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Finals > Liver/pancreas > Flashcards

Liver/pancreas Flashcards

1
Q

What is the substance that gallstones are most commonly formed by?

A

Cholesterol

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2
Q

What are the risk factors for gallstones?

A

Fat, fair, female, forty

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3
Q

What is the pain like that is associated with gallstones?

A

Severe, colickly epigastric or RUQ pain, triggered by meals (especially fatty meals), lasts between 30 minutes and 8 hours, can also radiate to shoulder

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4
Q

What LFTs are raised in a hepatic picture?

A

ALT and AST

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5
Q

What LFTs are raised in obstructive picture/biliary tree disease?

A

ALP, GGT and bilirubin (also get deranged clotting in obstruction)

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6
Q

What investigations can be done in someone presenting with RUQ pain?

A

1st line = USS abdomen
MRCP - sensitive and specific for biliary tract disease

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7
Q

When is a laparoscopic cholecystectomy indicated?

A

When the patient is symptomatic of gallstones or the gallstones are leading to complications

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8
Q

What pain relief can be given to patients with gallbladder pain whilst waiting for elective surgery?

A

If severe IM diclofenac
If mild/moderate - paracetamol plus NSAID

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9
Q

What is acute cholecystitis?

A

Inflammation of the gallbladder which is caused by blockage of the cystic duct preventing the gallbladder from draining (most often gallstones)

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10
Q

What features are present in acute cholecystitis?

A

RUQ pain, fever, nausea, vomiting, tachycardia, RUQ tenderness, Murphy’s sign positive, raised inflammatory markers and WBC

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11
Q

What management is done for those with acute cholecystitis?

A

Nil by mouth, IV fluids, antibiotics, NG tube, ERCP can be used to remove trapped stones

Cholecystectomy can be performed during acute admission or be delayed for 6-8 weeks

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12
Q

What complications can occur due to acute cholecystitis?

A

Sepsis, gallbladder empyema, gangrenous gallbladder, perforation

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13
Q

What are the two main causes of acute cholangitis?

A

Obstruction in bile ducts stopping bile flow or infection introduced during ERCP procedure

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14
Q

What are the most common organisms that cause acute cholangitis?

A

E.coli, Klebsiella, enterococcus

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15
Q

What is charcot’s triad?

A

RUQ pain, fever, jaundice = acute cholangitis

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16
Q

What is the management of acute cholangitis?

A

IV fluids, nil by mouth, IV antibiotics, blood cultures, ERCP to remove stones

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17
Q

What is decompensated liver cirrhosis?

A

When the liver is damaged to the point that is cannot function adequately and clinical complications such as jaundice are present

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18
Q

What examination findings are present in someone with severe liver disease?

A

Cachexia, jaundice, hepatomegaly, small nodular liver, splenomegaly, spider naevi, palmar erythema, gynaecomastia, bruising, excoriations, ascites, caput medusae, leukonychia, asterixis

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19
Q

When is a non-invasive liver screen performed?

A

In a patient with abnormal LFTs without a clear cause

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20
Q

What blood tests will be deranged in someone with severe liver disease?

A

Low albumin (due to reduced synthetic function of the liver)
Increased PT (due to reduced clotting production)
Thrombocytopenia (advanced disease)
Hyponatraemia (due to fluid retention)

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21
Q

What is a Fibroscan/transient elastogrpahy scan used for?

A

Assesses the stiffness of the liver to determine the degree of fibrosis

Used in all patients at risk of cirrhosis

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22
Q

What scores can be used in someone with end stage liver disease?

A

MELD score or the Child-Pugh score - done every 6 months

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23
Q

Why do patients with cirrhosis develop malnutrition?

A

Loss of appetite, protein metabolism in the liver is affected and therefore muscle tissue is broken down to be used as fuel

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24
Q

Why does portal hypertension occur in those with liver cirrhosis?

A

Liver cirrhosis increases the resistance to blood flow in the liver which thereby increases pressure in portal system and results in splenomegaly

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25
Q

Why do oesophageal varices form in liver cirrhosis?

A

Portal hypertension causes swollen and tortuous vessels at sites where collaterals form between portal and systemic venous systems = distal oesophagus

This also causes caput medusae

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26
Q

What prophylaxis is given to patients with oesophageal varices to prevent bleeding?

