Gastroenterology Flashcards

1
Q

What is Budd-Chiari syndrome?

A

Thrombotic or non-thrombotic obstruction of the hepatic venous outflow leading to (HAP):

  1. Hepatomegaly
  2. Ascites
  3. Pain in abdomen
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2
Q

True/False: aortic stenosis (AS) is associated with angiodysplasia, treatment of AS leads to regression of angiodysplasia.

A

True.

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3
Q

Which of the following treatments for ‘achalasia’ is best for symptom relief?

A. Medications (CCB, nitrates) to relax LOS
B. Surgical procedure (e.g. Heller myotomy)
C. Nissen fundoplication
D. Botox to the LOS

NB: LOS = lower oesophageal sphincter

A

A. Variable effect and with adverse effects

B. Best option - greater that 80% success with more than a year of persistent benefit

C. Used in conjunction with myotomy to alleviate the reflux that occurs from myotomy

D. Short-lived effect

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4
Q

What are the 4 risk factors for hepatotoxicity during a paracetamol overdose?

A
  1. Malnourished (anorexia/bulimia nervosa)
  2. Drugs that induce CYP3A4
  3. ‘Chronic’ EtOH abuse (not acute intake)
  4. HIV positive
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5
Q

Patient is obese with a diagnosis of NASH, what a simple intervention that will improve liver histology?

A

Weight-loss

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6
Q

Which of the following is a live vaccine and therefore should NOT be given in an immunosuppressed patient:

A. Infuenza
B. Conjugated meningococcal
C. Varicella/Zoster
D. Conjugated Pneumococcal
E. Hepatitis A
A

C. Varicella Zoster

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7
Q

What is the most common cause of severe B12 deficiency worldwide?

A

Pernicious anaemia

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8
Q

What is the pernicious anaemia?

A
  • Autoimmune gastritis due to destruction of gastric parietal cells and associated lack of intrinsic factor binding to vitamin B12.
  • Immune response directed at gastric H+/K+-ATPase which leads to achlorhydria
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9
Q

Regarding Rifaximin:

  1. MOA
  2. Indications
A
  1. MOA = inhibits bacterial RNA polymerase
  2. Used in prevention of encephalopathy in end-stage liver disease - reduces hospitalisations and maintains remission from encephalopathy.
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10
Q

T/F: Rifaximin is more effective at maintaining remission from encephalopathy in end-stage liver disease than non-absorbable dissacharides.

A

True

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11
Q

What are the risk factors for developing Barret’s oesophagus?

A
  1. Smoking
  2. Central obesity
  3. Caucasian
  4. Fhx in 1st degree relative

‘white smoking fat bloke whose brother had Barret’s oesophagus’ - Homer Simpson / Bart

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12
Q

T/F: alcohol consumption is a risk factor for developing Barret’s oesophagus.

A

False.

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13
Q

Which cells in the GIT secrete the following hormones:

  1. Gastrin
  2. CCK
  3. Secretin
  4. Somatostatin
A
  1. Gastrin = G-cells
    G for Gastrin
  2. CCK = I-cells
    I love hot ChiCKs
  3. Secretin = S-cells
    Secret Secretary
  4. Somatostatin = D-cells
    1’m SO Drunk
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14
Q

What is the definition of functional dyspepsia?

A

Rome III criteria require more than one of the following:

  1. postprandial fullness
  2. early satiation
  3. epigastric pain or burning

AND with no evidence of structural disease (including at upper endoscopy) to explain the symptoms

AND need symptoms for 3 month duration

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15
Q

Elderly patient presents with active haematemesis and malaena and is noted to be haemodynamically unstable.

  1. Within what timeframe should endoscopy be performed?
  2. Do PPI infusions reduce blood transfusion requirements in peptic ulcer bleeds?
  3. What is the utility of give the patient IV erythromycin?
  4. What prognostic score predicts risk of re-bleeding and mortality?
A
  1. Within what timeframe should endoscopy be performed?
    24h
  2. Do PPI infusions reduce blood transfusion requirements in peptic ulcer bleeds?
    Yes
  3. What is the utility of give the patient IV erythromycin?
    Promotes gastric emptying and therefore improves endoscopic visualisation.
4. What prognostic score predicts risk of re-bleeding and mortality?
Rockall score (Age above 80, BP below 100, HR above 100, IHD)
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16
Q

Patient with following serology:
HBsAb positive
HBcAB negative

Diagnosis?

