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GI > Liver, Biliary Tract and Pancreatic Diseases > Flashcards

Liver, Biliary Tract and Pancreatic Diseases Flashcards

1
Q

What causes pre-hepatic jaundice?

A

Too much haem to break down- unconjugated bilirubin enters small intestine

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2
Q

What will pre-hepatic jaundice show with regards to urine and stool colours?

A

Normal

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3
Q

What causes hepatic jaundice?

A

Hepatocyte damage means not enough bile is produced

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4
Q

What will hepatic jaundice show with regards to urine and stool colours?

A

Dark urine and may or may not cause pale stools

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5
Q

What causes post-hepatic jaundice?

A

Some kind of obstruction

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6
Q

What will post-hepatic jaundice show with regards to urine and stool colours?

A

Dark urine and pale stools

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7
Q

What can alcoholic liver disease cause?

A

Portal hypertension, malnutrition and increased risk of hepatocellular carcinoma

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8
Q

Which enzymes break down alcohol?

A

Alcohol dehydrogenase and aldehyde dehydrogenase

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9
Q

What is alcohol broken down to form?

A

Catalase and ketone bodies

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10
Q

What is an effective short term treatment for alcoholic liver disease?

A

Prednisolone

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11
Q

What class of LFTs will alcoholic liver disease show?

A

Mixed hepatic and cholestatic

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12
Q

What effect will alcohol have on the liver after 2-3 days and is this reversible?

A

Fatty liver- yes

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13
Q

What effect will alcohol have on the liver after 4-6 weeks and is this reversible?

A

Inflammation (hepatitis)- yes

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14
Q

What effect will alcohol have on the liver after months-years and is this reversible?

A

Fibrosis- no

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15
Q

What effect will alcohol have on the liver after many years and is this reversible?

A

Cirrhosis- no

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16
Q

How do fat vacuoles appear on histology?

A

White blobs in hepatocytes

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17
Q

What are essential features of alcoholic hepatitis?

A

Excess alcohol, bilirubin > 80, exclusion of other causes, AST < 500

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18
Q

What is laid down around cells in alcoholic fibrosis? What colour will this be when dyed?

A

Collagen- blue

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19
Q

What LFTs will NAFLD show?

A

Hepatitic- increased ALT and AST

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20
Q

What is significant about an ALT of above 300?

A

Unlikely to be NAFLD

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21
Q

What does steatosis (the first stage of NAFLD) mean?

A

Fat depositions in the liver

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22
Q

What does steatohepatitis (the second stage of NAFLD) mean?

A

Fat deposits have resulted in inflammation

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23
Q

What is NAFLD very closely associated with?

A

Metabolic syndrome

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24
Q

How is simple steatosis diagnosed?

A

Ultrasound

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25
Q

How is steato-hepatitis diagnosed?

A

Liver biopsy

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26
Q

What are the outcomes of steatosis?

A

If it doesn’t progress then there are no liver outcomes, however there is an increased CV risk

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27
Q

What are the outcomes of steato-hepatitis?

A

Risk of progression to fibrosis and cirrhosis

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28
Q

What is the main treatment for NAFLD?

A

Weight loss and exercise

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29
Q

What will any type of hepatitis show in terms of LFTs?

A

A predominant rise in aminotransferases (AST, ALT)

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30
Q

How is Hep A spread?

A

Faecal-oral spread

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31
Q

What is the incubation time of Hep A?

A

Short

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32
Q

Is hepatitis A directly cytopathic or is the damage caused by an inflammatory response?

A

Directly cytopathic

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33
Q

Is there a carrier state of Hep A?

A

No

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34
Q

What is the outcome of Hep A usually?

A

Mild illness with full recovery

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35
Q

How is Hep B spread?

A

Blood, blood products, sexually or vertically

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36
Q

What is the incubation time of Hep B?

A

Long (4-6 months)

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37
Q

Is hepatitis B directly cytopathic or is the damage caused by an inflammatory response?

A

Inflammatory response

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38
Q

Do carriers of Hep B exist?

A

Yes, but fairly infrequent

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39
Q

What is the outcome of Hep B?

A

Fulminant acute infection and death, chronic hepatitis, hepatocellular carcinoma

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40
Q

Is Hep B infectious?

