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Gastroenterology Flashcards

1
Q

Alcoholic liver disease results from the effects of the long term excessive consumption of alcohol on the liver. The onset and progression of alcoholic liver disease varies between people, suggesting that there may be a WHAT to the harmful effects of alcohol on the liver ?

A

Genetic predisposition

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2
Q

Stepwise process of progression of alcoholic liver disease ?

A
  1. ALCOHOL RELATED FATTY LIVER - drinking leads to a build up of fat in the liver (steatosis). If drinking stops this process reverses in around 2 weeks.
  2. ALCOHOLIC HEPATITIS - Drinking alcohol over a long period causes inflammation in the liver sites. Binge drinking is associated with the same effect. Mild alcoholic hepatitis is usually reversible with permanent abstinence.
  3. CIRRHOSIS - this is where fibrotic scar tissue replaces healthy tissue in the liver. This is irreversible. Stopping drinking can prevent further damage. Continued drinking has a very poor prognosis.
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3
Q

Recommended alcohol consumption ?

A

Not to regularly drink more than 14 units per week for both men and women. If drinking 14 units a week this should be spread evenly over 3 or more days and not more than 5 units in a single day.

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4
Q

Government guidelines state that any level of alcohol consumption increases the risk of cancers. Particularly which three ?

A

Breast, mouth and throat.

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5
Q

CAGE questions ? (what are the used for and what does CAGE stand for)

A

Used to quickly screen for harmful alcohol use

C - Cut down? Ever though you should?
A - Annoyed? Do you get annoyed at others commenting on your drinking?
G - Guilty? Ever feel guilty about drinking
E - Eye opener? Ever drink in the morning to help your hangover or nerves ?

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6
Q

What is the alcohol use disorders identification test (AUDIT) ?

A

Was developed by the WHO to screen people for harmful alcohol use. It involves 10 questions with multiple choice answers and gives a score. A score of 8 or more gives indication of harmful use.

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7
Q

Name 6 conditions caused by excessive alcohol use ?

A
  • Alcoholic liver disease
  • Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma
  • Alcohol dependence and withdrawal
  • Wernicke-Korsakoff syndrome (WKS)
  • Pancreatitis
  • Alcoholic cardiomyopathy
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8
Q

9 signs of liver disease ?

A
  • Jaundice
  • Hepatomegaly
  • Spider naevi
  • Palmar erythema
  • Gynaecomastia
  • Bruising (due to abnormal clotting)
  • Ascites
  • Caput medusae (engorged superficial epigastric veins)
  • Asterixis (“flapping tremor” in decompensated liver disease)
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9
Q

Blood investigations for alcoholic liver disease and what would these show ?

A
  • FBC - shows raised MCV
  • LFTts - shows elevated AST and ALT and particularly raised gamma GT. ALP will be elevated later in the disease. Low albumin due to reduced “synthetic function” of the liver. Elevated bilirubin in cirrhosis
  • CLOTTING - shows elevated prothrombin time due to reduced “synthetic function” of the liver (reduced production of clotting factors.
  • U&Es - may be deranged in hepatorenal syndrome.
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10
Q

Investigations for alcoholic liver disease (excluding bloods) ?

A
  • US of liver - may show fatty changes early on described as “increased echogenicity”. It can also demonstrate changes related to cirrhosis.
  • “FibroScan” - can used to check the elasticity of the liver by sending high frequency sound waves into the liver. It helps assess the degree of cirrhosis.
  • Endoscopy - can be used to assess for and treat oesophageal varices when portal HTN is suspected
  • CT and MRI scans - can be used to look for fatty infiltration of the liver, hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites.
  • Liver biopsy - can be used to confirm the diagnosis of alcohol related hepatitis or cirrhosis. NICE recommend considering a liver biopsy in pts where steroid treatment is being considered.
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11
Q

General management of alcoholic liver disease (6 bullet points) ?

A
  • Stop drinking alcohol permanently
  • Consider a detoxication regime
  • Nutritional support with vitamins (particularly thiamine) and a high protein diet
  • Steroids improve short term outcomes (over 1 month) in severe alcoholic hepatitis but infection and GI bleeding need to be treated first. Steroids do not improve outcomes over the long term.
  • Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy)
  • Referral for liver transplant in severe disease however they must abstain from alcohol for 3 months prior to referral
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12
Q

Alcohol withdrawal symptoms with time scale ?

A
  • 6-12 hrs: tremor, sweating, headache, craving and anxiety
  • 12-24 hrs: hallucinations
  • 24-48 hrs: seizures
  • 24-72 hrs: delerium tremens
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13
Q

What is delirium tremens (include presentation which has 9 bullet points)?

A

A medical emergency associated with alcohol withdrawal. Alcohol stimulates GABA receptors in the brain. GABA receptors have a relaxing effect on the rest of the brain. Alcohol also inhibits glutamate receptors ( also known as NMDA receptors) having a further inhibitory effect on the electrical activity of the brain.

Chronic alcohol use results in the GABA system becoming up-regulated and the glutamate system being down-regulated to balance the effects of the alcohol. When alcohol is removed from the system, GABA under-functions and glutamate over-functions causing an extreme excitability of the brain with excessive adrenergic activity. This presents as:

  • Acute confusion
  • Severe agitation
  • Delusions and hallucinations
  • Tremor
  • Tachycardia
  • HTN
  • Hyperthermia
  • Ataxia
  • Arrhythmias
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14
Q

Assessment tool used to score pt on their alcohol withdrawal symptoms and guide treatment ?

A

CIWA-Ar (clinical institute withdrawal assessment)

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15
Q

Treatment for alcohol withdrawal ?

A
  • Chlordiazepoxide (“Librium”) - is a benzodiazepine used to combat the effects of alcohol withdrawal. Diazepam is a less commonly used alternative. It is given orally as a reducing regime titrated to the required dose based on the local alcohol withdrawal protocol (e.g. 10-40mg every 1-4 hrs). This is continued for 5-7 days.
  • IV high dose B vitamins - this should be followed by regular lower dose oral thiamine. This is used to try and prevent Wernicke-Korsakoff syndrome.
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16
Q

How can alcoholism cause Wernicke-Korsakoff syndrome ?

A

Alcohol excess leads to thiamine (vitamin B1) deficiency. Thiamine is poorly absorbed in the presence of alcohol. Alcoholics tend to have poor diets and rely on the alcohol for their calories. Wernicke’s encephalopathy comes before Korsakoffs syndrome. These result from thiamine deficiency.

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17
Q

Features of Wernicke’s encephalopathy (3 points) ?

A
  • Confusion
  • Opthalmoplegia
  • Ataxia (difficulties with coordinated movements)
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18
Q

Features of Korsakoffs syndrome (2 points) ?

A
  • Memory impairment (retrograde and anterograde)

- Behavioural changes

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19
Q

Delirium tremens is a medical emergency with a mortality rate of what if left untreated ?

A

35%

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20
Q

Is Wernicke’s encephalopathy a medical emergency and does it have a high or low mortality rate if untreated ?

A

Yes it is a medical emergency and it has a high mortality rate if untreated

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21
Q

Is Korsakoffs syndrome reversible ? What does it result in ? What do prevention and treatment involve

A
  • It’s often irreversible
  • Results in pts requiring full time institutional care
  • Prevention and treatment involve thiamine supplementation and abstaining from alcohol.
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22
Q

Brief summary of liver cirrhosis ?

A

It’s the result of chronic inflammation and damage to liver cells. When the liver cells are damaged they are replaced with scar tissue (fibrosis) and nodules of scar tissue form within the liver. The fibrosis affects the structure and blood flow through the liver, which causes increased resistance in the vessels in to the liver. This is called portal hypertension.

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23
Q

Four most common causes of liver cirrhosis ?

A

Alcoholic liver disease
Non alcoholic fatty liver disease
Hepatitis B
Hepatitis C

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24
Q

7 less common causes of liver cirrhosis ?

A
  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Haemochromatosis
  • Wilsons disease
  • Alpha-1 antitrypsin deficiency
  • Cystic fibrosis
  • Drugs (e.g. amiodarone, methotrexate, sodium valproate)
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25
Q

Signs of cirrhosis (same as previous “signs of liver disease” card but with one additional bullet point, thats 10 in total) ?