A

Previous HBV vaccination

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17
Q

What is the timeframe for post-exposure prophylaxis in HIV?

A

72h

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18
Q

Cholestatic LFTs, p-ANCA positive, anti-mitochondrial antibody (AMA) positive.

What is the diagnosis?

A

Primary Biliary Cirrhosis (PBC)

P for p-ANCA
B for BAMA (i.e. AMA)
C for cholestatic LFTs

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19
Q

You suspect patient with CRC has Lynch syndrome, what test do you ask for first?

A

IHC for MMR genes

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20
Q

Patient with CRC is investigated for Lynch syndrome with IHC for MMR gene which is noted to be negative.

What is the next test?

A

No further testing unless patient has a strong clinical history

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21
Q

Patient with CRC is investigated for Lynch syndrome with IHC for MMR gene which is noted to be positive.

What test would be nest in the following scenarios:

  1. Absent MLH1 / PMS2 protein expression
  2. Absent MSH2 / MSH6 protein expression
  3. All proteins present
A
  1. Absent MLH1 / PMS2 protein expression
    BRAF V600E mutation analysis
  2. Absent MSH2 / MSH6 protein expression
    Germline mutational analysis
  3. All proteins present
    No further testing
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22
Q

Patient with CRC is investigated for Lynch syndrome with a positive IHC for MMR gene, absent MLH1 / PMS2 protein expression and negative BRAF V600E mutation.

What test should be consider next?

A

Germline mutational analysis

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23
Q

Patient with CRC is investigated for Lynch syndrome with a positive IHC for MMR gene, absent MLH1 / PMS2 protein expression and positive BRAF V600E mutation.

What test should be consider next?

A

No further testing

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24
Q

Patient X with CRC positive with:

  • Positive IHC for MMR gene
  • Absent MLH1 / PMS2 protein expression
  • Negative BRAF V600E mutation

Patient has germline mutational analysis - what are the 2 possible outcomes?

A
  1. MSI (microsatellite instability) = Lynch syndrome

2. MSS (microsatellite stability) = Familial CRC type X

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25
Q

Patient Y with CRC positive with:

  • Positive IHC for MMR gene
  • Absent MSH2 / MSH6 protein expression

Patient has germline mutational analysis - what are the 2 possible outcomes?

A
  1. MSI (microsatellite instability) = Lynch syndrome

2. MSS (microsatellite stability) = Familial CRC type X

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26
Q

What are the 3 genotypes associated with Lynch syndrome?

A

MLH1
MSH2
MSH6

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27
Q

T/F: Patient co-infected to HIV-1 and HCV have higher rates hepatic decompensation, liver cirrhosis, HCC and death.

A

True

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28
Q

T/F: Patient co-infected with HIV-1 and HCV genotypes 2 and 3 have high rates of virological response with 12 weeks of treatment with Ledipasvir and Sofobuvir.

A

False - wrong HCV genotypes

Patient co-infected with HIV-1 and HCV genotypes 1 and 4 have high rates of virological response with 12 weeks of treatment with Ledipasvir and Sofobuvir.

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29
Q

Once daily Sofosbuvir-velpatasvir for 12 weeks provides high rate of sustained virological response among both treated and untreated patients, including compensated cirrhotics, affected by which HCV genotypes?

A

HCV genotype 1, 2, 4, 5 or 6.

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30
Q

For autoimmune hepatitis:

  1. Which sex is more likely to get it?
  2. Which ethnicity is more likely to progress to cirrhosis?
A
  1. Which sex is more likely to get it?
    Female
  2. Which ethnicity is more likely to progress to cirrhosis?
    African Americans
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31
Q

Which of the 2 types of autoimmune hepatitis (AH) is more likely to be severe?

A

Type 1 AH - variable severity

Type 2 AH - always severe

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32
Q

What are the 4 autoantibodies found in type 1 autoimmune hepatitis (AH)?

A

ANCA
Anti-smooth muscle Abs
Soluble liver Ag
Soluble liver/pancreas Ag

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33
Q

What are the 4 autoantibodies found in type 2 autoimmune hepatitis (AH)?

A

Anti-liver kidney microsomal Ab Type 1 and 3

Anti-liver-cytosol Ab type 1

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34
Q

T/F: Autoimmune hepatitis (AH) is associated with hypergammaglobulinaemia.

