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FRACP Written Exam 2023 > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Rash with coeliac disease

A

Dermatitis herpetiformis
Mx: gluten free diet, steroids

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2
Q

Erythema nodosum - association with IBD?

A

Crohn’s > UC
Raised, tender, extensor surfaces

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3
Q

Pyoderma gangrenosum - association with IBD?

A

UC
Does not correlate with disease activity

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4
Q

5 classic endoscopic features of eosinophilic oesophagitis

A

Oedema
Longitudinal furrows
Concentric rings
White exudates
Strictures & mucosal tearing

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5
Q

Current therapies for eosinophilic oesophagitis (EoE)

A

PPI
Topical steroids (e.g. oral budesonide)
Six food elimination diet
Elemental diet

Emerging: dupilumab (anti IL-4/IL-13 therapy)

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6
Q

What type of cancer does achalasia increase your risk of?

A

10x increased risk of SCC

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7
Q

Risk factors for Barrett’s oesophagus

A

Male
Caucasian
Age
High BMI
Chronic heartburn
Smoking
Positive family history

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8
Q

Role for PPI in Barrett’s oesophagus

A

Epidemiological evidence that PPI reduces risk of progression to high grade dysplasia and oesophageal adenocarcinoma by 71% (Singh et al, Gut 2014)

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9
Q

Role of aspirin + PPI in Barrett’s oesophagus

A

AspECT trial - evidence to suggest combination PPI and aspirin therapy reduces risk of cancer development (primary end point: time to all cause mortality/oesophageal Ca/HGD)

Difficult to interpret this study - ?not definite evidence

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10
Q

Management of low grade dysplasia

A

Annual risk of progression to adenocarcinoma ~1.8%

  • Confirm LGD on 2 ocassions 6 months apart
  • RFA if present
    > Decreases rate of progression to HGD/adenocarcinoma
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11
Q

Preferred treatment for oesophageal flat dysplasia/intramucosal carcinoma

A

Radiofrequency ablation

Minimal complications
- Immediate: chest pain
- Long term: oesophageal strictures which are responsive to dilation

Studies show that it is associated with decreased neoplastic progression in patient’s with Barrett’s + LGD

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12
Q

Management for oesophageal high grade dysplasia

A

With HGD - annual risk of progression to adenocarcinoma is 10%

Oesophagectomy vs. endoscopic resectiono
- Preferred too ablative techniques (tissue samples allows for accurate staging)

Also need to treat rest of Barrett’s oesophagus

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13
Q

Role of surveillance post Barrett’s osophagus RFA?

A

Should do annual surveillance - at least for 5 years post

75% recurrences at OG junction and most are endoscopically visible

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14
Q

Who should have H Pylori testing?

A

<60 year old, uninvestigated dysepsia, no alarm features

All patients symptomatic of dyspepsia who have endoscopy
Pre-NSAID use
Ethnic groups with high gastric cancer risk (e.g. Japanese, Chinese, Koreans, Russians)
Patient’s with family history of gastric cancer
Active/history of PUD, MALT, endoscopic resection of early gastric cancer
Long term use of aspirin/NSAIDs
Unexplained iron deficiency after standard work up
Adults with ITP

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15
Q

Forrest ulcer classification

A

Forrest Ia - spurting
Forrest Ib - oozing
Forrest IIa - non bleeding visible vessel
Forrest IIb - adherent clot
Forrest IIc - flat red spot at ulcer base
Forrest III - clean ulcer base

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16
Q

When to use traditional triple therapy vs. quadruple therapy for H Pylori?

A

Triple therapy with clarithromycin only if clarithromycin resistance rates are known to be <15%

If clarithromycin levels are unknown - don’t use triple therapy

If known claritbhromycin resistance >15% or unknown:
- Quadruple therapy with:
(1) Clarithromycin + metro + amoxicillin + PPI
or
(2) Bismuth + metro + tetraccycline + PPI

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17
Q

At what INR is it safe to scope with bleed?

A

Safe to scope when INR ≤2.5
Don’t delay to prevent coagulopathy

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18
Q

Signs of cirrhosis clinically

A

Spider naevi
Gynecomastia
Feminisation - loss of axillary/chest hair
Palmar erythema
Testicular atrophy
Nail changes - clubbing, Terry nails
Hypertrophic osteoarthropathy (v rare)

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19
Q

What electrolyte derangement is associated with hepatic encephalopathy?

A

Hypokalaemia

Hypokalaemia increases renal ammonia production

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20
Q

MoA of lactulose in HE

A

Catabolisation of lactulose results in acidic pH which favors formation of NH4+ from NH3, traps NH4 in colon and reduces plasma ammonia concentrations.

Lactulose improves HE but no survival benefit

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21
Q

Diagnostic criteria for SBP

A

PMN/ >250 cells/mm3
Positive ascitic fluid bacterial culture
Absence of secondary causes of peritonitis

22
Q

SAAG interpretation

A

SAAG > 11g/L
- Likely portal hypertension
- E.g. cirrhosis etc.

SAAG <11 g/L
- E.g. peritoneal carcinomatosis, pancreatitis, nephrotic syndrome

23
Q

Most common bacteria isolated from SBP

A

E Coli (43%)
Klebsiella (11%)

24
Q

SBP treatment

A

IV ceftriaxone 2g daily or IV cefotaxime 2g Q8H
- If immediate non-severe/delayed non-severe hypersensitivity to penicillins, use above.
- If immediate/delayed severe HS to penicillins - ciprofloxacin.