A

Very

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41
Q

How is Hep C spread?

A

Blood, blood products, sexually

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42
Q

Is Hep C infectious?

A

Yes- but less so than hep B

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43
Q

What is the incubation time of Hep C?

A

Shorter (4-6 weeks)

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44
Q

What is the outcome of hep C?

A

It is commonly asymptomatic and becomes chronic hepatitis which can lead to cirrhosis and hepatocellular carcinoma

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45
Q

What is the most common hepatitis in the UK?

A

Hep C

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46
Q

Who are at risk groups for Hep C?

A

PWID, vast sexual history, tattoos, Pakistani/Indian ethnicity

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47
Q

What gives a fairly solid diagnosis of Hep C and what should be done if this is found?

A

Positive Hep C antibodies- find out the genotype and refer to hepatology for treatment

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48
Q

Who is autoimmune hepatitis most common in?

A

Females (peaks at 30-40 and 55-65) and people with other autoimmune disease

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49
Q

Autoimmune hepatitis is strongly associated with what?

A

Anti-smooth muscle antibodies

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50
Q

What is shown in terms of LFTs for autoimmune hepatitis?

A

Increased ALT and AST, increased PT

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51
Q

An increase in what antibody is also associated with autoimmune hepatitis?

A

IgG

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52
Q

What are common presentations of autoimmune hepatitis?

A

Hepatomegaly, splenomegaly, jaundice, stigmata of chronic liver disease

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53
Q

What treatment is used short and long term for autoimmune hepatitis?

A

Short- prednisolone

Long- azathioprine

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54
Q

What complications can develop from autoimmune hepatitis?

A

Cirrhosis or oesophageal varices

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55
Q

What are indicators of a poor prognosis in autoimmune hepatitis?

A

Ascites and encephalopathy

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56
Q

Who does primary biliary cholangitis occur most commonly in?

A

Women aged 50-65

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57
Q

What is primary biliary cholangitis strongly associated with?

A

Anti-mitochondrial antibodies

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58
Q

What antibody will potentially be raised in primary biliary cholangitis?

A

IgM

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59
Q

What is the mediator of primary biliary cholangitis?

A

T lymphocytes (CD4+ reacts to M2 target)

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60
Q

Primary biliary cholangitis is an inflammatory process of where?

A

Microscopic bile ducts

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61
Q

What may be seen on histology of primary biliary cholangitis?

A

Granulomas and bile duct loss

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62
Q

What disease is associated with numerous plasma cells?

A

Autoimmune hepatitis

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63
Q

What are common symptoms of primary biliary cholangitis?

A

Fatigue, itch, increased cholesterol and jaundice

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64
Q

What will primary biliary cholangitis show in terms of LFTs?

A

Cholestatic- increased ALP and slight increase of ALT and bilirubin

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65
Q

What is treatment for primary biliary cholangitis?

A

Ursodeoxcholic acid and treatment for itch

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66
Q

Who does primary sclerosing cholangitis occur more commonly in?

A

Males and people with ulcerative colitis

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67
Q

What is strongly associated with primary sclerosing cholangitis?

A

Anti-nuclear cytoplasmic antibodies

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68
Q

Which bile ducts does primary sclerosing cholangitis affect?

A

Intra and extra hepatic- large and small

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69
Q

How is a diagnosis of primary sclerosing cholangitis made?

A

Imaging of biliary tree (ERCP)

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70
Q

What is the outcome of primary sclerosing cholangitis?

A

Jaundice, periductal fibrosis and duct destruction

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71
Q

What is haemochromatosis?

A

Genetic condition causing excess iron in liver

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72
Q

What are secondary causes of haemochromatosis?

A

Excess iron in diet, blood transfusions and certain therapies

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73
Q

What other conditions can primary haemochromatosis predispose to?

A

Diabetes, cardiac failure, impotence and arthritis

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74
Q

What is a treatment option for haemochromatosis?

A

Venesection

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75
Q

What tests should always be done for haemochromatosis?

A

Serum iron and ferritin/transferrin saturations

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76
Q

What is the stain for iron known as?

A

Perl’s stain

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77
Q

What is Wilson’s disease?

A

Autosomal recessive disorder of copper metabolism which causes copper to accumulate in the liver and brain

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78
Q

Wilson’s disease is a loss of function of what?