A

1st line = non-selective beta blockers e.g. propranolol

2nd line = variceal band ligation

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27
Q

What is the management for bleeding oesophageal varices?

A

ABCDE and immediate senior help
Activate major haemorrhage protocol
Blood transfusions
Terlipressin or somatostatin can cause vasoconstriction
Prophylactic broad spectrum antibiotics
Urgent endoscopy with variceal band ligation

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28
Q

What is the most common complication of cirrhosis?

A

Ascites

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29
Q

How does ascites form in those with liver cirrhosis?

A

Increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and into the peritoneal cavity

The drop in circulating volume then activates RAAS leading to fluid and sodium retention

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30
Q

What kind of ascites is caused by cirrhosis?

A

Transudative

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31
Q

What is the management of ascites?

A

Low sodium diet, aldosterone antagonists, ascitic tap/drain, prophylactic antibiotics, TIPS

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32
Q

What is spontaneous bacterial peritonitis?

A

Infection within the asicitc fluid and peritoneal lining without a clear source of infection - most commonly caused by E.coli and Klebsiella

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33
Q

What is the management for spontaneous bacterial peritonitis?

A

Sample for ascitic fluid, IV broad spectrum antibiotics

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34
Q

How does liver disease lead to kidney disease? (hepatorenal syndrome)

A

Portal hypertension causes portal vessels to release vasodilators which leads to reduced BP

The kidneys therefore activate RAAS which leads to vasoconstriction of the renal vessels

Renal vasoconstriction and low systemic pressure results in kidneys being starved of blood and reduced kidney function

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35
Q

What toxin is built up during hepatic encephalopathy?

A

Ammonia - liver cells unable to metabolise ammonia into harmless waste products

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36
Q

How does hepatic encephalopathy present?

A

Reduced consciousness and confusion

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37
Q

What is the management for hepatic encephalopathy?

A

Lactulose, antibiotics (rifaximim), nutritional support

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38
Q

What are the progressive stages of alcoholic liver disease?

A

Alcoholic fatty liver –> alcoholic hepatitis –> cirrhosis

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39
Q

What LFTs are consistent with alcoholic liver disease?

A

ALT and AST will be raised
AST > ALT (2:1)
GGT also raised with high alcohol consumption

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40
Q

What investigations can be done in someone with alcoholic liver disease?

A

Liver USS, FibroScan, endoscopy to assess for varices, CT/MRI, liver biopsy

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41
Q

What nutritional support is given to those with alcoholic liver disease?

A

High protein diet, thiamine replacement

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42
Q

What tools can be used to assess for alcohol dependence?

A

CAGE questions, AUDIT questionnaire

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43
Q

What symptoms are present 6-12 hours following alcohol withdrawal?

A

Tremor, sweating, headache, cravings, anxiety

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44
Q

What symptoms occur 12-24 hours and 24-48 hours following alcohol withdrawal

A

12-24 = hallucinations
24-48 = seizures

45
Q

How long following alcohol withdrawal can delirium tremens develop?

A

24-72 hours

46
Q

Which receptors in the brain are affected with chronic alcohol use and are they down/up regulated?

A

GABA becomes downregulated and glutamate becomes upregulated

Both have relaxing effect of electrical activity of the brain

47
Q

What symptoms are associated with delirium tremens?

A

Confusion, agitation, delusions, hallucinations, tremor, tachycardia, hypertension, hyperthermia, ataxia, arrhythmias

48
Q

What can be prescribed to prevent alcohol withdrawal?

A

Chlordiazepoxide - given orally as a reducing regime titrated to the required dose (given for 5-7 days)

49
Q

What can be prescribed to prevent Wernicke-Korsakoff syndrome?

A

IM/IV Pabrinex (high dose vitamin B) followed by long term oral thiamine

50
Q

What causes Wernicke-Korsakoff syndrome?

A

Alcohol excess leads to thiamine deficiency and thiamine is poorly absorbed in the presence of alcohol

Wernicke-Korsakoff syndrome is a result of thiamine deficiency

51
Q

What are the features of Wernicke encephalopathy?

