GI Medicine 1

Question 1

Hepatocellular Carcinoma

1. What are the main risk factors?
2. What clinical features are seen?
3. When is screening considered and what would this be?
4. What should also be examined if the marker for this tumour is raised?

Answer 1

1. • cirrhosis (e.g. secondary to hep B or hep C)
   • alcohol
   • haemochromatosis
   • primary biliary cirrhosis
2. • features of liver cirrhosis or failure may be seen: jaundice, ascites, RUQ pain, hepatomegaly, pruritus, splenomegaly
   • possible presentation is decompensation in a patient with chronic liver disease
   • raised AFP

3.

• patients with liver cirrhosis secondary to hepatitis B & C or haemochromatosis
• men with liver cirrhosis secondary to alcohol

screening is US +/- AFP bloods

4. testes - as testicular tumour could also cause raised AFP in males

Question 2

Achalasia

1. What is it?
2. What clinical features are seen?
3. What can be seen n investigation?
4. How is it treated
   a) low surgical risk
   b) high surgical risk

Answer 2

1. disordered gastric motility I.e. lower oesophagus sphincter contracted and above oesophagus is dilated
2. • heartburn (body produces acid as it thinks food coming)
   • regurgitation (because food won’t go down)
   • dysphagia of solids and liquids (again because food won’t go down)
3. • oesophageal manometry
   • barium swallow - expanded oesophagus, fluid level, bird’s beak
   • CXR - widened mediastinum +/- fluid level
4. a) balloon dilatation
   if persistent symptoms consider hellers cardiomyotomy

b) botulin toxin injection

Question 3

Acute appendicitis

1. What clinical features are seen?
2. What investigations can be done?
3. How is it managed?

Answer 3

1.

• periumbilical pain radiating and then moving to RIF
• nausea
• appetite loss
• fever

2. FBC - neutrophil predominant leucocytosis
   urinalysis - can exclude renal cause and pregnancy
3. appendectomy
   +/- ABx to reduce chance of wound infection

Question 4

Acute liver failure

1. What can cause it?
2. What clinical features are seen?

Answer 4

1. • alcohol
   • paracetamol overdose
   • viral hepatitis
   • fatty liver in pregnancy
2. • jaundice
   • hypoalbuminaemia
   • coagulopathy - raised prothrombin time
   • hepatic encephalopathy
     +/- renal failure (hepatorenal syndrome)

Question 5

1. What can cause ketoacidosis other than diabetes?
2. What will differ on investigation?
3. How is it managed?

Answer 5

1. alcohol
2. normal / low glucose
3. • fluids
   • thiamine: to prevent wernicke’s + korsakoff

Question 6

Alcoholic Liver Disease

1. What conditions does this include?
2. What is seen on investigation?
3. How is it managed?

Answer 6

1.

• alcoholic liver disease
• alcoholic hepatitis
• cirrhosis

2. • raised Gamma GT
   • AST:ALT ratio >2, if >3 suggestive of acute alcoholic hepatitis
3. glucocorticoids (e.g. prednisolone) often used during acute episodes

NOTE: pentoxyphylline shown not to improve outcomes

Question 7

5-ASA drugs

e. g. mesalazine, sulphasalazine, olsalazine
1. What do they do?
2. What are their side effects?

3. a) What is sulphasalazine?
   b) What additional side effects are seen in this drug?

Answer 7

1. released into colon acting as anti-inflammatory and are not reabsorbed
2. • GI upset
   • pancreatitis (7x more common in mes over sulpha)
   • interstitial nephritis
   • agranulocytosis (therefore FBC key if patient unwell)
3. a) 5-ASA + sulphapyridine
   b)
   - rashes
   - Heinz body or megaloblastic anaemias
   - lung fibrosis
   - oligospermia

Question 8

Angiodysplasia

1. What is it?
2. How is it diagnosed?
3. How is it treated?

Answer 8

1. vascular deformity of GI tract causing bleeding and iron deficiency anaemia
   - generally seen in elderly patients

THINK: name tells you
angio = vessels
dysplasia = malformation

2. endoscopy
   (mesenteric angiography if bleeding)
3. • endoscopic cautery or argon plasma coagulation
   • antifibrinolytics e.g. tranexamic acid

Question 9

What are loperamide and diphenoxylate?

