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FRACP NOSH 2020 > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What does the term “extensive colitis” refer to in Ulcerative colitis?

A

Disease extending proximal to splenic flexure

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2
Q

What part of the GIT do Crohn’s Disease and UC affect respectively?

A

Crohn’s -> anywhere from mouth to anus. Transmural inflammation with skip lesions

UC -> involves colon, and rectum is almost always involved. Inflammation limited to mucosa

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3
Q

What biomarker is associated with UC?

A

pANCA

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4
Q

What biomarker is associated with Crohn’s Disease?

A

ASCA - anti Saccharomyces cerevisiae Ab

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5
Q

What is the peak age of onset of IBD?

A

20 - 30 years

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6
Q

What relationship does smoking have with Crohn’s and UC?

A

Crohn’s -> risk factor

UC -> decreases risk

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7
Q

What gene has been identified in ~40% of Crohn’s and is associated with more severe disease?

A

NOD2

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8
Q

What percentage of UC patients will end up proceeding to colectomy during the course of their disease?

A

20%

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9
Q

What percentage of Crohn’s patients end up requiring surgical resection?

A

50%

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10
Q

Which form of IBD is more associated with colorectal cancer?

A

UC

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11
Q

What is the colorectal cancer screening program for IBD patients?

A

Commence after 8 years of disease in UC or Crohn’s which involved >1/3 of colon

  • annually for active disease / FHx at age <50 / PSC / stricture / previous dysplasia
  • 3 yearly otherwise
  • 5 yearly if last two scopes normal
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12
Q

What is the main predictor at diagnosis of severe disease in Crohn’s ?

Name 3 other important predictors

A

Perianal disease

Requiring steroids at diagnosis
LOW >5kg
Fibro-stenosing disease

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13
Q

What are two laboratory markers used for monitoring disease activity in IBD?

A

CRP (aim <3)

Faecal calprotectin (aim <150)

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14
Q

What is the treatment goal for patients with IBD?

A

To achieve remission with complete mucosal healing

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15
Q

What is the first line treatment for mild-moderate UC left-sided/extensive colitis?

A

Oral + topical 5-ASA agent

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16
Q

What is the indication for immunomodulator therapy in UC?

A

Non-response to initial therapy with oral 5-ASA + steroid, or requiring more than one course of steroids in the year

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17
Q

What is the steroid regime typically used for induction in mild-moderate IBD?

A

Prednisolone 40mg for 1-2 weeks, slowly tapered over 6-8 weeks

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18
Q

What is the role of TPMT in thiopurine metabolism?

What happens in high TMPT activity?

What happens in low activity?

A

TMPT catalyses methylation of 6-MP to the inactive 6-MMP. Xanthine oxidase then catalyses 6-MP to the inactive 6-thiouracil

15% of all patients have high TPMT activity (shunters) → high 6-MMP → hepatotoxicity. Can use allopurinol in this setting.

Heterozygous mutation (11%) → low activity
Homozygous mutation (0.3%) → negligible activity → very high 6-TG → BM suppression
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19
Q

Which malignancies occur at increased rates with thiopurine use?

A

Lymphoma

Non-melanoma skin cancer

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20
Q

What is the first line treatment for rectal UC?

A

Topical + PO 5-ASA

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21
Q

What is the first line treatment for UC limited to proctitis?

A

Topical + PO 5-ASA (more effective than topical alone)

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22
Q

In Australia, what is the typical 1st line approach for induction in moderate to severe Crohn’s ?

A

Steroids + immunomodulator

Steroids - if severe then parenteral with hydrocort or methylpred

Immunomodulator - thiopurine or methotrexate

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23
Q

Which patient group in Crohn’s is budesonide preferred for, over prednisolone?

A

Mild ileocaecal disease

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24
Q

What is the route of escalation for a patient with Crohn’s who has failure of induction with first line therapy?

When is this change made?

A

Add on a biologic agent =

  • TNF inhibitor (infliximab IV / adalimumab SC
  • Alpha4beta7 integrin inhibitor (vedolizumab IV)

After 3 months of 1st line therapy

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25
Q

What is the treatment approach in perianal/fistulising Crohn’s disease?

A

Surgical consultation for possible drainage / Seton

Antibiotics (ciprofloxacin OR metronidazole)

Combination of anti-TNF (infliximab has strongest evidence) and Azathioprine

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26
Q

What is the medical management approach following surgical resection for Crohn’s?