A
  • Jaundice - caused by raised bilirubin
  • Hepatomegaly - however the liver can shrink as it becomes more cirrhotic
  • Splenomegaly - due to portal hypertension
  • Spider naevi - these are telangiectasia with a central arteriole and small vessels radiating away
  • Palmar erythema - caused by hyper dynamic circulation
  • Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
  • Bruising - due to abnormal clotting
  • Ascites
  • Caput medusae - distended paraumbilical veins due to portal hypertension
  • Asterixis - “flapping tremor” in decompensated liver disease.
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26
Q

Blood investigations for liver cirrhosis (excluding ELF blood test, 6 bullet points)

A
  • Liver biochemistry is often normal, however in decompensated cirrhosis all of the markers (ALT, AST, ALP and bilirubin) become deranged
  • Albumin and prothrombin time are useful markers of the synthetic function of the liver. The albumin level drops and the prothrombin time increases as the synthetic function becomes worse
  • Hyponatraemia indicates fluid retention in severe liver disease.
  • Urea and creatine become deranged in hepatorenal syndrome
  • Further bloods can hep establish the cause of cirrhosis if unknown (such as viral markers and autoantibodies)
  • Alpha-fetoprotein is a tumour marker for hepatocellular carcinoma and can be checked every 6 months as a screening test in pts with cirrhosis (along with a US)
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27
Q

Other investigations for liver cirrhosis (6 bullet points) ?

A
  • Enhanced liver fibrosis (ELF) blood test
  • US
  • FibroScan
  • Endoscopy - can be used to assess for and treat oesophageal varices when portal HTN is suspected
  • CT and MRI scans - can be used to look for hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites
  • Liver biopsy - can be used to confirm the diagnosis of cirrhosis
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28
Q

What is the ELF blood test ?

A

The first line recommended investigation for assessing fibrosis in non-alcoholic fatty liver disease but it is not currently available in many areas and cannot be used for diagnosing cirrhosis of other causes. It measures three markers (HA, PIIINP and TIMP-1) and uses an algorithm to provide a result that indicates the fibrosis of the liver:

  • less than 7.7 indicates = none to mild fibrosis
  • more than or equal to 7.7 to 9.8 = moderate fibrosis
  • more than or equal to 9.8 = severe fibrosis
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29
Q

What may an US show in liver cirrhosis (four points) + what is US used as a screening tool for relating to cirrhosis (include how often pts should be screened)?

A
  • Nodularity of the surface of the liver
  • A “corkscrew” appearance to the hepatic arteries with increased flow as they compensate for reduced portal flow
  • Enlarged portal vein with reduced flow
  • Ascites
  • Splenomegaly

US is also used as a screening tool for hepatocellular carcinoma (along with alpha-fetoprotein blood test). NICE recommend screening pts with cirrhosis for HCC every six months.

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30
Q

Why is a “FibroScan” used to investigate for liver cirrhosis and which pts should be retested ? (include how often)

A

It can be used to check the elasticity of the liver by sending high frequency sound waves into the liver and measuring how well they bounce back. It helps assess the degree of cirrhosis. This is called transient elastography and can be used to test for cirrhosis. NICE recommend retesting every 2 years in pts at risk of cirrhosis:

  • Hepatits C
  • Heavy alcohol drinkers (men drinking > 50 units or women drinking > 35 units per week)
  • Diagnosed alcoholic liver disease
  • Non alcoholic fatty liver disease and evidence of fibrosis on the ELF blood test
  • Chronic hepatitis B (they suggest yearly Fibroscan for hep B)
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31
Q

What is the Child-Pugh score for cirrhosis ?

A

Each factor is taken into account and given a score of 1, 2 or 3. the minimum score is 5 and the maximum score is 15. The score then indicates the severity of the cirrhosis and the prognosis.

Feature Score 1 Score 2 Score 3

Bilirubin <34 34-50 >50

Albumin >35 28-35 <28

INR <1.7 1.7-2.3 >2.3

Ascites None Mild Moderate to severe

Encehalopathy None Mild Moderate to severe

                    Class A           Class B            Class C

Total points 5-6 7-9 10-15

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32
Q

What is the MELD score ?

A

It’s recommended by NICE to be used every 6 months in pts with compensated cirrhosis. It is a formula that takes account the bilirubin, creatinine, INR and sodium and whether they are requiring dialysis. It gives a percentage estimated 3 month mortality and helps guide referral for liver transplant.

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33
Q

General follow up management of liver cirrhosis (6 bullet points) ?

A
  • US and alpha-fetoprotein every 6 months for hepatocellular carcinoma
  • Endoscopy every 3 years in pts without known varices
  • High protein, low sodium diet
  • MELD score every 6 months
  • Consideration fo a liver transplant
  • Managing complications as will follow on other cards.
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34
Q

Name 6 complications of liver cirrhosis ?

A
  • Malnutrition
  • Portal hypertension, varices and variceal bleeding
  • Ascites and spontaneous bacterial peritonitis (SBP)
  • Hepatorenal syndrome
  • Hepatic encephalopathy
  • Hepatocellular carcinoma
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35
Q

Give a simplified explanation of how liver cirrhosis causes malnutrition and muscle wasting ?

A

It leads to increased use of muscle tissue as fuel and reduces the protein available in the body for muscle growth. Cirrhosis affects protein metabolism in the liver and reduces the amount of protein produced. It also disrupts the ability of the liver to store glucose as glycogen and release it when required. This results in the body using muscle tissue as fuel, leading to muscle wasting and weight loss.

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36
Q

Management of of malnutrition caused by liver cirrhosis ?

A
  • Regular meals (every 2-3 hours)
  • Low sodium diet to minimise fluid retention
  • High protein and high calorie diet, particularly if underweight
  • Avoid alcohol
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37
Q

How does liver cirrhosis cause portal HTN, how does this cause varices and where do they occur ?

A

The portal vein comes from the superior mesenteric vein and the sphlenic vein and delivers blood to the liver. Liver cirrhosis increases the resistance of blood flow in the liver. As a result, there is increased back pressure into the portal system. This is called portal hypertension. This back-pressure causes the vessels at the sites where the portal system anastomoses with systemic venous system to become swollen and tortuous. These swollen, tortuous vessels are called varices. They occur at the:

  • Gastro oesophageal junction
  • Ileocaecal junction
  • Rectum
  • Anterior abdomina wall via the umbilical vein (caput medusae)
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38
Q

When do varices cause symptoms ?

A

Varices do not cause symptoms or problems until they start bleeding. Due to the high blood flow through the varices, once they start bleeding pts can exsanguinate (bleed out) very quickly.

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39
Q

Treatment for stable varices ?

A
  • Propanolol reduces portal HTN by acting as a non-selective B blocker
  • Elastic band ligation of varices
  • Injection of sclerosant (less effective than band ligation)
  • Transjugular intra-hepatic portosystemic shunt (TIPS)
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40
Q

What is a transjugular intra-hepatic portosystemic shunt (TIPS) and when is it used?

A

It is a technique where an interventional radiologist inserts a wire under xray guidance into the jugular vein, down the vena cava and into the liver via the hepatic vein. They then make a connection through the liver tissue between the hepatic vein and the portal vein and put a stent in place. This allows blood to flow directly from the portal vein to the hepatic vein and relieves the pressure in the portal system and varices. This is used if medical and endoscopic treatment of varices fail or if there are bleeding varices that cannot be controlled in other ways.

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41
Q

Management of a bleeding oesophageal varices ?

A

Resuscitation:

  • Vasopressin analogues (i.e. terlipressin) cause vasoconstriction and slow bleeding in varices
  • Correct any coagulopathy with vitamin K and fresh frozen plasma (which is full of clotting factors)
  • Giving prophylactic broad spectrum antibiotics has been shown to reduce mortality
  • Consider intubation and intensive care as they bleed very quickly and become life threateningly unwell

Urgent Endoscopy

  • Injection of sclerosant into the varices can be used to cause “inflammatory obliteration” of the vessel
  • Elastic band ligation of varices

A sengstaken-blakemore tube is an inflatable tube inserted into the oesophagus to tamponade the bleeding varices. This is used when endoscopy fails.

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42
Q

What is ascites and how does it affect the kidneys ?

A

Ascites is basically fluid in the peritoneal cavity. The increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and bowel into the peritoneal cavity. The drop in circulating volume caused by fluid loss into the peritoneal cavity causes a reduction in BP entering 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 reabsorption of fluid and sodium in the kidneys, leading to fluid and sodium overload. Cirrhosis causes a transudative, meaning low protein content, ascites.

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43
Q

Management of ascites caused by liver cirrhosis (6 bullet points) ?

A
  • Low sodium diet
  • Anti-aldosterone diuretics (spironolactone)
  • Paracentesis (ascitic tap or ascitic drain)
  • Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin or norfloxacin) in pts with less than 15g/litre of protein in the ascitic fluid
  • Consider TIPS procedure in refractory ascites
  • Consider liver transplantation in refractory ascites
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44
Q

What is spontaneous bacterial peritonitis (SBP) ?

A

It involves an infection developing in the ascitic fluid and peritoneal lining without any clear cause (e.g. not secondary to an ascitic drain or bowel perforation).

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45
Q

Presentation of SBP (6 bullet points) ?

