TorontoGiFellow

  Hb increment after blood transfusion  Ballpark:  77 / weight PS: The value is true to one decimal point Formula: 55 /  (weight female *0.065 + 0.350)                  55 / (weight male *0.075 + 0.350)   Source:  https://www.coreimpodcast.com/2022/01/05/1-to-1-prbc-bump-mind-the-gap-segment/

  Meta-analysis of nearly 850,000 patients 1 serve = 80 g (of fruit or vegetable) Mortality benefit plateaued after 5 fruit/vegetable servings per day Risk reduction arose from cardiovascular outcomes, no improvement in cancer-specific mortality Source:  https://www.bmj.com/content/bmj/349/bmj.g4490.full.pdf

Safety and Efficacy of different types of NOAC compared to Warfarin

  Source: https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/10.1111/anae.15179, https://www.breastfeedingnetwork.org.uk/colonoscopy/ https://www.asge.org/docs/default-source/education/practice_guidelines/doc-5c7150fd-910a-4181-89bf-bc697b369103.pdf?sfvrsn=d23a4a51_6

      Weight loss                               +                            +++                          None ⬇ CVD  Mortality                     +                               +                            None ⬇  MI / Stroke                          None                                   +                            None ⬇  CKD progression/Htn           +                             None                        None ⬇ HbA1c                                  0.5-0.7                     0.5-1.5                        0.5-0.8 GLP-1 analogues Mechanism of Action –  1) Decrease Glucagon secretion Usually in DM2, in addition to Beta cells (insulin), there is Alpha cell dysfunction as well, which leads to dysregulated glucagon secretion post prandially in diabetics, worsening hyperglycemia. GLP-1 agonists BLUNT glucagon secretion, thereby restoring glucagon levels 2) Increase Glucose mediated insulin secretion – insulin is secreted only in presence of hyperglycemia, thereby making hypog

 Genetics / Hereditary pancreatitis Suspect if 2nd episode of 'idiopathic' acute pancreatitis in patients <40 years of age Trypsin Dependent Pathway:  Trypsinogen (cationic / anionic forms) is a major protein produced in pancreas, which gets activated in dudoenum to trypsin and causes digestive proteolysis. Premature activation of Tryspin within pancreas is a major cause of development of hereditary pancreatitis. Genes: Dominant Gene:                           PRSS1   -  Autosomal dominant,   Gain of function mutation                                         Responsible for vast majority of cases of Hereditary pancreatitis                                         Causes  ⬆⬆ cationic trypsinogen, leading to premature activation within pancreas                                         80 -90% penetrance                                          First episode of pancreatitis is often by age 10                                         Dominant gene - can cause pancreatitis w/o other

  Really good discussion: https://www.youtube.com/watch?v=iHuIXVdOHrw&list=LL&index=1

 Traditional technique No. 1 Equipments: 10 Fr Cook Cystotome, 6-8mm CRE balloon, 2 JAG wires Step 1:  1) Remove the 10 Fr outer sheath. Then, puncture the cavity with the internal 0.038 needle knife (Autocut Effect 4/ 100W) inside the 5Fr sheath, and advance both in to cyst cavity 2) Once in the cavity, remove the 0.038 needle knife and advance a 0.035 JAG wire through the 5Fr sheath. 3) Then, advance the 10 Fr outer sheath (with diathermy ring) over the 5Fr sheath. The 10 Fr sheath is advanced in to the cyst cavity using ERBE (Forced coagulation, E2,30W). 4) The 5 Fr sheath is removed, and a second 0.035 JAG wire is inserted. 5) The 10 Fr sheath is then removed. The cyst-gastrostomy tract is then dilated by passing a 6-8 mm CRE balloon over one of the two 0.035 JAG wires, and dilating the tract to 8 mm. 6) Two pigtail stents are then inserted, one each over the JAG wire. Traditional Technique 2: Equipments needed: Optimos (Taewong), Oasis stent pusher system, 2 JAG wires, CRE balloon

 In patients with high Etoh intake: On an avg. 40g daily (♀) / 60g daily (♂) for 6 months Last intake within last 8/52 of presentation Grim outcome: AH a/w 20% mortality It is an immune-mediated hepatitis, thought to be secondary to  1) Immune activation directed at damaged hepatocytes from alcohol injury 2) High microbial load to liver, due to loss of integrity of tight-junctions in intestine Nutrition No strong evidence suggesting utility, but generally thought to be a good thing Calorie: Target 30 kcal/kg/day with night time snacks If not able to have enough calories orally,  consider enteral feeding Steroids: Consider using, once infection has been conclusively ruled out STOPAH - 1100 patients, showed HR 0.6 (28 days), and no benefit at 3 months (HR 1.02) or 1 yr (HR 1.01)

  Zenker's diverticulotomy HQ scope JAG wire in stomach Make a hole at tip of the long tongue of Cook overtube Feed the overtube over wire, with long tongue on tongue side, and short-tongue on hardpalate side Site it carefully in Zenker's Do myotomy using Zimmon needle knife papillotome (5.1Fr /  7 mm knife length Clip at the end Cefazolin 2g IV antibiotic

Usually treatment via CADS, christchurch Anti-Craving Medications Naltrexone - Opiod receptor Antagonist - **Funded in NZ via special authority, through CADS** NNT = 20 Does undergo hepatic metabolism, and no studies in AUD in liver disease, however generally considered safe in Cirrhotics up to CP-B Dose: 25-50mg daily Do Not use in patients on opiates - as this will result in opiate withdrawal Acamprosate. (Not available in NZ) NNT = 12 Dose: 333mg TDS No Hepatic metabolism Do Not use in patients with eGFR < 30 Baclofen  GABAb agonist The only drug studied in Cirrhotics Can be used in compensated and decompensated Cirrhotics Dose: Start at 10mg TDS - can be up-titrated, usually not more than 90mg daily Refernce: https://liverfellow.org/post/how-do-i-manage-alcohol-use-disorder-in-hepatology-clinic Core IM https://journals.lww.com/hep/Fulltext/2020/01000/Diagnosis_and_Treatment_of_Alcohol_Associated.25.aspx