Gastroenterology Flashcards
Alpha 1 antitrypsin deficiency causes liver damage by what mechansism?
Accumulation of unsecreted intracellular mutant AAT proteins leading to hepatocyte death.
What is the most likely type of glomerulonephritis to occur in patients with cirrhosis from any cause?
IgA nephropathy. This is likely due to the reduced clearance of IgA immune complexes by Kupffer cells in the liver.
What are the main recognised risk factors for gord?
Obesity, alcohol, hiatus hernia, smoking, drugs (e.g. bisphosphonates)
What other diseases are associated with GORD?
High acid production - Zollinger Ellison syndrome. Poor acid clearance- scleroderma, other connective tissue disease, gastroparesis.
Is helicobacter pylori associated with GORD?
No
What conservative management strategy for GORD is most effective?
Avoiding food at least 2hrs before sleep
What’s the incidence of Barrets amongst pts with chronic GORD?
10-15%
Which factors influence risk of progression to malignancy in Barrets oesophagus?
Segment length (>3cm worse), dysplasia grade (nil vs low grade vs high grade).
What treatment options are available for low (recetly treating more aggressively) and high grade dysplasia in Barrets oesophagus?
Endoscopic mucosa resection (effective for shallow disease), endoscopic mucosa dissection (for submucosal invasion). Surgery. If none of the above can be tolerated due to anaesthetic risk associated with longer procedure length, radiofrequency ablation can be performed quickly.
What is the first line treatment for eosinophilic oesophagitis?
PPIs. Then topical dispersible budesonide. Elimination diets sometimes work, but in adults the cause is often a swallowed aerosol (cf in kids where it is usually a dietary cause). Oral steroids or steroid agents can be used if topical steroids don’t work. Dupilmumab (targegs IL-4 and IL-13) is highly effective, but is only PBS funded for eczema (atypical dermatitis) at present, but can be paid for for off label use.
What is the demographic of pts with eosinophillic oesophagitis?
Young men with previous allergies.
Achalasia can be managed by a per oral endoscopic myotomy (POEM)- what pt demographic is this important for and what medication is required to start with it?
Young people. Is a long procedure, so need to have limited comorbidities to make it work from anaesthetic risk pov. Provides 80-90% cure with low complication rate. Can be associated with reflux after- treated with 8 weeks of PPI following procedure. Require a scope at 5 years to evaluate oesophagus.
Achalasia can be managed with pneumatic dilatation of the lower oesophageal sphincter (LOS). Who is this procedure good for and why?
Older patients who can still tolerate an endoscopy. The procedure is inflating a balloon in the LOS until the LOS ruptures. It’s quick, 80-90% curative, however it does carry a 3% perforation rate. Much faster than POEM, thus better for more comorbid pts.
How should you manage achalasia in patients who will only tolerate a brief endoscopy?
Botox injections to the lower oesophageal sphincter - provide 60-70% response, but need re-doing every 6 months. Pharmacotherapy can be used if endoscopy is contraindicated - nitrates and peripheral calcium channel blockers.
What percentage of cirrhosis patients will develop varicies?
50-60%
What percentage of cirrhosis patients diagnoses with varicies will bleed within 2 years of diagnosis?
30%
How much blood do you need to produce from the upper GI tract to produce malena?
150mls. Frank blood follow through from the upper GI tract suggests >500mls of blood loss.
What is the mortality risk associated with a first variceal bleed?
> 30%
In patients with oesophageal varicies, what treatment options are available to reduce the risk of having a first bleed?
Managing underlying portal hypertension with non-cardioselective beta blockade - carvedilol > propanolol - cam decrease risk by 50%. Target HR reduction of 25%.
Endoscopic banding of large varices may have additional benefit.
What are the interventions known to provide a mortality benefit in patients suspected of having an upper GI variceal bleed?
IV antibiotics (greatest impact on mortality, up to 50% reduction), terlipressin, octreotide, early endoscopy and banding.
What treatment options are available for variceal bleeding that is unable to be controlled initially with endoscopic banding?
Sengstaken-Blakemore or Linton tube - NGT that inflates in the lower third of the oesophagus to form a tamponade- can only be left in place for 12-24hrs. Danis stent - endoscopically inserted stent that tamponades the oesophagus- can be left for 7 days. Transjugular intrahepatic porto-systemic shunt (TIPSS) - rapidly addresses portal hypertension- carries risk of hepatic encephalopathy, especially in elderly pts and/or those with child’s B/C cirrhosis. Also can’t be done until bleeding tamponaded by one of the above methods.
After a variceal bleed is controlled, what options are available for secondary bleeding prophylaxis?
Beta blockers + band ligation is provided to all patients. In select patients, a transjugular intrahepatic porto-systemic shunt can be used. However a TIPSS procedure is usually a bridge procedure to get the patient to the most effective treatment- a liver transplant.
Is alcohol associated with an increased risk of peptic ulcer disease?
No. H. Pylori, smoking, NSAIDs and aspirin are.
Which drug is most greatly associated with peptic ulcer disease?
Aspirin. An alternative if pts are getting peptic ulcer disease might by clopidogrel for their cardiovascular disease.
What’s the first line treatment for H. Pylori treatment in Australia?
HP7- esomeprazole, amoxicillin and clarithromycin for 7 days- about 85% effective. For patients with a penicillin allergy, substitute amoxicillin with metronidazole. Most likely drug that h. Pylori will be resistant to in this regimen is clarithromycin (around 10%), and 30% for metronidazole. Rescue options are available that involve levofloxacin, bismuth, rifabutin, doxyxyline, or taking a specimen and assessing sens.