A
  • Can be asymptomatic so have a low threshold for ascitic fluid culture
  • Fever
  • Abdominal pain
  • Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
  • Ileus (reduce movement in the intestines)
  • Hypotension
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46
Q

Most common organisms that cause SBP (three bullet points) ?

A
  • Escherichia coli
  • Klebsiella pneumoniae
  • Gram positive cocci (such as staphylococcus and enterococcus)
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47
Q

Management of SBP ?

A
  • Take an ascitic culture prior to giving antibiotics

- Usually treated with an IV cephalosporin such as cefotaxime.

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48
Q

What is hepatorenal syndrome ?

A

It occurs in liver cirrhosis. HTN is the portal system leads to stretching of the portal blood vessels causing dilation. This leads to a loss of blood volume in other areas of the circulation, including the kidneys. Hypotension in the kidneys leads to activation of the renin-angiotensin system. This causes renal vasoconstriction, which combined with the low circulation volume leads to starvation of blood to the kidneys. This leads to rapidly deteriorating kidney function. Hepatorenal syndrome is fatal within a week or so unless a liver transplant is performed.

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49
Q

What is hepatic encephalopathy ?

A

Also known as portosystemic encephalopathy. It is thought to be caused by the build up of toxins that affect the brain. One toxin that is particularly worth remembering is ammonia, which is produced by intestinal bacteria when they break down proteins. Ammonia is absorbed in the gut. There are two reasons that ammonia builds up in the blood in pts with cirrhosis: Firstly, the functional impairment of the liver cells prevents them metabolising the ammonia into harmless waste products. Secondly, collateral vessels between the portal and systemic circulation mean that the ammonia bypasses the liver altogether and enters the systemic system directly.

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50
Q

How can hepatic encephalopathy present (both acutely and chronically) ?

A
  • Acutely, it presents with reduced consciousness and confusion.
  • It can present more chronically with changes to personality, memory and mood.
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51
Q

Name 6 precipitating factors of hepatic encephalopathy ?

A
  • Constipation
  • Electrolyte disturbance
  • Infection
  • GI bleeding
  • High protein diet
  • Medications (particularly sedative medications)
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52
Q

Management of hepatic encephalopathy ?

A
  • Laxatives (i.e. lactulose) promote the excretion of ammonia. The aim is 2-3 soft motions daily. They may require enemas initially.
  • Antibiotics (i.e. rifaximin) reduces the number of intestinal bacteria producing ammonia. Rifaximin is useful as it is poorly absorbed and so stays in the GI tract.
  • Nutritional support. They may need nasogastric feeding.
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53
Q

What is non alcoholic fatty liver disease (NAFLD) ?

A

Forms part of the “metabolic syndrome” group of chronic health conditions relating to processing and storing energy that increase the risk of heart disease, stroke and diabetes. It is estimated that up to 30% of adults have NAFLD. It is characterised by fat deposited in liver cells. These fat deposits can interfere with the functioning of the liver cells. NAFLD does not cause problems initially, however it can progress to hepatitis and cirrhosis.

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54
Q

Stages of NAFLD ?

A
  1. Non-alcoholic fatty liver disease
  2. Non-alcoholic steatohepatitis (NASH)
  3. Fibrosis
  4. Cirrhosis
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55
Q

Name 7 Risk factors for NAFLD ?

A

NAFLD shares the same risk factors as CVD and diabetes:

  • Obesity
  • Poor diet and low activity levels
  • Type 2 diabetes
  • High cholesterol
  • Middle age onwards
  • Smoking
  • High blood pressure
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56
Q

When a pt presents with abnormal liver functions tests without a clear cause you will often be advised to perform a “non-invasive liver screen”. This is used to assess for possible underlying causes of liver pathology. What does this include ?

A
  • US liver
  • Hep B and C serology
  • Autoantibodies (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)
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57
Q

Which four autoantibodies would be looked for when performing a non-invasive liver screen (NILS)

A
  • Antinuclear antibodies (ANA)
  • Smooth muscle antibodies (SMA)
  • Antimitochondrial antibodies (AMA)
  • Antibodies to liver kidney microsome type-1 (LKM-1)
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58
Q

Investigations for NAFLD ?

A
  • Liver US - can confirm the diagnosis of hepatic steatosis. It does not indicate the severity, the function of the liver or whether there is liver fibrosis.
  • ELF blood test - first line
  • NAFLD fibrosis score - the second line recommended assessment for liver fibrosis where the ELF test is not available.
  • Fibroscan - is the third line investigation. It involves a special type of US that measures the stiffness of the liver and gives an indication of fibrosis. This is pefromed if the ELF blood test or NAFLD fibrosis score indicate fibrosis.
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59
Q

What is the NAFLD fibrosis score ?

A

Based on an algorithm of age, BMI, liver enzymes, platelets, albumin and diabetes and is helpful in ruling out fibrosis. It is not helpful for assessing the severity when NAFLD is present.

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60
Q

Management of NAFLD (6 bullet points) ?

A
  • Weight loss
  • Exercise
  • Stop smoking
  • Control of diabetes, BP and cholesterol
  • Avoid alcohol
  • Refer pts with liver fibrosis to a liver specialist where they may treat with vit E or pioglitazone
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61
Q

What is hepatitis and how can it vary ?

A

Inflammation of the liver. This can vary from chronic low level inflammation to acute and severe inflammation that leads to large areas of necrosis and liver failure.

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62
Q

5 causes of hepatitis ?

A
  • Alcoholic hepatitis
  • Non alcoholic fatty liver disease
  • Viral hepatitis
  • Autoimmune hepatitis
  • Drug induced hepatitis (e.g. paracetamol overdose)
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63
Q

Presentation of hepatitis (7 bullet points) ?

A

It may be asymptomatic or could present with non-specific symptoms:

  • Abdominal pain
  • Fatigue
  • Pruritis (itching)
  • Muscle and joint aches
  • Nausea and vomiting
  • Jaundice
  • Fever (viral hepatitis)
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64
Q

Typical biochemical findings in hepatitis ?

A

LFts become deranged with high transaminases (AST and ALT) with proportionally less of a rise in ALP. This is referred to as a hepatitic picture. Transaminases are liver enzymes that are released into the blood as a result of inflammation of the liver cells. Bilirubin can also rise as a result of inflammation of the liver cells. High bilirubin causes jaundice.

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65
Q

What is the most common viral hepatitis worldwide but relatively rare in the UK ?

A

Hepatitis A

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66
Q

All viral hepatitis strains are RNA viruses accept which hepatitis + what is it ?

A

Hepatitis B. It is a DNA virus.

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67
Q

How is hepatitis A transmitted ?

A

Faecal-oral route, usually in contaminated water or food.

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68
Q

How does Hep A present (four points) and what can it cause ?

A

It presents with nausea, vomiting, anorexia and jaundice. It can cause cholestasis with dark urine, pale stools and moderate hepatomegaly.

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69
Q

Management of Hep A ?

A

It resolves without treatment in around 1 to 3 months. Management is with basic analgesia.

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70
Q

Is vaccination available for Hep A and is it a notifiable disease here in the UK ?

A

Yes vaccination is available. Yes it is a notifiable disease and Public Health need to be notified of all cases.

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71
Q

How is Hep B transmitted ?

A

By direct contact with blood or bodily fluids, such as during sexual intercourse or sharing needles (i.e. IV drug users or tattoos). It can also be passed through sharing contaminated household products such as toothbrushes or contact between minor cuts or abrasions. It can also be passed from mother to child during pregnancy and delivery (vertical transmission).

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72
Q

How does Hep B progress ?

A

Most people fully recover from the infection within 2 months, however 10-15% go on to become chronic hepatitis B carriers. In these pts the virus DNA has integrated into their own DNA and they continue to produce the viral proteins.

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73
Q

The 5 important viral markers in Hep B + what they show ?

A
  • Surface antigen (BSsAg) - active infection
  • E antigen (HBeAg) - marker of viral replication and implies high infectivity.
  • Core antibodies (HBcAb) - implies past or current infection
  • Surface antibody (HBsAb) - implies vaccination or past infection
  • Hep B virus DNA (HBV DNA) - direct count of viral load.
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74
Q

How should you screen for Hep B + would should you do if screen is positive?

A

Test HBcAb (for previous infection) and HBsAg (for active infection. If these are positive do further testing for HBeAg and viral load (HBV DNA).

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75
Q

What does HBsAb demonstrate and why isn’t it a useful test ?

A

It demonstrates an immune response to HBsAg. The HBsAg is given in the vaccine so having a positive HBsAb may simply indicate they have been vaccinated and created an immune response to the vaccine. The HBsAb may also be present in response to infection. The other viral markers are necessary to distinguish between previous vaccination or current infection.

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76
Q

What can HBcAb help distinguish and how can we do this ?

A

It can help distinguish between acute, chronic and past infections. We can measure IgM and IgG versions of the HBcAb. IgM implies an active infection and will give a high titre with an acute infection and a low titre with a chronic infection. IgG indicates a past infection where the HBsAg is negative.

