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General gastro Flashcards

1
Q

How long must antibiotics and PPIs be withheld before testing for H. pylori?

A

4 weeks Abx, 1-2 weeks PPI

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2
Q

What test is used to diagnose H. pylori?

A

C13 or C14 urea breath tests - better than faecal or serum tests

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3
Q

What is the biggest risk factor for cholangiocarcinoma?

A

Primary sclerosing cholangitis

Also: smoking, HBV, EtOH, fatty liver disease, DM, obesity, IBD

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4
Q

Risk of which cancers is increased with primary sclerosing cholangitis?

A

Colon, bile duct, gall bladder

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5
Q

What % of those with PSC also have IBD?

A

70-80%

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6
Q

What are the most common signs at PSC diagnosis?

A

Hepatomegaly and splenomegaly

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7
Q

What % of those with PSC have overlap with autoimmune hepatitis?

A

35% of children and 5% of adults

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8
Q

How does serum IgG4 level correspond with outcomes in PSC?

A

Elevated IgG4 levels => worse prognosis
Not to be confused with IgG4 disease, which can cause secondary sclerosing cholangitis, demonstrates IgG4-positive lymphoplasmacytic infiltration of organs, and is steroid-responsive.

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9
Q

Which IBD is more associated with PSC?

A

UC>CD

All new Dx PSC should have a colonoscopy

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10
Q

How is colon cancer risk affected by PSC?

A

Those with PSC + IBD are more likely to develop CRC compared with IBD alone

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11
Q

What deficiency causes porphyia cutanea tarda?

A

Uroporphyinogen decarboxylase

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12
Q

What factors contribute to porphyria cutanea tarda?

A

EtOH, HCV, haemochromatosis, oestrogen

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13
Q

Name 3 drugs associated with jejunal villous atrophy

A

Olmesartan, MMF and AZA

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14
Q

Why is ammonia elevated in liver failure?

A

It is usually produced in the colon, enters the portal system and is broken down via the urea cycle in the liver

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15
Q

How does hyperammoniaemia cause cerebral oedema?

A

Ammonia is converted to glutamine by astrocytic glutamine synthatase - this acts as an osmolyte.

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16
Q

What are the first line treatments for hepatic encephalopathy?

A

Lactulose 25mL BD - titrate to achieve 3 stools daily
IV L-ornithine-L-aspartate - provides alternative urea cycle substrate
Rifaximin 550mg BD
Probiotics

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17
Q

Which HLA genes are most strongly associated with coeliac disease?

A

DQ2 (95%) and DQ8 (80%)

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18
Q

What are the diagnostic tests in HCV?

A

HCV Ab

  • Screening test
  • Low false positive rate if risk factor/raised ALT
  • False negs if immunosuppressed or window period (6 weeks)
  • Does not distinguish between active and resolved disease

HCV RNA

  • Uses PCR
  • Most specific for active infection
  • Usually positive at 1-2 weeks
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19
Q

How are qualitative and quantitative HCV RNA tests used?

A

Qualitative
- Used to diagnose infection or test for cure

Quantitative

  • Reflective of viral burden
  • Predictor of response to IFN
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20
Q

What % of the world’s population has had HBV infection?

A

30%

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21
Q

What % of neonates, children and adults infected with acute HBV develop chronic infection?

A

95%, 20-30% and <5% respectively

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22
Q

What % of those infected with HBV seroconvert within a year?

A

10-20%

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23
Q

Which HBV genotype is most associated with HCC?

A

Genotype C

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24
Q

What is a precore mutant form of HBV?

A

HBeAg negative, increased risk of cirrhosis and HCC

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25
Q

What % of HBV-associated HCC develop without cirrhosis?

A

20%

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26
Q

Which HCV genotype is associated with steatosis and increased progression to cirrhosis and HCC?

A

Genotype 3

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27
Q

Which 2 extrahepatic manifestations are most associated with HCV?

A

Cryoglobulinaemia

Porphyria cutanea tarda

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28
Q

Name 3 non-invasive tests used to rule out cirrhosis

A

Fibroscan
APRI (AST:platelet ratio index)
Hepascore

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29
Q

Which direct acting antivirals cannot be used in severe liver failure?

A

Protease inhibitors

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30
Q

Which SE are reduced in tenofovir alafenamide (TAF) vs tenofovir disoproxil fumarate (TDF)?

A

Renal impairment and osteoporosis

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31
Q

When should treatment be stopped in HBV treatment?

A

In HBeAg negative – when HBsAg is cleared

In HBeAg positive – HBeAg seroconversion and 12 months consolidation

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32
Q

How should babies of HBsAg pos mothers be treated?