What medication should all patients generally receive?

A

All patients should receive 3 months of metronidazole.

For patients with risk factors, add thiopurine and/or a TNF inhibitor (infliximab or adalimumab)

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27
Q

What are the options for 1st line management for stricturing Crohn’s that is uncomplicated and <5cm?

A

May trial IV steroids and bowel rest if appears to be inflammatory component (based on clinical features/bloods/MRI)

If not - trial endoscopic dilatation

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28
Q

What are the management options for strictures in Crohn’s that are long or complicated in nature?

A

Strictureplasty or small bowel resection

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29
Q

What is the next line treatment in UC after failure of induction with oral 5-ASA and steroid?

A

Add an immunomodulator = thiopurine.

Methotrexate if intolerant to thiopurines

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30
Q

How is acute severe UC defined?

A

Truelove + Witts criteria =

The presence of 6 or more bloody stools per day, plus at least one of the following:

  • temperature more than 37.8ºC
  • HR >90
  • Hb less than 105
  • ESR > 30
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31
Q

What is the initial therapy for acute severe UC?

A
  • IV hydrocort / methylpred
  • IVF
  • clexane
  • exclude CMV infection by sigmoidoscopy
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32
Q

When should salvage therapy be considered for acute severe UC?

What are the options?

A

After 3-5 days of steroid therapy

Medical options:

  • infliximab
  • cyclosporin

Surgery is alternative

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33
Q

When would a biologic agent be added in UC therapy?

What are the options?

A

If failed 3 months of 5-ASA + immunomodulator

Options =

  • Infliximab
  • Vedolizumab
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34
Q

What are the pacemaker cells of the GIT which control peristalsis?

A

Interstitial cells of Cajal

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35
Q

What is the main acid-producing cell in the stomach?

A

Parietal cells

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36
Q

What are the main SEs of PPIs? (5)

A 
Enteric infections (C.diff)
Pneumonia
Hypomagnesaemia
Osteoporosis
Interstitial nephritis
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37
Q

What is the most common cause of hypergastrinaemia?

A

Prolonged acid suppression (PPI / H2RA)

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38
Q

How is Zollinger-Ellison Syndrome diagnosed?

A

Secretin Provocation Test -> measure gastrin levels following provocation

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39
Q

What genetic cancer syndrome is Zollinger-Ellison Syndrome associated with?

A

MEN1

  • Parathyroid
  • Pituitary
  • Pancreas
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40
Q

What is the gene involved in hereditary pancreatitis?

A

Trypsinogen gene PRSS1, on chromosome 7q35

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41
Q

What is the management of a symptomatic pancreatic pseudocyst?

A

Drainage (endoscopic or surgical)

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42
Q

What is ABCB4 disease associated with?

A

Biliary tract diseases

  • intrahepatic cholestasis of pregnancy
  • recurrent pancreatitis
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43
Q

What is the most common cause of Peptic ulcer disease in Australia?

A

H.Pylori (NSAIDs close 2nd)

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44
Q

What location of ulcers is H.Pylori more associated with?

A

Duodenal

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45
Q

What is the recommended 1st line therapy for H.pylori eradication?

A

esomeprazole 20 mg orally, twice daily for 7 days

PLUS

amoxicillin 1 g orally, twice daily for 7 days

PLUS

clarithromycin 500 mg orally, twice daily for 7 days

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46
Q

What is the gold standard for diagnosis of H.Pylori if not undertaking endoscopy?

A

C13- or C14-urea breath test.

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47
Q

What are most cases of Gastric mucosa–associated lymphoid tissue (MALT) lymphoma caused by?

A

Uncommon disease.

Most cases are caused by H. pylori infection.

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48
Q

What is the first-line treatment of choice for eosinophilic oesophagitis?

A

6-food elimination diet (wheat, egg, dairy, soy, nuts, seafood)

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49
Q

What are the most common triggers in eosinophilic oesophagitis?

A

Dairy and wheat are the most common triggers

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50
Q

What is first line medical therapy for eosinophilic oesophagitis (after diet)?

A

Standard dose PPI therapy

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51
Q

What element on dysphagia history indicates an oesophageal motility disorder rather than mechanical obstruction?

A

If there is dysphagia with both solids and liquids

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52
Q

Where does Zenker’s diverticulum arise from?