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77
Q

What can the level of HBeAg show ?

A

Where the HBeAg is present it implies the pt is in an acute phase of the infection where the virus is actively replicating. The level of HBeAg correlates with their infectivity. If the HBeAg is higher they are highly infectious to others. When the HBeAg is negative but the HBeAb is positive this implies they have been through a phase where the virus was replicating but the virus has now stopped replicating and they are less infectious.

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78
Q

How does vaccination for Hep B work ?

A

A vaccine is injected containing the HBsAg. Pts are tested for HBsAb to confirm the response to the vaccine. The vaccine requires 3 doses at different intervals. Vaccination to hep B is now included as part of the UK routine vaccination schedule (as part of the 6 in 1 vaccine).

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79
Q

Management of hep B (9 bullet points) ?

A
  • Have a low threshold for screening pts that are at risk of hep B
  • Screen for other blood born viruses (Hep C and HIV) and other sexually transmitted diseases
  • Refer to gastroenterology, hepatology or infectious diseases for specialist management
  • Notify Public Health (notifiable disease)
  • Stop smoking and alcohol
  • Education about reducing transmission and informing potential at risk contacts
  • Testing for complications: FibroScan for cirrhosis and US for hepatocellular carcinoma
  • Antiviral medication can be used to slow the progression of the disease and reduce infectivity
  • Liver transplantation for end-stage liver disease
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80
Q

How is hep C spread, is a vaccine available and is it curable ?

A

Spread by blood and bodily fluids, no vaccine is available and it is now curable with direct acting antiviral medications.

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81
Q

Disease course of Hep C

A
  • 1 in 4 fights off the virus and makes a full recovery

- 3 in 4 it becomes chronic

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82
Q

2 complications of Hep C ?

A
  • Liver cirrhosis and associated complications of cirrhosis

- Hepatocellular carcinoma

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83
Q

Testing for hep C ?

A
  • Hep C antibody screening test
  • Hep C RNA testing is used to confirm the diagnosis of hep C, calculate the viral load and assess for the individual genotype.
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84
Q

Management of hep C (9 bullet points) ?

A
  • Have a low threshold for screening pts that are at risk of hep C
  • Screen for other blood born viruses (hep B and HIV) and other sexually transmitted diseases
  • Refer to gastro, hepatology and ID for specialist management
  • Notify Public Health (it is a notifiable disease)
  • Stop smoking and alcohol
  • Education about reducing transmission and informing potential at risk contacts
  • Testing for complications: FibroScan for cirrhosis and US for hepatocellular carcinoma
  • Antiviral treatment with direct acting antivirals (DAAs) is tailored to the specific viral genotype. They successfully cure the infection in over 90% of pts. They are typically taken for 8 to 12 weeks
  • Liver transplantation for end-stage liver disease.
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85
Q

How does hep D infect pts, how common is it in the UK, what problems does it cause, treatment ? and is it a notifiable disease ?

A

It can only survive in pts who also have hep B infection. It attaches itself to the HBsAg to survive and cannot survive without this protein. There are very low rates in the UK. Hep D increases the complications and disease severity of hep B. There is no specific treatment for hepatitis D. It is a notifiable disease and Public Health need to be notified of all cases.

86
Q

How is Hep E transmitted, how common is it in the UK ?, how does it present/progress, treatment ?, any rare complications ?, is there a vaccination ? and is it a notifiable disease ?

A

It is transmitted by the faecal oral route. It is very rare in the UK. Normally it produces only a mild illness, the virus is cleared within a month and no treatment is required. Rarely it can progress to chronic hepatitis and liver failure, more so in pts that are immunocompromised. There is no vaccination. It is a notifiable disease and Public Health need to be notified of all cases.

87
Q

What is autoimmune hepatitis ?

A

A rare cause of chronic hepatitis. We are not sure of the exact cause, however it could be associated with a genetic predisposition and triggered by environmental factors such as a viral infection that causes a cell-mediated response against the liver cells. The T cells of the immune system recognise liver cells as being harmful and alert the rest of the immune system to attack these cells.

88
Q

Two types of autoimmune hepatitis ?

A

Type 1: Occurs in adults - typically women around their late 40s or 50s present around or after the menopause with fatigue and features of liver disease on examination. The presentation is less acute than type 2

Type 2: Occurs in children - typically pts in their teenage yrs or early 20s present with acute hepatitis with high transaminases and jaundice.

89
Q

What will investigations show in autoimmune hepatitis ?

A

Investigations will show raised transaminases and IgG levels. It is associated with many autoantibodies.

90
Q

Which autoantibodies are type 1 & 2 autoimmune hepatitis associated with ?

A

Type 1:

  • Anti-nuclear antibodies (ANA)
  • Anti smooth muscle antibodies (anti-actin)
  • Anti-soluble liver antigen (anti-SLA/LP)

Type 2:

  • Anti-liver kidney microsomes-1 (anti-LKM1)
  • Anti-liver cytosol antigen type 1 (anti-LC1)
91
Q

How can a diagnosis of autoimmune hepatitis be confirmed ?

A

By using a liver biopsy

92
Q

Treatment of autoimmune hepatitis ?

A

High dose steroids (prednisolone) that are tapered over time as other immunosuppressants, particularly azathioprine are introduced. Immunosuppressant treatment is usually successful in inducing remission, however it is usually required life long. Liver transplant may be required in end stage liver disease, however the autoimmune hepatitis can recur in transplanted livers.

93
Q

What is haemochromatosis ?

A

Its an iron storage disorder that results in excessive total body iron and deposition of iron in tissues

94
Q

The majority of cases of haemochromatosis relate to mutations in which gene ?

A

The human haemochromatosis protein (HFE) gene is located on chromosome 6. There are other genes that can cause the condition though.

95
Q

Is the haemochromatosis genetic mutation autosomal recessive or autosomal dominant ?

A

Autosomal recessive

96
Q

What does the HFE gene do ?

A

It is important in regulating iron metabolism

97
Q

When do symptoms of haemochromatosis usually present ?

A

After the age of 40 when iron overload becomes symptomatic. It presents later in females due to menstruation acting to regularly eliminate iron from the body.

98
Q

Name 7 symptoms of haemochromatosis ?

A
  • Fatigue
  • Joint pain
  • Pigmentation (bronze colouration)
  • Hair loss
  • Erectile dysfunction
  • Amenorrhoea
  • Cognitive symptoms (memory and mood disturbance)
99
Q

Diagnosis of haemochromatosis ?

A

The main diagnostic method is to perform a serum ferritin level. Ferritin is an acute phase reactant, meaning that it goes up with inflammatory conditions such as infection. Performing a transferrin saturation is helpful in distinguishing between a high ferritin caused by iron overload (in which case transferrin saturation is high) from a high ferritin due to other causes such as inflammation or NAFLD. If serum ferritin and transferrin saturation is high and there is no other reason then genetic testing can be performed to confirm haemochromatosis.

Liver biopsy with Perl’s stain can be used to establish the iron concentration in the parenchymal cells. This used to be the gold standard for diagnosis but it has been replaced by genetic testing.

A CT abdomen scan can show a non-specific increase in attenuation of the liver

MRI can give a more detailed picture of liver deposits of iron. It can also be used to look at iron deposits in the heart.

100
Q

7 complications of haemochromatosis ?

A
  • Type 1 diabetes (iron affects the functioning of the pancreas)
  • Liver cirrhosis
  • Iron deposits in the pituitary and gonads lead to endocrine and sexual problems (hypogonadism, impotence, amenorrhea and infertility)
  • Cardiomyopathy (iron deposits in the heart)
  • Hepatocellular carcinoma
  • Hypothyroidism (iron deposits in the thyroid)
  • Chrondocalcinosis (calcium deposits in the joints) causing arthritis
101
Q

Management of haemochromatosis ?

A
  • Venesection (a weekly protocol of removing blood to decrease total iron)
  • Monitoring serum ferritin
  • Monitoring and treatment of complications
102
Q

What is Wilson disease ?

A

The excessive accumulation of copper in the body and tissues.

Copper builds up in your liver until it overflows into the bloodstream.

103
Q

What mutation causes Wilsons disease (give both names) and is genetic inheritance of this mutation autosomal dominant or autosomal recessive?

A

It is caused by a mutation in the “Wilson disease protein” on chromosome 13. This protein is also called the “ATP7B copper-binding protein”. Genetic inheritance is autosomal recessive

104
Q

What does the ATP7B copper binding protein do (name two main functions) ?

A
  • Links copper to ceruloplasmin and releases it into the bloodstream
  • Removes excess copper by secreting it into bile
105
Q

Main features of Wilson disease (three areas) ?

