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2a > Liver > Flashcards

Liver 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 2 scores are used as as prognostic tools in liver cirrhosis? What information does each provide?

A
  • MELD score (Model for End-Stage Liver Disease): gives an estimated 3-month mortality as a percentage, should be calculated every 6 months in patients with compensated cirrhosis
  • Child-Pugh score: assesses the severity of cirrhosis and the prognosis
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3
Q

What are complications of liver cirrhosis?

A
  • Malnutrition and muscle wasting
  • Portal hypertension -> oesophageal varices -> bleeding varices
  • Ascites -> spontaneous bacterial peritonitis
  • Hepatorenal syndrome
  • Hepatic encephalopathy
  • Hepatocellular carcinoma
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4
Q

How does cirrhosis lead to malnutrition and muscle wasting?

A
  • Patients often have a LOA resulting in reduced intake
  • Cirrhosis affects protein metabolism in the liver -> reduces the amount the liver produces -> less protein available to maintain muscle tissue
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5
Q

What is used for bleeding prophylaxis in stable oesophageal varices?

A
  • Beta blockers (e.g. propranolol) first-line
  • Variceal band ligation (if BB are contraindicated)
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6
Q

What is the management of bleeding oesophageal varices?

A
  • Immediate senior help
  • Consider blood transfusion (activate the major haemorrhage protocol)
  • Treat any coagulopathy (e.g. with fresh frozen plasma)
  • Vasopressin analogues (e.g. terlipressin or somatostatin) cause vasoconstriction and slow bleeding
  • Prophylactic broad-spectrum antibiotics (shown to reduce mortality)
  • Urgent endoscopy with variceal band ligation
  • Consider intubation and intensive care
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7
Q

What is ascites?

A

Abnormal accumulation of fluid in the abdomen

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8
Q

How can ascitic fluid be classified?

A

According to serum-ascites albumin gradient (SAAG)

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9
Q

How do you calculate serum-ascites albumin gradient?

A

Serum albumin - ascitic fluid albumin = SAAG

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10
Q

How do you interpret SAAG?

A
  • High SAAG (>11g/L) = transudate
  • Low SAAG (<11g/L) = exudate
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11
Q

What are causes of a high serum-ascites albumin gradient?

A

High SAAG indicates portal hypertension (fluid pushes out, albumin remains)

  • Liver disorders - cirrhosis, ALD, acute LF, liver mets
  • Cardiac - RHF, constrictive pericarditis
  • Other - Budd-Chiari syndrome
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12
Q

What are causes of a low serum-ascites albumin gradient?

A

Low SAAG implies an aetiology that causes increased vascular permeability of the portal system

  • Malignancy
  • Infections - tb peritonitis
  • Hypoalbuminamia - nephrotic syndrome, severe malnutrition
  • Other - pancreatitis, bowel obstruction, biliary ascites
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13
Q

What is the management of ascites?

A
  • Low sodium diet
  • Aldosterone antagonists (spironolactone)
  • Paracentesis
  • Prophylactic antibiotics (ciprofloxacin) when there is <15 g/litre of protein in the ascitic fluid
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14
Q

Why are aldosterone antagonists given in ascites?

A
  • Fluid loss into the peritoneal cavity decreases circulating volume
  • This decreases renal blood pressure, triggering renin release
  • Aldosterone is secreted which causes fluid and sodium reabsorption in the kidneys
  • This results in fluid and sodium retention
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15
Q

What is a complication of ascites?

A

Spontaneous bacterial peritonitis

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16
Q

How do you diagnose SBP?

A
  • Paracentesis - neutrophil >250 cells/ul
  • Ascitic fluid culture
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17
Q

What are the most common causative organisms of SBP?

A
  • E. Coli
  • Klebsiella pneumoniae
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18
Q

What is the management of SBP?

A

IV abx (normally cefotaxime)

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19
Q

What is one toxin that can build up in patients with liver cirrhosis and cause hepatic encephalopathy?

A

Ammonia

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20
Q

How does hepatic encephalopathy present acutely and chornically?

A

Acutely - reduced consciousness, confusion
Chronically - changes to personality, memory and mood

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21
Q

What is the management of hepatic encephalopathy?

A
  • Lactulose (aiming for 2-3 soft stools daily)
  • Antibiotics
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22
Q

What is the role of antibiotics in the management of hepatic encephalopathy? What is the first line antibiotic?

