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Medicine (Year 5) > Gastroenterology (Liver) > Flashcards

Gastroenterology (Liver) Flashcards

1
Q

Non-alcoholic fatty liver disease (NAFLD)

A

describes the excess accumulation of fat in the liver (steatosis) which is not due to excessive alcohol consumption or other secondary causes. NAFLD is strongly associated with insulin resistance.

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2
Q

NAFLD often progresses through the following stages:

A
  1. Non-alcoholic fatty liver disease
  2. Non-alcoholic steatohepatitis (NASH)
  3. Fibrosis
  4. Cirrhosis
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3
Q

RF for NAFLD

A

Risk Factors

  • Obesity
  • Impaired glucose tolerance and diabetes mellitus
  • Hypertension
  • Hyperlipidaemia
  • Family history
  • Polycystic ovary syndrome
  • Hypothyroidism
  • Total parenteral nutrition (TPN)
  • Jejunoileal bypass surgery
  • Rapid weight loss
  • Refeeding syndrome
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4
Q

presentation of NAFLD

A

Most patients have no symptoms but have deranged liver function tests. Features may be:

  • Hepatomegaly
  • Fatigue
  • Splenomegaly
  • Features of risk factors (e.g. obesity)
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5
Q

investigations for NAFLD

A
  • LFT - raised ALT
  • liver US (hyper-echgenic bright imaging)
  • FibroScan- measures degree of liver stiffness
  • Liver biopsy- definitive diagnosis
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6
Q

management of NAFLD

A

Management involves:

  • Weight loss
  • Healthy diet (Mediterranean diet is recommended)
  • Exercise
  • Avoid/limit alcohol intake
  • Stop smoking
  • Control of diabetes, blood pressure and cholesterol
  • Refer patients where scoring tests indicate liver fibrosis to a liver specialist
  • Specialist management may include vitamin E, pioglitazone, bariatric surgery and liver transplantation
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7
Q

Alcohol recommendations

A

A summary of the recommendations surrounding alcohol are as follows:

  • Both men and women should drink no more than 14 units of alcohol per week
  • If people are to drink 14 units of alcohol per week, they should spread it evenly over 3 days
  • Pregnant people should not drink
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8
Q

stages of alcohol-related liver disease

A
  1. Alcoholic fatty liver (also called hepatic steatosis)

Drinking leads to a build-up of fat in the liver. This process is reversible with abstinence.

  1. Alcoholic hepatitis

Drinking alcohol over a long period causes inflammation in the liver cells. Binge drinking is associated with the same effect. Mild alcoholic hepatitis is usually reversible with permanent abstinence.

  1. Cirrhosis

Cirrhosis is where the functional liver tissue is replaced with scar tissue. It is irreversible. Stopping drinking can prevent further damage. Continued drinking has a very poor prognosis.

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9
Q

Complications of Alcohol

A
  • Alcohol-related liver disease
  • Cirrhosis and its complications (e.g., hepatocellular carcinoma)
  • Alcohol dependence and withdrawal
  • Wernicke-Korsakoff syndrome (WKS)
  • Pancreatitis
  • Alcoholic cardiomyopathy
  • Alcoholic myopathy, with proximal muscle wasting and weakness
  • Increased risk of cardiovascular disease (e.g., stroke or myocardial infarction)
  • Increased risk of cancer, particularly breast, mouth and throat cancer
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10
Q

presetation of alcohol related liver disease

A
  • Right upper quadrant abdominal pain
  • Hepatomegaly

Features of advanced liver disease:

  • Jaundice
  • Palmar erythema
  • Spider naevi
  • Haematemesis and/or melaena due to varices or coagulopathy
  • Engorged paraumbilical veins (caput medusae)
  • Splenomegaly
  • Asterixis – flapping tremor when the hands are outstretched and dorsiflexed
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11
Q

blood tests for alcoholic liver disease

A
  • Raised mean cell volume (MCV)
  • Raised alanine transaminase (ALT) and aspartate transferase (AST)
  • AST:ALT ratio above 1.5 particularly suggests alcohol-related liver disease
  • Raised gamma-glutamyl transferase (gamma-GT) (particularly notable with alcohol-related liver disease)
  • Raised alkaline phosphatase (ALP) later in the disease
  • Raised bilirubin in cirrhosis
  • Low albumin due to reduced synthetic function of the liver
  • Increased prothrombin time due to reduced synthetic function of the liver (reduced production of clotting factors)
  • Deranged U&Es in hepatorenal syndrome
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12
Q

other investigations for alcoholic liver disease

A
  • liver US
  • FibroScan
  • Endoscopy - oesophageal varices (portal hypertension)
  • liver biopsy
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13
Q

management of alcoholic liver disease

A
  • Stop drinking alcohol permanently (drug and alcohol services are available for support)
  • Psychological interventions (e.g., motivational interviewing or cognitive behavioural therapy)
  • Consider a detoxication regime
  • Nutritional support with vitamins (particularly thiamine – vitamin B1) and a high-protein diet
  • Corticosteroids may be considered to reduce inflammation in severe alcoholic hepatitis to improve short-term outcomes (but not long-term outcomes)
  • Treat complications of cirrhosis (e.g., portal hypertension, varices, ascites and hepatocellular carcinoma)
  • Liver transplant in severe disease (generally 6 months of abstinence is required)
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14
Q