A

True

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35
Q

What is the typical histopathology of autoimmune hepatitis (AH)?

A
  • Infiltration of lymphocytes and plasma cells extending from the portal tract to surrounding parenchyma.
  • ‘Interface hepatitis’ - sharp difference between normal parenchyma and inflammatory zone
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36
Q

Which biochemical and histopathological feature suggests that an autoimmune hepatitis (AH) should be treated?

What is the treatment?

Is the condition likely to relapse with withdrawal of treatment?

A

Indications for treatment:

  1. Elevated aminotransferase more than 2x upper limit
  2. Interface hepatitis on biopsy

Treatment:
Steroids and AZA +/- liver transplant if unresponsive (esp. Type 2 AH)

Relapsing disease is common if treatment is withdrawn.

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37
Q

T/F: Formal diagnosis of coeliacs disease requires a duodenal biopsy.

A

True

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38
Q

All patients about to undergo chemotherapy or immunosuppression should be screened with HBsAg and anti-HBc.

Patient is seronegative for HBV. What is recommended?

A

HBV vaccination

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39
Q

All patients about to undergo chemotherapy or immunosuppression should be screened with HBsAg and anti-HBc.

Patient is HBaAg positive. What is recommended?

A
  1. Test for HBV DNA levels
  2. Start NA (nucleoside analogues) pre-emptively regardless of HBV DNA levels
  3. Continue for 12m post cessation of therapy (i.e. chemo or immunosuppression)
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40
Q

All patients about to undergo chemotherapy or immunosuppression should be screened with HBsAg and anti-HBc.

Patient is HBsAG negative, anti-HBc positive with detectable HBV DNA. What is recommended?

A

SAME as for HBsAg positive patients:

  1. Test for HBV DNA levels
  2. Start NA (nucleoside analogues) pre-emptively regardless of HBV DNA levels
  3. Continue for 12m post cessation of therapy (i.e. chemo or immunosuppression)
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41
Q

Patient is HBsAG negative, anti-HBc positive with UNDETECTABLE HBV DNA. What is recommended?

A
  • Regardless of HBsAb status (i.e. immunity) should be monitored closely with ALT and HBV DNA.
  • NA (nucleoside analogues) to be commenced if HBV DNA is positive even if ALT is NOT elevated.
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42
Q

What is the MOA lamivudine?

A

Antiretroviral - analogue of cytadine

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43
Q

63M with weight loss on normal diet complains of diarrhoea 3-4x per day, including overnight. Denies abdominal pain or rectal bleeding. Background of 2x episodes of gallstone pancreatitis 15 yrs ago.

What is the diagnosis?

How should it be investigated?

A

Pancreatic insufficiency (often asymptomatic) - investigate with faecal elastase

44
Q

You suspect protein-losing gastroenteropathy - what test can confirm this?

A
  • alpha-1-antitrypsin clearance (paired 24h stool sample and serum level)
  • alpha-1-antitrypsin concentration is NOT reliable
45
Q

T/F: Coeliac serology (IgA, EMA, IgA tTG or IgG DGP) are sufficient to confidently diagnose coeliac disease.

A

False - need small bowel biopsy for diagnosis.

46
Q

ABSENCE of which genotype is useful in EXCLUDING coeliac disease?

A

HLA DQ2/DQ8

47
Q

Which type of diet is beneficial in IBS?

A

low FODMAP diet

FODMAP

Fermentable
Oligo--saccharides
Dissacharides
Monosaccharides
And
Polyol
48
Q

What is the concern with long-term use of PPIs?

A

Hypochlorhydria and hypergastrinaemia that may lead to gastric atrophy

49
Q

What are the potential complications of PPIs upon the following:

  1. Risk of infection
  2. Electrolyte imbalance
  3. Metabolic bone disease
  4. Renal complications
A
  1. Risk of infection - C. difficile and pneumonia from upper GI colonisation
  2. Electrolyte imbalance - hypomagnesaemia and hypocalcaemia
  3. Metabolic bone disease - decreased bone density and increased fractures
  4. Renal complications - AIN
50
Q

Patient has primary sclerosing cholangitis (PSC), what 4 types of cancers is the patient at risk of getting?

A
  • Gallbladder and cholangiocarcinoma cancer
  • HCC
  • CRC
51
Q

What is the pathophysiological substrate for pruritus that occurs in liver disease.

A

Failure to excrete bile salts.

52
Q

Which region of the bowel does Yersinia usually affect?

