Digestive System
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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.

Alcohol intake is a strong and well-established risk factor for esophageal squamous cell carcinoma (SCC), but the association with esophageal adenocarcinoma  or adjacent tumors of the esophagogastric junction (EGJA), is not clear.

There is evidence of dietary factors being protective against both adenocarcinoma and squamous cell.  This seems to have a protective effect in both, and probably reduces obesity which is a known  risk factor for adenocarcinoma

Chronic GERD can lead to Barrett´s oesophagus which is a factor for adenocarcinoma, but not for SCC.

High compsumption of hot beverages have been linked to SCC, not adenoca.

Interestingly, Mate te (very common in Argentina) seems to have a increased risk for SCC.

Even in 2019, 38.9% of the HCC- liver transplant  had Hepatitis C etiology (vs 24% NASH and 16.3% ALD) . This is completely different in patients without HCC (the majority of liver transplant candidates, which only 7% had hepatitis C , 28% NASH and the leading cause with 37.7 %  was ALD.  https://doi.org/10.1016/j.cgh.2020.05.0

Misty mesentery refers to a non-specific radiological finding characterized by increased attenuation within the mesenteric fat on computed tomography  imaging.  It mimics mistiness as localised fat stranding in the mesentery.  Many processes can lead to the appearance including infiltration by inflammatory cells, oedema, lymphatic accumulation, haemorrhage, tumour infiltration, and fibrosis.  Tipically reflects mesentery panniculitis  ( rare  benign condition characterized by chronic inflammation  of adipose tissue mainly of the small bowel mesentery) But can be the results of any inflammatory or neoplasic process. That is why it is needed to consider also vasculitis, lymphomas, inflammatory process or GI neoplasia.

Check the guidelines

Delirium tremens is a form of severe withdrawal syndrome in which, long term alcohol has chronically bound to GABA receptors and modified its expression( GABA is the inhibitory neurotransmitter which normally reduces neuronal excitability) . This leads to  GABA downregulation of α1- and α3-containing GABA-A receptors (Liang and Olsen, 2014). GABAA receptor downregulation may contribute to anxiety and shakes of withdrawal once alcohol is not present in the nervous system. Also, chronic hyperestimulation of the GABA system by alcohol leads to brain mechanism of up-regulation of the postsynaptic N-methyl-D-aspartate (NMDA) type of glutamate receptor, which mediates the postsynaptic excitatory effects of glutamate to counteract this inhibitory effect of GABA, and once alcohol is suppressed this excitatory system takes over causing autonomic hyperactivity, tachicardia, cardiovascular collapse, seizures or even comma and death.