Gastroenterology Flashcards
What is the triad of Budd-Chiari syndrome?
Ascites, abdominal pain, and hepatomegaly
Key features in Wernicke’s encephalopathy?
Triad
1. Ataxia
2. Ocuomotor dysfunction
i. Nystagmus
ii. Opthalmoplegia
3. Encephalopathy
i. Confusion, disorientation, inattentiveness
(Also sensory neuropathy)
Korsakoff syndrome
- Antero- and retrograde amnesia with confabulation
Positive anti-mitochondrial antibodies (AMA), raised IgM, and cholestatic LFTs (esp. raised ALP) suggests what diagnoses? And what treatment delays progression?
Primary biliary cholangitis
- Ursodeoxycholic acid
Middle aged, itchy lady with autoimmune condition (Sjogren, CREST, RA etc.)
Increased cholesterol but nil IHD due to increased HDL
Imaging: ultrasound or magnetic resonance cholangiopancreatography to exclude extrahepatic obstruction
What gene is associated with higher rates of NASH, and which ethnic group is implicated?
rs738409 in PNPLA3
- in Hispanic groups
What are key SE of long term PPI?
• Hyponatraemia,hypomagnasaemia
• Osteoporosis → increased risk of fractures
• Microscopic colitis
• Increased risk ofC. difficileinfections
What scoring system is used to alcoholic hepatitis, and what is the cut off for administration of prednisolone?
Maddrey’s Discriminant Function
- Score >/= 32
What are endoscopy findings which are high risk of bleeding?
• Actively bleeding peptic ulcers
• Ulcers with nonbleeding visible vessels
• Ulcers with adherent clots
Which dermatological condition is associated with coeliac disease, and what is its treatment?
Dermatitis herpetiformis
- Treatment with dapsone
Which HLA markers are associated with coeliac disease?
HLA-DQ2 and HLA-DQ8
Which autoimmune conditions are associated with coeliac disease?
What are the SEROLOGICAL screening tests for coeliac disease?
What are the most common causes of portal HTN in
a) Western world
b) Africa
Cirrhosis and schistosomiasis respectively
What is antimicrobial treatment for life-threatening toxic megacolon?
ORAL vancomycin and IV metronidazole
What are factors that may indicate severe pancreatitis?
Factors:
• Age > 55 years
• Hypocalcaemia
• Hyperglycaemia
• Hypoxia
• Neutrophilia
• Elevated LDH and AST
Only thing low are the UMMs (calcium, oxygumm)
What are the genetics of Wilson’s disease? What is the treatment
Autosomal recessive - characterised by excessive copper deposition in the tissues
- Defect in theATP7Bgene located onchromosome 13
Treatment: penicillamine, chelates copper
What is the most common site affected in ischaemic colitis, and what is seen on AXR
The splenic flexure with ‘thumbprinting’ on AXR due to mucosal oedema/haemorrhage
Watershed area (minimal collateral supply)
What is the genetic inheritance of HNPCC/Lynch syndrome?
Autosomal dominant
What causes defective bilirubin conjugation in Gilbert’s syndrome?
Deficiency of UDP glucuronosyltransferase (UGT1A1)
Classic histological finding in hepatocytes in patients with alcoholism?
Mallory bodies
What are implications of TPMT gene when treating IBD?
Genetic variants alter drug metabolism
- Low enzyme activity = risk of toxicity due to slow metabolism
Treatment of CMV colitis?
Ganciclovir
- Tx valganciclovir in renal transplant
Dysphagia with solids alone suggests which of the following?
- Mechanical obstruction, or
- Motility disorder?
Mechanical
- Benign or malignant
- Masses, strictures, eosophageal ring e.g. Schatzki ring, webs, hiatus hernia
Causes of strictures
- Chronic reflux oesophagitis
- Eosinophilic oesophagitis
- Radiation
- Caustic injury
Dysphagia that progresses from occuring only with solids to both solids and liquids is concerning for what?
Most importantly - malignancy
- DDx: benign stricture that has become high grade obstruction
Where are Schatzki rings located?
A Schatzki ring is a circular membrane of mucosa and submucosa that forms at the squamocolumnar junction of the distal esophagus
- Do not contain any muscularis propria
- Always associated with hiatal hernias
Does achalasia present as dysphagia to liquids or solids first?
70-97% will have both upon initial presentation
Classic achalasia
- Hypertonic lower oesophageal sphincter + aperistalsis
Longstanding achalasia associated with SCC
Goblet cells make what?
Mucous
- Goblets are gross and make mucous
Chief cells secrete what?
Pepsinogen
- Pepsi is king
- Pepsinogen is the inactive form of pepsin, which digests protein into polypeptides
Parietal cells secrete what?
- Gastric acid e.g. HCl
- Keep it PG, Ga
- Primary cell - Intrinsic factor - required for B12 absorption in terminal ileum
D cells secrete what?
Somatostatin; inhibits acid secretion
- Don’t Secrete
Suppresses gastrin
G cells (a neuroendocrine cell) secrete what?
Gastrin; stimulates acid secretion
- Good to go on a acid trip on the gasTRaIN
MOA
- Stimulates parietal cells directly, and
- Stimulates ECL cells to release histamine > works on parietal cells
In Barrett oesophagus, which cells are replaced with what?
Squamous epithelial cells as replaced with metaplastic columnar epithelium
- Precursor to oesophageal Ca
- EtOH itself is not a RF for Barrett (although EtOH is a RF for sqamous cell carcinoma)
What are the 2 types of oesophageal cancer, and which is most common?
Squamous cell and adenocarcinoma
- SCC is ~90% and found in PROXIMAL oesophagus; assoc. EtOH
- Adenocarcinoma usually found in DISTAL oesophagus; assoc. with GORD or Barrett’s
Most common causes of PUD?
NSAIDS and H. pylori
First line regime for H. pylori eradication in Australia?
ACE
- Amoxicillin 1 g orally, twice daily for 7 to 14 days
- Clarithromycin 500 mg orally, twice daily for 7 to 14 days
- Esomeprazole 20 mg orally, twice daily for 7 to 14 days
If allergic to penicillin, use metronidazole
What are standard follow up post H. pylori eradication treatment?
C13- or C14-urea breath test
- Antibiotic therapy and bismuth should not be taken for at least 4 weeks
- PPI therapy should be withheld for at least 1 week (and preferably 2 weeks)
OK to have H2-receptor antagonists (ranitidine, famotidine etc.)
What is second line H. pylori eradication?
- PPI BD for 10/7
- Amoxicillin 1 g BD 10/7
- Levofloxacin BD OR moxifloxacin BD for 10/7
NB: secondary Helicobacter pylori resistance to clarithromycin is common after failure of first-line therapy
What is MOA of azathioprine? Which metabolite causes immunosuppression?
Azathioprineinhibits purine synthesis (purines are needed to produce DNA and RNA)
- Inhibit purine synthesis > less DNA and RNA are produced for synthesis of WBC > immunosuppression
6TGN
Which type of hepatorenal syndrome has the best prognosis?
Type 2
Anti-smooth muscle Ab is suggestive of which condition?
Autoimmune hepatitis
What MHC gene promotes spontaneous HCV clearance?
MHC IL28B
Other factors: young, female
Which skin condition is associated with hepatitis C?
Porphyria cutanea tarda
- blistering disease on sun-exposed skin esp. hands
What is a normal FibroScan result?
<7 kPA
How and when do you check for cure of HCV post treatment?
Negative HCV RNA 12 weeks post completion of treatment
Sustained virological response = cure