A

HBIG and 3 x vaccinations

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33
Q

What is the most common cause of acute hepatitis globally?

A

HEV

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34
Q

What are the criteria for radiographic diagnosis of HCC?

A

> 1cm AND MDCT/Gad-enhanced MRI with arterial hyperintensity AND washout on delayed or venous phase.

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35
Q

What are the therapeutic options in HCC?

A
  • 1 nodule < 2cm => Transplant if portal HTN / high bili. Resect if not. Ablate if resection contraindicated.
  • 1 nodule < 3cm => Transplant if portal HTN / high bili. Resect if not.
  • Up to 3 nodules < 3cm => Transplant if possible. Otherwise ablate.
  • Multinodular => TACE
  • Portal invasion, extrahepatic spread => sorafenib
  • Child-Pugh C => supportive care
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36
Q

What is the most common cause of acute liver failure?

What are other common differentials?

A

HBV
DDx:
- HAV, HEV, HSV, EBV, Parvovirus B19
- Paracetamol, antiepileptics, anti-TB drugs
- Amanita phalloides (death cap mushroom)

Uncommon DDx:
- AIH, malignancy, ischaemic hepatitis, Wilson’s disease, acute fatty liver of pregnancy, Reye syndrome, Budd-Chiari syndrome

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37
Q

What are the King’s College criteria for liver transplant in paracetamol overdose?

A
  1. pH < 7.25 after fluids + NAC + 24hrs
    OR
  2. INR > 6.5 AND Cr > 300/anuric AND grade 3/4 encephalopathy
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38
Q

What are the King’s College criters for liver transplant in non-paracetamol overdose?

A 
INR > 6.5
OR
3 out of 5:
- INR > 3.5
- Bili > 300
- Jaundice to encephalopathy > 7 days
- Age < 10 or > 40
- Unfavourable aetiology (seronegative, drugs)
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39
Q

What is the most significant variable predictive of death in acute liver failure?

A

Encephalopathy

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40
Q

What is the most common cause for liver transplantation in Australia?

A

Hepatitis C

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41
Q

What are the 4 most common causes of cirrhosis?

A

EtOH > Hep C > Hep B > NAFLD

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42
Q

What are the components of the Child-Pugh-Turcotte score?

A 
A BEAP:
Albumin
Bili
Encephalopathy
Ascites
PT (INR)

Predictive of 2yr survival

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43
Q

What are the cut-off scores for Child A, B and C?

A 
5 = A
7 = B
10 = C
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44
Q

What are the components of the MELD score?

What is it used for?

A

Cr, bili and INR

MELD 20 or more = transplant candidate

45
Q

What portal pressure is necessary for ascites to develop?

A

12mmHg

46
Q

What should be used to treat spontaneous bacterial peritonitis?

A

Ceftriaxone or cefotaxime

47
Q

What is the difference between Type 1 and Type 2 hepatorenal syndromes? Which has a poorer prognosis?

A

Type 1 = acute
Type 2 = chronic (eGFR<60 for >3months)

Type 1 is worse

48
Q

What hepatic-venous-portal gradient and what variceal pressure is predictive of variceal bleeding?

A

HVPG > 12mmHg (normal 1 - 5mmHg)

Variceal pressure > 15mmHg

49
Q

At what hepatic-venous-portal gradient (HVPG) do varices form?

A

10mmHg

50
Q

Who should receive primary prophylaxis against variceal haemorrhage?

A

Cirrhotics
- Child B or C
Large varices
- Red wale sign

51
Q

What is first choice for primary prophylaxis against variceal haemorrhage?

A

Propranolol > endoscopy band ligation > carvedilol

52
Q

What is the pathological hallmark of NASH?

A

Hapatocyte ballooning

- Also Mallory body formation (damaged intracellular intermediate filaments)

53
Q

What is used in secondary prophylaxis of spontaneous bacterial peritonitis?

A
  1. Bactrim

2. Norfloxacin

54
Q

What is the most important determinant of survival in NAFLD?

A

Fibrosis

55
Q

What are the 2 most common causes of death in NAFLD?

A

Malignancy and IHD

56
Q

What genetic variant is most associated with NAFLD?

A

PNPLA3

57
Q

What is the mechanism of action of acamprosate in alcoholism?

A

It stimulates GABA receptors, thereby inhibiting glutaminergic activity. This minimises withdrawal symptoms.

58
Q

How does baclofen work in alcohol dependence?

A

Stimulates GABA (B) receptors, reducing cravings for EtOH.

