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FRACP > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Give 2 antibiotics that classically cause cholestatic LFTs.

A

Augmentin (due to clavulonic acid) and macrolide

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2
Q

What are the prognostic factors in the context of a paracetamol overdose?

A

Most important: time to NAC instigation being under 8h.

Others (GLAD):

  • Glutathione deficiency: fasting/malnutrition, acute illness, HIV/AIDs
  • Liver injury: viral / EtOH (acute intake)
  • Alcohol use (chronic intake)
  • Drugs that induce p450 (CRIB): carbamazepine, rifampicin, isoniazid, barbituates
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3
Q

Give 2 drugs that classically cause hepatocellular LFT derangement.

A

Diclofenac and isoniazid

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4
Q

What does Dubin-Johnson syndrome do to LFTs?

A

Genetic cause of elevated CONJUGATED bilirubin due to inability of hepatocyte to SECRETE bilirubin into bile.

NO changes in ALT/AST.

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5
Q

Which type of iron, haem vs. non-haem iron has higher bioavailability? What are the sources of these types of iron in the diet?

A

Haem iron (meat and fish) has higher bioavailability than non-haem (vegetables) iron.

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6
Q

What 4 ‘alarm bell’ clinical features that prompt one to think IBD rather than IBS?

A

B-PAW:

  1. Blood derangements: UEC/FBC/ESR/CRP
  2. PR bleeding
  3. Abdominal pain that is worsening
  4. Weight loss
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7
Q

What are 3 useful tests to ‘exclude’ coeliacs disease (i.e. high sensitivity)? What immunogloblin deficiency affects the sensitivity of one of these tests?

A

Excluding coeliac disease (unlikely if both negative):

  1. Serology:
    EMA (endomysial Ab – IgA) - affect by IgA deficiency.
    tTGA (tissue-transglutamase Ab)
  2. Genotype: HLA-DQ2 or HLA-DQ8
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8
Q

What happens to the level of hepcidin with the following scenarios:
Increased body iron levels
Infection
Inflammation

A

Hepcidin levels increases congruently with increases in bodily iron levels, infection or inflammation.

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9
Q

What type of iron is dietary iron, ferrous or ferric?

A

Dietary iron is Fe2+ - ferrous/food/two (all have ‘o’ in it).

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10
Q

What are the DDx for atrophic villi on a bowel biopsy (6)? Which is most likely

A

CE-SCAM (think caecum):

Coeliac’s disease (most likely), Eosinophilic enteritis, Sprue (collagenous, tropical, hypogammaglobulinic), Crohn’s disease, Adult-onset autoimmune enteropathy, Malnutrition.

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11
Q

What are the most common long-term complications of liver transplantation?

A

Most common long-term complication of liver transplantation = metabolic syndrome (HOLD): HTN, obesity, lipid disorder, DM.

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12
Q

What is the significance of NOD1/CARD15 mutations?

A

NOD1 / CARD15 gene polymorphisms are implicated in Crohn’s diseases and suggest increased risk of need for Sx at a younger age and strituring disease.

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13
Q

What is Zollinger-Ellison syndrome (give 3 points).

A

Zollinger-Ellison Syndrome:

  1. Tumour of pancreatic islet of Langerhans (non-beta cells) that secretes gastrin which in turn stimulates parietal cells in the stomach to cause GI mucosal ulcerations.
  2. Part of MEN1 or sporadic
  3. Primary tumours = pancreas, duodenum and LN of abdomen (ectopics possible)
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14
Q

Which bacteria is known to cause terminal ileitis?

A

Yersinia may cause acute terminal ileitis

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15
Q

What are the 2 most common causes of pancreatitis?

A

Common causes of pancreatitis:
Gallstones and EtOH 80%
Idopathic 10%
Other (all) 10%

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16
Q

Give 3 GI causes of clubbing.

A
  1. IBD
  2. Coeliac’s disease
  3. Whipple’s disease
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17
Q

True/False: most cases of acute hepatitis are symptomatic.

A

False.

Acute hepatitis does NOT necessarily present with florid symptoms, as only 25% present with acute hepatitis and the rest are asymptomatic until they present with chronic liver failure.

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18
Q

Give 4 inherited disorders of bilirubin metabolism. Elucidate upon whether they are conjugated or unconjugated.