A
  • Ammonia is produced in the intestinal bacteria when they break down proteins and is (normally) metabolised and excreted by the liver
  • Antibiotics are used to reduce the number of intestinal bacteria producing ammonia

Rifaximin is used as it is poorly absorbed and stays in the GI tract

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23
Q

What is the step-wise progression of alcohol-related liver disease?

A
  1. Hepatic steatosis
  2. Alcoholic hepatitis
  3. Cirrhosis
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24
Q

What can be used to quickly screen for harmful alcohol use?

A

CAGE questions:

C – CUT DOWN? Do you ever think you should cut down?
A – ANNOYED? Do you get annoyed at others commenting on your drinking?
G – GUILTY? Do you ever feel guilty about drinking?
E – EYE OPENER? Do you ever drink in the morning to help your hangover or nerves?

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25
Q

What withdrawal symptoms 6-12 hrs after alcohol consumption ceases?

A
  • Tremor
  • Sweating
  • Headache
  • Craving
  • Anxiety
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26
Q

What withdrawal symptoms 12-24 hrs after alcohol consumption ceases?

A

Hallucinations

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27
Q

What withdrawal symptoms 24-48 hrs after alcohol consumption ceases?

A

Seizures

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28
Q

What withdrawal symptoms 24-72 hrs after alcohol consumption ceases?

A

Delirium tremens

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29
Q

What 2 medications are used in alcohol withdrawal? What are their roles?

A
  • Chlordiazepoxide - combat the effects of alcohol withdrawal
  • Pabrinex followed by long-term oral thiamine - used to prevent Wernicke-Korsakoff syndrome
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30
Q

What causes Wernicke-Korsakoff Syndrome?

A
  • Thiamine deficiency (vit B1) due to excess alcohol
  • Thiamine is poorly absorbed in the presence of alcohol
  • Alcoholics typically have poor diets -> decreased intake
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31
Q

What are features of Wernicke’s encephalopathy?

A
  • Confusion
  • Oculomotor disturbances (disturbances of eye movements)
  • Ataxia
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32
Q

What are features of Korsakoff’s syndrome?

A
  • Memory impairment (retrograde and anterograde)
  • Behavioural changes
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33
Q

What is Non-alcoholic fatty liver disease (NAFLD)?

A

Excess fat (namely triglycerides) in liver cells. These fat deposits interfere with the functioning of liver cells. NAFLD can progress to hepatitis and cirrhosis

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34
Q

NAFLD is associated with metabolic syndrome. What is this?

A

A combination of HTN, obesity and diabetes

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35
Q

NAFLD has stages of disease. What investigation findings indicate each stage? What investigation is diagnostic?

A
  1. NAFLD
    - Raised ALT is often the first indication of NAFLD
  2. Non-alcoholic steatohepatitis (NASH)
    - Liver USS confirms hepatic steatosis (seen as increased echogenicity)
  3. Fibrosis
    - Enhanced liver fibrosis (ELF) blood test indicates advanced liver fibrosis
  4. Cirrhosis
    - Transient elastography (“FibroScan”) determines the degree of fibrosis to test for liver cirrhosis

Liver biopsy is diagnostic

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36
Q

What two scores can be used to assess liver fibrosis in NAFLD? What do they use? What result would indicate advanced fibrosis? What would indicate an alternate diagnosis?

A
  • NAFLD Fibrosis Score (NFS) and Fibrosis 4 (FIB-4) score
  • Both use AST:ALT ratio to assess severity of fibrosis
  • Ratio > 0.8 suggests advanced fibrosis
  • Ratio greater than 1.5 indicates ALD rather than NAFLD
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37
Q

What does NAFLD management entail?

A
  • Lifestyle changes
  • Managing co-morbidities
  • If scoring test indicate fibrosis, refer to specialist
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38
Q

When is liver transplantation considered?

A
  • Acute liver failure
  • Decompensated liver disease (?same as chronic liver failure)
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39
Q

What is acute liver failure?

A

The rapid onset of hepatocellular dysfunction leading to a variety of systemic complications

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40
Q

What are the causes of acute liver failure?

A
  • Paracetamol overdose
  • Viral hepatitis (usually A/B)
  • Alcohol
  • Acute fatty liver of pregnancy
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41
Q

What are features of acute liver failure?

