Digestive System
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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)

Scores of 8-14 represent Hazardous or Harmful range. In those cases, the recommendation is to explain to the patient that they may be drinking too much on occasions, and the likely negative impact the alcohol can cause as it is carcinogenic, can help developing cardiovascular disease, can cause dependence and can put you or others at risk.

Any  score of 15 or above associates high risk (drinking could cause harm and it is important a clear determination to cut down or stop alcohol). Any score of 20 or above indicates likely dependence and needs referral to specialist and supervised detoxification

Based on this study by O Sullivan et al where 2451 LNPCPs (Large non pedunculated colonic polyps)  were analyzed after resection and found and average of 10% had submucosal invasive cancer (SMIC).  Previously, overall described SMIC had been reported around 7.6%–8.5% of endoscopically resected LNPCPs.   The higher risk were the depressed polyps ( 60%) followed by non granular (20%) or granular in rectosigmoid (20%)

We need to differenciate between non dysplastic (the majority of Barrett's do not have any dysplasia, just metaplasia) versus dysplastic changes (proliferative changes that is characterized by a loss in the uniformity of individual cells in a tissue and loss in the architectural orientation )

The overall yearly incidence of  eosphageal adenocarcinoma in non dysplasitc  is 0.3% (. This is approximate and based on a metanalysis, although we know that factors such a age, smoking or obesity increase the overall risk of adenocarcinoma in Barrett's patients, and equally, the risk lowers when short segment (<3cm) - down to 0.19 % per year)

9.1% is the overall incidence of progression (to either HGD or adenoca) in those who already present low grade dysplasia, up to   9.1% per patient/year  with pooled annual incidence of adenocarcinoma of 0.54% per year

The majority of pancreatic cancers are due to spontaneous mutations in a complex combination of usually several mutations ((KRAS) mutations are common in 90% of pancreatic cancers, but in combination with different other mutations, DNA damage and usually other risk factors.

There is however a very important percentage (5%-10%) of new PC which associate familial pancreatic cancer (Defined by two first-degree-relatives with pancreatic cancer), There are indeed genes involved such as BRCA2 gene  mutations  ( 3.5-fold increased risk of pancreatic cancer ).  Other inherited mutations in the STK11 gene cause the Peutz-Jeghers syndrome, and individuals with Peutz-Jeghers have a 130-fold increased risk of pancreatic cancer

To put in context,

One degree relative with PC  makes relative having an 80% increased risk of developing pancreatic adenocarcinoma (this is RR: 1.8)

individuals with 2 degree relatives with PC have a nine fold risk , and this rises to thirty-two times greater risk if three or more first degree relatives have been previously diagnosed

Mucosal xantoma - benign lesion composed of foamy macrophages within the lamina propria. fibrovascular. They presents as discrete single to multiple yellowish-white patches, most commonly in the antrum or pyloric region of the stomach . Endoscopically it sometimes can resemble candidiasis, polyp, lymphangiectasia, Russell body gastritis, and Pseudoxanthoma elastic or gastric malignancy.

Lymphangiectasia would have showed prominent dilated lymphatics in the lamina propria region of the villous structure, often with extension into submucosa . These are more commonly seen in duodenum or terminal ileum

This image  impedance pH study showing a proximal then distal increase in impedance with air clearing from the esophagus orally. Arrows indicate direction of air flow down and then up. This is supragastric Belching. (B) High-resolution manometry showing repetitive supragastic belching with upper esophageal sphincter opening then air propagating through the esophagus, contraction of diaphragm with aborad (away from the mouth) movement of lower esophageal sphincter.   The treatment for this is behavioural therapy and adding central neuromodulators in cases of linked psychological disorders

Calcium channel inhibitors and other antispasmodic therapy has been used for spastic disorders such as diffuse oesophageal spasm and nutcracker (hypercontractile) oesophagus.

POEM and Hellers myotomy are well known treatments for Achalasia.

EGJOO(Esophagogastric junction outflow obstruction )  can respond well to balloon dilation or botox (63-70%, although POEM is not commonly used it has been described very effective)

Andexanet is factor Xa inhibitor which is approved to reverse Rivaroxaban and Apixaban. However, it has not being proved to be efficacious against Edoxaban. Dabigatran is  a direct thrombin (factor IIa) inhibitor, not a Xa inhibitor.

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