Albumin 20% IV within 6 hours of diagnosis IV + single dose on day 3

25
Q

SBP prophylaxis/prevention

A

After 1st episode of SBP, prophylaxis reduces risk of subsequent episodes + all cause mortality - secondary prophyalxis

Primary prophylaxis recommended only for high risk patients: cirrhosis, ascites, ascitic. fluid protein <15g/L and at least one of:
- Impaired kidney function (Cr >110, urea >8.9, Na <130)
- Liver failure (CPC >9 or Bili >50)

(1) Trimethoprim/sulfamethoxazole 160/800mg DAILY

Or

(2) Norfloxacin 400mg daily

26
Q

Causes of portal hypertension (prehepatic, intrahepatic, posthepatic)?

A

Prehepatic: portal/splenic vein thrombosis, splenomegaly

Intrahepatic: schistosomiasis, PBC/PSC, sarcoid, drugs (amiodarone, MTX), amyloid, Budd-Chiari

Posthepatic: cardiac disease, constrictiver pericarditis, IVC obstruction *Budd Chiari)

27
Q

Portal hepatic pressure gradient if varices present?

A

> 12mmHg

28
Q

Primary prophylaxis for varices - management?

A

Screening endoscopy every 1-3 years (if meeting Baveno criteria, i.e. do not need if platelets >150 AND fibroscan <20kPa)

NSBB or carvedilol
Endoscopic variceal ligation (if cannot tolerate BB)

Need to band until eradication is received

If large varix, some studies suggest EVL better than BB

28
Q

Primary prophylaxis for varices - management?

A

Screening endoscopy every 1-3 years
NSBB or carvedilol
Endoscopic variceal ligation (if cannot tolerate BB)

Need to band until eradication is received

If large varix, some studies suggest EVL better than BB

29
Q

Secondary prophylaxis for varices - management?

A

EVL + NSBB

30
Q

Management of varices

A
  1. Resuscitation
  2. Antibiotic prophyalxis - IV ceftriaxone
  3. Octreotide/terlipressin
  4. Avoid over transfusion, aim Hb >70
  5. Consider TIPPS if appropriate
  6. Endoscopy
    - Variceal ligation/banding
    - Sclerotherapy
    - Ballon tamponade - SB tube
31
Q

Timing of screening/surveillance endoscopies for varices

A

Compensated cirrhosis + no varices: every 2-3 years

Compensated cirrhosis + small varices: every 1-2 years

Decompensated cirrhosis: anually

32
Q

C/I for terlipressin

A

Diagnosed/suspected IHD

33
Q

Management of HRS

A

Terlipressin + albumin

34
Q

PSC association with IBD?

A

90% of patients with PSC have UC
Only 5% of patients with UC have PSC

35
Q

Definition of hyperacute, acute and subacute fulminant hepatic failure?

A

Hyperacute < 7 days
Acute 7-21 days
Subacute >21 days and <26 weels

35
Q

Definition of hyperacute, acute and subacute fulminant hepatic failure?

A

Hyperacute < 7 days
Acute 7-21 days
Subacute >21 days and <26 weels

36
Q

Components of Kings College Criteria?

A

pH <7.30
INR >6.5 (PT >100s)
Serum Cr >300
Grade III/IV encephalopathy

37
Q

Management of Hep A exposure

A

Post exposure prophylaxis with single dose of vaccine within 2 weeks in healthy persons 1-40

Vaccine + IgG in <1 and >40, immunocompromised or if liver disease

38
Q

What are the 4 phases of chronic HBV?

A

Immune tolerance: high HBV DNA, normal LFTs, HbsAg positive

Immune clearance: high HBV DNA, abnormal LFTs, HbeAg positive - should be referred for consideration of treatment

Immune control: low HBV DNA, normal LFTs, HBeAg negative, anti-HBe positive

Immune escape: high HBV DNA, abnormal LFTs, HbeAg negative, anti-HBe positive - should be referred for consideration of treatment

39
Q

Extrahepatic manifestations of Chronic Hep B?

A

Polyarteritis nodosa
Glomerular disease
Serum sickness

40
Q

When do you start treatment for HBV?

A

HBV + cirrhotic
Immune active chronic HBV
HBV DNA >2000 + ALT 2x ULN if HBeAg neg
HBV DNA >20000 + ALT 2x ULN if HBeAg pos

41
Q

What Hep B medication can you use in pregnancy?

A

Tenefovir

Entecavir is teratogenic

42
Q

Extrahepatic manifestations of HCV?

A

Lichen planus
Essential mixed cryoglobulinaemia
Porphyria Cutaneous Tarda

43
Q

Treatment of Hep C in treatment naive, non-cirrhotics/cirrhotics? Genotype not known.

A

Maviret or Epclusa.

Maviret: glecaprevir + pibrentavir
Epclusa: sofosbuvir + velpatasvir

44
Q

Scoring systems for alcoholic hepatitis

A

Maddrey’s score: if ≥32, consider steroids
Lille score on day 7

45
Q

Most common variants in hereditary haemochromatosis?

A

Homozygosity for C282Y variant in HFE gene
Homozygosity in H63D

Both are substitution mutations

46
Q

What is the number one cause of death in individuals with non alcoholic steatohepatitis (NASH)?

A

Cardiovascular disease

47
Q

What is Peutz-Jeghers syndrome?

A

Hamartomas in GI tract

48
Q

Ulcerative colitis - histology features?

A

Crypt abscesses/branching
Crypt atrophy
Mucin depletion
Paneth cell metaplasia

FRACP Written Exam 2023 (20 decks)

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