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.

It has always been agreed that High grade dysplasia should merit ablation, however clasically LGD would be offered endoscopic surveillance until progressed to HGD. This approach has changed over the last years to the point that Both ESGE and AGA suggest eradication with ablation to prevent progression to HGD/cancer. BSG recommends repeating endoscopy in 6 months and if confirmed again, offering eradication vs 6 -monthly surveillance.  The AGA 2024 guidelines favous ablation over surveillance.

All societies agree that he biopsies should be reviewed by an expert pathologist (ESGE suggest 2 experts) before embarking into eradication.  Remember that the incidence of progression (to HGD or adenoca) is estimated around   9.1%/year  with reported incidence of adenocarcinoma of 0.54% per year. The overall yearly incidence of Eosphageal adenocarcinoma is 0.3% (0.19 in short segment )

-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

If someone has IgA deficiency and celiac disease, the IgA deficiency can cause a false negative on a celiac disease antibody test.  (As IgA anti transglutaminase antibodies may be falsely normal) In this case it is important to perform IgG-specific antibody tests for endomysium, gliadin, and tissue transglutaminase

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

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.

The proportion of AST to ALT in hepatocytes is about 2.5:1, but because AST is removed from serum by the liver sinusoidal cells twice as quickly (serum half-life t1/2 = 18 hr) compared to ALT (t1/2 = 36 hr), so the resulting serum levels of AST and ALT are about equal in healthy individuals, resulting in a normal AST/ALT ratio around 1. See here.

B6 is more essencial for ALT synthesis than AST, that is why in chronic alcohol (low B6) we will see a reduction of ALT in proportion to AST, increasing the AST/ALT ratio>2

Check the ESGE  guidelines

The AGA guidelines recommend random biopsies of the cardia and distal 2 cm of the tubular esophagus.

In general, EMR recurrence  (presence of residual polypoid tissue at the level of the scar in control colonoscopy) is described as high as 20-30%.    Currently it is recommended to treat the margins of the scar immediately after polyp resection to reduce this rate.  Treating with APC or soft snare coagulation (this latter is preferred in the ESGE guidelines) help significantly reduce the recurrence

See Bourkes group RCT

See metanalisis

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)