Gastroenterology Flashcards by Abigail Sim

Rash with coeliac disease

Dermatitis herpetiformis
Mx: gluten free diet, steroids

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Erythema nodosum - association with IBD?

Crohn’s > UC
Raised, tender, extensor surfaces

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Pyoderma gangrenosum - association with IBD?

UC
Does not correlate with disease activity

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5 classic endoscopic features of eosinophilic oesophagitis

Oedema
Longitudinal furrows
Concentric rings
White exudates
Strictures & mucosal tearing

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Current therapies for eosinophilic oesophagitis (EoE)

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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What type of cancer does achalasia increase your risk of?

10x increased risk of SCC

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Risk factors for Barrett’s oesophagus

Male
Caucasian
Age
High BMI
Chronic heartburn
Smoking
Positive family history

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Role for PPI in Barrett’s oesophagus

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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Role of aspirin + PPI in Barrett’s oesophagus

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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Management of low grade dysplasia

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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Preferred treatment for oesophageal flat dysplasia/intramucosal carcinoma

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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Management for oesophageal high grade dysplasia

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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Role of surveillance post Barrett’s osophagus RFA?

Should do annual surveillance - at least for 5 years post

75% recurrences at OG junction and most are endoscopically visible

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Who should have H Pylori testing?

<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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Forrest ulcer classification

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

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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At what INR is it safe to scope with bleed?

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

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Signs of cirrhosis clinically

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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What electrolyte derangement is associated with hepatic encephalopathy?

Hypokalaemia

Hypokalaemia increases renal ammonia production

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MoA of lactulose in HE

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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Diagnostic criteria for SBP

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

SAAG interpretation

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

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

Most common bacteria isolated from SBP

E Coli (43%)
Klebsiella (11%)

SBP treatment

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

SBP prophylaxis/prevention

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

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

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)

Portal hepatic pressure gradient if varices present?

>12mmHg

Primary prophylaxis for varices - management?

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

Primary prophylaxis for varices - management?

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

Secondary prophylaxis for varices - management?

EVL + NSBB

Management of varices

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

Timing of screening/surveillance endoscopies for varices

Compensated cirrhosis + no varices: every 2-3 years Compensated cirrhosis + small varices: every 1-2 years Decompensated cirrhosis: anually

C/I for terlipressin

Diagnosed/suspected IHD

Management of HRS

Terlipressin + albumin

PSC association with IBD?

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

Definition of hyperacute, acute and subacute fulminant hepatic failure?

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

Definition of hyperacute, acute and subacute fulminant hepatic failure?

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

Components of Kings College Criteria?

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

Management of Hep A exposure

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

What are the 4 phases of chronic HBV?

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

Extrahepatic manifestations of Chronic Hep B?

Polyarteritis nodosa Glomerular disease Serum sickness

When do you start treatment for HBV?

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

What Hep B medication can you use in pregnancy?

Tenefovir Entecavir is teratogenic

Extrahepatic manifestations of HCV?

Lichen planus Essential mixed cryoglobulinaemia Porphyria Cutaneous Tarda

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

Maviret or Epclusa. Maviret: glecaprevir + pibrentavir Epclusa: sofosbuvir + velpatasvir

Scoring systems for alcoholic hepatitis

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

Most common variants in hereditary haemochromatosis?

Homozygosity for C282Y variant in HFE gene Homozygosity in H63D Both are substitution mutations

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

Cardiovascular disease

What is Peutz-Jeghers syndrome?

Hamartomas in GI tract

Ulcerative colitis - histology features?

Crypt abscesses/branching Crypt atrophy Mucin depletion Paneth cell metaplasia