What condition does it mimic?

A

Terminal ileum - often mimic appendicitis.

53
Q

Patient returns from India with abdominal pain, stool MCS reveals Entamoeba histolytica (endemic to India). Which part of the bowel does it tend to affect?

A

Colon - causes colitis.

54
Q

Patient returning from India is thought to have Ileal Crohn’s disease. What is an important differential?

A

M. tuberculosis (residents or frequent travellers to India)

55
Q

CMV colitis only occurs in immunocompromised patients, HIV AIDS or drug-iunduced immunosiuppression (steroids, biologics). What part of the bowel does it tend to affect?

A

Colon - usually CMV colitis.

56
Q

T/F: Untreated Hereditary Haemochromatosis is associated with increased incidence of coronary artery disease.

A

False - reduced CAD is suggested in studies.

57
Q

Acute uncomplicated pancreatitis is best treated conservatively with IVF and analgesia. Which of the following additional interventions should be considered:

  1. Commencing TPN nutrition rather than PO
  2. Routine Abx
A

Neither

58
Q

Is an FOBT sensitive or specific for diagnosis of CRC?

A

Neither.

59
Q

Most patients with a single adenoma can have repeat colonoscopies in 5 years time. Presence of 3 or more adenomas will reduce this period.

What 2 other features of the adenoma might also warrant closer surveillance?

A
  • Villous pattern

- Greater than 10mm in diameter

60
Q

Having a first degree relative with CRC increases the risk of CRC by which of the following:

  1. 2x
  2. 5x
  3. 10x
  4. 100x
A

2x

61
Q

What percentage of coeliac patients are IgA deficient?

A

5%

62
Q

Patient is less than 40 years of age, presents with pancreatitis and is WITHOUT a history of smoking, gall stones or alcohol consumption.

What 2 rare genetic mutations might be considered?

A

CF and SPINK1 mutations.

63
Q

T/F: H. pylori is a risk factor for GORD.

A

False.

64
Q

H. pylori infection increases the risk of which 4 gastrointestinal conditions?

A
  1. Duodenal ulcers
  2. Gastric carcinoma
  3. Gastric MALT lymphoma
  4. Intestinal metaplasia
65
Q

Describe the enterohepatic circulation of bile salts.

A
  • Bile salts are synthesised in liver and stored in the gall bladder
  • Released into the duodenum post-prandially to aid digestion.
  • Travel to terminal ileum and reabsorbed (95%) into the hepatic portal vein and return to the liver.
66
Q

What percentage of bile salts that arise from the liver are recycled vs. newly synthesised?

A
  • 95% recycled

- 5% newly synthesised

67
Q

Describe the synthesis of bilirubin.

A

Reticuloendothelial system (macrophages and liver kupffer cells) salvage heme:

  • RBC (85%)
  • Myoglobin cytochromes (15%)

Heme –[ heme oxydase ]–> Biliverdin (green)

Biliverdin –[ biliverdin reductase ] –> UNCONJUGATED bilirubin (red/orange)

Unconjugated bilirubin binds to albumin and enter the liver

Unconjugated bilirubin –[ ? ]–> bilirubin diglucuronide (CONJUGATED bilirubin)

Conjugated bilirubin enters the biliary system.

68
Q

Describe the recycling and excretion of bilirubin.

A
  • Conjugated bilirubin enters the small intestines as bile.
  • Enteric bacteria action creates urobilinogen that then undergoes 3 pathways:
    1. Oxidises in the large intestines and forms urobilin stercolin and is faecally excretion
    2. Urobilinogen enters the portal vein and may be renally excreted as urinary urobilinogen.
    3. Urobilinogen may be returned to liver and be recycled
69
Q

Patient with Crohn’s disease has a terminal ileum resection during an exacerbation.

What complication would you anticipate?

How is this complication treated?

A

Bile salt diarrhoea

Cholestyramine sequested the bile salts.

70
Q

What are the mechanisms of bile salt diarrhoea in patient with terminal ileum resection?

