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It is expected that up to 1 in 2 patients who are positive in faecal inmunochemistry test  (FIT) can have pathology (polyps or cancer) This can be seen in  results such as the QUALISCOPIA group or the UK bowel screening  report

Smoking and obesity are probably the most important modifiable risk factors for panc cancer (Smoking 74% higher risk, whereas every 5 points of increased BMI  increases risk in 10% )

Diabetes is an independent factor associated with higer risk of pancreatic cancer.

Alcohol is known to increase the risk although there is different evidence in regards of the association (It is known to be dose dependant, plus also alcohol can increase the risk of adquired chronic pancreatitis, which in itself increases the overal risk of cancer in about 4%)

The evidence of Hpylori is controversia, it was described in this review however further evidence fails to suppor this. It is thought to be  through secondary mucosal inflammation and immune evasion rather than Hpylori per se.

However it is known that there is an association with ABO blood groups in several large epidemiological studies. Non 0 blood types have a higher risk of developing pancreatic cancer compared to A/B/AB

In this article they summarised the current evidence.

The protective effect on colon cancer has been suggested in <70 yo. A meta-analysis of five RCTs showed a 24% decrease in the risk for developing CRC (HR 0.76, CI 95% 0.60–0.96). Daily low-dose aspirin also showed a 40% reduction for the risk of CRC mortality (HR 0.60, CI 95% 0.42–0.86). However, the ASPREE trial studied low-dose aspirin among >70yo without cardiovascular disease. Secondary analyses demonstrated that aspirin use was associated with a higher risk for cancer-related mortality (HR 1.31, CI 95% 1.10–1.56) and colorectal cancer-related mortality.  This significance is uncertain and we should be cautious. Check preliminary results here. DOI: 10.1056/NEJMoa1803955

The protective effect preventing HGD and adenocarcinoma in Barrett’s was seen in several studies such as Aspect trial (DOI:https://doi.org/10.1016/S0140-6736(18)31388-)

The lower cutoff for FIB 4   >1.3.  Less than 1.3 rules out advanced fibrosis, and >1.3 needs further investigations.

In elderly patients (>65 yo) this threlsholds has low especificity (many false positive patients who do not really have advanced fibrosis) therefore the cutoff proposed in those is 2 (Fib 4 <2 rules out significant fibrosis)

>2.67 is the upper threshold for advanced fibrosis. Patients scoring this have high chance of advance fibrosis and should be referred to liver clinic

Check AGA guidelines and ESGE, BSG  and Asia Pacific and  international consensus group

This is a Forrest III (clean based) duodenal ulcer in a healthy and stable patient. (Rebleeding risk <5% )

Patient could be discharged if stable and toleranting oral diet (AGA recommends in low risk endoscopic findings considerning discharge in stable cases with stable vitals and Hb and  no other reason for hospitalization).  PPI should be initiated orally, but given it is a low risk finding (F-III) only standard dose would be enough.  If it was a high risk such as Forrest I-IIa, then 72h of  IV PPI (Or oral high dose PPI in selected cases) is recommended as well as keeping the patient under observation.

In high risk (Forrest I-IIb) American and International guidelines advise commencing a two week course of twice daily high dose PPI,  based on a trial that showed 40 mg esomeprazole BD significantly reduced rebleeding compared  40 mg esomeprazole once daily  ( 10.8% v 28.7%,)

So the endoscopist gave good advice in general. So why is it false then? Because:

•  ESGE recommends in bleeding secondary to peptic ulceration,H pylori test at index endoscopy.   In the event of a negative result,  like this case, advise  retesting within four weeks and eradication of H pylori if positive (given the low-ish sensitivity of clotest or histology in acute bleeding, about 0.7)
• Do not forget iron replacement, either orally or if patient does not tolerate, then iron infusion to correct the anaemia.
• Smoke cessation is advised too!  Especially if Hpylori is really negative, then smoking could be a main trigger factor.

both Left main bronchus and left atrium are compressions   visualized anterior to the oesophagus. See image

In the guidelines they mention the increasing resistance of  Hpylori strains in the US to Clarithromycin (20-30%)  and Levofloxacin (approaching 40%) , therfore supporting antibiotics with much lower resistance rates (such as amoxicillin, tetracycline, and rifabutin that are all 5%)

That is why this guidelines say Clarithromycin- and levofloxacin-containing treatment regimens should be avoided in the absence of demonstrated macrolide and quinolone susceptibility, respectively.