A

Caeruloplasmin

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79
Q

What are characteristics of Wilson’s disease?

A

Low caeruloplasmin and Kayser-Fleisher rings

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80
Q

When does Wilson’s disease typically present?

A

Young age

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81
Q

What can Wilson’s disease result in?

A

Chronic hepatitis and neurological symptoms

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82
Q

What should you always test for in Wilson’s disease?

A

Serum and urine copper/serum caeruloplasmin

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83
Q

How can you treat Wilson’s disease?

A

Copper-chelation drugs

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84
Q

What can occur as a result of alpha 1 anti-trypsin deficieny?

A

Lung emphysema, liver deposition of mutant protein

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85
Q

What is the treatment for alpha 1 anti-trypsin deficiency?

A

Supportive

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86
Q

What is Budd-Chiari?

A

Thrombosis of hepatic veins

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87
Q

What deficiencies are common in Budd Chiari?

A

Protein S or C

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88
Q

What are acute presentations of Budd Chiari?

A

Jaundice and tender hepatomegaly

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89
Q

What can chronic Budd Chiari cause?

A

Ascites

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90
Q

How is Budd Chiari diagnosed?

A

Ultrasound of hepatic veins

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91
Q

What is treatment of Budd Chiari?

A

Recanalisation or stent

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92
Q

What is methotrexate and what does it cause?

A

Drug used to treat rheumatoid arthritis and psoriasis which can cause progressive fibrosis

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93
Q

What is the treatment for liver disease secondary to methotrexate?

A

Stop the drug

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94
Q

What is the cause of cardiac cirrhosis?

A

High right sided pressure (incompetent tricuspid valve, congenital, rheumatic fever, constrictive pericarditis)

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95
Q

What does cardiac cirrhosis cause clinically?

A

Ascites and liver impairment from CCF

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96
Q

How do you treat cardiac cirrhosis?

A

By treating the cardiac condition

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97
Q

What is the common final end point for any chronic liver disease?

A

Cirrhosis

98
Q

Cirrhosis is scarring of the liver which causes what?

A

Obstruction

99
Q

Cirrhosis is a vascular disease, associated with what?

A

Hyperdynamic circulation and portal hypertension

100
Q

What is portal hypertension?

A

Portal pressure >5mmHg

101
Q

What causes pre-hepatic portal hypertension?

A

Blockage of portal vein before the liver (e.g. portal vein thrombosis)

102
Q

What causes intra-hepatic portal hypertension?

A

Distortion of liver architecture (e.g. Budd Chiari)

103
Q

What is compensated cirrhosis?

A

Usually clinically normal and often an incidental finding

104
Q

What can patients with compensated cirrhosis present with?

A

Haematemesis

105
Q

What is decompensated cirrhosis?

A

Liver failure as a result of end stage liver disease

106
Q

What are 5 signs of compensated cirrhosis?

A

Spider naevi, palmar erythema, clubbing, gynecomastia, hepato/splenomegaly

107
Q

What are 4 signs of decompensated cirrhosis?

A

Jaundice, ascites, encephalopathy, bruising

108
Q

What are treatment options for decompensated cirrhosis?

A

Treat underlying cause, prevent NaCl retention, small frequent meals, vitamin B supplements

109
Q

Patients with a UKELD score of what can be listed for transplant?

A

49 or more

110
Q

What are the major complications of cirrhosis?

A

Ascites, encephalopathy and oesophageal varices

111
Q

How does ascites occur?

A

Vasodilation results in driving the action of vasoconstrictors which causes increased fluid retention

112
Q

How is ascites diagnosed?

A

Shifting dullness and darkness on ultrasound

113
Q

What are treatment options for ascites?

A

Treat underlying disease, decrease salt intake, prevent NaCl reabsorption, spironolactone, paracentesis, shunt, transplant

114
Q

What is a complication of ascites and what should you do to test for it?

A

Spontaneous bacterial peritonitis- WCC

115
Q

What does encephalopathy cause?

A

Confusion, hepatic flap, neurological symptoms

116
Q

When is a common time to see encephalopathy?

A

Alcohol withdrawal

117
Q

How does encephalopathy occur?

