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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

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)

Solid pseudopapillary neoplasm account for around 5% of pancreatic neoplasm. They are almost exclusively found in females (f:m ratio 10:1) and usually appear in their 20s.  CT and EUS can show well-encapsulated mass with varying solid and cystic components, caused by hemorrhagic degeneration. Peripheral calcification may occur.  They appearance can vary from solid to purely cystic- therefore even a small cystic lesion in a young female without previous pancreatitis episodes must make us consider this diagnosis

These lesion have a potential for malignant degeneration (Around 15%) therefore surgical removal is recommended . Cytology can show cluster  or sheets of papillary cells, PAS + and Vimentin.

• CLINICAL CASE AND Image: Dr Hajar Adil
• Source: Endosonography, 5th Edition by Shyam Varadarajulu, MD, Paul Fockens, MD, PhD and Robert H. Hawes, MD.
• Learning point brought by Dr Sarto Paquin

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

- Gastric lesions. Even though ESGE guidelines do not specifically mention EUS in the flowchart staging, the reality is that EUS can clarify lymph nodes and the layer invasion, so realistically can be  useful for all the answers mentioned.

Smoking and obesity are probably the most important modifiable risk factors for panc cancer (Smoking 74% higher risk, whereas every 5 points of increased BMI  increases risk in 10% )

Diabetes is an independent factor associated with higer risk of pancreatic cancer.

Alcohol is known to increase the risk although there is different evidence in regards of the association (It is known to be dose dependant, plus also alcohol can increase the risk of adquired chronic pancreatitis, which in itself increases the overal risk of cancer in about 4%)

The evidence of Hpylori is controversia, it was described in this review however further evidence fails to suppor this. It is thought to be  through secondary mucosal inflammation and immune evasion rather than Hpylori per se.

However it is known that there is an association with ABO blood groups in several large epidemiological studies. Non 0 blood types have a higher risk of developing pancreatic cancer compared to A/B/AB

In this article they summarised the current evidence.

According to the Haraldsson  classification, Type 2 and 3 are usually the most difficult- Type 3 is normally quite challenging as papilla is  protruding or bulging into the duodenal lumen or sometimes hanging down, pendulous , mobile and with the orifice oriented caudally. This papilla asociates a higher risk of failure OR 7.4 compared to type 1, followed closely by type 2 which is flat and small and associates also more risk of pancreatitis.
See image and data from retrospective database

In grade C-D reflux oesophagitis we should initiate PPI longlife (or increase the dose if patient already taking) and repeat endoscopy in 6-8 weeks to confirm healing and rule out underlying Barrett's (British recommend 6 weeks, american recommend 8weeks)

Biopsies, however, are controversial. ASGE  recommends bx  of irregular or deep oesophageal ulcerations or nodularity. ESGE does not mention them, whereas BSG recommends taking samples of any oesophageal ulcer or severe grade D oesophagitis.

Is the opinion of the author that any suspicious ulcer (despite of the grade of esophagitis) should be biopsied in the moment, whereas in  typical grade D oesophagitis biopsies might have a low diagnostic yield, atypia is difficult to assess due acute inflammation, and samples will be best targeted after improvement of the inflammation.

-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