A

Confusion, oculomotor disturbances, ataxia

52
Q

What are the features of Korsakoff syndrome?

A

Memory impairment and behavioural changes

53
Q

What are the progressive stages of NAFLD?

A

NAFLD –> non-alcoholic steatohepatitis (NASH) –> fibrosis –> cirrhosis

54
Q

What are the risk factors for NAFLD?

A

Obesity, poor diet, low activity levels, T2DM, high cholesterol, high BP, smoking

55
Q

What is found on the LFTs of someone with NAFLD?

A

AST and ALT raised
ALT > AST

56
Q

What is the first line investigation for assessing fibrosis in NAFLD?

A

Enhanced liver fibrosis blood test (>10.51 is advanced)

57
Q

What is the gold standard for diaganosing NAFLD?

A

Liver biopsy

58
Q

What is the management for NAFLD?

A

Weight loss, healthy diet, exercise, avoid alcohol, control any co-morbidities, refer to specialist if fibrosis

59
Q

What are the main causes of pancreatitis?

A

Alcohol, gallstones, ERCP

60
Q

What is the presentation of someone with pancreatitis?

A

Severe sudden onset epigastric pain radiating to the back, vomiting, abdominal tenderness, fever, tachycardia, eccyhmoses

61
Q

What blood tests results are raised in pancreatitis? (used to diagnose)

A

Amylase and lipase
Lipase is more sensitive and specific but amylase is used more often

62
Q

What scoring system is used to assess severity and what are the components of it?

A

Glasgow score - PANCREAS
PaO2 <8kpa
Age >55
Neutrophils (WBC >15)
Calcium <2
uRea >16
Enzymes - LDH >600 or AST/ALT >200
Albumin <32
Sugar (glucose >10)

63
Q

How is pancreatitis managed?

A

IV fluids, analgesia, IV antibiotics if evidence of infection, ERCP to treat gallstones, nutritional support

64
Q

What complications can occur due to acute pancreatitis?

A

Necrosis of pancreas, infection in a necrotic area, abscess formation, peripancreatic fluid collections, pseudocysts, chronic pancreatitis

65
Q

What is the most common cause of chronic pancreatitis?

A

Alcohol

66
Q

What complications can occur due to chronic pancreatitis?

A

Loss of exocrine function - lack of pancreatic enzymes (notably lipase)

Loss of endocrine function - diabetes

67
Q

How is chronic pancreatitis managed?

A

Abstinence from alcohol and smoking, analgesia, Creon (replacement pancreatic enzymes), insulin

68
Q

What is the presentation of hepatitis?

A

Abdominal pain, fatigue, flu-like illness, itching, muscle and joint aches, N+V, jaundice

69
Q

How is hepatitis A spread and how is it managed?

A

Transmitted in contaminated water (faecal-oral route), vaccination to prevent, management is supportive

70
Q

How is hepatitis B spread and how is it managed?

A

Transmitted by direct contact with blood or bodily fluids and vertical transmission, supportive treatment and antivirals, vaccine is available

71
Q

Which antigen shows active infection with hepatitis B?

A

HBsAg

72
Q

Which viral marker shows vaccination with hepatitis B vaccine?

A

HbsAb

73
Q

How is hepatitis C spread and how is it managed?

A

Spread by blood and bodily fluids, no vaccine is available but now curable with direct-acting antivirals, without treatment develops into chronic hepatitis C

74
Q

When is someone likely to develop a hepatitis D infection?

A

Can only get hepatitis D infection when there is a concurrent hepatitis B infection, increases complication and severity of hepatitis B

75
Q

How is hepatitis E spread and how is it managed?

A

Transmitted by faecal oral route, mild illness and no treatment is required, there is no vaccine

76
Q

Which antibodies are associated with type 1 autoimmune hepatitis?

A

ANA, anti-actin, anti-SLA/LP

77
Q

Which antibodies are associated with type 2 autoimmune hepatitis?

A

anti-LKM1, anti-LC1

78
Q

What are the typical LFTs of someone with autoimmune hepatitis?

A

High AST/ALT with minimal change in ALP

Raised IgG levels

79
Q

What are the presenting features of haemochromatosis?