A

Ammonia is taken to the brain without being metabolised which causes disturbances in neurotransmitters of the brain

118
Q

What is treatment for encephalopathy?

A

Treat underlying cause, give lactulose and maintain nutritional status

119
Q

What should be done if encephalopathy occurs spontaneously?

A

Transplant

120
Q

What can varices lead to?

A

Decompensation, liver failure and death

121
Q

What is primary prophylaxis for varices?

A

Beta blockers (propranolol) and endoscopic ligation

122
Q

What is the emergency treatment for varices? What are the risks?

A

Balloon tamponade- aspiration and perforation which is usually fatal

123
Q

What are primary liver tumours?

A

Hepatocellular carcinoma/adenocarcinoma

124
Q

Where is metastases to the liver commonly from?

A

Colon, pancreas, stomach, breast and lung

125
Q

What is a liver tumour in an old patient most likely to be?

A

Malignant metastases

126
Q

What is a liver tumour in an CLD patient most likely to be?

A

Primary liver cancer

127
Q

What is a liver tumour in a non-cirrhotic patient most likely to be?

A

Haemangioma

128
Q

What is a haemangioma?

A

Commonest liver tumour, mostly found in women

129
Q

Are there symptoms of haemangioma?

A

No

130
Q

How can a diagnosis of haemangioma be made?

A

MRI, CT, ultrasound

131
Q

Is there treatment for haemangioma?

A

No treatment needed

132
Q

What is focal nodular hyperplasia?

A

Benign nodule formation in normal tissue

133
Q

Who is focal nodular hyperplasia most common in?

A

Women but has no relation to sex hormones

134
Q

Does focal nodular hyperplasia have symptoms?

A

Usually not but may cause slight RUQ pain

135
Q

How is focal nodular hyperplasia diagnosed and does it need treatment?

A

US, CT, MRI, FNA- no treatment

136
Q

Who are adenomas most common in?

A

Woman

137
Q

What are a common cause of adenomas?

A

Sex hormones and other steroidal therapies

138
Q

Are there symptoms of adenomas?

A

Usually not, but could cause some pain, or rupture/bleed

139
Q

Where are adenomas most often found?

A

Right lobe

140
Q

What is associated with multiple adenomas?

A

Glycogen storage disease

141
Q

How are adenomas diagnosed?

A

CT, US, MRI, FNA

142
Q

What is 1st line treatment for adenomas?

A

Stop taking hormones and lose weight

143
Q

When do adenomas need to be removed?

A

Always in males and if they are >5cm in women (regular reviews)

144
Q

What is a cyst?

A

Liquid collection lined by epithelium

145
Q

Do cysts have symptoms?

A

Mostly asymptomatic but can cause haemorrhage, infection, rupture or compression

146
Q

What are treatment options for cysts?

A

No treatment, follow ups or surgery

147
Q

What is a hyatid cyst? How does it present?

A

Caused by a tapeworm- may present with spread disease or erosion into other structures

148
Q

What is treatment for hyatid cysts?

A

Surgery, percutaneous drainage, albendazole (anti-helminth)

149
Q

What are some signs are symptoms of a liver abscess?

A

High fever, leucocytosis, abdominal pain, complex liver lesions

150
Q

When are liver abscesses common?

A

After abdominal or biliary infection or a dental procedure

151
Q

What is treatment for a liver abscess?

A

Broad spectrum antibiotics, drainage and operate if no improvement

152
Q

What is hepatocellular carcinoma associated with?

A

Any form of chronic hepatitis

153
Q

Hepatocellular carcinoma can be asymptomatic, but how can it present?

A

Mass, RUQ pain, weight loss or obstruction

154
Q

Where is hepatocellular carcinoma likely to metastasise to?

A

Other parts of liver, portal vein, lymph nodes, lung, bone and brain

155
Q

Alfa Ferroprotein levels above what is highly suggestive of hepatocellular carcinoma?

A

> 100

156
Q

How can a diagnosis of hepatocellular carcinoma be made?

A

History, ultrasound, triphasic CT, MRI, biopsy

157
Q

What does the prognosis of hepatocellular carcinoma depend on?

A

Tumour size, spread, underlying disease and patient performance

158
Q

What is the best treatment for hepatocellular carcinoma?

A

Liver transplant

159
Q

What requirements must be met for a liver transplant?