A
  • Jaundice
  • Hepatic encephalopathy
  • Renal failure
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42
Q

What investigations indicate acute liver failure?

A
  • Coagulopathy - raised PTT
  • Hypoalbuminaemia

LFTs do not always accurately the synthetic function of the liver

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43
Q

Which pts benefit from activated charcoal following paracetamol overdose?

A
  • Pts who present within 1 hr of overdose
  • May reduce absorption of the drug
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44
Q

What is a complication of acetylcysteine treatment for paracetamol overdose? What is the management?

A
  • Anaphylactic reaction
  • Stop infusions, restart at a slower rate
45
Q

What is the King’s College Hospital criteria for liver transplantation (in paracetamol overdose)?

A

Arterial pH <7.3 (24 hrs after ingestion)

Or all of:
- Raised PTT
- Raised Cr
- Encephalopathy

46
Q

What features indicate decompensated liver disease?

A

A – Ascites
H – Hepatic encephalopathy
O – Oesophageal varices bleeding
Y – Yellow (jaundice)

47
Q

Give 3 complications of gallstones

A
  • Acute cholecystitis
  • Acute cholangitis
  • Pancreatitis
48
Q

What is biliary colic?

A

Intermittent RUQ pain caused by gallstones irritating bile ducts

49
Q

Biliary tract disease definitions:
1. Cholestasis
2. Cholelithiasis
3. Cholecystitis
4. Gallbladder empyema
5. Cholecystectomy
6. Cholecystostomy

A
  1. Blockage to flow of bile
  2. Gallstones present
  3. Inflammation of the gallbladder
  4. Pus in gallbladder
  5. Removal of gallbladder
  6. Drain inserted into gallbladder
50
Q

What are the risk factors for gallstones?

A
  • Fat
  • Fair
  • Female
  • Forty
51
Q

Why are patients with gallstones and biliary colic advised to avoid fatty foods?

A
  • Fat entering the digestive system triggered CCK secretion from the duodenum
  • CCK triggers contraction of the gallbladder
  • This exacerbates symptoms
52
Q

What is the first line Ix for gallstones? What is second line if this fails to show stones but is still suggestive of disease?

A
  • USS
  • MRCP
53
Q

What is the main indication for endoscopic retrograde cholangio-pancreatography? What else is ERCP used for?

A

To clear stones in the bile ducts

Other roles:
- Insert stents to improve bile drainage
- Take biopsies of tumours
- Inject contrast and take XR to visualise the biliary system

54
Q

What is the management of gallstones in asymptomatic and symptomatic patients?

A
  • Asymptomatic: no intervention required
  • Symptomatic: cholecystectomy
55
Q

What is the main cause of acute cholecystitis?

A

Gallstones in the head of the gallbladder or cystic duct, preventing the gallbladder from draining

56
Q

How does acute cholecystitis present?

A
  • RUQ pain
  • Fever
  • N+V
  • Tachycardia
57
Q

What is a key examination finding in acute cholecystitis?

A

Murphy’s sign

58
Q

What is the first line investigation for acute cholecystitis? What will it show?

A
  • USS
  • Thicken gallbladder wall
  • Stones/sledge in gallbladder
  • Fluid around gallbladder
59
Q

What is the management of acute cholecystitis?

A
  • Admit
  • IV fluids
  • Abx
  • ERCP/cholecystectomy
60
Q

What are possible complications of acute cholecystitis?

A
  • Sepsis
  • Gallbladder empyema
  • Gangrenous gallbladder
  • Perforation
61
Q

What is acute cholangitis?

A

Infection and inflammation in the bile ducts

62
Q

What are the 2 main causes of acute cholangitis?

A
  • Obstruction in the bile ducts e.g. gallstones
  • Infection introduced during an ERCP procedure
63
Q

What are the common causative organisms of acute cholangitis?

A
  • E coli
  • Klebsiella species
  • Enterococcus species
64
Q

How does acute cholangitis present?

A
  • RUQ pain
  • Fever
  • Jaundice
65
Q

What is the name for the triad of symptoms seen in acute cholangitis?

A

Charcot’s triad

66
Q

What is the management of acute cholangitis?