A

Bile salt is usually absorbed in the terminal ileum, unabsorbed bile salts cause diarrhoea via:

  • sodium and water secretion
  • increased colonic motility
  • increased mucous secretion
  • direct mucosal damage
71
Q

Compare type 1 and type 2 Autoimmune Hepatitis (AIH) in terms of:

  1. Age of onset
  2. IgG elevated
  3. Sex
  4. Distinguishing autoantibodies present
  5. HLA haplotype associations
  6. Prognosis
  7. Frequency
A

Type 1 AIH vs. Type 2 AIH:

  1. Age of onset: old vs. young (< 18yrs)
  2. IgG elevated: +++ vs. +
  3. Sex: both have female preponderance
  4. Distinguishing autoantibodies present:
    - Type 1 AIH = p-ANCA / ANA / ASMA (often both)
    - Type 2 AIH = Anti-LKM / Anti-LC-1
  5. HLA haplotype associations: Type 1 AIH = DR3, DR4
  6. Prognosis: good vs. bad
    Steroids: responsive vs. less responsive
    Progression to cirrhosis: 40% vs. 80%
  7. Frequency: 95% vs. 5%
72
Q

What is the clinical significance of a positive AMA (Anti-Mitochondrial Ab)?

A

2 DDx:

  • PBC (primary biliary cholangitis) - AMA highly sensitive and specific for this
  • Type 1 AIH - AMA also seen in Type 1 AIH
73
Q

Interpret the following Hep B serology:

HBsAg - negative
anti-HBc - negative
anti-HBs - negative

A

Susceptible

HBsAg - negative = no active infection
anti-HBc - negative = no natural Hep B infection
anti-HBs - negative = no immunity

74
Q

Interpret the following Hep B serology:

HBsAg - negative
anti-HBc - positive
anti-HBs - positive

A

Immune due to natural infection

HBsAg - negative = no active infection
anti-HBc - positive = natural Hep B infection
anti-HBs - positive = immunity

75
Q

Interpret the following Hep B serology:

HBsAg - negative
anti-HBc - negative
anti-HBs - positive

A

Immune due to Hep B vaccination

HBsAg - negative = no active infection
anti-HBc - negative = no natural infection
anti-HBs - positive = immunity

76
Q

Interpret the following Hep B serology:

HBsAg - positive
anti-HBc - positive
anti-HBs - negative
IgM anti-HBc - positive

A

Acutely infected

HBsAg - positive = active infection
anti-HBc - positive = natural Hep B infection
anti-HBs - negative = no immunity
IgM anti-HBc - positive = acute infection

77
Q

Interpret the following Hep B serology:

HBsAg - positive
anti-HBc - positive
anti-HBs - negative
IgM anti-HBc - negative

A

Chronically infected

HBsAg - positive = active infection
anti-HBc - positive = natural Hep B infection
anti-HBs - negative = no immunity
IgM anti-HBc - negative = no acute infection

78
Q

Interpret the following Hep B serology:

HBsAg - negative
anti-HBc - positive
anti-HBs - negative

A

Difficult to interpret - 4 possibilities

  • resolved infection (most likely)
  • false positive anti-HBc
  • low-level chronic infection (false negative HBsAg)
  • resolving acute infection (false negative HBsAg)

HBsAg - negative = no active infection
anti-HBc - positive = natural Hep B infection
anti-HBs - negative = no immunity

79
Q

Compare Hep B vaccination schedules in the following 3 populations:

  1. 0-19yrs
  2. > 20 yrs
  3. CKD with haemodialysis
A
  1. 0-19 yrs either:
    - Engerix-B - 10ug x3 doses (day 0, 1m, 6m)
    - H-B-Vax II - 5ug x3 doses (day 0, 1m, 6m)
  2. > 20 yrs either (double 0-19 yrs):
    - Engerix-B - 20ug x3 doses (day 0, 1m, 6m)
    - H-B-Vax II - 10ug x3 doses (day 0, 1m, 6m)
  3. CKD with haemodialysis (double >20 yrs):
    - Engerix-B - 40ug x3 doses (day 0, 1m, 6m)
    - H-B-Vax II - 30ug x3 doses (day 0, 1m, 6m)
80
Q

Patient is noted to have fistulising Crohn’s disease. Which 2 Abx may be of benefit?

A

Metronidazole / Ciprofloxacin

81
Q

T/F: EUA (examination under anaesthetic) is compulsory for ALL patients suspected of fistulising Crohn’s disease and may be of symptomatic benefit.

A

True

82
Q

Which biologic is useful in the treatment of fistulising Crohn’s disease?

A

Infliximbab (anti-TNF mAb)

83
Q

T/F: Sulphasalazine is useful in the treatment of fistulising Crohn’s disease?

A

False - not effective.

