Digestive System
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GERD is a well known risk factor for adenocarcinoma of esophagus, but not for squamous cell carcinoma.

Risk factors for SCC are low socioeconomic status, consumption of tobacco, alcohol, hot beverages, and nitrosamines (e.g cured or smoked) . Additionally, micronutrient deficiencies have also been linked to the development of esophageal squamous cell cancer. These include vitamin C, vitamin E, and folate

Plummer-Vinson syndrome (PVS) is a rare condition characterized by the classic triad of dysphagia, iron-deficiency anemia, and esophageal webbing.  Approximately 10% of patient can develop SCC.

Remember Achalasia as other importart pathology in which there is an increased risk of esophageal cancer, particularly SCC

This is likely a lower GI bleed, however, the fact that is so abrupt and has caused   haemorrhagic shock makes us wonder if he is not having a severe upper GI bleed – frail patient taking clopidogrel - Severe upper GI bleed sometimes can be so brisk and profuse that blood travels the intestine fast wihtout being digested, so patient passes per rectum red bright blood instead of black melaena. (Blood is laxative too) As many as 10–15% of patients suspected initially to have lower GI bleed are ultimately found to have an UGI source.

Once OGD is done and clear, the next step should be depending on the clinical and hemodinamic status. Either prepare the patient for colonoscopy/ video capsule (If clinically stable)  or repeat CT angio (If clinically worse)-->If bleeding point is located and there is no access to IR (interventional radiology) the surgeons may want to proceed with exploration and colectomy but this is the last resource as obviously this is an elderly patient with cardiovascular factors (Clopidogrel) whose surgery would be high risk of mortality and morbidity.

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

They recommend dual therapy in bleeding ulcers- Forrest Ia, Ib -(except selected cases of big excavated vascular ulcers that can be considered straight for cap-mounted clip).   In Forrest IIa (non bleeding vessel) they recommend thermal therapy, mechanical therapy, or injection of a sclerosing agent, each as monotherapy or in combination with epinephrine injection

DOI: 10.1055/a-1369-5274

Endoscopy 2021; 53(03): 300 - 332

Check guidelines 

It has always been agreed that High grade dysplasia should merit ablation, however clasically LGD would be offered endoscopic surveillance until progressed to HGD. This approach has changed over the last years to the point that Both ESGE and AGA suggest eradication with ablation to prevent progression to HGD/cancer. BSG recommends repeating endoscopy in 6 months and if confirmed again, offering eradication vs 6 -monthly surveillance.  The AGA 2024 guidelines favous ablation over surveillance.

All societies agree that he biopsies should be reviewed by an expert pathologist (ESGE suggest 2 experts) before embarking into eradication.  Remember that the incidence of progression (to HGD or adenoca) is estimated around   9.1%/year  with reported incidence of adenocarcinoma of 0.54% per year. The overall yearly incidence of Eosphageal adenocarcinoma is 0.3% (0.19 in short segment )

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 US Hpylori Guidelines, BQT  is the first option for both standard and penicillin allergic patients.  This is a PPI (standard dose)  b.i.d.   Bismuth subcitrate (120–300 mg) or subsalicylate (300 mg) q.i.d. Tetracycline (500 mg)e q.i.d. and Metronidazole (500 mg) t.i.d. or q.i.d

In treatment-experienced patients with persistent H. pylori infection  , they recommend O+L+  either Amoxicillin or Metronidazole

Check the guidelines

ESGE recommends offering treatment to all the patients with CBD stones (symptomatic or not) who are fit enough to undergo procedure.
This is true that we should explain always the option of intervention, and we should at least talk about risks of complication from leaving untreated biliary stones (Roughly about 25%  - biliary colic, pancreatitis, cholangitis- vs 12% if we clear the bile stones) this is  based on this  Gallrisk sweddish cohort   where they followed 3969 patients with untreated CBD stones, during follow-up ranging from 0 to 4 years. 

In summary: Explain why there is an indication to treat, which risks ERCP associates, what the alternatives may be  (ie Cholecystectomy plus surgical bile duct exploration in the same setting when approppriate) and their own risks.  And last but not least, explain the alternative of not treating and only monitoring, and the risks of this approach as well.

1. True.  Around 80%  of AIH will be either ANA or ASMA+, 8% AMA+, 2% LKM+. 30% SLA+
2.  True. Less than 50% in reduction of transaminases in 4 weeks after treatment is considered Non-response. (Occurs in 17% of treated patients and assoiciates a 7-fold risk of liver related death )
3.  False. Previous guidedlines suggested this parameter, but now we consider response when complete normalisation of transmanisases and IgG.   Liver biopsy is very useful to asses histological response if Modified Ishak hepatitis activity index (mHAI) <4 /18, however histology response lags behind biochemical response by several months: in one  RCT, only 28% and 50% of patients receiving prednisolone±azathioprine achieved histological remission after 6 and 12 months, respectively. Thus, repeat biopsy to confirm remission is not recommended over the first 2 years

4.  True. Since the response criteria are more strict, there will be 20-30% who wont achieve complete biochemical remission.  These scenarios are tricky, we need to compare the overall response, patient adeherence to treatment, considering Azathioprine adeherence and metabolism:  Measuring Thioguanin nucleotides- TGN-  to see that they are in therapeutic range(>220 pmol/8×10) and  Metilmercaptoruine ( MeMP) > 5700 can confirm that the patient is taking the right dose,  Also there are specific situations in which transaminases can remain slightly abnormal due to other causes like MASLD or drug related, and IgG is commonly raised in conditions like cirrhosis.

Check BSG guidelines AIH