What’s the treatment for h pylori negative peptic ulcer disease?
PPI BD for 2 weeks, then daily for 8 weeks followed by repeat gastroscopy- must make sure ulcer was not actually malignancy!
What treatment is used to manage a bleeding gastric ulcer after it is visualised endoscopically?
Clipping, adrenaline injection and heater probe coagulation on combination has the best outcome under endoscopic guidance. This should be accompanied by high dose IV PPI infusion for atbleast 72hrs.
What are the antibodies tested for coeliac disease?
Antigliadin (least sensitive and specific), antitransglutaminase - very sensitive and specific, antireticulin - very sensitive and specific, antiendomysial, specific and sensitive. Remember that IgA and IgG antibodies should be tested due to the ~5% prevalence of IgA deficiency in patients with ceoliac disease.
What HLA haplotypes are associated with coeliac disease?
HLA-DQ2 and DQ8. Almost always positive in pts with coeliac disease, but positive in many other people without the disease. Good negative predictive value. Remember that small bowel biopsy is necessary for diagnosis.
What are the other diseases associated with coeliac disease?
Autoimmune thyroiditis, alopecia, atrophic gastritis, reduced fertility and miscarriage, osteoporosis, autoimmune hepatitis, primary biliary sclerosis, IgA deficiency, Down Syndrome, type 1 diabetes, cardiomyopathy, dermatitis herpetiformis.
What disease is dermatitis herpetiformis associated with?
Coeliac disease
If a patient with coeliac disease presents with symptom recurrence despite strict adherence to a gluten free diet, what should you be worried about?
Small bowel non-Hodgkin’s lymphoma. Peak incidence 6th decade of life. Less often, small bowel adenocarcinoma.
How do you manage refractory coeliac disease?
Two types:
Type 1: has the usual population of intraepithelial t cells on biopsy of the small bowel. These pts usually respond to steroids of steroid sparing agents.
Type 2: clonal immature lymphocyte population in small bowel biopsy. Do poorly. May need some haematological treatment.
What’s the most effective method for reducing post ercp pancreatitis?
Indomethacin suppository
IgG4 disease- how is it detected?
Usually a mass seen, concerning for malignancy. Then someone thinks of IgG4 disease and does a IgG subclass test on the pts plasma, and it’s elevated in 70% of pts with IgG4 deposition disease. The ‘tumour’ is then hopefully biopsied and found on histopathology to have IgG4 throughout.
How do you manage IgG4 disease?
Steroids. If it recurs, consider traditional steroid sparing agents (MMF or AZA) for longer term immunosuppresion. If ongoing recurrence, rituxumab.
In patients with hepatitis C, what factors are associated with an increased risk of developing liver fibrosis?
Diabetes, obesity, MAFLD, alcohol, younger age at infection, HCV genotype 3, HIV co-infection, post menopausal women, host genetic factors
What is the APRI score?
AST to Platlet Ratio Index (APRI). A score that can be used to exclude fibrosis in patients with hepatitis c. Less than 1.0 is considered to exclude fibrosis.
In liver elastography, what mean liver stiffness (MLS) is considered abnormal?
> 12.5kPa
What non-hepatic complications are associated with hepatitis C infection?
Mixed cryoglobulinaemia, CKD, porphyria cutanea tarda (blistering skin on sun exposure), diabetes mellitus, non-hodgkin lymphoma, lichen planus, sjogrens, inflammatory arthritis, depression.
For the purpose of hepatitis c treatment, what are protease inhibitors? What’s important to know when prescribing them?
Inhibit the NS3/NS4A viral protein protease- critical to viral protein production. They are contraindicated in decompensated liver failure.
How is hepatitis B typically transmitted in low endemicity countries?
Parenteral, percutaneously or sexualising.
Which hepatitis B genotypes
is associated with the greatest risk of cirrhosisand HCC?
Genotype C.
B is associated with slower progression and lower rates of HCC. A and D sit somewhere in between B and C. F is associated with fulminant liver failure, but is very rare.
What is the HBeAg, and why is it helpful?
It’s a protein secreted by actively replicating hepatitis B virus- correlates with higher Hep B DNA plasma levels. Some patients with Hep B E Ag clearance may still have high levels of viral DNA due to having variant with a mutation in the promoter region for the E antigen. Cf Hep B core ab which simply suggests prior infection that may have been completely cleared. Pts with HBeAg positivity and viral DNA >20k should be treated with antiviral medication. Pts without HBeAg with DNA>2k should be treated with antivirals.
What serology and LFT profile would a pt with chronic hepatitis B have in immune active and inactive phases?
HBsAg positive for >6 months is required to diagnose hep b. Hep B core ab will also be positive. If so, Hep B e Ag, positivity with DNA > 1 million and normal ALT is the immune tolerance phase and doesnt eequire treatment. Hep B e Ag positivity with DNA > 20000 and raised ALT equates to immune active phase requiring treatment. If Hep B e Ag negative with DNA > 2000 with anti-hep B e ag ab and raise ALT, this also equates to immune active phase and requires treatment. If Hep B e Ag negative, Hep B e Ag antibody positive, DNA <2000, and ALT negative, this is inactive chronic Hep B and doesn’t require treatment.
In hepatitis B chronic infection, what increases risk of progression to cirrhosisand HCC?
HBeAg negative with DNA +ve , high DNA, genotype C, HIV, Hep C, Hep D, male, older age, recurrent flares, high ALT, diabetes, history of HCC, heavy alcohol intake, smoking, exposure to aflatoxins (mould toxins).
