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Gastroenterology for Finals Flashcards

1
Q

What is the criteria for 2WW referral in suspected upper GI malignancy?

A
  • Dysphagia
    OR
  • Age over 55 with weight loss and: Reflux symptoms, dyspepsia or epigastric pain
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2
Q

What is the eradication therapy for H. pylori in patients who are not allergic to penicillin?

A

Omeprazole 20mg BD
Amoxicillin 1g BD
Clarithromycin 500mg BD
All for 7 days

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3
Q

What is the eradication therapy for H. pylori in patients who are allergic to penicillin?

A

Omeprazole 20mg BD
Metronidazole 400mg BD
Clarithromycin 500mg BD
All for 7 days

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4
Q

What is the inheritance pattern of Wilson’s disease?

A

Autosomal recessive

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5
Q

What is the pathophysiology of Wilson’s disease?

A

Normally, the small amount of copper that is ingested is absorbed in the small intestine and incorporated into a carrier protein ‘caeruloplasmin’ in the liver. In Wilson’s disease, the absorption process is normal but there is a problem when incorporating the copper into the carrier protein and subsequently it’s excretion. Copper therefore accumulates.

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6
Q

What is a Kayser-Fleischer ring?

A

Copper deposition in the iris seen in Wilson’s disease

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7
Q

What are the stages of hepatic encephalopathy?

A 
I = Lethargy, insomnia
II = Confusion
III = Drowsiness
IV = Coma
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8
Q

Which part of the GI tract does ulcerative colitis affect?

A

Colon and rectum - rectum is ALWAYS affected

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9
Q

True / False: Smoking has a protective effect in ulcerative colitis

A

True

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10
Q

Which tool is used to assess the severity of ulcerative colitis?

A

Truelove - Witts criteria

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11
Q

What is measured in the Truelove-Witts criteria?

A 
Number of bowel motions per day
Rectal bleeding
Temperature
Haemoglobin
Resting pulse
ESR (and/or CRP)
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12
Q

What is the management of acute severe colitis?

A
  • Blood cultures to rule out infective cause
  • Monitor observations and stool habit
  • Daily bloods (especially FBC, U+E, CRP)
  • Flexible sigmoidoscopy
  • Steroids 100mg hydrocortisone QDS IV then switch to oral
  • VTE prophylaxis
  • AXR to rule out toxic megacolon
  • Good response to steroids: Switch to oral steroids and add 5-ASA
  • No response to steroids: Consider surgery e.g. subtotal colectomy, consider rescue therapy i.e. cyclosporin and infliximab
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13
Q

Which drugs are used in the medical ‘rescue’ therapy of acute severe colitis?

A

Infliximab

Cyclosporin

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14
Q

True / False: Colonoscopy is a useful investigation in acute severe colitis?

A

False - There is a high risk of perforation so not performed in acute severe colitis…do a flexible sigmoidoscopy instead

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15
Q

Which part of the GI tract is affected in Crohn’s?

A

The entire GI tract can be affected, but particularly affects terminal ileum

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16
Q

Do ‘Skip lesions’ occur in Crohn’s or ulcerative colitis?

A

Crohn’s

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17
Q

What antibodies are important in Coeliac disease?

A

Anti-TTG (tissue transglutaminase) antibodies

Anti-endomysial antibodies

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18
Q

What is the ‘gold standard’ test for Coeliac disease?

A

Biopsy of the D2 section of duodenum

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19
Q

Which antibodies are important in primary biliary cirrhosis?

A

Anti-mitochondrial antibodies

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20
Q

Which LFTs are usually raised in a ‘cholestatic’ picture?

A

ALP and GGT

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21
Q

What is jaundice?

A

Visble hyperbilirubinaemia

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22
Q

Does jaundice of a pre-hepatic cause give a conjugated or unconjugated hyperbilirubinaemia?

A

Pre-hepatic jaundice = Unconjugated

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23
Q

The presence of bilirubin in the urine excludes WHAT as a cause of jaundice?

A

Presence of bilirubin in urine excludes pre-hepatic causes of jaundice, as unconjugated bilirubin (as seen in pre-hepatic causes) is too large to be excreted via kidneys

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24
Q

What are the causes of unconjugated hyperbilirubinaemia?

A

Pre-hepatic causes…

  • Haemolysis
  • Impaired conjugation e.g. Gilbert’s syndrome, Crigler-Najjar syndrome
  • Drugs e.g. gentamicin, contrast agents, rifampicin, chloramphenicol
  • Physiological neonatal jaundice
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25
Q

Are the levels of urobilinogen high or low in post-hepatic (conjugated) hyperbilirubinaemia?

