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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

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.

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.

The proportion of AST to ALT in hepatocytes is about 2.5:1, but because AST is removed from serum by the liver sinusoidal cells twice as quickly (serum half-life t1/2 = 18 hr) compared to ALT (t1/2 = 36 hr), so the resulting serum levels of AST and ALT are about equal in healthy individuals, resulting in a normal AST/ALT ratio around 1. See here.

B6 is more essencial for ALT synthesis than AST, that is why in chronic alcohol (low B6) we will see a reduction of ALT in proportion to AST, increasing the AST/ALT ratio>2

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.

Underwater EMR offers the advantage of keeping the polyp surface small in flat polyps (opposite to when we inject lifting solution where the polyp keeps spreading and this makes grabbing the polyp en bloc more difficult) this explains why is a good method to remove en bloc lesions bigger than 10mm (Ideally even bigger than 20mm, although even with U-EMR the bigger the polyp, the more difficult to obtain full resected piece en bloc. This results are published in endoscopy in this meta analysis

Underwater EMR is a technique in which instead of gas, the colon is insuflated with liquid (usually water, less common saline). The water makes the mucosa 'float' by reducing the wall tension and this separates the layers of the mucosa-submucosa naturally without injecting lifting solution.  This makes flat polyps easy to get grasped. Scar appears small after resection, but when water is aspirated and air insuflatted, one can see the scars are usually much bigger than they appear with water.  See this image from Spadaccini et al 

Check the ESGE  guidelines

The AGA guidelines recommend random biopsies of the cardia and distal 2 cm of the tubular esophagus.

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

<2cm visible lesion without deep invasion: Offer EMR first and then ablation for Barretts eradication if lesion has been cured

Low grade dysplasia is a difficult diagnosis and should be always  confirmed by at second endoscopy and ideally by two pathologist (sometime LGD is actually downgraded to non displasia , or sometimes when reviewed can be upgraded to HGD)

HGD, on the contrary, does not necessarily need repeating endoscopy but always needs to be confirmed by a expert GI pathologist.  If any doubt, it is always reasonable to repeat endoscopy.

Patients with early-stage esophageal adenocarcinoma need treatment depending on many factors ( EMR, ESD, surgery or Radio-chemotherapy , discuss in the MDT)

If Check the guidelines