TorontoGiFellow

 https://www.youtube.com/watch?v=3cP2kvPq7iQ m.c form of acquiring Hep B in Asia - Vertically m.c form of acquiring Hep B in western coutnries: Parenterally (sexual / needles etc) Neonates have immature immune system, so they cant 'fight-off' vertically acquired virus. Over 90% of babies infected with Hep B, go on to have chronic Hep B infection 95% of adults if they acquire Hep B - fight it off! HBV is a DNA virus - replicates efficiently. But is error-prone. Plagued with mutants.  e-antigen negative mutant - tend to be in older patients, tend to be more aggressive. 30-50% of HCC in HBV occurs in absence of cirrhosis Reveal study - 15 year follow-up study of untreated patients with HEp B. The only factor that was relevant in predicting risk of HCC was viral load at base-line! Viral load more than 10*4 (2000 IU/ml) was predictive of risk of HCC or Cirrhosis (similar graph for Cirrhosis as for HCC) Immune Tolerant Phase: typically after vertical infection. DNA remains very high,

  If starting antiviral prophylaxis: - Continue for atleast 18-24 months in total - Conitnue for atleast 6-12 months after cessation of immunosuppressive therapy During antiviral prophylaxis :Check LFT, HbsAg, HBV DNA q3 monthly After completing antiviral prophylaxis :Check LFT, HbsAg, HBV DNA q3 monthly for 1 year

Source: https://www.igibdscores.it/en/info-rutgeerts.html  The Original Rutgeerts score was described in a paper published in Gastroenterology in 1990 This was based on 89 patients, followedup between 1979 and 1984. The Rutgeerts score, when measured within a year out of surgery, predicts risk of symptomatic recurrence at 5 years after surgery

 Source- UTD https://www.jtcvs.org/action/showPdf?pii=S0022-5223%2818%2931859-2 Endoscopic Sphincterotomy  - Risk of bleeding persist for upto 3 to 5 days after sphincterotomy           Low to Mod risk of Thrombosis: Delay attaining therapeutic anticoagulation for 3 to 5 days after                                                                 For eg: Re-start Warfarin at day 3 / Restart DOAC at day 5                      High risk of Thrombosis:  Re-start Warfarin on the evening of procedure / LMWH 48H after / DOAC day 5  - UFH 24-48H post.                     Mechanical Heart valves: Mechanical Mitral / Pulmonary vaalve - HIGHEST risk Mechanical Aortic valve - low to moderate risk based on presence of concurrent stroke risk (chadvasc) After high-risk procedure (sphincterotomy), regardless of the valve, DO NOT re-start LMWH within 48-72H after procedure! As per Journal of Thoracic & Cardiovascular surgery guideline (2019) for non-cardiac procedures: Metallic Heart valve with no

  S ource: https://www.youtube.com/watch?v=tn_UP-Ec0yA&t=1758s

Normal human A1AT is a 52-kDa glycoprotein of the serpin (serine proteinase inhibitor) family, predominantly produced in the liver and released into the blood.  In affected patients, circulating levels of mutant A1AT are ≤15% of normal protein levels.  A1ATD is unique in that it is a proteinopathy that impacts the lungs and the liver by different mechanisms [ 9 ]. In the lungs, it is a loss-of-function mutation, where A1AT is an inhibitor of neutrophil elastase. Emphysema results when A1AT is not present to inhibit the serine proteinase, allowing it to freely destroy the lung tissue [ 10 ].  The liver disease associated with A1ATD is a gain-of-toxic function mechanism. The misfolded insoluble globular proteins (ATZ) accumulate in the endoplasmic reticulum (ER), leading to hepatic fibrosis and even hepatocellular carcinoma (HCC) [ 11 ] Liver transplant is the only curative treatment. Source:  Alpha-1 antitrypsin deficiency: A re-surfacing adult liver disorder - Journal of Hepatology (jo

  70 patients randomized to each EUS-CDS (6x8 mm axios) and ERCP arm EUS-CDS was quicker (14 mins vs 24 mins), had similar technical and clinical success Same rate of early adverse events, and delayed stent obstruction 5-8% underwent Whipples - no increased difficulty with whipple in EUS-CDS arm (similar surgical duration, similar adverse event, similar post-op hospitalization duration) when compared to ERCP Zero risk of pancreatitis - as expected.