A
  • Admit
  • IV fluids
  • Blood cultures
  • IV abx
  • ERCP/percutaneous transhepatic cholangiogram (PTC)

PTC is an option where ERCP has failed, it involves inserting a drain through the skin and liver into bile ducts and relieves the immediate obstruction

67
Q

What are the top 3 causes of pancreatitis?

A
  • Gallstones
  • Alcohol
  • Post-ERCP
68
Q

What drugs can cause pancreatitis?

A
  • Steriods
  • Furosemide
  • Thiazide diuretics
  • Azathioprine
69
Q

How does acute pancreatitis present?

A
  • Severe epigastric pain
  • Radiates to back
  • Vomiting
  • Systemically unwell
70
Q

What investigations are useful in pancreatitis?

A
  • Amylase - raised >3x upper limit of normal in acute pancreatitis, can be normal in chronic
  • Lipase - more sensitive and specific than amylase
  • CRP - useful for monitoring inflammation
  • USS - first line for assessing gallstones
  • CT abdo - not required unless suspect complications of pancreatitis
71
Q

What score can be used to assess the severity of pancreatitis? What are the criteria?

A

Glasgow score

Criteria –> PANCREAS (1 point per criteria)
- PaO2 <8 KPa
- Age >55
- Neutrophils (WBC >15)
- Calcium <2
- uRea >16
- Enzymes (LDH >600 or AST/ALT >200)
- Albumin <32
- Sugar (Glucose >10)

Scores:
- 0-1 = mild pancreatitis
- 2 = moderate
- 3 or more = severe

72
Q

What is the management of acute pancreatitis?

A
  • ABCDE
  • IV fluids
  • Analgesia
  • Treatment of cause e.g. gallstones
  • Abx if evidence of specific infections
  • Treatment of complications
73
Q

What are potential complications of acute pancreatitis?

A
  • Necrosis of pancreas
  • Abscess formation
  • Acute peripancreatic fluid collections
  • Pseudocyst (collections of pancreatic juice that can develop 4 wks after acute pancreatitis)
  • Chronic pancreatitis
74
Q

What are potential complications of chronic pancreatitis?

A
  • Chronic epigastric pain
  • Loss of exocrine function
  • Loss of endocrine function -> lack of insulin production -> diabetes
  • Damage and strictures in the duct system -> obstruction in excretion of pancreatic juice and bile
  • Pseudocysts and abscesses
75
Q

What is involved in the management of chronic pancreatitis?

A
  • Analgesia if required

Management of complications:
- Replacement of pancreatic enzymes (Creon) if lose of enzymes (reduced exocrine function)
- Insulin regime if diabetes
- ERCP with stenting to treat strictures and obstruction
- Surgery to manage cysts, abscesses, obstruction

76
Q

What is the most common site of pancreatic tumour?

A

The head of the pancreas

77
Q

How does pancreatic cancer present?

A
  • Painless obstructive jaundice
  • Wt loss
  • Non-specific abdo pain/back pain
  • Palpable epigastric mass
  • N+V
  • Loss of endocrine function - new onset diabetes/worsening of T2DM (in exam if pt has worsening glycaemic control despite good lifestyle measures and medication)
  • Loss of exocrine function - steatorrhoea
78
Q

What are the referral guidelines for pancreatic cancer?

A
  • > 40 with jaundice = 2ww
  • > 60 with wt loss plus an additional symptoms = GP can refer directly for a CT abdo (suspected pancreatic cancer is the only situation GPs can do this)
79
Q

What is a differential to pancreatic cancer?

A

Cholangiocarcinoma

80
Q

What does Courvoisier’s law state?

A
  • A palpable gallbladder along with jaundice is unlikely to be gallstones
  • Cause is usually cholangiocarcinoma/pancreatic cancer
81
Q

How do you investigate pancreatic cancer?

A
  • USS
  • High resolution CT is Ix of choice if diagnosis is suspected
  • Imaging may demonstrate ‘double duct’ sign - presence of simultaneous dilation of the common bile and pancreatic ducts
  • MRCP to assess the billiard system
  • ERCP to put a stent in and relieve obstruction and to obtain a biopsy
  • Biopsy under US/CT guidance or during ERCP
82
Q

What is the tumour marker of pancreatic cancer?