A

Sac-like outpouching of mucosa and submucosa through Killian’s triangle (area of muscular weakness in the hypopharynx b/w the transverse fibres of the cricopharyngeus and the oblique fibres of the lower inferior constrictor)

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53
Q

What is the classic presentation of Zenker’s diverticulum?

A

Foul breath, gurgling in the throat, regurgitation of food into the mouth

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54
Q

How is Zenker’s diverticulum diagnosed?

A

Barium swallow

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55
Q

What is the management of Zenker’s diverticulum?

A

Surgery (diverticulotomy or cricopharyngeal myotomy), with some endoscopic options available (but not performed everywhere)

56
Q

What are the hallmark manometry findings in achalasia?

What is the difference between Type 1 and Type 2?

A

No peristalsis
Incomplete or absent LOS relaxation

Type 2 is more painful, with pan-oesophageal pressurisation

57
Q

What are the management options for achalasia?

A

Medical = GTN, CCBs

Surgical = pneumatic dilatation, botox, POEM myotomy

Last line = PEG, oesophagectomy

58
Q

What is a Schatzki ring?

How does it present?

A

Lower oesophageal ring at squamocolumnar junction
Almost always associated with hiatus hernia

Presents with intermittent dysphagia for solids

59
Q

What HLA genotype is associated with Coeliac?

A

HLA DQ2, DQ8

60
Q

What is the prevalence of Coeliac?

A

1/200

61
Q

What are the characteristics small bowel biopsy findings in Coeliac?

A

Intra-epithelial lymphocytosis
Crypt hyperplasia
Villous atrophy

62
Q

What is the first line serology in suspected Coeliac?

A

Old -> IgA TTG + total IgA

New -> IgG TTG (and can correlate with IgG DGP)

63
Q

What test should be sent for in suspected Coeliac with IgA deficiency?

A

IgG Deamidated Gliadin Peptide (DGP)

64
Q

What is the likely culprit in non-Coeliac self-reported gluten sensitivity?

A

Fructans

65
Q

Which nutrient is most likely to be deficient in a Coeliac patient not compliant with gluten-free diet?

A

Iron - absorbed in proximal small bowel

66
Q

What phenomenon is usually responsible for mild reflux?

A

Transient lower oesophageal relaxations

67
Q

What is the metaplastic change that occurs in Barrett’s oesophagus?

A

Stratified squamous epithelium to columnar epithelium

68
Q

What is the management approach to Barrett’s oesophagus?

What is the treatment of choice for dysplasia?

A

Regular endoscopic surveillance (3-5 yearly if no dysplasia)
Lifelong PPI

Low or high grade dysplasia -> endoscopic eradication with radiofrequency ablation

69
Q

What is the most common risk factor present in oesophageal SCC?

A

Smoking

70
Q

What type of virus is Hep C?

A

RNA flavivirus

71
Q

What is the definition of sustained virological response in Hep C?

A

Undetectable HCV RNA on PCR, 12 weeks post completion of treatment

72
Q 
Which class of DAAs for Hep C can only be used for Child-Pugh A cirrhosis? 
Why?
A

Protease inhibitors

They can precipitate liver decompensation

73
Q

What are the pan-genotypic regimes of DAAs used for initial Hep C treatment?

A

Epclusa -> Sofosbuvir + Valpatasvir for 12 weeks

Mavyret -> Glecaprevir + pibrentasvir for 8 weeks (can be used in advanced CKD)

74
Q

What test indicates active Hep C infection, rather than past exposure?

A

HCV RNA PCR +ve

75
Q

Which drug interacts with essentially all HCV treatment options?

A

Carbamazepine

76
Q

Where are amino acids absorbed?

A

Duodenum, jejunum, colon

77
Q

Where are carbs absorbed?

A

Require salivary and pancreatic amylase

Small bowel

78
Q

Where is thiamine absorbed?

A

Proximal small bowel

79
Q

What are the signs of active inflammation in IBD? (4)

A

Large joint arthralgia
Episcleritis
Erythema nodosum
Sweets Syndrome

80
Q

Which class of DAAs can precipitate liver decompensation, and thus should only be used in Child Pugh A?

A

NS3/4A protease inhibitors

81
Q

What are the most common HCV genotypes in Australia?

A

1, 3

82
Q

Which drug interacts with essentially all DAAs for HCV, and thus makes treatment extremely difficult?

A

Carbamazepine

83
Q

How should virologic response to HCV treatment with DAAs be assessed?