Clarithromycin- and levofloxacincontaining treatment regimens remain an important option for selected patients, especially treatment-experienced patients with confirmed persistent H. pylori infection with strains that are known to be susceptible to these antibiotics

Vonoprazan is potassium-competitive acid blocker (PCAB) that inhibits the H⁺, K⁺-ATPase enzyme system in a potassium-competitive manner.    This is the same target as PPI but this class  of drugs  are acid-stable and thus do not require enteric coating or optimal dosing administration 30 minutes prior to meals , are more potent acid suppression, rapid onset of action, and long-lasting half-life.   Penicillin dual therapy was superior to lansoprazole-clarithromycin triple therapy among patients with clarithromycin-resistant H. pylori strains (70% vs 32%, P , 0.0001).

When treating with Vonoprazan + Amoxicillin, exceptionally we can add Clarithromycin as first line even in naive patients.

Based on the KSGE (Korean society of GI endoscopy) 2021 guidelines : Repeat EUS-guided acquisition provides a conclusive diagnosis in the majority of cases with indeterminate cytopathological diagnoses and, therefore, should be strongly recommended ahead of other modalities, such as biopsy under computed tomography-guidance or diagnostic surgical exploration.

Also common sense will tell us repeating EUS is the less invasive option and has high chances of being successful in tissue adquisition. If persisting negative/inconclusive material, MDT re-discussion should take place and possibly surgical team should speak to the patient regarding risks and benefits of  laparoscopic examination or even proceeding to pancreatectomy -the incidence of benign disease among patients undergoing pancreatic resection for suspicion of malignancy is extremely variable, ranging  from roughly 4-13% , but in some series has been reported up to 35%.

If patient had HGD / Adenoca on a Barrett´s oesophagus, then the lesion is removed or ablated and afterwards the Barretts is fully ablated, we should perform regular gastroscopies for surveillance after Barretts eradication- yearly for 5 years and then at year 7 and 10-  Check the guidelines

If the reason for the ablation was only low grade dysplasia, then the surveillance can be 1,3 and 5 years and than surveillance can be stopped.

1. True.  Around 80%  of AIH will be either ANA or ASMA+, 8% AMA+, 2% LKM+. 30% SLA+
2.  True. Less than 50% in reduction of transaminases in 4 weeks after treatment is considered Non-response. (Occurs in 17% of treated patients and assoiciates a 7-fold risk of liver related death )
3.  False. Previous guidedlines suggested this parameter, but now we consider response when complete normalisation of transmanisases and IgG.   Liver biopsy is very useful to asses histological response if Modified Ishak hepatitis activity index (mHAI) <4 /18, however histology response lags behind biochemical response by several months: in one  RCT, only 28% and 50% of patients receiving prednisolone±azathioprine achieved histological remission after 6 and 12 months, respectively. Thus, repeat biopsy to confirm remission is not recommended over the first 2 years

4.  True. Since the response criteria are more strict, there will be 20-30% who wont achieve complete biochemical remission.  These scenarios are tricky, we need to compare the overall response, patient adeherence to treatment, considering Azathioprine adeherence and metabolism:  Measuring Thioguanin nucleotides- TGN-  to see that they are in therapeutic range(>220 pmol/8×10) and  Metilmercaptoruine ( MeMP) > 5700 can confirm that the patient is taking the right dose,  Also there are specific situations in which transaminases can remain slightly abnormal due to other causes like MASLD or drug related, and IgG is commonly raised in conditions like cirrhosis.

Check BSG guidelines AIH