Source: https://www.gastrojournal.org/action/showPdf?pii=S0016-5085%2804%2900195-7 

  Baveno 7   1)     Portal hypertension = HVPG >5 mm hg 2)     In viral & alcoholic hepatitis – CSPH = HVPG >=10 3)     In PBC, CSPH likely develops at lower HVPH, due to (unmeasured) component of pre-sinusoidal PH 4)     Similarly, in NASH, CSPH may develop at HVPG < 10     Reduction in HVPG secondary to Betablockers predicts clinical response!   In patients undergoing TIPS, HVPG <12 affords near-complete protection from PH complications     Compensated advanced chronic liver disease (cACLD) ( a.k.a cirrhosis) <10 kPa = unlikely cACLD      (<1% 3-year risk of decompensation or liver-related death) >15 Kpa = highly likely cACLD     Clinically significant reduction in LSM defined as either: 1)     20% reduction, such that LSM <20 Kpa 2)     Or LSM <10 Kpa   CSPH (based on LSM) LSM <15 + Platelet >150 – unlikely CSPH (>90% negative predictive value) LSM >25 – Definite CSPH   Baveno indicatio

 Refer to UTD Following is an easy excerpt as of July 2023 from UTD ALT = 35 (men), 25(women) regardless of laboratory cut-ff 1 IU = 5 copies /ml

IDA   Ferritin: (BSG 2021 / UTD)   Ferritin is the universal intracellular protein containing Iron – a soluble and non-toxic form. It is the primary iron storage protein in prokaryotes and eukaryotes. Ferritin w/o iron is called apo-ferritin . Each ferritin molecule can store up to 4,500 atoms of iron within it.     Iron deficiency anaemia:   1)     Low MCH is more sensitiv e for Iron deficiency than Low MCV. 2)     Low Ferritin is single most important serological marker of IDA. Serum ferritin assessed by assays is usually apo-ferritin, but reflects intra-cellular ferritin stores in RES (macrophages in liver, spleen, LN etc ) in absence of inflammation.   Fe < 15 – indicative of absent iron stores Fe <45 – indicative of low iron stores   In anaemia of chronic disease / CHF  - TSat <20% with Fe <100 is suggestive of Fe deficiency     Fe > 150 unlikely to represent low iron stores even in face of inflammation .   3)     Transf

In rectal LST (>20 mm insize) with at least a 10 mm nodular component, the overall risk of SMI malignancy is 12%.  Patients with LST (Mixed or NG) (IIa + Is or Is) with nodule atleast 10 mm in size should be conisdered for upfront ESD than EMR 33% of cancers resected by ESD can be potentially curative (the others harboring high-risk histological features, or >1000 micron invasion) Number of ESD needed for 1 curative cancer resection = 12

  Source: https://www.youtube.com/watch?v=6c4qiecpYPg

  CEA Levels:   CEA >192 is 60% sensitive and 90% specific for mucinous cysts (ipmn/mcn) This was based on a study of 70 lesions in 2004 and has stuck till date   CEA < 5 has excellent negative predictive value for mucinous cysts   CEA > 5, therefore can still be a mucinous neoplasm and needs to be taken in context. Other markers such as Ca 72-4, CA 19-9, CA 15-3, CA 125 have lower accuracy than CEA   Amylase levels: ·        Amylase < 250 IU/L is highly unlikely to be connected to PD (eg  SCA) ·        MCN usually have very low / low amylase (one study suggested it has similar amylase to ipmn)   Glucose: ·        Glucose is very low in mucinous tumors & pseudocysts (those with communication to PD)– usually less than 2.8 mmol/l     Glucose < 2.8 mmol/l has Sens/Spec of 90/90 ( more accurate)  compared to CEA >192 (sens/spec 60/90) for identification of mucinous cysts

 MCN - (Mother cyst) >95% in pre-menopausal women Mostly in body and tail of pancreas Thick-walled cyst, lined by Ovarian type stroma. Cyst contains mucinous / hemorrhagic material. Does not communicate with PD (unlike IPMN) 10-20% have in-dwelling cancer One review found - no dysplasia in cysts <3 cm in size LN mets is rare. Distal pancreatectomy usually suffices.  Doesnt result in metachronous lesions. Surveillance isnt really necessary SCA - (Grandmother cyst) 75% of SCAs seen in post-menopausal women Can be anywhere in pancreas Honeycombing, with tiny cysts containing clear fluid distributed around central scarring. Central scarring may bear calcification in 30% cases Microcystic SCAs can undergo degeneration and become macrocystic variants zero risk of malignancy, but they can continue to grow and cause obstructive symptoms SPN - (daughter lesion) - Solid Pseudopapillary Neoplasm 90% of lesion occur in young women, in teens / twenties Anywhere  in pancreas Solid / Solid-cys