A

4 inherited disorders of bilirubin metabolism:

Conjugated (DC - has ‘C’):

  1. Dubin-Johnson syndrome
  2. Crigler-Najjar syndrome (types I and II)

Unconjugated (GR):

  1. Gilbert syndrome
  2. Rotor syndrome
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19
Q

Where is bilirubin normally conjugated?

A

Bilirubin is conjugated in the liver hepatocytes and catalysed by gluconyl transferase.

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20
Q

Give lots of causes of pancreatitis.

A

Causes of pancreatitis (IGETSMASHED)

Idiopathic approx 10%
Gall stones / EtOH approax 80%

Rest approx 10%:
Trauma/tumours
Scorpion/Snake venom
Microbiology (CHEP: CMV, hepatitis, EBV, paramyxovirus)
Autoimmune (PAN, SLE)
Steroids
Hypercalcaemia/Hypertriglyeridaemia/Hypothermia/Hereditary
ERCP/Estrogen
Drugs (sulphonamides, AZA, NSAIDs, diuretics) / Duodenal ulcers

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21
Q

What is the clinical triad for Zollinger-Ellison syndrome? What is the mechanism?

A

Clinical triad (PIG):

  1. PUD
  2. Isle of Langerhans cell tumour
  3. Gastric acid hypersecretion

Mechanism: Islet of Langerhans cell tumour → gastric hypersecretion → PUD

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22
Q

What is the significance of CAGA+ in PUD?

A

CAGA+ in H. pylori confer worse disease (PUD/GUD or gastric cancers)

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23
Q

What is Whipple’s disease?

A

Whipple’s disease is a chronic infection from Tropheryma Whipplei

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24
Q

What is the genetics of hereditary haemachromatosis?

A

Herediatary haemachromatosis has autosomal RECESSIVE inheritance and involve C282Y/H63D genetic mutations

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25
Q

What are constituents of total bilirubin?

A

delta bilirubin (conjugated bilirubin bound to albumin)

conjugated bilirubin

unconjugated bilirubin

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26
Q

True/False: anorexia nervosa leads to hypoalbuminaemia.

A

False.

Albumin levels remain normal in anorexia nervosa.

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27
Q

Patient has fatigue, pruritus and abdominal pain with jaundice. Bloods reveal positive anti-mitochondrial antibodies. Diagnosis?

A

Primary biliary cirrhosis.

Jaundice is a late sign.

28
Q

What is the cell that is responsible for causing fibrosis in the liver?

A

Stellate cell

29
Q

Patient presents with red-crusted lesions around the mouth and finger pulps 3m after SB resection for Crohn’s disease. What is the diagnosis?

A

Zinc deficiency – Acrodermatitis

Peri-oral dermatitis
Acral involvement
Occasionally alopecia

30
Q

What is the IL28B genotype?

A

IL28B is a PATIENT genotype that affects Hep C viral kinetics

2 types:
CC (good) - responds well to treatment, so treat immediately
TT (bad) - responds poorly to treatment (Africans), no date for best treatment regimen.

Remember:
‘yum, these CCs are good!’
‘Tsk, Tsk! Don’t do that - that’s bad!’

31
Q

IL28B genotype is an important predictive factor for which condition and what does it predict?

A

Hep C - IL28B is the single most important predictive factor.

  1. Treatment response to Peg-Riba (pegylated interferon and ribavirin)
  2. Sustained or spontaneous viral clearance.
32
Q

What does it mean to have Hep C Genotype 1?

A

Genotype 1-3 are VIRAL genotypes that influence response to treatment:

Genotype 1 = BAD (type 1A is worse than 1B)
Genotype 2 + 3 = GOOD (but less common)

Remember: ‘Type A personalities almost wanna be no. 1 and are the worst!’

33
Q

What is the new standard of care for Hep C with Genotype 1?

A

Pegylated interferon + Ribavirin + Protease inhibitors (triple therapy)

Example: Pega-Riba-Telaprevir or Pega-Riba-Boceprevir

34
Q

What are the SEs of using triple-therapy in Hep C with Genotype 1?

A

Example: Pega-Riba-Telaprevir or Pega-Riba-Boceprevir

Both:

  1. Myelosuppression
  2. Riba (ribavirin) causes severe haemolytic anaemia.

SEs of Telaprevir:
1. ‘Fire-a-rrhoea’ - diarrhoea with anal pain
2. Rash 6%
Remember: ‘if you watch TELAvision all day, your ass will hurt’

SEs of Boceprevir:
1. Dygeusia - bad taste
2. Nausea
Remember: ‘this BOCconcini cheese left a bad taste in my mouth - it’s dyguesting!!’

