Digestive System
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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.

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.

 Low amplitude propagated contractions (LAPC) Haustral contractions, triggered by chyme, facilitate the slow movement and mixing of food to enhance water absorption. Those are slow, segmenting movements that further mix chyme, most comoon in proximal colon.  (5 to 40 mm Hg) and last about 3  seconds.They happen  about every 30 minutes. 

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

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.

Paquet (Or Modified Paquet that contains 3 categories insted of 4) is the classification used for esophageal varices. Zargar is used for caustic injury

EREFS (EoE reference endoscopic score) is used to grade Eosinophilic esophagitis.

Kodsi is used for staging Candidiasis:

Grade I, a few raised white plaques up to 2 mm in size without edema or ulceration.

Grade II, multiple raised white plaques greater than 2 mm in size without ulceration.

Grade III, confluent, linear, and nodular elevated plaques.

Grade IV, finding of grade III with increased friability of the mucous membranes and occasional narrowing of the lumen

Should be endoscopic ablation (Radiofrequency or similar).  We cannot resect endoscopically a lesion that we cannot see.  Check the guidelines

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