A

Single tumour < 5cm, less than 3 tumours < 3cm

160
Q

Apart from liver transplant, what other treatment options are available for hepatocellular carcinoma?

A

Resection, local ablation

161
Q

Who is fibrolaminar carcinoma most common in?

A

Young patients, mostly children

162
Q

What is fibrolaminar carcinoma NOT to do with?

A

Alcohol or cirrhosis

163
Q

What is the AFP value in fibrolaminar carcinoma?

A

Normal

164
Q

What is the treatment for fibrolaminar carcinoma?

A

Surgical resection or transplant

165
Q

What does normal bile contain?

A

Bile salts, cholesterol, bilirubin and phospholipids

166
Q

Where is bile released?

A

2nd part of the duodenum through common bile duct and Ampulla of Vater

167
Q

What causes cholesterol stones?

A

Imbalance between the ratio of cholesterol to bile salts during micelle formation

168
Q

Who are cholesterol stones more common in?

A

Women, obesity and diabetes

169
Q

What causes pigment stones?

A

Excess bilirubin cannot be solubilised into bile salts

170
Q

In reality, what are gallstones most commonly?

A

A mix of cholesterol and pigment cells

171
Q

How does gallstones present?

A

Pain, jaundice, anorexia, nausea, abnormal cholestatic LFTs

172
Q

How do you confirm a diagnosis of gallstones?

A

ERCP

173
Q

What increases the risk of gallstones?

A

Fat, female, forty, fertile, fair

174
Q

What are complications of gallstones?

A

Biliary colic, acute pancreatitis and gallstone ileus

175
Q

What causes biliary colic?

A

Stone impacts the cystic duct

176
Q

How does biliary colic present?

A

Gradual build up of pain in RUQ which radiates to the back and shoulders and may be associated with indigestion and nausea

177
Q

How is biliary colic diagnosed?

A

Bloods (LFTs), ultrasound, ERCP

178
Q

What is the treatment for uncomplicated biliary colic?

A

Painkillers, weight loss, low fat diet

179
Q

If symptoms of biliary colic are persisting, what is the treatment?

A

Refer for cholecystectomy or if this isn’t possible use ursodeoxycholic acid

180
Q

What is acute cholecystitis?

A

Inflammation of the gallbladder which causes obstruction

181
Q

How do you diagnose cholcystitis?

A

Ultrasound

182
Q

What is the treatment for cholecystitis?

A

IV antibiotics and fluids and urgent cholecystectomy (within a week)- if not possible do interval cholecystectomy after 3 months

183
Q

What is gallstone ileus?

A

Fistula has occurred between the gallbladder and duodenum which causes a gallstone to enter the small bowel and cause obstruction

184
Q

How does gallstone ileus present?

A

Intermittent colic followed by full blown pain and a swollen tummy

185
Q

What is the treatment for gallstone ileus?

A

Urgent laparotomy

186
Q

When should you do a follow up cholecystectomy following a gallstone ileus?

A

Only if there are more stones present- check with ultrasound first

187
Q

What type of carcinoma is found in the gallbladder?

A

Adenocarcinoma

188
Q

What is gallbladder carcinoma most likely to be?

A

Metastases

189
Q

What is cholangiocarcinoma?

A

Adenocarcinoma of large or small bile ducts

190
Q

What is cholangiocarcinoma associated with?

A

UC and primary sclerosing cholangitis

191
Q

How does cholangiocarcinoma present?

A

Obstructive jaundice

192
Q

What are the main causes of acute pancreatitis?

A

Alcohol and gallstones

193
Q

What are all the causes of acute pancreatitis?

A

Idiopathic, gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion bites, hypercalcaemia/parathyroidism/lipidaemia, ERCP, drugs

194
Q

Where does the gallstone blockage occur which causes pancreatitis?

A

Sphincter of Oddi

195
Q

How does acute pancreatitis present?

A

Sudden onset severe abdominal pain, nausea, vomiting, jaundice

196
Q

What tests should be done for acute pancreatitis?

A

ABG, FBC, coagulation, U and E, LFT, Ca++, glucose, amylase/lipase, CRP

197
Q

What is important about serum amylase in pancreatitis?