A

Low

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26
Q

What are the causes of post-hepatic jaundice?

A
  • Gallstones
  • Tumour
  • Biliary atresia
  • Cholecystitis and cholangitis
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27
Q

Does jaundice of a post-hepatic cause give a conjugated or unconjugated hyperbilirubinaemia?

A

Post hepatic jaundice = Conjugated

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28
Q

Does jaundice of an intra-hepatic cause give a conjugated or unconjugated hyperbilirubinaemia?

A

Intra-hepatic jaundice = Conjugated

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29
Q

Give 3 causes of a massive transaminitis

A

Acute viral hepatitis
Drug induced liver failure
Ischaemic hepatitis

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30
Q

What are the different types of gallstones?

A

Pigment stones
Cholesterol stones
Mixed

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31
Q

True / False: Most gallstones appear on x-ray

A

False - Most gallstones are radiolucent so do not appear on x-ray

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32
Q

What is Charcot’s triad?

A

Sign of cholangitis - RUQ pain, fevers jaundice

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33
Q

Which blood marker(s) is classically raised in acute pancreatitis?

A

Amylase

Serum lipase - more specific for pancreatitis

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34
Q

Give some drug causes of acute pancreatitis

A 
Steroids
5-ASAs e.g. sulphasalazine, mesalazine
Azathioprine
Sodium valproate
Furosemide
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35
Q

What are the causes of acute pancreatitis?

A 
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Mumps
Autoimmune e.g. SLE
Scorpion bites
Hyperlipidamia, hyperparathyroidism
ERCP, emboli
Drugs e.g 5-ASAs (sulphasalazine, mesalazine), azathioprine
Neoplasm
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36
Q

Which tool can be used to assess severity of pancreatitis?

A

Glasgow Score

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37
Q

What parameters are measured in the Glasgow score for acute pancreatitis?

A 
PaO2 less than 8kPa (respiratory failure)
Age over 55
Neutrophilia
Calcium low (less than 2mmol/L)
Renal function (urea more than 16)
Enzymes (AST or LDH raised)
Albumin less than 32
Sugar (glucose!) more than 10mmol/L
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38
Q

Give 3 investigations which might be done in the assessment of a patient with dysphagia

A

Endoscopy
Barium swallow
Manometry

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39
Q

What are the features of Plummer-Vinson Syndrome?

A

Iron deficiency anaemia
Oesophageal webs
Dysphagia
Glossitis

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40
Q

What is the most common histology of oesophageal cancer?

A

65% are adenocarcinomas

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41
Q

What is the appearance of achalasia on barium swallow?

A

‘Bird beak’ or ‘rats tail’

42
Q

What is the mechanism by which achalasia occurs?

A

Failure of the lower oesophageal sphincter to relax due to abnormality of the nerve supply

43
Q

What is the treatment for achalasia?

A
  • Nitrates or calcium channel blockers relax the sphincter if not too severe
  • Botox lasts about 6/12
  • Endoscopic dilatation
  • Heller’s cardiomyotomy cuts the muscle at the lower oesophageal sphincter
44
Q

Which is more common, duodenal or gastric ulcers?

A

Duodenal ulcers are more common

45
Q

What is haemochromatosis?

A

Autosomal recessive disorder of iron metabolism, causing increased iron deposition in tissues

46
Q

Which tissues might be particularly affected in haemochromatosis?

A 
Liver
Joints
Heart
Pituitary
Pancreas
Adrenals
Skin
47
Q

Give some clinical features of haemochromatosis

A 
Slate-grey skin appearance
Arthralgia
Tiredness
Hypogonadism, erectile dysfunction, gynacomastia
Chronic liver disease - cirrhosis and hepatomegaly
Dilated cardiomyopathy
Arrhythmias
Diabetes
Low renin, low aldosterone
48
Q

What is the treatment for haemochromatosis?

A

Venesection
Monitor LFTs, glucose
Low iron diet
Screening for 1st degree relatives

49
Q

Which parameters are assessed in the Child-Pugh score?

A 
Remember ABCDE:
Albumin
Bilirubin
Clotting (Prothombin time)
Distension i.e. ascites
Encephalopathy
50
Q

What does the Child-Pugh score assess?

A

The severity of liver cirrhosis and the risk of variceal bleeding

51
Q

What is the Blatchford score?

A

Risk stratification tool for determining whether patients with upper GI bleed require urgent endoscopy or whether it can be outpatient

52
Q

What is the Rockall score?

A

Mortality predictor for patients with upper GI bleed

53
Q

What is used for secondary prevention of variceal bleeding?

