Gastroenterology Flashcards
Rash with coeliac disease
Dermatitis herpetiformis
Mx: gluten free diet, steroids
Erythema nodosum - association with IBD?
Crohn’s > UC
Raised, tender, extensor surfaces
Pyoderma gangrenosum - association with IBD?
UC
Does not correlate with disease activity
5 classic endoscopic features of eosinophilic oesophagitis
Oedema
Longitudinal furrows
Concentric rings
White exudates
Strictures & mucosal tearing
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)
What type of cancer does achalasia increase your risk of?
10x increased risk of SCC
Risk factors for Barrett’s oesophagus
Male
Caucasian
Age
High BMI
Chronic heartburn
Smoking
Positive family history
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)
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
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
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
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
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
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
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
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
At what INR is it safe to scope with bleed?
Safe to scope when INR ≤2.5
Don’t delay to prevent coagulopathy
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)
What electrolyte derangement is associated with hepatic encephalopathy?
Hypokalaemia
Hypokalaemia increases renal ammonia production
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
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
- Resuscitation
- Antibiotic prophyalxis - IV ceftriaxone
- Octreotide/terlipressin
- Avoid over transfusion, aim Hb >70
- Consider TIPPS if appropriate
- 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