A

Chronic tiredness, joint pain, bronze pigmentation to skin, testicular atrophy, erectile dsyfunction, amenorrhoea, hepatomegaly

79
Q

What is the treatment for autoimmune hepatitis?

A

High dose steroids or immunosuppressants, liver transplant

80
Q

What results will be found on an iron study of someone with haemochromatosis?

A

Raised ferritin, high transferrin, low total iron binding capacity

High transferrin differentiates it from other differentials of high ferritin

81
Q

What is the management of haemochromatosis?

A

Venesection at regular intervals, monitoring

82
Q

What is the pathophysiology of Wilson’s disease?

A

Autosomal recessive condition resulting in excessive accumulation of copper in the body especially in the liver and CNS

83
Q

What are the features of Wilson’s disease?

A

Chronic hepatitis which can lead to cirrhosis, tremor, dysarthria, dystonia, Parkinsonism, Kayser-Fleischer rings in cornea

84
Q

What is the initial screening test for suspected Wilson’s disease?

A

Serum caeruloplasmin (will be reduced)

85
Q

What is the management for Wilson’s disease?

A

Copper chelation using penicilliamine or trientene

86
Q

What are the features of alpha-1-antitrypsin deficiency?

A

COPD and bronchiectasis in the lungs
Dsyfunction, fibrosis and cirrhosis of the liver

87
Q

What investigations are performed in alpha-1-antitrypsin deficiency?

A

Serum alpha-1-antitrypsin levels, genetic testing, high resolution CT, liver biopsy

88
Q

What is the management of alpha-1-antitrypsin deficiency?

A

Stop smoking, symptomatic management of COPD, liver/lung transplant, monitoring for complications

89
Q

What are the symptoms of pancreatic cancer?

A

Painless obstructive jaundice, diarrhoea, N+V, abdo/back pain, new onset diabetes

90
Q

What surgical procedure is done in early pancreatic cancer?

A

Whipple’s resection is performed (done in head of pancreas tumours = most common)

91
Q

What investigations are done in those with suspected pancreatic cancer?

A

CT = 1st line, biopsy for definitive diagnosis

92
Q

What is the main risk factor for developing cholangiocarcinoma?

A

Primary sclerosing cholangitis

93
Q

What are the features of cholangiocarcinoma?

A

Painless obstructive jaundice, persistent biliary colic symptoms, palpable mass in RUQ, weight loss

94
Q

What investigations are done in someone with suspected cholangiocarcinoma?

A

USS upper abdo = 1st line, biopsy = definitive

95
Q

What tumour marker is raised in cholangiocarcinoma?

A

CA19-9

96
Q

What is the most common type of liver cancer?

A

Hepatocellular carcinoma

97
Q

What are the risk factors for developing HCC?

A

Alcoholic liver disease, NAFLD, hepatitis B/C, liver cirrhosis

98
Q

What tumour marker is used for HCC?

A

Alpha-fetoprotein

99
Q

What symptoms are seen in liver cancer?

A

Enlarged liver, worsening liver function, jaundice, abdo pain, abdo mass

100
Q

What investigations are done in liver cancer?

A

USS = 1st line, CT/MRI, biopsy = definitive

101
Q

What medications can be used to manage severe alcoholic hepatitis?

A

Corticosteroids such as prednisolone to reduce mortality - used during acute episodes

102
Q

What sign is seen on CT imaging in someone with pancreatic cancer?

A

Double duct sign

103
Q

Bile acid malabsorption is a complication following cholecystectomy, what are the symptoms and how is it managed?

A

Watery green diarrhoea
Treated with cholestyramine

104
Q

What investigations are done in primary sclerosing cholangitis and what is found?

A

MRCP will show beaded appearance of bile duct

105
Q

What are the features of primary biliary cholangitis?

A

Fatigue, pruritus, cholestatic jaundice, hyperpigmentation, xanthelasmas, hepatosplenomegaly (associated with autoimmune conditions)

106
Q

How is primary biliary cholangitis diagnosed?

A

mitochondrial antibodies, abdo USS or MRCP done to exclude extra hepatic biliary obstruction

107
Q

How is primary biliary cholangitis managed?

A

1st line - ursodeoxycholic acid, cholestyramine for itching

108
Q
A

Finals (21 decks)

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