84
Q

Patient has HCV.

What 5 important questions need to be considered before commencing treatment?

A
  1. Which HCV genotype?
  2. Is cirrhosis present?
  3. Is HBV–HCV or HIV-HCV coinfection present?
  4. Are there potential drug-drug interactions?
  5. What is the eGFR (renal function)?
85
Q

Below what eGFR is Sobosbuvir NOT recommended?

A

eGFR < 30 ml/min/1.73^2

86
Q

Below what eGF does Ribavirin need dose reduction?

What other risk factor need to be considered for this durg?

A

eGFR < 50 ml/min/1.73^2

IHD - patient > 50 or with h/o CVS risk factors need an Echo prior to Ribavirin

87
Q

Which 3 co-infections need to be considered prior to treatment of HCV?

If seronegative, which of these require vaccinations prior to commencing HCV treatment.

A

HBV (HBsAg / anti-HBc / anti-HBs)
HAV
HIV

HBV / HAV require vaccinations

88
Q

Which 2 modalities may be used to determine presence of liver cirrhosis?

What are the parameters that suggest NO cirrhosis in each of these?

A

Fibroscan (liver stiffness) < 12.5 kPa (no cirrhosis)

APRI (AST to Platelet Ratio Index) < 1.0

89
Q

How is APRI (AST to Platelet Ratio Index) calculated?

A

APRI = 100 x [AST / ULN AST] / platelet count (10^9)

NB: ULN AST = 40

Examples:

Cirrhotic: AST 100 / plts 50
APRI = 100 [ (100/40) / 50 ] = 100 x 2.5/50 = 5
Greater than 1

Non-cirrhotic: AST 20 / plts 200
APRI = 100 [ (20/40) / 200 ] = 100 x 0.5/200 = 0.25
Less than 1

90
Q

Most HCV treatment regimens are 12 weeks.

Give the timing of the 4 episodes of follow-up and the blood tests required for each.

A

Week 0 = FBE / UEC / LFT / HCV RNA (quantitative)
Week 4 = LFT and determine adherence
Week 12 = LFT +/- HCV RNA - if adherence a concern
Week 24 = LFT+ HCV RNA (qualitative) - to determine SVR

Week 12 = end of treatment
SVR = sustained virological response

91
Q

What type of follow-up is required after successful HCV treatment in the following scenarios:

  1. SVR + no cirrhosis + normal LFTs (male AST < 30, female AST < 19)
  2. SVR + abnormal LFTs (male AST > 30, female AST > 19)
  3. SVR + cirrhosis
A
  1. SVR + no cirrhosis + normal LFTs (male AST < 30, female AST < 19)
    - no follow-up
  2. SVR + abnormal LFTs (male AST > 30, female AST > 19)
    - liver screen and refer to gastroenterologist
  3. SVR + cirrhosis
    - longterm follow-up due to risk of HCC / oesophageal varices / osteoporosis
92
Q

What are the genotypes that the following HCV regimens suitable for:

  1. Sofosbuvir / Velpatasvir
  2. Sofosbuvir / Ledipasvir
  3. Elbasvir / Grazoprevir +/- Ribavirin
  4. Partiaprevir-Ritonavir / Ombitasvir / Dasabuvir +/- Ribavirin
  5. Sofosbuvir / Daclatasvir +/- Ribavirin

Given MOA for all drugs

A
  1. Sofosbuvir / Velpatasvir (NS5Bi / NS5Ai)
    Genotypes 1-6
  2. Sofosbuvir / Ledipasvir (NS5Bi / NS5Ai)
    Genotype 1 only
  3. Partiaprevir-Ritonavir / Ombitasvir / Dasabuvir +/- Ribavirin (NS3i / NS5Ai / NS5Bi +/- NA)
    Genotype 1 only
  4. Sofosbuvir / Daclatasvir +/- Ribavirin (NS5Bi / NS5Ai +/- NA)
    Genotypes 1 + 3
  5. Elbasvir / Grazoprevir +/- Ribavirin (NS5Ai / NS3i +/- NA)
    Genotypes 1 + 4

NB:
…prEvir = NS3 protease inhibitor - three/E
…Asvir = NS5A inhibitors - A
…Buvir = NS5B RNA polymerase inhibitor - B

Sofosbuvir = NIP (nucleotide)
Dasabuvir = NNPI (non-nucleotide)
Ribavirin = guanosine nucleoside analogue (NA)
93
Q

Prior to current direct acting HCV treatment regimens, what was previously used?