A

Most pts with Wilson disease present with one or more of:

  • Hepatic problems (40%)
  • Neurological problems (50%)
  • Psychiatric problems (10%)
106
Q

Hepatic problems caused by Wilson disease ?

A

Copper deposition in the liver leads to chronic hepatitis and eventually liver cirrhosis.

107
Q

What does copper deposition in the CNS lead to (two things) ?

A

Neurological and psychiatric problems.

108
Q

Neurological symptoms caused by Wilson disease ?

A

Neurological symptoms can be subtle and range from concentration and coordination difficulties to dysarthria (speech difficulties) and dystonia (abnormal muscle tone). Copper deposition in the basal ganglia leads to Parkinsonism (tremor, bradykinesia and rigidity). These Parkinsonism symptoms are symmetrical, differentiating them from the asymmetrical symptoms in Parkinson disease.

109
Q

Psychiatric symptoms caused by Wilson disease ?

A

Vary from mild depression to full psychosis and the underlying cause of Wilson disease is often missed and treatment delayed.

110
Q

Kayser-Fleischer rings can be present in Wilson disease, what are these and how can they be assessed ?

A

They are brownish circles surrounding the iris. They are due to copper deposition in the cornea (Descemet’s membrane). They can usually be seen by the naked eye but proper assessment is made using slit lamp examination

111
Q

Name 3 other features of Wilson disease ?

A
  • Haemolytic anaemia
  • Renal tubular damage leading to renal tubular acidosis
  • Osteopenia (loss of bone mineral density)
112
Q

Diagnosis of Wilson disease ?

A

The initial investigation of choice is the serum caeruloplasmin. Caeruloplasmin is the protein that carries copper in the blood. Serum caeruloplasmin is normally low in Wilson disease. It can be falsely normal or elevated in cancer or inflammatory conditions, therefore it is not specific to Wilson disease.

Liver biopsy to check liver copper content is the definitive gold standard test for diagnosis Diagnosis can also be established if the 24hr urine copper assay is sufficiently elevated. Alternatively there are scoring systems that take into account various features and laboratory tests to establish a diagnosis of Wilson disease.

113
Q

Why is serum caeruloplasmin low in the majority of Wilson disease cases ?

A

As it cant bind to copper so (termed apocaeruloplasmin) and is rapidly degraded in the bloodstream.

114
Q

Management of Wilson disease ?

A

Treatment is with copper chelation

  • Penicillamine
  • Trientine
115
Q

What is alpha 1 antitrypsin deficiency ?

A

It is an inherited deficiency of a protease inhibitor called alpha 1 antitrypsin. This leads to an excess of protease enzymes that attack the liver an lung tissue and cause liver cirrhosis and lung disease.

116
Q

Pathophysiology of A1AT deficiency ?

A

Elastase is an enzyme secreted by neutrophils. This enzyme digests connective tissues. A1AT is present in tissues to inhibit the neutrophil elastase and protect tissues. A1AT is coded for on chromosome 14. In A1AT deficiency, there is an autosomal recessive defect in the gene for A1AT. This results in a lack of protection against neutrophil elastase, leading to connective tissue damage.

117
Q

The main organs affected by A1AT deficiency are the liver and the lungs, what does it lead to ?

A
  • Liver cirrhosis after 50 years old

- Pulmonary basal emphysema after 30 years old

118
Q

Diagnosis of A1AT deficiency (4 bullet points) ?

A
  • Low serum alpha 1 antitrypsin. This is the screening test of choice.
  • Liver biopsy shows cirrhosis and acid-Schiff-positive staining globules (this is a test to stain the breakdown products of the action of the proteases) in hepatocytes
  • Genetic testing for A1AT gene
  • High resolution CT thorax diagnoses pulmonary emphysema
119
Q

Management of A1AT deficiency (5 bullet points) ?

A
  • Stop smoking (smoking dramatically accelerates emphysema)
  • Symptomatic management
  • NICE recommend against the use of alpha 1 antitrypsin, however the research and debate is ongoing regarding the possible benefits
  • Organ transplant for end stage liver disease or lung disease
  • Monitoring for complications (e.g. hepatocellular carcinoma)
120
Q

What is primary biliary cirrhosis

?

A

It is a condition where the immune system attacks and progressively destroys the small bile ducts in the liver. The first parts to be affected are the intralobular ducts, also known as the Canals of Hering. This causes obstruction of the outflow of bile, which is called cholestasis. The back pressure of the bile obstruction and overall disease process ultimately leads to fibrosis, cirrhosis and liver failure.

121
Q

How are bile acids, bilirubin and cholesterol affected by PBC ?

A

They are usually excreted through the bile ducts into the intestines. When there is obstruction to flow of these chemicals they build up in the blood as they are not being excreted. Raised bile acids cause itching and raised bilirubin causes jaundice. Raised cholesterol causes cholesterol deposits in the skin called xanthelasma. Xanthoma are larger nodular deposits of cholesterol in the skin or tendons. Cholesterol deposits in the blood vessels increase the risk of cardiovascular disease.

Bile acids are normally responsible for helping the gut digest fats. Having a lack of bile in the stool causes GI disturbance, malabsorption of fat and steatorrhoea. Bilirubin normally causes the dark colour of stools, so a lack of bilirubin causes pale stools.

122
Q

Presentation of PBC (7 bullet points) ?

A
  • Fatigue
  • Pruritis
  • GI disturbance and abdominal pain
  • Jaundice
  • Steatorrhoea
  • Xanthoma and xanthelasma
  • Signs of cirrhosis and failure (e.g. ascites, splenomegaly, spider naevi etc)
123
Q

Name 3 associations of PBC ?

A
  • Middle aged women
  • Other autoimmune diseases (e.g. thyroid, coeliac)
  • Rheumatoid conditions (e.g. systemic sclerosis, Sjogrens and rheumatoid arthritis)
124
Q

Diagnosis of PBC ?

A

Liver function tests:

  • Alkaline phosphatase is the first liver enzyme to be raised (as with most obstructive pathology)
  • Other liver enzymes and bilirubin are raised later in the disease

Autoantibodies:

  • Anti-mitochondrial antibodies are the most specific to PBC and form part of the diagnostic criteria
  • Anti-nuclear antibodies are present in about 35% of pts

Other blood tests:

  • Raised ESR
  • Raised IgM

Liver biopsy is used in diagnosing and staging the disease

125
Q

Treatment of PBC (4 bullet points) ?

A
  • Ursodeoxycholic acid reduces the intestinal absorption of cholesterol
  • Cholestyramine is a bile acid sequestrate. It binds to bile acids to prevent absorption in the gut which reduces the amount of bile in the blood. Also causes liver to use cholesterol to replace bile salts which reduces cholesterol levels.
  • Liver transplant in end stage liver disease
  • Immunosuppression (e.g. with steroids) is considered in some pts.
126
Q

Disease progression of PBC ?

A

Disease course and symptoms vary significantly. Some people live decades without symptoms. The most important end results of the disease are advanced liver cirrhosis and portal HTN.

Some other issues and complications are:

  • Symptomatic pruritis
  • Fatigue
  • Steatorrhoea
  • Distal renal tubular acidosis
  • Hypothyroidism
  • Osteoporosis
  • Hepatocellular carcinoma
127
Q

What is primary sclerosing cholangitis ?

A

A condition where the intrahepatic OR extrahepatic ducts become strictured and fibrotic. This causes obstruction to the flow of bile out of the liver and into the intestines. Sclerosis refers to the stiffening and hardening of the bile ducts, and cholangitis is the inflammation of the bile ducts. Chronic bile obstruction eventually leads to hepatitis, fibrosis and cirrhosis.

128
Q

Cause of PSC ?

A

Mostly unclear although there is likely to be a combination of genetic, autoimmune, intestinal microbiome and environmental factors. There is an established association with ulcerative colitis, with around 70% of cases being alongside pre-existing ulcerative colitis.

129
Q

Name four risk factors for PSC ?

A
  • Male
  • Aged 30-40
  • Ulcerative colitis
  • Family history
130
Q

Presentation of PSC (5 bullet points) ?

A
  • Jaundice
  • Chronic right upper quadrant pain
  • Pruritis
  • Fatigue
  • Hepatomegaly
131
Q

Would would LFTs show in PSC ?

A

They show a “cholestatic” picture. This means ALP is the most deranged LFT and may be the only abnormality at first.

There may be a rise in bilirubin as the strictures become more severe and prevent bilirubin from being excreted through the bile duct. Other LFTs (i.e. ALT and AST)n can also be deranged, particularly as the disease progresses to hepatitis.

132
Q

Talk through the relevance of autoantibodies to PSC ?

