Digestive System
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Based on this  article of the NEJM

Check AGA guidelines and ESGE, BSG  and Asia Pacific and  international consensus group

This is a Forrest III (clean based) duodenal ulcer in a healthy and stable patient. (Rebleeding risk <5% )

Patient could be discharged if stable and toleranting oral diet (AGA recommends in low risk endoscopic findings considerning discharge in stable cases with stable vitals and Hb and  no other reason for hospitalization).  PPI should be initiated orally, but given it is a low risk finding (F-III) only standard dose would be enough.  If it was a high risk such as Forrest I-IIa, then 72h of  IV PPI (Or oral high dose PPI in selected cases) is recommended as well as keeping the patient under observation.

In high risk (Forrest I-IIb) American and International guidelines advise commencing a two week course of twice daily high dose PPI,  based on a trial that showed 40 mg esomeprazole BD significantly reduced rebleeding compared  40 mg esomeprazole once daily  ( 10.8% v 28.7%,)

So the endoscopist gave good advice in general. So why is it false then? Because:

•  ESGE recommends in bleeding secondary to peptic ulceration,H pylori test at index endoscopy.   In the event of a negative result,  like this case, advise  retesting within four weeks and eradication of H pylori if positive (given the low-ish sensitivity of clotest or histology in acute bleeding, about 0.7)
• Do not forget iron replacement, either orally or if patient does not tolerate, then iron infusion to correct the anaemia.
• Smoke cessation is advised too!  Especially if Hpylori is really negative, then smoking could be a main trigger factor.

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.

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

-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

 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. 

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

It is not 2 times higher, it is actually > 10 times higher!!

This is the reason ADR is probably  the most important surrogate marker of a good  quality colonoscopy, (others are bowel preparation, caecal intubation and withdrawal time) and we need to maintain ADR  at least >20%

Difficult case with patient older than 65 and comorbidities with moderately to severely active ulcerative colitis.

Vedolizumab should be indicated in his case as it performs better than anti TNFs in ulcerative colitis, confirming the results of the Varsity study.   ( Over a 5 year period, drug persistence is higher in patients treated with vedolizumab as compared to anti-TNF therapies and loss of response is less frequent again in the vedolizumab group). Age or previous TIA /AV block are not contraindications for anti-TNF (only Moderate-severe heart failure, which is not the case) So even though Adalimumab would be a valid option, it should be ideally used if Vedolizumab fails.

JAK inhibitor (Tofacitinib) should not be prescribed in people with a history of cardiovascular disease (eg. heart attack or stroke) at increased risk of cardiovascular problems (eg. current or past long-time smokers) at increased risk of cancer or aged 65 years and over unless no suitable alternative

Ozanibod could be an oral alternative , however second-degree Mobitz type II atrioventricular (AV) bloc and TIA within the previous 6 months contraindicates its use.

Off the quizz options, another good one would be Ustekinumab (interleukin 12&23 antagonist drug ) as not contraindicated here and equally valid to Vedolizumab.

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