Answer 9

opioid agonists acting as anti-diarrhoeal agents

do not interact with CNS like other opioids

Question 10

Ascites

1. a) How is it grouped?
   b) What can cause each group type?
2. How is it managed?

Answer 10

1.
a) serum ascites albumin gradient
b)
>11 g/l - indicates portal hypertension

liver problems:

• mets
• acute liver failure
• cirrhosis / alcoholic liver disease

heart: HF or constrictive pericarditis
other: budd-chiari, portal vein thrombosis, vino-occlusive disease, myxoedema

<11g/l
hypoalbuminaemia
- nephrotic syndrome
- severe malnutrition

malignancy

other: pancreatitis, bowel obstruction

2. • limit dietary sodium
   • fluid restriction if Na <125
   • aldosterone antagonist +/- loop diuretic
   • if tense ascites: drainage
   • antibiotic prophylaxis to prevent bacterial peritonitis if cirrhosis + ascites

NOTE: drainage of >5L highly can cause circulatory dysfunction associated with recurrence, hepatorenal syndrome, dilution hyponatraemia

Question 11

Autoimmune Hepatitis

1. What clinical features are seen?
2. What antibodies are seen and age groups effected in
   a) type I
   b) type II
   c) type III
3. How is it managed?

Answer 11

1. • chronic liver disease
   • acute hepatitis (fever, jaundice etc)
   • amenorrhea

2.

a) ANA / ASMA antibodies
- adults and children

b) anti- liver/kidney microsomal type 1 antibodies
- children only

c) soluble liver/kidney antigen
- middle-aged adults

3. • steroids or other immunosuppressants e.g, azathioprine

liver transplant

Question 12

Barrett’s oesophagus

1. What happens histologically?
2. What are the RFs?
3. How is it managed if
   a) metaplasia
   b) dysplasia

Answer 12

1. squamous epithelium of oesophagus converts to columnar epithelium seen in cardiac region of stomach / small intestine
2. • GORD
   • male
   • central obesity
   • smoking
3. a) surveillance: endoscopy + biopsy every 3-5 years

b) intervention: mucosal removal / radio frequency ablation

Question 13

Bile-acid malabsorption

1. a) What is it?
   b) What clinical features will be seen?
   c) What can it lead to?
2. What can cause it?
3. What investigation is done?
4. How is it managed?

Answer 13

1. a) hyper secretion of bile acid

b) chronic diarrhoea +/- stearrhoea

c) malabsorption of vitamins A, D, E and K
(the fat solubles!)

2. • Crohn’s (ileal disease so therefore NOT UC)
   • cholecystectomy
   • coeliac
   • overgrowth of gut bacteria
3. SeHCAT
   (nuclear medicine test involving 2 scans 7 days apart)
4. cholestyramine

SEs:

• constipation
• decreases fat soluble vitamin absorption
• cholesterol stones / raises level of triglycerides

Question 14

Bilirubin

1. What is meant by conjugated bilirubin?
2. What bilirubin levels will be seen in
   a) pre-hepatic jaundice (e.g. excess haemolysis)
   b) hepatic jaundice
   c) post-hepatic jaundice

Answer 14

1. bilirubin which has been made water soluble by glucuronyl transferase to help its excretion

(osly this happens in liver cells)

2. a) raised unconjugated bilirubin
   (because too much bilirubin for liver to conjugate)

b) mix of raised unconjugated and conjugated bilirubin

c) raised conjugated bilirubin
(as liver can conjugate the bilirubin by not enough can be excreted)

Question 15

1. Why can hepatic jaundice cause a “mixed picture” of raised unconjugated and conjugated bilirubin?
2. a) When will pale stools and dark urine occur with jaundice?
   b) Why?

Answer 15

1. liver cells lose ability to conjugate bilirubin (raised unconjugated)
   AND
   unhealthy liver results in compressing of intra-hepatic portions of biliary tree causing obstruction to excretion (raised conjugated)
2. a) obstructive

b)
pale stools: as less stercobillin (product of bilirubin breakdown in gut) which gives poo its dark colour

dark urine: conjugated bilirubin (as its water soluble) can be excreted via urine and this is only way of excretion meaning much more bilirubin in urine giving it ‘coco-cola’ appearance