A

No antibodies are highly sensitive or specific to PSC. They aren’t very helpful in diagnosis but they can indicate where there is an autoimmune element to the disease that may respond to immunosuppression. The main autoantibodies are:

  • Antineutrophil cytoplasmic antibody (p-ANCA) in up to 94%
  • Antinuclear antibodies (ANA) in up to 77%
  • Anticardiolipin antibodies (aCL) in up to 63%
133
Q

Diagnosis of PSC ?

A

The gold standard investigation for diagnosis is a magnetic resonance cholangiopancreatography (MRCP). The involves an MRI scan of the liver, bile ducts and pancreas. In PSC it may show bile duct lesions or strictures.

134
Q

Name 6 associations and complications of PSC ?

A
  • Acute bacterial cholangitis
  • Cholangiocarcinoma develops in 10-20% of cases
  • Colorectal cancer
  • Cirrhosis and liver failure
  • Biliary strictures
  • Fat soluble vitamin deficiencies
135
Q

Management of PSC ?

A

Liver transplant can be curative but is associated with its own problems (around 80% survival at 5 years)

  • ERCP can be used to dilate and stent any strictures
  • Ursodeoxycholic acid is used and may slow disease progression
  • Cholestyramine is a bile acid sequestrate. It binds to bile acids to prevent absorption in the gut which reduces the amount of bile in the blood.
  • Monitoring for complications such as cholangiocarcinoma, cirrhosis and oesophageal varices.
136
Q

What is ERCP (Endoscopic retrograde cholangiopancreatography) ?

A

It involves inserting a endoscope through the persons oesophagus, stomach, and duodenum to the point in the duodenum where the bile ducts empty into the GI tract. They then go through the sphincter of Oddi into the ampulla of Vater. From the ampulla of Vater they can enter the bile ducts and inject contrast and use X-rays to identify any strictures. These strictures can then be dilated and stented during the same procedure, providing improved flow through those ducts and an improvement in symptoms.

137
Q

What is primary liver cancer and what are the two main types ?

A

Cancer that originates in the liver. The two main types are hepatocellular carcinoma (80%) and cholangiocarcinoma (20%).

138
Q

What is secondary liver cancer ?

A

Cancer that originates outside the liver and metastasises to the liver. Metastasis to the liver can occur in almost any cancer that spreads.

139
Q

Prognosis of secondary liver cancer ?

A

There is a poor prognosis when there is cancer with liver metastasis. The first stage is to search for the primary (e.g. full body CT scan and thorough history and examination of the skin and breasts). It is not uncommon to have liver metastases of unknown primary.

140
Q

Main risk factor for HCC ?

A

Liver cirrhosis due to:

  • Viral hep (B and C)
  • Alcohol
  • NAFLD
  • Other chronic liver disease

Pts with chronic liver disease are screened for HCC.

141
Q

Risk factors for cholangiocarcinomas ?

A

They are associated with primary sclerosing cholangitis. However, only 10% of pts with cholangiocarcinoma had PSC. Cholangiocarcinoma usually presents in pts more than 50 years old, unless related to PSC.

142
Q

Presentation of liver cancer ?

A

Liver cancer often remains asymptomatic for a long time and then presents late, making the prognosis poor.

There are non specific symptoms associated with liver cancer:

  • Weight loss
  • Abdominal pain
  • Anorexia
  • N&V
  • Jandice
  • Pruritis

Cholangiocarcinoma often presents with painless jaundice in a similar way to pancreatic cancer.

143
Q

Investigations for liver cancer (5 bullet points) ?

A
  • Alpha-fetoprotein is a tumour marker for HCC
  • CA19-9 is a tumour marker for cholangiocarcinoma
  • Liver US can identify tumours
  • CT and MRI scans are used for diagnosis and staging of the cancer
  • ERCP can be used to take biopsies or brushings to diagnose cholangiocarcinoma.
144
Q

Treatment of HCC ?

A

HCC has a very poor prognosis unless diagnosed early. Resection of early disease in a in a resectable area of the liver can be curative. Liver transplant when the HCC is isolated to the liver can be curative.

There are several kinase inhibitors that are licensed as medical treatment for HCC. They work by inhibiting the proliferation of cancer cells. Some examples of these are sorafenib, regorafenib and lenvatinib. They can potentially extend life by months.

HCC is generally considered resistant to chemotherapy and radiotherapy. In certain circumstances they are used as part of palliative treatment or clinical trials.

145
Q

Treatment of cholangiocarcinoma ?

A

Cholangiocarcinomas have a very poor prognosis unless diagnosed early. Early disease can potentially be cured with surgical resection.

ERCP can be used to place a stent in the bile duct where the cholangiocarcinoma is compressing the duct. This allows for the drainage of bile and usually improves symtpoms.

Cholangiocarinomas are also generally considered resistant to chemotherapy and radiotherapy.

146
Q

What are haemangiomas in relation to the liver ?

A

Common benign tumours of the liver. They are often found incidentally. They cause no symptoms and have no potential to become cancerous. No treatment or monitoring is required.

147
Q

What is focal nodular hyperplasia ?

A

It is a benign liver tumour made of fibrotic tissue. This is often found incidentally. It is usually asymptomatic and has no malignant potential. It can be related to oestrogen and therefore is more common in women and those on the oral contraceptive pill. No treatment or monitoring is required.

148
Q

What is an orthotopic liver transplant

A

When an ENTIRE liver is transplanted from a deceased pt to a recipient. This translates as straight (ortho) in place (topic)

149
Q

What is a living donor liver transplant ?

A

Due to the fact that the liver can regenerate as an organ it is possible to take a portion of the organ from a living donor, transplant it into a pt and have both regenerate to become two fully functioning organs.

150
Q

What is a split liver donation ?

A

When the liver of a deceased person is split into two and transplanted into two pts where the livers regenerate to their normal size in each recipient.

151
Q

Indications for liver transplant can be split into which two categories ?

A

Acute liver failure or chronic liver failure.

152
Q

Acute liver failure usually requires an immediate liver transplant, and these pts are placed on top of the transplant list. What are the two most common causes ?

A

Acute viral hepatitis and paracetamol overdose.

153
Q

Chronic liver failure pts can wait longer for their liver transplant and are put on a standard transplant list. It is normal for it to take how many months for a liver to become available ?

A

5 months.

154
Q

Name 5 factors suggesting unsuitability for liver transplantation ?

A
  • Significant co-morbidities (e.g. severe kidney or heart disease)
  • Excessive weight loss and malnutrition
  • Active hepatitis B or C or other infection
  • End stage HIV
  • Active alcohol use (generally 6 months of abstinence is required)
155
Q

Where are liver transplant surgeries carried out, what kind of incision does it involve and what else happens during the surgery ?

A

It is carried out in a specialist transplant clinic. It involves a “rooftop” or “Mercedes Benz” incision along the lower costal margin for open surgery. The liver is mobilised away from the other tissues and excised. The new liver, biliary system and blood supply is then implanted and connected.

156
Q

Post liver transplantation care ?

A

Pts will require livelong immunosuppression (e.g. steroids, azathioprine and tacrolimus) and careful monitoring of these drugs. They are required to follow lifestyle advice and require monitoring and treatment for complications:

  • Avoid alcohol and smoking
  • Treating opportunistic infections
  • Monitoring for disease recurrence (i.e. hepatitis or primary biliary cirrhosis)
  • Monitoring for cancer as there is a significantly higher risk in immunocompromised pts
157
Q

Following a liver transplant pts need to be monitored for evidence of transplant rejection, name 4 S/S of this ?

A
  • Abnormal LFTs
  • Fatigue
  • Jaundice
  • Fever
158
Q

What is gastro-oesophageal reflux disease (GORD) ?

A

It is where acid from the stomach refluxes through the lower oesophageal sphincter and irritates the lining of the oesophagus.

159
Q

Which type of epithelium lines the oesophagus ?

A

Squamous epithelium (it is more sensitive to the effects of stomach acid)

160
Q

Which type of epithelium lines the stomach, is it more protected against stomach acid ?

A

Columnar epithelium (it is more protected against stomach acid)

161
Q

Presentation of GORD (term used to describe indigestion + 6 bullet points) ?

A

Dyspepsia is a non-specific term used to describe indigestion. It covers the symptoms of GORD:

  • Heartburn
  • Acid regurgitation
  • Retrosternal or epigastric pain
  • Bloating
  • Nocturnal cough
  • Hoarse voice
162
Q

Endoscopy can be used to assess for peptic ulcers, oesophageal or gastric malignancy if there are concerning features. Pts with evidence of a GI bleed (i.e. melaena or coffee ground vomiting) need what ?

A

Admission and an urgent endoscopy.

163
Q

Referral for endoscopy:

Pts with symptoms suspicious of cancer should have a 2WW referral for an endoscopy. The NICE guidelines have various criteria for when to refer urgently and when to refer routinely. The key red flag features indicating referral are (8)?

