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ALD is the most common diagnose on referral for liver transplant in men but the second for women after MASLD.  MASLD is the most rapidly increasing indication for liver transplant worldwide.

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.

Whenever an HCC (Hepatocelullar carcinoma) is resected in an early starge, 5-year recurrence occurs in up to 60-70% of the cases,  either as a result of intrahepatic metastases (true recurrent disease) or de novo cancer in the remaining cirrhotic liver .  However, similar rates of reccurence occurs if we use ablation instead of surgical resection (  between 60% and 85% recurrence with ablation) via the same mechanisms (either incomplete tumor erradication, or new tumor formation)

5-year recurrence after liver transplant is way lower (8-20%) and of course varies depending on the tumoral burden --> potential microvascular invasion at the time of the transplant.

See BSG guidelines

For standard colonoscopies,  ASGE  and ESGE  agree that it should be an overall > 25% (for men ≥30%, for women ≥20%)

The  BSG minimum standard is slightly lower to > 15% (aspirational 20%)

Based on this metanalysis of real life Colonoscopy findings in >3.5 million patients, this percentage are pooled to real life colonoscopies

This rate is for standard colonoscopies, does not take into account FIT/FOBT  positive patients (Positive faecal blood patients in bowel screening) in which the aspirational should be at least 40-50% of adenoma or cancer detection. (See report from bowel screening in the UK)

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

See AASLD  and BSG guidelines

Difficult case. In this patient, option A is false- This is a very early stage ≤2cm (BCLC 0)

HCC requieres always an individualised treatment. Knowing that patient is fit and wihtout portal hypertension, he could be amenable for resection. However ablation has been proved to be as effective as surgery with less adverse events, so it would probably be indicated in such as small lesion as first line. The bigger the lesions, the less efficacious ablation is as can leave tumoral tissue untreated. In this case, transplant  certainly could be considered but would not be an ideal first line option as still is <2cm and Child A does not warrant the inclusion in list.

If this HCC was between 2-5cm, treatment could be trasplant (however Child A has per se no indication for transplant, being in the list with modify MELD can be tricky and has risk of tumour progression) surgical resection or ablation, based on radiological features , patient background and preferences

If multifocal HCC,  transplant is ususally the recommended 1st line therapy, whereas TACE/SIRT would be an option in non transplant candidates, unless the lesions are in the same lobe and accesible, in which case occasionally surgical resection can be offered.

If mass>7cm, this surpasses even the Expanded Milan criteria, and we know the risks of HCC invasion, recurrence and mortality after transplant are too high, therefore TACE/ SIRT/ Stereotactic resection or surgical resection are options based on patients features.

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)

The caliber of the duodenoscope is 11.3mm  (shaft) with a 13.5mm distal end outer diameter.

This can help us  estimating the size of the biliary duct and the stones. We should use a balloon no bigger than  the size of the biliary duct at level of the trapped  stone, and ideally no  bigger than the duct diameter proximal to the ampullary segment.

In this case  biliary duct is approx the same size as the shaft , perhaps slightly less(10-11mm) therefore it is reasonable to start with the size balloon of 10mm (for 30-60 secs, although this is not well stablished) and keep inflating in ranges of 1mm per minute, until the waist of the balloon (see arrow)  disappears completely on fluoroscopic examination (see added picture  of a real balloon at the right to see how it should look at the end of the procedure) . Once balloon waist is gone, sphincter is considered to be adequately dilated .

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.

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)