A

Propranolol

54
Q

What is the treatment for active variceal bleeding?

A
  • DR ABCDE approach
  • Group and save, crossmatch 6 units
  • Resuscitation, including transfusion if necessary
  • IV antibiotics recommended for all patients with variceal bleeding
  • Terlipressin until 5/7 after bleed stops
  • Use Blatchford score to decide whether patient needs urgent or outpatient endoscopy
  • Endoscopy for banding, scleotherapy
    Stengstachen-Blackemore tube to tamponade bleeding
  • TIPS procedure
55
Q

What is the pathological process in liver cirrhosis?

A

Fibrosis of hepatocytes, formation of nodules due to direct insult to hepatocytes

56
Q

What is the King’s College Criteria for drug-induced liver failure?

A
  • Arterial pH less than 7.3 less than 24 hours after ingestion
    OR ALL of the following:
  • Prothrombin time more than 100s or INR more than 6.5
  • Creatinine more than 300
  • Grade III or IV encephalopathy
57
Q

What is the King’s College criteria for non-drug induced liver failure?

A
  • Prothrombin time more than 100s or INR more than 6.5
    OR 3 out of 5 of the following:
  • Drug-induced liver failure
  • Prothrombin time more than 50s or INR more than 3.5
  • Bilirubin more than 300
  • Age less than 10 or more than 40
  • More than 1 week from first jaundice to encephalopathy
58
Q

What drug might be useful in the treatment of ascites and why?

A

Spironolactone - Secondary hyperaldosteronism in liver failure due to low albumin states stimulating aldosterone production

59
Q

How might ascites be managed?

A

Spironolactone
Loop diuretics
Salt and fluid restriction
Ascitic drain

60
Q

What are the signs of decompensated liver disease?

A

Ascites
Jaundice
Hepatic encephalopathy

61
Q

What drug is useful in the treatment of hepatic encephalopathy?

A

Lactulose - Reduces ammonia production

62
Q

Why does hepatic encephalopathy occur in advanced liver disease?

A

Varices can open up in portal hypertension, and these varices can bypass the portal venous system and travel directly into the systemic circulation (a portal-systemic shunt). The liver normally filters out toxins e.g. ammonia, so blood from varices are unfiltered and so toxins can accumulate.

63
Q

What is rifaximin used for?

A

Secondary prevention of hepatic encephalopathy

64
Q

What are the causes of chronic liver disease?

A

Alcoholic liver disease
Metabolic liver disease: Wilson’s, haemochromoatosis, NASH, NAFLD
Drug-related liver disease

65
Q

What is erythema ab igne?

A

Mottled dusky greyness on the abdomen seen in chronic pancreatitis

66
Q

What are the causes of toxic megacolon?

A

Ulcerative colitis
Crohn’s disease
Pseudomembranous colitis

67
Q

What is the main cause of chronic pancreatitis?

A

Alcohol

68
Q

What does imaging show in chronic pancreatitis?

A

X-ray and CT show pancreatic calcification

69
Q

What is the difference between a Mallory-Weiss tear and Boerhaave’s syndrome?

A 
Mallory-Weiss = Linear lacerations at the gastro-oesophageal junction - not full thickness.
Boerhaave's = Full thickness perforation of oesophagus
70
Q

Compare the nature of the pain in a gastric ulcer to a duodenal ulcer

A

Gastric ulcer = Worsened by eating

Duodenal ulcer = Relieved by eating

71
Q

What is Zollinger-Ellison Syndrome?

A

High levels of gastrin, usually from gastrinoma (might be seen in MEN1) which cause multiple gastroduodenal ulcers, diarrhoea, malabsorption.

72
Q

What is Barrett’s oesophagus?

A

Metaplasia of oesophageal squamous epithelium into columnar cells due to chronic reflux and associated inflammation. Associated with increased risk of oesophageal malignancy so annual OGD required. High-dose PPI given.

73
Q

List some causes of dysphagia

A 
Neuromuscular e.g. myasthenia gravis
Motility problem e.g. achalasia, oesophageal spasm
Pharyngeal pouch
Stricture
- Benign: Oesophageal web
- Malignant: Oesophageal cancer
74
Q

What is Coeliac disease?

A

An autoimmune condition affecting the small bowel where an intolerance to gluten causes villous atrophy and malabsorption.

75
Q

Which condition of the skin has an associated with coeliac disease?

A

Dermatitis herpetiformis

76
Q

List some complications of coeliac disease

A 
Anaemia
Hyposplenism
Dermatitis herpetiformis
Osteoporosis
Intestinal T cell lymphoma
77
Q

What are the pathological features of Crohn’s disease?