35
Q

What is the duration of therapy of Hep C triple therapy?

A

Trick question - depends.

Duration dictated by ‘response guided therapy’ - HCV RNA checked at 8 weeks:

  1. Undetectable then 24 weeks Rx
  2. Detectable then 48 weeks Rx
36
Q

What is a new treatment available for Hep C?

How does it differ from the old regimen in terms of duration of treatment and indications?

A

Sofosbuvir and Ledipasvir.
Remember: ‘If nothing else works for Hep C then just hit themover the head with SOFT-LED’

Sofosbuvir is a polymerase inhibitor - direct antiviral agent.

  • Duration of Rx = 12 weeks only
  • 90% effective ALL genotypes with good SEs profile.
37
Q

What are the phases of Hep B infection?

A

Phases of Hep B:

Phase I: immunotolerant (no liver disease, occurs in 80%)

Phase II: acute infection (first or acute flare on chronic Hep B)

Phase III: latent disease

Phase IV: pre-core mutant infection

38
Q

What is occurs in phase IV Hep B?

A

Pre-core mutant infection:

  • Host directs a lot of immune pressure towards eAG (eAg is only present in wild type virus
  • Resulting in negative eAg but positive eAb
  • Patient remains susceptible to flares of hepatitis from pre-core mutant therefore core IgM positive.
39
Q

True/False: in the treatment of Hep C with triple therapy, failure of one type of protease inhibitor warrant the trial of another.

A

False.

Resistance to protease inhibitors is an issue in Hep C treatment.

40
Q

What phase of Hep B infection does the following patients have: sAg+, eAg+, core IgM+/-, core IgG+, HBV DNA+, sAb-, eAb-

A

Active hepatitis: acute flare of chronic infection (phase II)

NB:
eAg indicates infection with wild-type virus
sAg indicated infection with any type (i.e. wild or mutant)

41
Q

What phase of Hep B infection does the following patients have: sAg+, eAg-, core IgM+, core IgG+, HBV DNA+, sAb-, eAb+

A

Active hepatitis: pre-core mutant infection (phase IV)

NB:
eAg indicates infection with wild-type virus
sAg indicated infection with any type (i.e. wild or mutant)

42
Q

What phase of Hep B infection does the following patients have: sAg+, eAg-, core IgM-, core IgG+, HBV DNA-, sAb-, eAb-

A

Latent disease (phase III)

NB:
eAg indicates infection with wild-type virus
sAg indicated infection with any type (i.e. wild or mutant)

43
Q

What is the standard of care for a young patient with Hep B with Hep D coinfection?

How many respond well?

Is there risk of of decompensated liver disease?

A

Remember: ‘Be quick, you need to PEG the SINGLE YOUNG guy!’

Single agent PEG (pegylated interferfon) for 48 weeks.

1/3 of patient with sustained viral response.

Risk of decompensated liver disease.

44
Q

What is the standard of care for an older patient with Hep B?

What types of drugs are used?

How many respond well?

Is there risk of decompensated liver disease?

A

Remember: ‘You can Be LATE for older guys!’

Lamivudine - problems with resistance
Adefovir
Tenofovir
Entecavir

All NARTi (nucleoside analogue reverse transcriptase inhibitors) that prevent viral replication.

95% with viral suppression but only 6% with sustained viral response.

Not much risk of decompensated liver disease.

45
Q

What is the treatment of Hep B reactivation in pregnancy?

What is the perinatal consideration?

A

Lamivudine and Tebivudine (Lam-Telbi) at 32 weeks to prevent vertical transmission (10% risk if untreated)

12 prior to delivery give Hep B immunoglobulin,

46
Q

What % of people with Hep B will develop cirrhosis?

What is the most important risk factor for this?

A

20% (high)

Hep B DNA viral load

47
Q

What need to be found on the biopsy of the distal oesophagus to diagnose Barrett’s oesophagus?

A

Intestinal dysplasia.

48
Q

What are the 6 risk factors for Barrett’s oesophagus?

A

‘Old fat white guy that smokes and has reflux’

>50yrs
Overweight
Male
Caucasian
Smoking 
GORD
49
Q

True/False: PPIs are beneficial in the treatment of Barrett’s oesophagus.