A
  • Dysphagia - at any age
  • Aged over 55
  • Weight loss
  • Upper abdominal pain and reflux
  • Treatment resistant dyspepsia
  • Persistent vomiting
  • Low haemoglobin
  • Raised platelet count
164
Q

Management of GORD ?

A

LIFESTYLE ADVICE:

  • Reduce tea, coffee and alcohol
  • Weight loss
  • Avoid smoking
  • Smaller, lighter meals
  • Avoid heavy meals before bed time
  • Stay upright after meals rather than lying flat

ACID NEUTRALISING MEDICATION WHEN REQUIRED:

  • Gaviscon
  • Rennie

PROTON PUMP INHIBITORS (reduce acid secretion in the stomach):

  • Omeprazole
  • Lansoprazole

RANITIDINE:

  • This is an alternative to PPIs
  • It is a H2 receptor antagonist (antihistamine)
  • Reduces stomach acid

Surgery for reflux is called laparoscopic fundoplication. This involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.

165
Q

What is H. pylori ?

A

A gram negative aerobic bacteria.

166
Q

Where does H. pylori live ?

A

In the stomach

167
Q

Talk through what H. pylori does to they body ?

A

It causes damage to the epithelial lining of the stomach resulting in gastritis, ulcers and increasing the risk of stomach cancer. It avoids the acidic environment by forcing its way into the gastric mucosa. The breaks it creates in the mucosa exposes the epithelial cells underneath to acid.

It also produces ammonia to neutralise the stomach acid. The ammonia directly damages the epithelial cells. Other chemicals produced by the bacteria also damage the epithelial lining.

168
Q

A H. pylori test is offered to anyone with dyspepsia, what are the conditions for this test and why ?

A

Pts need 2 weeks without using a PPI before testing for H. pylori for an accurate result.

169
Q

Name 3 tests for H. pylori ?

A
  • Urea breath test using radiolabelled carbon 13
  • Stool antigen test
  • Rapid urease test can be performed during endoscopy.
170
Q

What is a rapid urease test a.k.a. a CLO test (campylobacter-like organism test) ?

A

It is performed during endoscopy and involves taking a small biopsy of the stomach mucosa. Urea is added to this sample. If H. pylori are present, they produce urease enzymes that converts the urea to ammonia. The ammonia makes the solution more akaline giving a positive result when the pH is tested.

171
Q

How is a H.pylori infection in the stomach eradicated + what test can be used to see if this is successful ?

A

A regime involving triple therapy with a PPI plus 2 antibiotics (e.g. amoxicillin and clarithromycin) for 7 days.

The urea breath test can be used as a test of eradication after treatment. This is not routinely necessary.

172
Q

What is Barretts oesophagus, does this affect reflux symptoms, what type of condition is it considered to be and how is it monitored?

A

It is where the constant reflux of acid results in the lower oesophageal epithelium undergoing metaplasia from a squamous to columnar epithelium.

When this happens pts typically get improvement in reflux symptoms.

It is considered to be a “premalignant” condition and is a risk factor for the development of adenocarcinoma of the oesophagus.

Pts identified as having Barretts oesophagus are monitored for adenocarcinoma by regular endoscopy.

Note: In some pts there is a progression from Barretts oesophagus with no dysplasia to low grade dysplasia to high grade dysplasia and then to adenocarcinoma.

173
Q

Treatment of Barretts oesophagus ?

A

With PPIs

Ablation therapy during endoscopy using photodynamic therapy, laser therapy or cyrotherapy is used to destroy the epithelium so that it is replaced with normal cells. This is not recommend in pts with no dysplasia but has a role in low and high grade dysplasia in preventing progression to cancer.

174
Q

What are peptic ulcers + which type is more common ?

A

Ulceration of the mucosa of the stomach or duodenum. Duodenal ulcers are more common.

175
Q

Pathophysiology of peptic ulcers ?

A

The mucosa is prone to ulceration from:

  • Breakdown of the protective layer of the stomach and duodenum
  • Increase in stomach acid

There is a protective layer in the stomach and duodenum comprised of mucus and bicarbonate secreted by the mucosa. The protective layer can be broken down by:

  • Medications (e.g. steroids or NSAIDs)
  • H. pylori

Increased acid can result from:

  • Stress
  • Alcohol
  • Caffeine
  • Smoking
  • Spicy food
176
Q

Presentation of a peptic ulcer ?

A
  • Epigastric discomfort or pain
  • Nausea and vomiting
  • Dyspepsia
  • Bleeding causing haemetemsis “coffee ground” vomiting and melaena
  • Iron deficiency anaemia (due to constant bleeding)

TOM TIP: In your MCQ exams, eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.

177
Q

Diagnosis of peptic ulcers ?

A

They are diagnosed by endoscopy.

Note :During endoscopy a rapid urease test (CLO test) can be performed to check for H. pylori. Biopsy should be considered during endoscopy to exclude malignancy as cancers can look similar to ulcers during the procedure.

178
Q

Treatment for peptic ulcers ?

A

Medical treatment is the same as with GORD, usually with high dose proton pump inhibitors. Endoscopy can be used to monitor the ulcer to ensure it heals and to assess for further ulcers.

179
Q

Complications of a peptic ulcer ?

A
  • Bleeding - common and potentially lie threatening
  • Perforation - resulting in an “acute abdomen” and peritonitis. This requires urgent surgical repair (usually laparoscopic)
  • Scarring and strictures of the muscle and mucosa - This can lead to pyloric stenosis. This presents with upper abdominal pain, distention, nausea and vomiting particularly after eating.
180
Q

Bleeding from the upper GI tract is a medical emergency that you will see often on the wards as a junior doctor. It involves some form of bleeding from the oesophagus, stomach or duodenum. Name four causes ?

A
  • Oesophageal varices
  • Mallory-Weiss tear, which is a tear of the oesophageal mucous membrane
  • Ulcers of the stomach or duodenum
  • Cancers of the stomach or duodenum
181
Q

Presentation of an upper GI bleed ?

A
  • Haematemesis
  • “Coffee ground vomit” - This is caused by vomiting digested blood that looks like coffee grounds.
  • Melaena - tar like, black, greasy and offensive stools caused by digested blood.
  • Haemodynamic instability occurs in large blood loss, causing a low blood pressure, tachycardia and other signs of shock. Bear in mind that young, fit pts may compensate well with normal obs until they have lost a lot of blood.

The pt may have symptoms related to the underlying pathology:

  • Epigastric pain and dyspepsia in peptic ulcers
  • Jaundice or ascites in liver disease with oesophageal varices.
182
Q

What is the Glasgow-Blatchford score ?

A

A scoring system used in suspected upper GI bleed on their initial presentation. It establishes their risk of having an upper GI bleed to help you make a plan.

NOTE: 
Using an online calculator is the easiest way to calculate the score.  A score > 0 indicates high risk for an upper GI bleed.  It takes into account various features indicating an upper GI bleed:
-Drop in Hb
-Rise in urea
-BP
-HR
-Malaena
-Syncopy
183
Q

TOM TIP:

A

The reason urea rises in upper GI bleeds is that the blood in the GI tract gets broken down by the acid and digestive enzymes. One of the breakdown products is urea and this urea is then absorbed into the intestines.

184
Q

What is the Rockall score ?

A

It is used for pts that have had a bleed and an endoscopy. It provides a % risk of rebleeding and mortality.

NOTE:
Use an online calculator to calculate the score. It takes into account RF’s from the clinical presentation and endoscopy findings such as:
-Age
-Features of shock
-Co-morbidities
-Cause of bleeding
-Endoscopic stigmata of recent haemorrhage such as clots or visible bleeding vessels

185
Q

Management of an upper GI bleed ?

A

ABATED

A - ABCDE approach to immediate resuscitation
B - Bloods
A - Access (ideally 2 large bore cannula)
T - Transfuse
E - Endoscopy (arrange urgent endoscopy within 24 hours)
D - Drugs (stop anticoagulants and NSAIDs)

186
Q

Which bloods would you send for following an upper GI bleed ?

A
  • Hb (FBC)
  • Urea (U&Es)
  • Coagulation (INR, FBC for platelets)
  • Liver disease (LFTs)
  • Crossmatch 2 units of blood
187
Q

TOM TIP:

A

“Group and save” is where the lab simply checks the pts blood group and keeps a sample of their blood saved incase they need to match blood to it. “Crossmatch” is where the lab actually finds blood, tests that it is compatible and keeps it ready in the fridge to be used if necessary.

188
Q

Note regarding transfusion following an upper GI bleed:

A

Transfusion is based on the individual presentation:

  • Transfuse blood, platelets and clotting factors (fresh frozen plasma) to pts with massive haemorrhage
  • Transfusing more blood than necessary can be harmful
  • Platelets should be given in active bleeding and thrombocytopenia (platelets < 50)
  • Prothrombin complex concentrate can be given to pts taking warfarin that are actively bleeding.
189
Q

Note:

A

Following an upper GI bleed there are some additional steps if oesophageal varices are suspected, for example in pts with a history of chronic liver disease:

  • Terlipressin
  • Prophylactic broad spectrum antibiotics
190
Q

Definitive treatment of an upper GI bleed ?

