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-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

Even though only 10% of hep B infections will become chronic and we have an effective vaccination that can virtually prevent infection, the reality is that hepatitis B incidence and prevalence is very high.  WHO estimates that 254 million people were living with chronic hepatitis B infection in 2022, with 1.2 million new infections each year. Maternal-to-newborn perinatal transmission of the virus can be high (70 to 90% in HBeAg-positive-indicating high viral replication-, or 10% to 30% if the mother is HBeAg-negative )

Hepatitis C , despite easy to become chronic (80% of infections) and no effective vaccine, is less common, (Estimated 50 million worldwide) partly because the vertical transmission is low and also because the new  direct-acting antiviral (DAA) tablets are highly effective at clearing the infection in more than 90% , reducing transmission.

Kudo II (asteroid or stellate pits) which are star or cross-shaped.  This is very typical of hyperplastic polyps (non neoplastic)  or serrated lesions.

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 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

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

Check the guidelines

Hb needs to be kept 7-8g/dl at least,  and a target of >9-10g/dl  if significant cardiovascular disease.  Andenaxet is recommended if life threatening or uncontrolled bleeding, like this case which is responding only partially to resucitation with fluids and continues to pass blood, so it could be prescribed.  If not available, 4-F PCC can be used instead.  Urgent sigmoidoscopy in general has no role and it would likely be useless without an adequate bowel preparation as we would expect to have very poor visibility due to stool and blood remains.

Unprepped colonoscopy or any form of sigmoidoscopy is NOT recommended in acute lower GI Bleeding unless very clear that the source is known to be anorectal or very distal colon (see American Guidelines) BSG guidelines also recommneds Colonoscopy as  inpatient with adequate bowel preparation, not urgently but  ideally after stabilising the patient.

If after resucitation and transfusion the patient remains unstable, then a joined plan with intensivist and surgical colleagues should be made (i.e, Interventional radiology, vs quick preparation with movicol, vs enema and salvage lower endoscopy, vs surgical approach)

Difficult question.  This response is based on Waterfall trial that compared moderate resucitation (1.5ml per Kg) vs aggressive (3ml per Kg) and showed no difference in worsening pancreatitis  but a tendency of fluid overload in the aggresive group (20.5% vs. 6.3%).

Ringer lactate or Hartmanns have been proved to have benefit ovver saline due to an anti-inflammatory effect which was attributed to the properties of lactate and to have a higher pH that can help counteract acidosis.

This indeed is a subject of debate. American guidelines still mentions that most patients with acute pancreatitis & hypovolaemia could have a deficit of 3-4 L to replace in 24h (Like it is our patient with vomiting and  mild hypotension and tachycardia) . If patient has no evidence of hypovolemia, an initial resuscitation rate of no more than 1.5 mL/kg of body weight per hour should be administered. However, in patients with hypovolemia, clinicians should administer a bolus of 10 mL/kg which in this case is 750ml per hour (1500ml in 2 hours)

So, the answer is  Goal-directed rehydration with Ringer’s lactate solution (or Hartmann’s).  In this case of Hypovolemia, our first step should be resucitate until volume is stable (normal BP, HR and clinical status) looking closely to avoid overfluid, and once patient is stable, keep her on 1.5ml per Kg per 24 h with clinical re-checking every few hours to ensure she is not hyper or overhydrated.

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.