A

True.

PPIs need to be lifelong.

50
Q

For the following case of Barrett’s oesophagus comment on the timing of endoscopic surveillance:

  1. No dysplasia
  2. Low-grade dysplasia
  3. High-grade dysplasia in absence of eradication therapy.
A
  1. No dysplasia = 3-5yrs
  2. Low-grade dysplasia = 6-12m
  3. High-grade dysplasia in absence of eradication therapy = 3m
51
Q

What is the risk of Barrett’s oesophagus with high-grade dysplasia progressing to cancer?

52
Q

Patient wil deranged LFTs (mixed picture) has a liver biopsy that reveals marked steatosis, portal and lobular inflammation and hepatocyte ballooning. What is the likely diagnosis?

53
Q

What is the difference between NAFL (non-alcoholic fatty liver) and NASH (non-alcoholis steatohepatitis)?

A

NAFL = hepatic steatosis WITHOUT significant inflammation, benign.

NASH = hepatic steatosis WITH hepatic inflammation +/- fibrosis.

54
Q

True/False: the majority of deaths from in patients with NASH are due to liver-related mortality.

A

False:

Most due to CVD and T2DM.

1/3 cases have liver-related mortality:

  • Complication of liver cirrhosis
  • HCC
55
Q

What is the metabolic syndrome?

A

HOLD:

HTN
Obesity (central)
Lipid derangement (high TG and low HDL)
DM / insulin resistance

56
Q

What are the principle in NASH management?

A

Treat metabolic and cardiovascular comorbidities.

57
Q

A patient with Hep C infection is at increased risk of developing which condition?

A

T2DM

HCV causes insulin resistance by affecting insulin signalling pathways

58
Q

Patient is noted to have both chronic HCV infection (treated) and T2DM, what is the patient at risk of (3)?

A
  1. Accelerated progression of liver fibrosis (via stimulation of stellate cells)
  2. Reduced SVR (sustained viral response) rates with PEG-Riba
  3. HCC development
59
Q

In Crohn’s disease management, what is the utility of Budesonide?

A

Used as an alternative to prednisone for active ileitis or right-sided Crohn’s colitis.

60
Q

Metabolite testing is often used in thiopurine (AZA, 6-MP) use in IBD. What do the following metabolites suggest:

  1. 6-TG
  2. 6-MMP
A
  1. 6-TG: therapuetic efficacy, high levels (>400) may cause bone marrow suppression
  2. 6-MMP: liver toxicity (>5000)
61
Q

Explain the phenomena of shunting in AZA metabolism?

How is this addressed clinically?

A

Certain patients have low TMPT activity, this leads to excessive shunting of AZA to 6-TG (theperautic moiety).

At-toxic levels (>400) this causes marrow suppression and leucopenia.

If shunt is noted then reduced dose of AZA/6-MP +/- allopurinol (block XO but also inhibits TPMT)

62
Q

Is the dosing of AZA and 6-MP equivalent?

A

No

1mg AZA = 0.5mg 6-MP

(only 50% of AZA metabolises to become 6-MP

63
Q

TNFi are effective in what types of Crohn’s disease?

A

Luminal and fistulising Crohn’s Disease.

64
Q

Define the following:

  1. Severe UC (ulcerative colitis)

2. Fulminant UC

A 
1. Severe UC (ulcerative colitis)
>6 stools/d
Severe cramps
Systemic toxicity (febrile and tachycardic)
Anaemia Hb < 105
ESR > 30
2. Fulminant UC
>10 stools/d + continous bleeding
abdominal pain +/- acute abomen
Systemic toxicity + anorexia
Risk of toxic megacolon and bowel perforation
65
Q

What is the treatment of severe UC?

If not responsive at 3-5d?

If still not responsive at 4-7d?

A
  1. IV hydrocortisone / Abx (broad) / supplements (fluid/electrolytes)
  2. Surgical review
  3. DVT prophylaxis

Not responsive at 3-5d = cyclosporin or TNFi (infliximab)

Not responsive at 4-7d = colectomy

66
Q

Patient has stage 2 colon cancer, what are the risk factors for relapse?

A

Pathology:

  1. lymphovascuar invasion
  2. poorly differentatiated cells
  3. T4 disease

Clinical:
4. presents with obstructione

67
Q

T/F: LN involvement is a feature suggestive of relapse in stage 2 colon cancers.

FRACP (20 decks)

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