A

Transmural inflammation, granulomas, increased goblet cells

78
Q

What are the endoscopic findings in Crohn’s disease?

A

‘Cobblestone appearance’
Deep ‘rose thorn’ ulcers
Skip lesions

79
Q

What are the main complications of Crohn’s disease?

A 
Perforation
Small bowel obstruction
Abscess formation
Fistulae formation (due to full-thickness involvement)
Toxic megacolon
Colon cancer
80
Q

What are the pathological findings in ulcerative colitis?

A
  • Continuous disease
  • Does not extend proximal to ileocaecal valve
  • Inflammation is NOT transmural
  • Inflammatory infiltrates
  • Reduced goblet cells
  • Crypt abscesses
  • Glandular distortion
  • Mucosal ulcers
81
Q

Are pseudopolyps typical of ulcerative colitis or Crohn’s?

A

Ulcerative colitis

82
Q

What is a useful investigation to distinguish inflammatory bowel disease from IBS?

A

Faecal calprotectin - raised in IBD but not IBS

83
Q

List some features which might be visible on abdominal x-ray of a patient with ulcerative colitis

A

Lead-pipe appearance of transverse colon
Loss of haustral markings
Thumb-printing
Toxic megacolon

84
Q

What are the features of toxic megacolon?

A

Toxic: Fever, neurophilia, tachycardia, anaemia, dehydration, U+E disturbance, hypotension
Dilatation of the colon more than 6cm on AXR

85
Q

What is the treatment for toxic megacolon?

A

Stool culture for ?infective cause
Fluid resuscitation
Drip and suck
Antibiotics

86
Q

List some complications of ulcerative colitis

A

Perforation
Toxic megacolon
VTE
Colon cancer

87
Q

What is the treatment for mild ulcerative colitis?

A

5-ASAs e.g. sulphasalazine, mesalazine

Short (2 week) course of steroids e.g. prednisolone

88
Q

What test is required before commencing azathioprine therapy? Why?

A

TPMT (Thiopurine methyltransferase) test required as some patients may be prone to toxicity from azathioprine

89
Q

Give some side effects of azathioprine

A

Bone marrow suppression
Pancreatitis
Hepatotoxicity
Nausea, vomiting

90
Q

Primary sclerosing cholangitis is associated with ulcerative colitis or Crohn’s?

A

Ulcerative colitis

91
Q

Which antibodies are associated with primary sclerosing cholangitis?

A

p-ANCA

92
Q

Which antibodies are associated with primary biliary cirrhosis?

A

Anti mitochondrial antibodies

93
Q

Give some features of primary sclerosing cholangitis

A

Fatigue
Itching
Cholestatic jaundice picture
Increased risk of colon cancer and cholangiocarcinoma

94
Q

What investigations might you perform in suspected primary sclerosing cholangitis, and what might they show?

A

Bloods: p-ANCA, hypergammaglobulinaemia, LFTs show post-hepatic picture
ERCP: Beaded appearance of ducts
Liver biopsy: ‘Onion skin’ appearance

95
Q

What is the treatment of primary sclerosing cholangitis?

A

Symptomatic e.g. cholestyramine for itching
Ursodeoxycholic acid
Liver transplantation

96
Q

Compare the pathological process in primary biliary sclerosis and primary sclerosing cholangitis

A

PBC: Autoimmune inflammatory disorder of intra-lobular ducts where there is granulomatous inflammation causing cholestatis
PSC: Inflammation of intra- and extra-hepatic bile ducts causing fibrosis and stricture formation causing cholestasis

97
Q

What is the treatment of primary biliary sclerosis?

A

Symptomatic:
- Itching = Cholestyramine, naltrexone, rifampicin
- Diarrhoea = Codeine phosphate
- Fat soluble vitamin prophylaxis = Vit A, D, K
Ursodeoxycholic acid may improve survival
Liver transplantation for end-stage disease

98
Q

What is the most common cause of liver disease in the developed world?

A

NAFLD i.e. Non-alcoholic fatty liver disease

99
Q

What might investigations show in Wilson’s disease?

A

Raised 24 hour urinary copper excretion
Low serum caeruloplasmin
Liver biopsy: High concentration of hepatic copper

100
Q

What is the treatment for Wilson’s disease?

A

Low copper diet
Lifelong penicillamine
Liver transplantation
Screening for siblings

101
Q

What are the causes of Duputren’s contracture?

A 
Liver disease
Alcohol excess
Familial
Manual labour
Phenytoin

Gastroenterology (3 decks)

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