59
Q

Which 2 HLA alleles are associated with Type 1 Autoimmune Hepatitis? How do the 2 groups differ?

A 
HLA-DR3: 
- Early-onset, severe form, seen in girls and young women.
HLA-DR4: 
- Older patients
- More extrahepatic manifestations
- Better response to steroids
60
Q

What is required for diagnosis of primary biliary cholangitis (PBC)?

A

ALP > 1.67xULN for 6 months
AMA positive
Typical liver biopsy

61
Q

Which autoimmune condition is most associated with autoimmune hepatitis?

A

Thyroid disease

62
Q

What is the first line treatment for autoimmune hepatitis?

A

Prednisone + Azathioprine

63
Q

Who should have a liver biopsy in PSC?

A
  1. To exclude other causes of liver disease if diagnosis uncertain
  2. To determine the stage of PSC for therapeutic purposes
  3. To diagnose small duct PSC:
    - IBD + cholestatic LFTs + normal imaging => biopsy
64
Q

How does smoking affect risk of development of PSC, and risk of cholangiocarcinoma in those with PSC?

A
  • Smoking reduces risk of PSC developing

- Smoking increases risk of cholangioacarcinoma in those with PSC

65
Q

What is the sensitivity of bloody stools in ulcerative colitis?

A

95%

66
Q

What is the distribution of disease in Crohn’s Disease in different parts of the GIT?

A

Terminal ileum only > ileocolic > colonic only > small bowel

67
Q

Which patients with ulcerative colitis would benefit from appendicectomy?

A

Age < 20 years old with Hx of appendicitis or mesenteric adenitis

68
Q

Where is calprotectin produced?

A

Neutrophils and monocytes

69
Q

How are anti-Saccharomyces cerevesiae antibodies (ASCA) and pANCA used in the diagnosis of IBD?

A

CD: ASCA + / pANCA -
UC: ASCA - / pANCA +

70
Q

In which form of IBD are aminosalicylates (5-ASA) more effective?
What are the available options?

A

UC

  • Sulfasalazine
  • Mesalamine
  • Olsalazine
  • Balsalazide

Give topical (suppositories/foams/enemas) in left sided disease.

Mnemonic: UCASA (UC = 5-ASA treatment)

71
Q

When should budesonide be used in IBD?

A

UC to control disease flare, while awaiting immunomodulators to kick in.
CD as initial therapy

72
Q

Which IBD patients benefit from thiopurines (AZA and 6-MP)?

A 
CD
- At diagnosis
- With first course of steroids
UC
- In severe UC requiring hospitalisation
- Steroid-refractory UC despite optimal dose ASA`
73
Q

What are the side effects of thiopurines?

A 
Nausea
Leucopenia
Fever, rash, arthritis
Infections
Hepatitis (hepAZAtitis)
Pancreatitis (pancreAZAtitis)
74
Q

Which IBD patients benefit from methotrexate?

A
  • CD unresponsive to or intolerant of optimised thiopurine.

- Young males: increased risk of hepatosplenic T cell lymphoma with long term anti-TNF agents and thiopurines.

75
Q

Which IBD patients benefit from cyclosporin?

A

Acute UC requiring hospitalisation

- Use in thiopurine naive patients until maintained on thiopurine.

76
Q

What is the treatment algorithm for Crohn’s Disease?

A

Induction Rx:

  • Budesonide first line
  • Prednisone or 5-ASA second line

Maintenance Rx:

  • Induction with steroids => taper off
  • Induction with 5-ASA => continue 5-ASA
  • AZA, 6-MP, MTX, Anti-TNFα, or Vedolizumab in moderate to severe CD
  • Anti-TNFα: infliximab, adalimumab or certolizumab
  • Vedolizumab (as alternative to TNF blockers)
  • Ustekinumab - IL-12 and IL-23 receptor blocker
77
Q

What is the treatment algorithm for Ulcerative Colitis?

A

Induction Rx:

  • 5-ASA (topical>oral)
  • Resistant to above => topical 5-ASA + topical steroid foam
  • Resistant to above => oral and topical 5-ASA + topical steroid
  • Resistant to above => oral steroids
  • Steroid-resistant => cyclosporin, Anti-TNFα, or Vedolizumab

Maintenance Rx:

  • No Rx if first episode proctitis
  • Topical 5-ASA
  • If resistant to above => topical + oral 5-ASA
  • If resistant to above => AZA, 6-MP, Anti-TNFα, or Vedolizumab
78
Q

What is the mechanism of action of vedolizumab?

A
  • Selective blockage of α4β7 integrin, which binds to MADCAM1 in the gut wall.
  • Largely used in UC.
79
Q

What is the treatment of IgG4 disease?