CAGE questionnaire for alcoholism

A
  • 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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15
Q

alcohol withdrawal timeline

A
  • 6-12 hours: tremor, sweating, headache, craving and anxiety
  • 12-24 hours: hallucinations
  • 24-48 hours: seizures
  • 24-72 hours: delirium tremens
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16
Q

delirium tremens

A

Associated with alcohol withdrawal
35% mortality

Pathophysiology: Chronic alcohol use results in the GABA system becoming down-regulated and the glutamate system becoming up-regulated to balance the effects of alcohol. When alcohol is removed, the GABA system under-functions and the glutamate system over-functions, causing extreme excitability of the brain and excessive adrenergic (adrenalin-related) activity.

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17
Q

presentation of delirium tremens

A
  • Acute confusion
  • Severe agitation
  • Delusions and hallucinations
  • Tremor
  • Tachycardia
  • Hypertension
  • Hyperthermia
  • Ataxia (difficulties with coordinated movements)
  • Arrhythmias
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18
Q

management of alcohol withdrawal

A

reducing dose of chlordiazepoxide

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19
Q

Wernicke-Korsakoff Syndrome

A

Alcohol excess leads to thiamine (vitamin B1) deficiency. Thiamine is poorly absorbed in the presence of alcohol. Alcoholics often have poor diets and get many of their calories from alcohol. Thiamine deficiency leads to Wernicke’s encephalopathy and Korsakoff syndrome.

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20
Q

Features of Wernicke’s encephalopathy include:

A

Confusion
Oculomotor disturbances (disturbances of eye movements)
Ataxia (difficulties with coordinated movements)

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21
Q

Features of Korsakoff syndrome include:

A
  • Memory impairment (retrograde and anterograde)
  • Behavioural changes
  • Korsakoffs psychosis
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22
Q

Liver cirrhosis

A

is the result of chronic inflammation and damage to liver cells. The functional liver cells are replaced with scar tissue (fibrosis). Nodules of scar tissue form within the liver.

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23
Q

portal hypertension and cirrhosis

A

is the result of chronic inflammation and damage to liver cells. The functional liver cells are replaced with scar tissue (fibrosis). Nodules of scar tissue form within the liver.

  • oesphageal varies
24
Q

The four most common causes of liver cirrhosis are:

A
  • Alcohol-related liver disease
  • Non-alcoholic fatty liver disease (NAFLD)
  • Hepatitis B
  • Hepatitis C
25
Q

Cirrhosis also has many rarer causes:

A
  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Haemochromatosis
  • Wilsons disease
  • Alpha-1 antitrypsin deficiency
  • Cystic fibrosis
  • Drugs (e.g., amiodarone, methotrexate and sodium valproate)
26
Q

Signs of liver cirrhosis on examination include:

A
  • Cachexia (wasting of the body and muscles)
  • Jaundice caused by raised bilirubin
  • Hepatomegaly (enlargement of the liver)
  • Small nodular liver as it becomes more cirrhotic
  • Splenomegaly due to portal hypertension
  • Spider naevi (telangiectasia with a central arteriole and small vessels radiating away)
  • Palmar erythema caused by elevated oestrogen levels
  • Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
  • Bruising due to abnormal clotting
  • Excoriations (scratches on the skin due to itching)
  • Ascites (fluid in the peritoneal cavity due to hypoalbuminaemia)
  • Caput medusae (distended paraumbilical veins due to portal hypertension)
  • Leukonychia (white fingernails) associated with hypoalbuminaemia
  • Asterixis (“flapping tremor”) in decompensated liver disease
27
Q

Compensated liver cirrhosis

A

Where cirrhosis is present, but the liver synthetic function is preserved (normal clotting and albumin), and there is no evidence of complications as a result of portal hypertension (ascites, oesophageal varies, variceal bleeding, jaundice etc.).

28
Q

Decompensated liver cirrhosis

A

Where cirrhosis is present, but there is evidence of liver dysfunction, such as impaired synthesis (deranged clotting and low albumin), and complications as a result of portal hypertension.