A

By checking the viral load at 12 weeks following the cessation of therapy

84
Q

What form of Hep B transmission poses highest risk for chronic infection?

A

Vertical (HBeAg mother to baby)

85
Q

What are the 4 phases of Hep B infection?

What is the HBeAg status in each?

A

Immune tolerance

Immune clearance

Immune control

Immune escape

HBeAg is positive in first 2 phases, negative in 3-4.

86
Q

What are the 2 main antivirals used in Hep B treatment?

A

Entecavir

Tenofovir

87
Q

What is the clinical significant of pre-core mutant / basal core mutants?

A

Both of these confer risk of advanced cirrhosis and HCC

88
Q

Who is recommended to undergo treatment for HBV? (6)

A
  • cirrhosis
  • HCC
  • HBeAg positive -> HBV DNA >20,000 and ALT >2 x ULN (after having waited 6 months to ensure no spontaneous seroconversion
  • HBeAg negative -> HBV DNA >2,000 and ALT >2 x ULN
  • Immunosuppression
  • Pregnant women with high viral loads in 3rd trimester
89
Q

What is the definition of chronic Hep B?

A

The diagnosis of chronic HBV infection is based upon the persistence of hepatitis B surface antigen (HBsAg) for greater than six months

90
Q

What is the usual treatment endpoint for treatment in HBV HBeAg positive disease?

A

Seroconversion from HBeAg to anti-HBe

91
Q

What is the usual treatment endpoint for treatment in HBV HBeAg negative disease?

A

HBsAg loss

92
Q

What is the preferred Hep B treatment agent in pregnancy?

What is alternative?

A

Tenofovir disoproxil fumarate

Lamivudine

93
Q

Who needs HCC screening in HBV? (6)

A 
Cirrhosis 
FHx HCC
ATSI > 50 years
Asian men >40 years
Asian women >50 years
African patients >20 years
94
Q

How should infants born to HBV positive mothers be managed to reduce risk of infection?

A

Routine hepatitis B vaccination

+ hepatitis B immunoglobulin (HBIG) given within 12 hours of birth

95
Q

What is mainstay of treatment for Hep D infection?

A

Peginterferon alfa for >48 weeks

96
Q

Which antibodies are most associated with Type 1 AIH?

A

ANA

Anti-Smooth Muscle Ab

97
Q

Which antibody is most associated with Type 2 AIH?

A

Anti-LKM1

98
Q

What is the initial treatment for mild to mod AIH?

A

Prednisolone + azathioprine

99
Q

What antibody is often positive in PBC?

A

Anti-mitochondrial ab

100
Q

What is the only disease-modifying agent for PBC?

A

Ursodeoxycholic acid

101
Q

What condition is PSC very closely associated with?

A

Ulcerative colitis in 70-80%

102
Q

What is the Maddrey score used for?

A

Scoring system to identify patients who may respond to prednis(ol)one.
Maddrey score more than 32 -> consider starting prednis(ol)one.

103
Q

What is the treatment used in Alcoholic Hepatitis if appropriate?

What is the role of the Lille score?

A

Prednis(ol)one 40 mg orally, daily for 28 days, ?taper after

The Lille score should be calculated on day 7 of prednis(ol)one treatment to identify patients who are not responding and should have prednis(ol)one stopped

104
Q

What are some treatment options for Wilson’s disease?

A

Penicillamine / Trientine (chelating agents)

Zinc (to decrease copper absorption)

105
Q

Worldwide, what is the primary cause of HCC?

A

HBV infection

106
Q

What is the classic contrast pattern seen on CT/MRI with HCC?

Why is this?

A

Hyperenhancement in the arterial phase and washout in venous or delayed phases

Benign lesions are supplied by branches of the portal system, whereas malignant nodules are supplied by blood from the hepatic artery

107
Q

What is the Milan criteria for liver transplantation in HCC?

A

A single nodule ≤5 cm in diameter or

up to three nodules, none larger than 3 cm in diameter

108
Q

For patients with advanced HCC and compensated cirrhosis, what agent has been shown to prolong survival?

A

Sorafenib (multikinase inhibitor) has been shown to prolong survival and is regarded as the standard of care.
Use sorafenib 400 mg orally, twice daily

109
Q

When is terlipressin used in hepatorenal syndrome?