A

OGD to provide interventions to stop the bleeding. This could involve variceal banding or cauterisation of the bleeding vessel.

191
Q

Features of Crohn’s disease that are distinct from UC ?

A

crows NESTS

N - No blood or mucus (less common)
E - Entire GI tract
S - “Skip lesions” on endoscopy
T - Terminal ileum is most affected and Transmural inflammation
S - Smoking is a risk factor (don’t set the nest on fire)

Crohns is also associated with weight loss, strictures and fistulas.

192
Q

Features of UC that are distinct from Crohn’s disease ?

A

U - C - CLOSEUP

C - Continuous inflammation
L - Limited to colon and rectum
O - Only superficial mucosa affected
S - Smoking is protective
E - Excrete blood and mucus
U - Use aminosalicylates 
P - Primary sclerosing cholangitis
193
Q

Name 4 common presenting features of IBD ?

A
  • Diarrhoea
  • Abdominal pain
  • Passing blood
  • Weight loss
194
Q

Investigations for IBD (include diagnostic test)?

A
  • Routine bloods for anaemia, infection, thyroid, kidney and liver function
  • CRP indicates inflammation and active disease
  • Faecal calprotectin is released by the intestines when inflamed. It is a useful screening test and is more than 90% sensitive and specific to IBD in adults
  • Endoscopy (OGD and colonoscopy) with biopsy is diagnostic
  • Imaging with US, CT and MRI can be used to look for complications such as fistulas, abscesses and strictures
195
Q

Management of Crohn’s disease ?

A

INDUCING REMISSION:
-First line: Steroids (e.g. oral prednisolone or IV hydrocortisone)

If steroids don’t work, consider adding immunosuppressant medication under specialist guidance:

  • Azathioprine
  • Mercaptopurine
  • Methotrexate
  • Infliximab
  • Adalimumab

MAINTAINING REMISSION:
Treatment is tailored to individual pts based on risks, side effects, nature of the disease and pt wishes. It is reasonable not to take any medications whilst well.

First line:

  • Azathioprine
  • Mercaptopurine

Alternatives:

  • Methotrexate
  • Infliximab
  • Adalimumab

SURGERY:
-When the disease only affects the distal ileum it is possible to surgically resect this area and prevent further flares. Crohn’s typically involves the entire GI tract. Surgery can also be used to treat strictures and fistulas secondary to Crohn’s.

Note: This section is based on NICE guidelines last update My 2016. Please see full guidelines and talk to seniors before treating pts.

196
Q

Management of UC ?

A

INDUCDING REMISSION
Mild to moderate disease
-First line: aminosalicylates (e.g. mesalazine oral or rectal)
-Second line: corticosteroids (e.g. prednisolone)

Severe disease

  • First line: IV corticosteroids (e.g. hydrocortisone)
  • Second line: IV ciclosporin

MAINTAINING REMISSION

  • Aminosalicylate (e.g. mesalazine oral or rectal)
  • Azathioprine
  • Mercaptopurine

SURGERY
UC typically only affects the colon and rectum. Therefore ,removing the colon and rectum (panproctocolectomy) will remove the disease. The pt is then left with either a permanent ileostomy or something called an ileo-anal anastomosis (J-pouch). This is where the ileum is folded back on itself and fashioned into a larger pouch that function a bit like a rectum. This “J-pouch” is then attached to the anus and collects stools prior to the person passing the motion.

197
Q

What is irritable bowel syndrome ?

A

A functional bowel disorder. This means there is no identifiable organic disease underlying the symptoms. The symptoms are a result of the abnormal functioning of an otherwise normal bowel.

Note:

  • It is often described as a diagnosis of exclusion.
  • It is very common and occurs in up to 20% of the population. It affects women more than men and is more common in younger adults.
198
Q

Name 7 symptoms of IBS ?

A
  • Diarrhoea
  • Constipation
  • Fluctuating bowel habit
  • Abdominal pain
  • Bloating
  • Worse after eating
  • Symptoms improved by opening bowels.
199
Q

Diagnosis of IBS ?

A

NICE GUIDELINES

Other pathology should be excluded:

  • Normal FBC, ESR and CRP blood tests
  • Faecal calprotectin negative to exclude IBD
  • Negative coeliac disease serology (anti-TTG antibodies)
  • Cancer is not suspected or excluded if suspected

SYMPTOMS SHOULD SUGGEST IBS:
Abdominal pain and/or discomfort:
-Relieved on opening bowels, or
-Associated with a change in bowel habit

AND 2 OF:

  • Abnormal stool passage
  • Bloating
  • Worse symptoms after eating
  • Mucus with stools
200
Q

Management of IBS ?

A

Making a positive diagnosis and providing reassurance that there is no serious pathology present is important.

General healthy diet and exercise advice:

  • Adequate fluid intake
  • Regular small meals
  • Reduced processed foods
  • Limit caffeine and alcohol
  • Low “FODMAP” diet guided by a dietician
  • Trial of probiotic supplements for 4 weeks.

First line medication:

  • Loperamide for diarrhoea
  • Laxatives for constipation. Avoid lactulose as it can cause bloating. Linaclotide is a specialist laxative for pts with IBS not responding to first line laxatives.
  • Antispasmodics for cramps e.g. hyoscine butylbromide (Buscopan)

Second line medication:
-Tricyclic antidepressants (i.e. amitriptyline 5-10mg at night)

Third line medication:
-SSRI antidepressants

CBT is also an option to help pts psychologically manage the condition and reduce distress associated with symptoms.

201
Q

What is coeliac disease ?

A

An autoimmune condition where exposure to gluten causes an autoimmune reaction that causes inflammation in the small intestine

202
Q

Pathophysiology of coeliac disease ?

A

Autoantibodies are created in response to exposure to gluten that target the epithelial cells of the intestine and lead to inflammation.

Inflammation affects the small bowel, particularly the jejunum. It causes atrophy of the intestinal villi meaning there is a lower SA for absorption of nutrients. Thus inflammation causes malabsorption of nutrients and the symptoms of the disease.

203
Q

Presentation of coeliac disease ?

A

It is often asymptomatic, so have a low threshold for testing for coeliac disease in pts where it is suspected.

Symptoms can include:

  • Failure to thrive in young children
  • Diarrhoea
  • Fatigue
  • Weight loss
  • Mouth ulcers
  • Anaemia secondary to iron, B12 or folate deficiency
  • Dermatitis herpetiformis

Rarely coeliac disease can present with neurological symptoms:

  • peripheral neuropathy
  • Cerebellar ataxia
  • Epilepsy
204
Q

TOM TIP:

A

Remember for your exams that we test all new cases of type 1 diabetes for coeliac disease even if they don’t have symptoms, as the conditions are often linked.

205
Q

Genetic associations of coeliac disease ?

A
  • HLA-DQ2 gene (90%)

- HLA-DQ8 gene

206
Q

3 main autoantibodies associated with coeliac disease ?

A
  • Anti-tissue transglutaminase antibodies (anti-TTG)
  • Anti-endomysial antibodies (anti-EMA)
  • Deaminated gliadin peptides antibodies (anti-DGPs)
207
Q

TOM TIP:

A

Anti-TTG and anti-EMA antibodies are IgA. Some patients have an IgA deficiency. When you test for these antibodies, it is important to test for total IgA levels because if total IgA is low the coeliac test will be negative even when they have coeliacs. In this circumstance, you can test for the IgG version of anti-TTG or anti-EMA antibodies or do an endoscopy with biopsies.

208
Q

Diagnosis of coeliac disease ?

A

Investigations must be carried out whilst the pt remains on a diet containing gluten otherwise it may not be possible to detect antibodies or inflammation in the bowel.

Check total IGA levels to exclude IgA deficiency before checking for coeliac disease specific antibodies:

  • Raised anti-TTG antibodies (first choice)
  • Raised anti-endomysial antibodies

Endoscopy and intestinal biopsy show:

  • Crypt hypertrophy
  • Villous atrophy
209
Q

Coeliac disease is associated with many other autoimmune conditions. Name 5 of these ?

A
  • Type 1 diabetes
  • Thyroid disease
  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis
210
Q

Complications of untreated coeliac disease ?

A
  • Vitamin deficiency
  • Anaemia
  • Osteoporosis
  • Ulcerative jejunitis
  • Enteropathy-associated T-cell lymphoma (EATL) of the intestine
  • Non-hodgkin lymphoma (NHL)
  • Small bowel carcinoma (rare)
211
Q

Treatment of coeliac disease ?

A

A lifelong gluten free diet.

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