A
  • CA19-9 (carbohydrate antigen)
  • Also raised in cholangiocarcinoma and other malignant/non-malignant conditions
83
Q

What is the management if pancreatic cancer

A
  • Less than 20% are suitable for surgery at diagnosis
  • Whipple’s resection (pancreaticoduodenectomy) for resectable lesions at the head of the pancreas
  • Chemo
  • ERCP with stunting is used for palliation
84
Q

What are causes of hepatitis?

A
  • Viral hepatitis
  • Autoimmune hepatitis
  • Alcoholic hepatitis
  • Non-alcoholic steatohepatitis (NASH)
  • Drug induced hepatitis (e.g. paracetamol overdose)
85
Q

What are the 5 types of viral hepatitis? Which have vaccines?

A
  • Hep A (vaccine)
  • Hep B (vaccine)
  • Hep C
  • Hep D
  • Hep E
86
Q

Which viral hepatitis is a DNA virus?

A
  • Hep B
  • Double stranded DNA virus
  • Rest are all RNA
87
Q

Which types of viral hepatitis have faecal-oral transmission?

A
  • Hep A
  • Hep E
88
Q

How is Hep B transmitted?

A

Blood/bodily fluids

89
Q

How is Hep C transmitted?

A

Blood

90
Q

How is Hep D transmitted?

A

Always with Hep B

91
Q

What is the most common viral hepatitis worldwide?

A

Hep A

92
Q

How is Hep A diagnosed?

A

IgM antibodies

93
Q

Which types of viral hepatitis are managed supportively?

A
  • Hep A
  • Hep E
94
Q

How does hepatitis present?

A
  • Abdo pain
  • Fatigue
  • Flu like illness
  • Pruritis
  • Muscle/joint aches
  • N+V
  • Jaundice
95
Q

How do you screen for Hep B?

A
  • HBcAb (vaccination/past/current infection)
  • HBsAg (active infection)
96
Q

How do you confirm a diagnosis of Hep B?

A

If positive screening tests:
- HbeAg (marker of viral replication and implies high infectivity)
- HBV DNA (viral load)

97
Q

What is the management of Hep B?

A
  • Refer to gastro/hepatology/ID
  • Screen for other viral infections
  • Avoid alcohol
  • Contact tracing
  • Testing for complications (FibroScan for cirrhosis and USS for hepatocellular carcinoma)
  • Antiviral meds to slow progression of disease and reduce infectivity
  • Transplant for liver failure
98
Q

How do you test for Hep C?

A
  • Hep C antibody (screening test)
  • Hep C RNA testing (confirm diagnosis)
99
Q

What is the management of Hep C?

A

Same general principles as for Hep B

100
Q

Is Hep C curable?

A
  • Yes - with direct-acting antiviral meds
  • Without treatment 1 in 4 make a full recovery and 3 in 4 develop chronic Hep C
101
Q

What are complications of Hep C?

A
  • Liver cirrhosis and associated complications of cirrhosis
  • Hepatocellular carcinoma

?same for Hep B

102
Q

Why id Hep D always associated with Hep B?

A

Hep D attaches itself to HBsAg and cannot survive without it

103
Q

How is Hep D treated?

A
  • Pegylated interferon alpha for > 48 weeks
  • Tx is not very effective = has sig side effects
104
Q

What is autoimmune hepatitis?

A

A rare cause of chronic hepatitis due to a combination of genetic and environmental factors

105
Q

What are the two types of autoimmune hepatitis? Who do they affect? How do they present?

A

Type 1:
- Women in their late 40s/50s
- Presents around menopause with fatigue and features of liver disease
- Less acute than type 2

Type 2:
- Children/young people
- F>M
- Presents with acute hepatitis with high transaminases and jaundice

106
Q

How do you investigate autoimmune hepatitis?

A
  • LFTs - hepatic picture
  • Raised IgG
  • Autoantibodies
  • Liver biopsy (showing interface hepatitis and plasma cell infiltration)
107
Q

What autoantibodies are present in Type 1 autoimmune hepatitis?

A
  • Anti-nuclear antibodies
  • Anti-smooth muscle antibodies
  • Anti-soluble liver antigen
108
Q

What autoantibodies are present in Type 2 autoimmune hepatitis?

A
  • Anti-liver kidney microsomes-1
  • Anti-liver cytosol antigen type 1
109
Q

What is the management of autoimmune hepatitis?

A
  • Immunosuppressants (usually successful in inducing remission) - high dose steroids, azathioprine
  • Liver transplant - required in end-stage liver disease

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