A

After correction of precipitants (infection / drugs / UGIB / hypovolaemia), if renal function still not improving

110
Q

What are the main indications for liver transplant in chronic liver disease? (7)

A
  • refractory ascites
  • SBP
  • hepatorenal syndrome
  • recurrent or chronic hepatic encephalopathy
  • small hepatocellular carcinomas
  • Child-Turcotte-Pugh score of B7 or above
  • Model for End-stage Liver Disease (MELD) score of 13 or above
111
Q

What are some key contraindications to liver transplant? (6)

A
  • advanced HCC
  • extrahepatic malignancy
  • uncontrolled extrahepatic infection
  • active alcohol or substance abuse
  • significant coronary or cerebrovascular disease
  • inadequate social support
112
Q

What are the main treatments for chronic/recurrent hepatic encephalopathy?

A

Lactulose 30 mL orally, 3 to 4 times daily, aiming for 2 or 3 semisoft stools per day.

For patients with repeated episodes of hepatic encephalopathy despite lactulose therapy, add:
rifaximin 550 mg orally, twice daily.

113
Q

How can we differentiate between cirrhotic and non-cirrhotic causes of ascites?

A

Serum-to-ascites albumin gradient (SAAG) of more than 11 g/L suggests cirrhosis

A SAAG of 11 g/L or less suggests a noncirrhotic cause of ascites (eg malignancy, pancreatitis, tuberculosis), or the presence of complications, such as spontaneous bacterial peritonitis or hepatocellular carcinoma

114
Q

King’s College Criteria for Liver Transplant in acute liver failure?

A

Paracetamol ->

  • pH <7.3 OR
  • INR >6.5 + Creatinine >300 + encephalopathy grade 3-4

Other cause ->

  • INR >6.5 OR 3 of the following:
  • Age <10 or >40
  • INR >3.5
  • Bili > 300
  • Jaundice to encephalopathy time >7 days
  • Hep C, drug-induced
115
Q

What kind of diet should a patient with chronic liver disease be on?

A

Low salt, high-protein, high energy

116
Q

What are the key diagnostic tests for Wilson’s disease, other than liver biopsy?

A 
Serum ceruloplasmin (low)
24 hour urinary copper (high)
117
Q

What is the most common HFE gene mutation observed with hereditary haemachromatosis?

A

Homozygosity for C282Y

118
Q

What are the measures included in calculation of Child-Pugh score?

A 
Albumin
Ascites
Encephalopathy
INR
Bilirubin
119
Q

What test for HCV tells us about active disease status?

A

Viral RNA PCR

120
Q

What GN is associated most with HCV?

A

MPGN

121
Q

What is the most common troubling SE of sorafenib?

A

Palmar-plantar erythrodysesthesia (Hand-foot syndrome)

122
Q

Which component of Aug DF is most associated with DILI?

A

Clavulanate

123
Q

What is the best statin in terms of avoiding DILI?

A

Pravastatin

124
Q

What are 2 alternative medicines closely linked with DILI?

A

Valerian

Black cohosh

125
Q

Which HLA alleles are closely associated with Coeliac’s?

A

HLA-DQ2 / DQ8

126
Q

What are the 1st line investigations for coeliac disease?

What is the gold standard for confirming the diagnosis?

A

IgA anti-TTG, and total IgA

Upper endoscopy with small bowel biopsy showing Marsh 2-3 lesions

127
Q

Which kind of polyps are thought to be highest risk for progression to cancer?

A

Adenomatous polyps

128
Q

What information does the SAAG give?

How is a SAAG of >11 interpreted?

A

Serum to ascites albumin gradient accurately identifies the presence of portal hypertension

SAAG = (Serum albumin) – (Ascitic fluid albumin)

SAAG >11 suggests portal HTN as the cause of ascites

129
Q

What Child Pugh score denotes B, and C?

A

B - 7-9

C - 10 and above

130
Q

What are the extra-intestinal manifestations of IBD that are associated with active disease? (4)

A

Arthritis
Episcleritis
Oral ulcers
Erythema nodosum

131
Q

Which 3 hormones are key in stimulating appetite?

A

Ghrelin
Ag-RP
NPY

132
Q

What classic endoscopic finding is seen with chronic laxative abuse?

A

Melanosis coli

133
Q

What is the mutation in FAP?

A

APC gene, which codes for beta catenin (involved in cell-to-cell adhesions)

134
Q

Which types of duodenal polyps are most severe?

A

Villous

135
Q

When do those with FAP need screening to commence?

A

Age 10 years

FRACP NOSH 2020 (18 decks)

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