duodenum.

35
Q

Define cholestasis

A

Blockage of flow of bile

36
Q

Define cholelithiasis

A

Presence of gallstones within gallbladder.

37
Q

Define choledocholithiasis

A

Gallstones present in bile duct.

38
Q

Define gallbladder empyema

A

Pus in gallbladder.

39
Q

Are gallstones normally symptomatic?

A

No normally asymptomatic.

40
Q

What are the complications of gallstones?

A

Biliary colic, acute cholecystitis, ascending cholangitis, acute pancreatitis.

41
Q

Define Mirrizi syndrome

A

Common hepatic duct obstruction caused by extrinsic compression from an impacted stone in the cystic duct or infundibulum of the gallbladder. Patients can present with jaundice, fever RUQ pain.

42
Q

What are the most common type of gallstones made of?

A

Cholesterol

43
Q

What causes black pigment gallstones?

A

Calcium bilirubinate - in haemolytic anaemias.

44
Q

What are the synthetic liver function tests?

A

Bilirubin, albumin and clotting factors.

45
Q

A raised ALP is a sign of…

A

Biliary obstruction in presence of RUQ pain and/or jaundice.
But can also be raised in liver or bone malignancy, primary biliary cirrhosis and Paget’s disease.

46
Q

ALT and AST are useful markers of…

A

Hepatocellular injury.

47
Q

When would a MRCP be indicated?

A

To investigate further if the ultrasound scan does not show stones in the bile duct, but there is bile duct dilatation or raised bilirubin suggestive of obstruction.

48
Q

What is the main indications for ERCP?

A

Clear stones in bile ducts, take biopsies of tumours, inject contrast for X-rays, or insert stents or balloon dilation to improve biliary drainage.

49
Q

What is the management for asymptomatic gallstones?

A

No intervention required.

50
Q

Describe the complications of a cholecystectomy

A

Bleeding, infection, pain and scars.
Damage to the bile duct including leakage and strictures.
Stones left in the bile duct.
Damage to the bowel, blood vessels or other organs.
Anaesthetic risks.
Venous thromboembolism (DVT/PE).
Post-cholecystectomy syndrome (diarrhoea, indigestion, epigastric/RUQ pain, nausea, intolerance of fatty foods, flatulence).

51
Q

Compensated vs. Decompensated liver cirrhosis

A

Compensated: asymptomatic as small residual function of liver still left.
Decompensated: liver no longer has capacity to carry out its normal functions, resulting in complications.

52
Q

List the stigmata of chronic liver disease

A

Spider naevi, palmar erythema, jaundice, leukonychia (due to low albumin), asterixis, ascites, oesophageal varices, caput medusae, hepatosplenomegaly, Dupuytren’s contracture, gynaecomastia, bruising.

53
Q

What are the features of hepatic decompensation?

A

Encephalopathy, ascites, jaundice, GI bleeding, coagulopathy.

54
Q

List the tests in a non-invasive liver screen after a patient receives abnormal LFTs

A

Ultrasound liver.
Hepatitis B and C serology.
Auto-Abs: ANA, SMA, AMA, LKM-1 (autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis).
Immunoglobulins (autoimmune hepatitis and primary biliary cirrhosis).
Caeruloplasmin (Wilsons disease).
Alpha 1 Anti-trypsin levels (alpha 1 anti-trypsin deficiency).
Ferritin and transferrin saturation (hereditary haemochromatosis).

55
Q

Describe the hepatic picture vs cholestatic picture of LFT derangement

A

Hepatic (liver parenchyma): a predominant rise in ALT/AST.
Cholestatic (biliary system): a predominant rise in gGT/ALP.

56
Q

What are the markers of synthetic liver function?

A

Bilirubin, albumin and clotting factors.

57
Q

A rise in liver enzymes reflects what?

A

Liver injury or inflammation.

58
Q

What is a haemangioma?

A

Common benign tumours of the liver.

59
Q

What is focal nodular hyperplasia?

A

Benign liver tumour made of fibrotic tissue. Often related to oestrogen and therefore more common in women taking the OCP.

60
Q

Describe the main functions of the liver

A

Storage of glycogen, release of glucose and gluconeogensis.
Synthesis of albumin and clotting factors.
Catabolism of amino acids and urea production.
Detoxification of nitrogenous molecules from GI tract.
Drug metabolism.
Conjugation and excretion of bilirubin.
Production and excretion of bile salts.
Immune function e.g. production of acute phase proteins.

61
Q

Describe the 3 types of liver transplant

A

Orthotopic transplant - entire liver transplanted from deceased patient to recipient.
Living donor transplant - portion of liver from living donor transplanted to recipient.
Split donation - split liver from deceased patient into 2 and transplant it into 2 patients.

62
Q

What are the indications for a liver transplant?

A

Acute liver failure - acute viral hepatitis and paracetamol overdose. Patients placed at top of transplant list.
Chronic liver failure.

63
Q

What are the 2 types of incision for a liver transplant?

A

Rooftop or Mercedes Benz.

64
Q

Why does haemochromatosis present later in females?

A

Due to menstruation acting to regularly eliminate iron from the body.

65
Q

What is the most common cause of acute liver failure in UK?

A

Paracetamol overdose (drug-induced liver injury).

66
Q

What are the normal metabolites of paracetamol?

A

Sulphate or glucuronide, which are excreted via urine.

67
Q

What metabolite builds up in paracetamol overdose causing hepatotoxicity?

A

NAPQI

68
Q

When do patients develop clinical features of hepatic necrosis following a paracetamol overdose?

A

48-72 hours.

69
Q

Describe the features of hepatic necrosis

A

RUQ pain, nausea, vomiting, jaundice, AKI (i.e. oligo-/anuria) and hepatic encephalopathy.

70
Q

What is the treatment for a paracetamol overdose?

A

N-acetylcysteine (via IV).

71
Q

What are the features of acute liver failure?

A

Coagulopathy, jaundice and alerted levels of consciousness/confusion (hepatic encephalopathy).

72
Q

What is Budd-Chiari syndrome?

A

A classic triad of hepatomegaly, abdominal pain and ascites due to hepatic venous obstruction (from thrombus - hypercoagulable states).

73
Q

What is Gilbert syndrome?

A

Autosomal recessive disorder that causes abnormal bilirubin processing in the liver, due to a mutation in the enzyme that conjugates bilirubin. This leads to recurrent episodes of unconjugated hyperbilirubinaemia. It is the most common cause of inherited jaundice and is benign. Episodes of jaundice are precipitated by febrile illness, exercise and stress.

74
Q

What is the M rule for primary biliary cholangitis?

A

IgM, anti-Mitochondrial antibodies, Middle aged females.

75
Q

Refeeding syndrome can result in…

A

Abnormal fluid balance and arrhythmias.

76
Q

Coma is what grade of hepatic encephalopathy?

A

Grade IV

77
Q

What is the management for hepatic encephalopathy?

A
  • Lactulose (first line) - excretion of ammonia.
  • Plus rifaximin (secondary prophylaxis).
78
Q

Management of severe alcoholic hepatitis?

A

Corticosteroids