A

3xULN is diagnostic

198
Q

What will pancreatitis sometimes show on imaging?

A

Pleural effusion of sentinel loop

199
Q

What test should all patients with pancreatitis receive?

A

Ultrasound

200
Q

What test can be used to assess severity of pancreatitis?

A

CT

201
Q

If pancreatitis was caused by gallstones, should a cholecystectomy be performed?

A

Yes, within 2 weeks to prevent recurrence

202
Q

What are complications of pancreatitis?

A

Death, shock, pseudocysts, necrosis, haemorrhage, abscess, hypocalcaemia, hyperglycaemia

203
Q

How are 80% of cases of pancreatitis managed?

A

Analgesia and fluids

204
Q

A score of what on the Glasgow criteria for pancreatitis is indicative of severe pancreatitis?

A

3 or more

205
Q

What causes pseudocysts?

A

Leakage of pancreatic juices

206
Q

What do pseudocysts present with?

A

Nausea, vomiting, jaundice, weight loss

207
Q

What is the treatment for pseudocysts?

A

None, or drainage

208
Q

What are causes of chronic pancreatitis?

A

Alcohol, gallstones, cystic fibrosis, hyperparathyroidism, familial

209
Q

What is treatment for chronic pancreatitis?

A

Treat acute cases and Creon can be given as enzyme replacement

210
Q

What are complications of chonic pancreatitis?

A

Splenic vein thrombosis, pseudocysts, pleural effusion, ascites, pancreatic cancer, obstruction

211
Q

What does a calcified pancreatic duct suggest?

A

Tropical pancreatitis

212
Q

What type of cancer is in the pancreas?

A

Adenocarcinoma

213
Q

What does pancreatic cancer commonly present as?

A

Jaundice with no pain

214
Q

What are investigations for pancreatic cancer?

A

US, triple phase CT, MRI, MRCP

215
Q

What are treatment options for pancreatic cancer?

A

Resect if possible, if not then maybe stent

216
Q

What type of LFTs does pancreatic cancer cause?

A

Mixed

217
Q

What does treatment of acute viral hepatitis include?

A

No antivirals, monitoring for encephalopathy and resolution

218
Q

What are precautions that should take place when a case of acute viral hepatitis is diagnosed?

A

Notify public health and immunise contacts

219
Q

What vaccinations should be given to chronic viral hepatitis patients?

A

Other hepatitis vaccines and if they are cirrhotic then also influenza and pneumococcal

220
Q

What are the most commonly used antivirals?

A

Adefovir and entecavir

221
Q

What environmental factors are often associated with Hep A?

A

Poor hygiene and overcrowding

222
Q

When is the peak incidence of SYPTOMATIC Hep A?

A

Older children and young adults

223
Q

What is the main laboratory test for Hep A?

A

Bloods for serology to looks for hep A IgM

224
Q

When is chronic infection of Hep B more likely?

A

When the first exposure is in childhood

225
Q

When is HBsAg present?

A

In the blood of all infectious individuals?

226
Q

When is HBeAg present?

A

Usually present in highly infectious individuals

227
Q

When is hep B viral DNA present?

A

Always in highly infectious individuals

228
Q

When is hepatitis B IgM most likely to be present?

A

Recently infected cases

229
Q

When is Anti-HBs present?

A

Immunity

230
Q

Is there a vaccine for Hep B?

A

Yes

231
Q

Is there a vaccine for Hep C?

A

No

232
Q

If the test for Hep C antibody is positive, what test should you do?

A

Hep C virus RNA by PCR

233
Q

When is the only time Hep D will be found?

A

alongside hepatitis B virus

234
Q

What does Hepatitis D do?

A

Exacerbates hep B

235
Q

When can hep D infect?

A

At the same time as hep B or after

236
Q

Where is Hep E more common?

A

Tropics

237
Q

Where can Hep E be contracted?

A

Food, commonly found in pigs

238
Q

How is Hep E spread?

A

Faecal-oral

239
Q

Hep E is clinically similar to what?

A

Hep A

240
Q

Tropical genotypes of Hep E are associated with what?

A

Severe disease in pregnant women

241
Q

Is there a vaccine for Hep E?

A

No

242
Q

Who can develop a chronic infection from Hep E?

A

Immunocompromised

GI (17 decks)

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