29
Q

investigations for cirrhosis

A

Liver function tests (LFTs):

  • ALT and AST are increased, however normal ALT and AST do not exclude cirrhosis as a diagnosis
  • Generally speaking, ALT>AST in most liver diseases except for alcohol where AST>ALT

Liver ultrasound:

  • Patients with cirrhosis should have a liver ultrasound every 6 months + alpha-fetoprotein measurement to screen for the development of hepatocellular carcinoma

Ultrasound-based elastography:

  • A non-invasive method of assessing fibrosis and cirrhosis

Liver biopsy:

  • The definitive test, however not always necessary if the features and findings are suggestive of cirrhosis

Other
- Endoscopy
- CT and MRI
- Liver biopsy

30
Q

common blood test results in cirrhosis

A
  • Low albumin due to reduced synthetic function of the liver
  • Increased prothrombin time due to reduced synthetic function of the liver (reduced production of clotting factors)
  • Thrombocytopenia (low platelets) is a common finding and indicates more advanced disease
  • Hyponatraemia (low sodium) occurs with fluid retention in severe liver disease
  • Urea and creatinine become deranged in hepatorenal syndrome
  • Alpha-fetoprotein is a tumour marker for hepatocellular carcinoma
31
Q

MELD Score

A

NICE recommend using the MELD (Model for End-Stage Liver Disease) score every 6 months in patients with compensated cirrhosis. The formula considers the bilirubin, creatinine, INR and sodium and whether they require dialysis, giving an estimated 3-month mortality as a percentage.

32
Q

scoring system for assessing severity of cirrhosis and prognosis

A

Child-Pugh score

33
Q

Child-Pugh Score

A

The Child-Pugh scores uses 5 factors to assess the severity of cirrhosis and the prognosis. Each factor is considered and scored 1, 2 or 3. The minimum overall score is 5 (scoring 1 for each factor), and the maximum is 15 (scoring 3 for each factor). You can remember the features with the “ABCDE” mnemonic:

A – Albumin
B – Bilirubin
C – Clotting (INR)
D – Dilation (ascites)
E – Encephalopathy

34
Q

management of cirrhosis

A

There are four principles of management:

  • Treating the underlying cause
  • Monitoring for complications
  • Managing complications
  • Liver transplant
35
Q

managing underlying cause of cirrhosis

A
  • Stop drinking alcohol
  • Lifestyle changes for non-alcohol fatty liver disease
  • Antiviral drugs for hepatitis C
  • Immunosuppressants for autoimmune hepatitis
36
Q

monitoring for complications of cirrhosis

A
  • MELD score every 6 months
  • Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
  • Endoscopy every 3 years for oesophageal varices
37
Q

liver transplantation

A

Liver transplantation is generally considered when there are features of decompensated liver disease. The four key features can be remembered with the “AHOY” mnemonic:

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

38
Q

key complucations of cirrhosis

A
  • Malnutrition and muscle wasting
  • Portal hypertension, oesophageal varices and bleeding varices
  • Ascites and spontaneous bacterial peritonitis
  • Hepatorenal syndrome
  • Hepatic encephalopathy
  • Hepatocellular carcinoma
39
Q

malnutrition

A

Cirrhosis leads to malnutrition and muscle wasting. Patients often have a loss of appetite resulting in reduced intake. Cirrhosis affects protein metabolism in the liver and reduces the amount of protein the liver produces. It also disrupts the ability of the liver to store glucose as glycogen and release it when required. Overall, less protein is available for maintaining muscle tissue and muscle tissue is broken down for use as fuel.

Management involves nutritional support guided by a dietician, with:

  • Regular meals
  • High protein and calorie intake
  • Reduced sodium intake to minimise fluid retention
  • Avoiding alcohol
40
Q

Portal Hypertension and Varices

A

The portal vein comes from the superior mesenteric and splenic veins and delivers blood to the liver. Liver cirrhosis increases the resistance to blood flow in the liver. As a result, there is increased back pressure on the portal system. This is called portal hypertension. The back pressure of blood results in splenomegaly.

Back pressure in the portal system causes swollen and tortuous vessels at sites where collaterals form between the portal and systemic venous systems. These collaterals can occur at several locations, notably the:

  • Distal oesophagus (oesophageal varices)
  • Anterior abdominal wall (caput medusae)
41
Q

management of varices

A

Prophylaxis
- Propanolol
- Variceal band ligation ( if BB contraindicated)

42
Q

Bleeding Oesophageal Varices management

A

Bleeding oesophageal varices is a life-threatening emergency. Initial management involves:

  • 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

other:
- TIPS

43
Q

TIPS

A

Transjugular intrahepatic portosystemic shunt (TIPS) is a technique where an interventional radiologist inserts a wire under x-ray guidance into the jugular vein, down the vena cava and into the liver via the hepatic vein. A connection is made through the liver between the hepatic vein and portal vein, and a stent is inserted. This allows blood to flow directly from the portal vein to the hepatic vein, relieving the pressure in the portal system.

