Digestive System
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Pancreatic cancer tends to have an ominous character, partly cause disease is a) advanced age, so even in resectable cases many patients are unfit for surgery and b) most cancers are borderline resecable, irresectable or metastatic. (80% of the pancreatic cancers are diagnosed in advanced stages)

Even in patient with surgical resection, the 5-year survival is quoted as 27%

A recent review showed that 5-year survival is 30% in Ia (T1 N0 M0- single 2cm or less panc mass)  dropping to 11.8% in Ib ( T2 N0 M0, this is single mass 2-4cm). When putting all the stages together, the 5 year survival is only 5%.

The best possible outcome would theorically be in an early cancer, 2cm or less (T1), found either incidentally (or if it gives symptoms very early), resectable (non conctacting vessels and not involving other anatomical structures, as well as surgically accesible)  and in a fit patient amenable for surgery.

GERD is a well known risk factor for adenocarcinoma of esophagus, but not for squamous cell carcinoma.

Risk factors for SCC are low socioeconomic status, consumption of tobacco, alcohol, hot beverages, and nitrosamines (e.g cured or smoked) . Additionally, micronutrient deficiencies have also been linked to the development of esophageal squamous cell cancer. These include vitamin C, vitamin E, and folate

Plummer-Vinson syndrome (PVS) is a rare condition characterized by the classic triad of dysphagia, iron-deficiency anemia, and esophageal webbing.  Approximately 10% of patient can develop SCC.

Remember Achalasia as other importart pathology in which there is an increased risk of esophageal cancer, particularly SCC

ESGE recommends offering treatment to all the patients with CBD stones (symptomatic or not) who are fit enough to undergo procedure.
This is true that we should explain always the option of intervention, and we should at least talk about risks of complication from leaving untreated biliary stones (Roughly about 25%  - biliary colic, pancreatitis, cholangitis- vs 12% if we clear the bile stones) this is  based on this  Gallrisk sweddish cohort   where they followed 3969 patients with untreated CBD stones, during follow-up ranging from 0 to 4 years. 

In summary: Explain why there is an indication to treat, which risks ERCP associates, what the alternatives may be  (ie Cholecystectomy plus surgical bile duct exploration in the same setting when approppriate) and their own risks.  And last but not least, explain the alternative of not treating and only monitoring, and the risks of this approach as well.

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.

Difficult case with patient older than 65 and comorbidities with moderately to severely active ulcerative colitis.

Vedolizumab should be indicated in his case as it performs better than anti TNFs in ulcerative colitis, confirming the results of the Varsity study.   ( Over a 5 year period, drug persistence is higher in patients treated with vedolizumab as compared to anti-TNF therapies and loss of response is less frequent again in the vedolizumab group). Age or previous TIA /AV block are not contraindications for anti-TNF (only Moderate-severe heart failure, which is not the case) So even though Adalimumab would be a valid option, it should be ideally used if Vedolizumab fails.

JAK inhibitor (Tofacitinib) should not be prescribed in people with a history of cardiovascular disease (eg. heart attack or stroke) at increased risk of cardiovascular problems (eg. current or past long-time smokers) at increased risk of cancer or aged 65 years and over unless no suitable alternative

Ozanibod could be an oral alternative , however second-degree Mobitz type II atrioventricular (AV) bloc and TIA within the previous 6 months contraindicates its use.

Off the quizz options, another good one would be Ustekinumab (interleukin 12&23 antagonist drug ) as not contraindicated here and equally valid to Vedolizumab.

According to the Haraldsson  classification, Type 2 and 3 are usually the most difficult- Type 3 is normally quite challenging as papilla is  protruding or bulging into the duodenal lumen or sometimes hanging down, pendulous , mobile and with the orifice oriented caudally. This papilla asociates a higher risk of failure OR 7.4 compared to type 1, followed closely by type 2 which is flat and small and associates also more risk of pancreatitis.
See image and data from retrospective database

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.

-Sporadic Pancreatitis: Episode of acute pancreatitis from any ethiology (Ethanol, Obstructive, drug-related..)  There is no strong identified genetic factors. Incidence is 5-12 per 100000

-Idiopathic Pancreatitis: When Acute recurrent pancreatitis (ARP)  on more than one occasion and no cause identified. SPINK1 and CFTR mutations predispose the pancreas to develop pancreatitis from other genetic or environmental factors. It has been  shown that 16%-23% of patients with apparent idiopathic pancreatitis have SPINK1 mutations, compared with only about 2% of healthy controls. Heterozygotes for CFTR mutations are generally healthy but still have a 3 to 4-fold risk over the general population for pancreatitis.

-Autoimmune pancreatitis: THis is an autoimmune condition with type 1 (lymphoplamocytic infiltrate, IgG 4 associated) and 2 segmental or focal narrowing)  As many autoimune conditions, some multi-gene mutations have been described but no specific strong association genetics proved.

-Hereditary pancreatitis :Rare entity that tends to manifest in early ages. HP is a rare cause of acute, recurrent acute, and chronic pancreatitis. Up to 80% of patients with HP have been found to have a mutation in the PRSS1 gene.  A diagnosis  requires (a) demonstration of a clear pattern of autosomal dominant inheritance in a family and/or (b) finding a known disease-causing variant in the PRSS1 gene. This presentation of disease in a family should be consistent with autosomal dominant inheritance – i.e. two or more individuals with recurrent acute or chronic pancreatitis across two or more generations of a family.   Do not confuse with familial pancreatitis, in which  families with a higher incidence of pancreatitis than expected by chance (2 or more 1st or 2nd degree relative with idiophatic pancreatitis)  but no autosomal dominant pattern or PRSS1 is found

Many chronic pancreatitis causing biliary stricture are asymptomatic or associate minimal changes in liver blood tests particularly ALP. In order to call cholestasis we have to see an increase in of usually >3 times ULN of alkaline phosphate (this is about >350-400 U/L)  As long as it does not cause significant cholestasis or cholangitis, there is no indication of biliary draining. IF they associate biliary stones , episodes of repeating infection or biliary pain (his pain seems more due to chronic pancreatitis) then it is justifed to drain the biliary tree.

Despite some increases in ALP, Conservative management with close monitoring is still adequate in this case, as well as recommend complete alcohol abstinence. If his bloods worsen or the bile dilation progresses during the next months, ERCP could be dicussed in a multidisciplinary meeting (risk of stenosis progression and cholestasis vs risk of ERCP adverse events)