A

Steroids +/- AZA

80
Q

High serum level of what are predictors of severe disease in Crohn’s Disease?

A

ASCA, OmpC, Cbir-1

81
Q

What do 6-MMP and 6-TG levels correspond with in Azathioprine use?

A 
6-MMP = hepatotoxicity
6-TG = therapeutic / myelosuppression
82
Q

When should allopurinol be used with thiopurines?

A
  • Use in shunters, where 6-MMP/6-TG>11.

- Allopurinol increases 6-TG and reduces 6-MMP

83
Q

Name 4 adverse effects of PPIs

A

Hypomagnesaemia
Hypocalcaemia
Interstitial nephritis
Accelerated development of gastric atrophy and gastric cancer

84
Q

What is first line Rx for Barrett’s oesophagus with high grade dysplasia?

A

Radiofrequency ablation

85
Q

What does the oesophagus look like on endoscopy in eosinophilic oesophagitis?

A

White specks (eosinophilic exudates), “Corrugated iron”, longitudinal furrows, mucosal oedema and strictures

86
Q

What is 1st, 2nd and 3rd line Rx for eosinophilic oesophagitis?

A
  1. Elimination diet avoiding: wheat, milk, soy, nuts, eggs, and seafood
    PPI => PPI + topical steroids => oral steroids if losing weight
87
Q

Which intervention has the greatest effect on reducing mortality in variceal haemorrhage?

A 
Antibiotics for 2 days
- norfloxacin (PO) 
OR 
- ceftriaxone (IV) 
OR
- ciprofloxacin (IV)
88
Q

How much bleeding is required to produce melaena?

A

150mL

89
Q

In coeliac disease with rapid weight loss, what is the necessary next test?

A

Abdo/pelvis CT scan – to investigate for small bowel lymphoma

90
Q

How is IgG4 disease diagnosed?

A
  • Lymphoplasmacytic infiltrate on histopath

- Positive staining for IgG4

91
Q

What can be given to reduce risk of pancreatitis associated with ERCP?

A

PR indomethacin

92
Q

What are the main characteristics of eosinophilic oesophagitis clinically and on biopsy?

A
  • Dysphagia and food impaction

- Eosophageal mucosal eosinophils > 15 per high power field

93
Q

Which cytokines are predominantly involved in eosinophilic oesophagitis?

A

IL-5 and IL-13

94
Q

What % of patients having endoscopy following food bolus have eosinophilic oesophagitis?

A

54%

95
Q

What HPVG defines portal hypternsion?

A

HPVG > 5 mmHg

96
Q

What should be used as secondary prophylaxis for spontaneous bacterial peritonitis?

A

Bactrim or norfloxacin

97
Q

Granulomas are found in which type of IBD?

A

Crohn’s Disease

98
Q

What do NOD2 / CARD 15 confer in Crohn’s Disease?

A

Worse survival, earlier onset, more small bowel involvement

99
Q

What are the criteria for acute severe colitis in UC?

A

Bloody stool frequency > 6/day PLUS at least one of:

  • Pulse > 90
  • Temp > 37.8
  • Hb < 105
  • ESR > 30
100
Q

Where is B12 absorbed?

A

Distal ileum

101
Q

Which levels of Transferrin Sats and ferritin should prompt investigation for hereditary haemochormatosis?

A

TSAT > 45%

Ferritin > 150 for females, > 200 for males

102
Q

What findings on small bowel biopsy are supportive of a diagnosis of Whipple’s Disease?

A

PAS-positive macrophages

103
Q

What changes in B12 and folate levels are associated with small intestinal bacterial overgrowth?

A

Low B12, high folate

Luminal bacteria tend to consume cobalamin but produce folate

104
Q

Which patients should receive pharmacological treatment in alcoholic hepatitis?

A

Maddrey score ≥ 32

Treat with prednisolone 40mg daily for 28 days

105
Q

What is the mechanism of action of pentoxifylline?

A

Inhibition of TNF synthesis

106
Q

What SAAG is highly specific for portal hypertension?

A

≥ 1.1 g/dL

107
Q

In those with a low ascitic WCC and SAAG ≥ 1.1 g/dL, how can cirrhosis and CCF be differentiated?

A

Total protein ≥ 2.5g/L = cardiac ascites

Total protein < 2.5g/L = cirrhotic ascites

108
Q

What is TMPRSS6, where is it secreted from, and what is its function?

A

Protein secreted by hepatocytes, in response to iron.

Suppresses hepcidin.

Gastro (3 decks)

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