The two main indications are:

  • Bleeding oesophageal varices
  • Refractory ascites
44
Q

ascites

A

1) Ascites refers to fluid in the peritoneal cavity. The increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and other abdominal organs into the peritoneal cavity. The drop in circulating volume caused by fluid loss into the peritoneal cavity causes reduced blood pressure in the kidneys. The kidneys sense this lower pressure and release renin, which leads to increased aldosterone secretion via the renin-angiotensin-aldosterone system. Increased aldosterone causes the reabsorption of fluid and sodium in the kidneys, leading to fluid and sodium retention.

2) Cirrhosis causes transudative (low protein content) ascites.

45
Q

management of ascites

A
  • Low sodium diet
  • Aldosterone antagonists (e.g., spironolactone)
  • Paracentesis (ascitic tap or ascitic drain)
  • Prophylactic antibiotics (ciprofloxacin or norfloxacin) when there is <15 g/litre of protein in the ascitic fluid
  • Transjugular intrahepatic portosystemic shunt (TIPS) is considered in refractory ascites
  • Liver transplantation is considered in refractory ascites
46
Q

Spontaneous Bacterial Peritonitis

A

Spontaneous bacterial peritonitis (SBP) occurs in 10-20% of patients with ascites. It has a mortality of 10-20%. It involves an infection developing in the ascitic fluid and peritoneal lining without a clear source of infection (e.g., an ascitic drain or bowel perforation).

Most common organisms
- E.coli
- Klebsiella pneumoniae

47
Q

presentation of SBP

A
  • Fever
  • Abdominal pain
  • Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
  • Ileus (reduced movement in the intestines)
  • Hypotension
48
Q

management of SBP

A
  • Taking a sample of ascitic fluid for culture before giving antibiotics
  • Intravenous broad-spectrum antibiotics according to local policies (e.g., piperacillin with tazobactam)
49
Q

Hepatic Encephalopathy

A

Ammonia is produced when bacteria in the gut digest proteins

Hepartic encephalopathy is caused by a build of ammonia in the blood due to:

1) poor metabolism by the liver
2) collateral veels bypass the liver and send ammonia straight into systemic blood flow

50
Q

presentation of hepatic encephalopathy

A

Acutely, hepatic encephalopathy presents with reduced consciousness and confusion.

It can present more chronically with changes to personality, memory and mood.

51
Q

management of hepatic encephalopathy

A

Management involves:

  • Lactulose (aiming for 2-3 soft stools daily)- reduces the amount of time bacteria has to digest proteins and produce ammonia
  • Antibiotics (e.g., rifaximin) to reduce the number of intestinal bacteria producing ammonia- stays in the GI tract due to poor absorption
  • Nutritional support (nasogastric feeding may be required)
52
Q

acute liver failure

A

rapid development of hepatocellular dysfunction (juandice, coagulopathy and hepatic encephalopathy) in patients with no prior liver disease

(can also cause acute on chronic liver failure)

53
Q

acute liver failure can be classified as

A

Liver failure can be classified as:

  • Hyperacute – within 7 days
  • Acute – between 8 to 28 days
  • Subacute 29 days to 12 weeks
54
Q

causes of acute liver failure

A

Causes

  • Viral hepatitis
  • Paracetamol overdose
  • Chronic alcohol abuse
  • Reye’s syndrome
  • Hepatocellular carcinoma
  • Liver metastases
  • Wilson’s disease
  • Alpha-1 antitrypsin deficiency
  • Acute fatty liver of pregnancy
  • Budd-Chiari syndrome
  • Ischaemic hepatitis
  • Autoimmune hepatitis
55
Q

presentation of acute liver failure

A
  • Jaundice
  • Hepatic encephalopathy
  • Coagulopathy
  • Right upper quadrant pain
  • Nausea
  • Vomiting
  • Hyperdynamic circulation – hypotension and tachycardia
  • Kidney failure – hepatorenal syndrome may develop due to reduced perfusion
56
Q

investigations for acute liver failure

A

Liver function tests (LFTs):

  • Increased bilirubin
  • Elevated liver enzymes – usually very high

Prothrombin time or INR:

  • Prolonged

U&Es:

  • May be deranged if hepatorenal syndrome develops

Arterial blood gases:

  • May show metabolic acidosis
  • May show increased lactate

Other investigations to decipher cause:

  • Viral hepatitis serology
  • Autoimmune hepatitis antibodies
  • Paracetamol levels
  • Serum/urine toxicology
  • Pregnancy tests for acute fatty liver of pregnancy and HELLP syndrome
  • Abdominal ultrasound – for Budd-Chiari syndrome

Medicine (Year 5) (34 decks)

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