A

Ribavirin + IFN-alpha

94
Q

Donald Trump wore a Good CAP to the PROM and took his PPIs.

What are the many SEs of PPIs?

A

GI-related (G-CAP):

Gastroenteritis
C. Difficile colitis
Atrophic gastritis
Pseudomembranous colitis

Non GI-related (PROM):

Pneumonia
Renal (AIN)
Osteoporosis
Mg low

95
Q

Of the following 3 Abx used in the treatment of H. Pylori, grade them in terms of most to least likely to be resistant:

Amoxicillin
Clarithromycin
Metronidazole

A

Metronidazole (50%) > Clarithromycin (8%) > Amoxicillin (rare)

96
Q

Compare the Abs for type 1 and type 2 autoimmune chronic hepatitis.

A

Type 1 (SN):
ASMA (anti-smooth muscle antibody)
ANA (anti-nuclear antibody)

Type 2 (Ls):
ALKM-1 (anti-liver/kidney microsome-1)
ALC-1 (anti-liver cytosol-1)

97
Q

AXR suggests a volvulus, what radiological sign might be found?

A

Coffee-bean sign = volvulus

98
Q

What are the 3 components of HELLP syndrome?

How is HELLP graded?

A

H - Haemolysis
EL - Elevated LFTs
LP - Low Platelets

Mild - plts >100
Moderate - plts 50-100
Severe - H / EL / LP (plts < 50)

99
Q

Pregnant woman has moderate/severe HELLP syndrome.

What treatment is indicated in the following scenarios?

  1. Stable < 34/40 weeks
  2. Stable > 34 weeks
  3. Unstable at any gestation
A
  1. Stable < 34 weeks - steroids and conservative Mx for Pre-eclampsia
  2. Stable > 34 weeks - deliver
  3. Unstable at any gestation - deliver
100
Q

Which of the following medications are useful in PBC:

UDCA (Ursodeoxycolic acid)
MTX
Colchicine
Prednisone 
AZA
Cyclosporine
Penicillamine
Silymarin
A

UDCA (Ursodeoxycolic acid) - slows progression of PBC

Equivocally useful: AZA / Colchicine

The rest: NOT useful

101
Q

Barett’s oesophagus diagnosis requires a biopsy suggesting intestinal metaplasia.

What does this mean?

A

Columnar epithelium replacing squamous cell epithelium in the lower oesophagus.

102
Q

Patient is investigated for Barrett’s Oesophagus with confirmed intestinal metaplasia, when should the follow-up endoscopy occur in the following scenarios:

  1. Intestinal metaplasia + absence of dysplasia
  2. Low-grade dysplasia
  3. High-grade dysplasia
  4. Adenocarcinoma
A
  1. Intestinal metaplasia + no dysplasia
    - repeat in 6-12m to confirm absence of dysplasia then repeat every 3y
  2. Low-grade dysplasia
    - repeat in 6m to confirm low-grade dysplasia then repeat every 12m +/- endoscopic Rx
  3. High grade dysplasia
    - confirm with 2 pathologists then every 3m +/- endoscopic/surgical Rx
  4. Adenocarcinoma
    - oesophegectomy +/- palliation
103
Q

What are the CAGE questions for alcoholic disorders?

What score is considered positive?

What is the sensitivity of this instrument?

A

Cut down - have you ever considered the need to cut down?
Annoyed - do people annoy you by criticising your drinking?
Guilty - do you feel guilty about drinking?
Eye opener - do you need to drink early in the morning or need it to steady your nerves.

Out of 4 points - positive is 2 or greater

> 90% sensitivity of alcohol disorder

104
Q

Most causes of liver cell injury causes greater increase in ALT than AST.

What are the likely causes of liver injury in the following scenarios:

  1. AST:ALT > 2
  2. AST:ALT = 1
  3. AST:ALT < 1
A
  1. AST:ALT > 2
    - Alcoholic hepatitis (esp. if GGT also raised, due to reduction in pyridoxal phsophate)
    - Wilson’s disease
  2. AST:ALT = 1
    - Ischaemia (CCF / necrosis / hepatitis)
  3. AST:ALT < 1 (hepatocellular damage)
    - Viral hepatitis
    - NASH
    - Paracetamol OD
    - DILI
105
Q

Gastro CA Q11

A

Gastro CA Q11