Gastroenterology Flashcards
Most common cause of peptic ulcers
Medications (Previously H. Pylori)
How much blood loss does postural drop reflect
>10%
In acute resuscitation of upper GI bleed, when to start bloods
Blood after 1-2 L of isotonic fluids
Ongoing upper GI haemorrhage and all else fails
Recombinant activated factor VII
Hb treatment aim in acute GI bleed
Aim Hb >70
Indication for urgent endoscopy in acute upper GI bleed
Ongoing massive bleeding, no response to normal saline
Varices acute bleeding medical therapy
Octreotide 50 mcg/hr for 5 days (but no mortality benefit despite reducing rebleeding) Terlipressin 1-2mg IV bolus (not good for peripheral \vascular disease) Antibiotics - ceftriaxone for 3 days (MOST EFFECTIVE) Endoscopy Rx with banding
Secondary prophylaxis for oesophageal varices
1) Subsequent variceal banding sessions every 2-4 weeks for 3-4 sessions to eradicate them 2) Beta blockers (propanolol) - poorly tolerated but shown to reduce rebleeding and mortality
What condition can cause isolated gastric varices without cirrhosis
Thrombosed splenic vein - as gastric varices are the anastamoses between short gastric and splenic vein branch
How is endoscopic therapy different in gastric and oesophageal varices
Gastric varices are injected with cyanoacrylat glue mixed with lipiodol (radiological agent used that can show hardening of the glue during injection) Oesophageal varices are banded
Nutritional subjective global assessment (SGA) Grade C
Muscle wasting, fat wasting, peripheral oedema
What muscle area has high correlation with complications of malnutrition?
L3/4 retroperitoneal muscle bulk
Red flags in anorexia - very high refeeding risk likely requiring ICU admission
Bradycardia and hypotension
Physiology of refeeding syndrome
Hyperinsulinaemia causing potassium to go intracellular and also phosphate going intracellular to balance out the negative charge. Insulin also has effects on the distal tubule and causes salt retention and peripheral and pulmonary oedema
Minimum amount of small bowel (with colon present) required before needing TPN
60cm
What effect does bile acid have on the colon
Bile acid stimulates water secretion in the colon
What kind of stones can massive small bowel resections lead to
Oxalate stones - as steatorrhea loses calcium and calcium normally binds oxalate. Manage with calcium loading and low oxalate diet
Action of glucagon like peptide 2
Produced in the distal small bowel and colon - provides feedback to upper intestine to optimize the nutrient and fluid absorption. GLP-2 analogus is teduglutide, which has demonstrated clinical utility in SBS trials
What positive antibodies is autoimmuen hepatitis associated with
ANA, Anti LKM, anti SMI
What part of the portal triad does autoimmune hepatitis affect
peri-portal
Clinical phenotype of viral hepatitis
middle-aged women, non-drinker without viral hepatitis
which type of autoimmune hepatitis is worse
Type 2 younger onset LKM-1 antibody (liver kidney muscle)
pathonemonic sign of autoimmune hepatitis on histology
rosette sign
Treatment of autoimmune hepatitis - first line
Pred Azathioprine
What is the biggest sign on histology for relapse in autoimmune hepatitis
portal plasma cells
biomarker for primary biliary cholangitis
AMA - anti-mitochondrial antibody
What is a marker of disease activity in PBC
symptomatic patients (fatiguem pruritis, sicca
What liver function test is elevated the most in PBC
ALP - 3-4x ULN AST, ALT <200 Bilirubin rises late HIgh cholesterol (lack of absorption of bile salts)
Medical management of primary biliary cholangitis
UCDA - Ursodeoxycholic acid (first line) 13-15mg/kg/day split dose 2-3x/day Only medication with survival advantage (OCA, fibrates only have biochemical effect)
What is obeticholic acid, what is it used for and what’s its main side effect
semi-synthetic analogue of cheno-deoxycholic acid PBC Itch
what other gastro disease is PSC associated with
IBD (90% of PSC will have IBD) - UC more common than crohn’s 4-5% of UC patients have PSC associated with cholangiocarcinoma, bowel cancer
What is the appearance of ducts for PSB on imaging and what is the best mode of diagnosis
Beading of ducts - inflammation and fibrosis of the intrahepatic duct MRCP
What is more symptomatic out of PBC and PSC
PSC - jaundice, itch, ascending cholangitis PBC is generally asymptomatic on presentation and symptoms indicate poor prognosis
What’s a secondary cause of sclerosing cholangitis
IgG4 disease
What autoantibodies is associated with PSC
p-ANCA 80% AMA <2% ANA 50-60%
Histological feature of PSC
Periductal fibrosis - looks like onion peeling Ductpaenia - lack of small bill ducts
Management of PSC
Cancer surveillance - reg colonoscopies Pruritis - symptomatic tx: antihistamines, rifampicin, naltrexone no disease specific medical therapy
What is the role of ERCP in PSC
to dilate dominant strictures to prevent recurrent infections
How to grade UC
Mayo clinic score Stool frequency Rectal bleeding Mucosal appearance at endoscopy Physician rating of disease activity
What is 5-ASA
Mesalazine, for UC
How to manage mild to mod flare of UC
- optimise existing medication - topical mesalazine more effective than topic steroids - oral steroids for those who fail to respond to optimised mesalazine escalation of therapy in those requiring more than 1 course of steroids a year
Faecal calprotectin
Neutrophil-derived alcium binding protein Non invasive marker of intestinal inflammation Done early in the morning as there is higher levels Useful to differentiate between IBS and IBD Monitoring of disease activity in IBD Can be falsely elevated by blood
Iron deficiency in IBD - how common and why
60-80% losses through bleeding, reduced intake, inflammatory mediated side note // if CRP is elevated, cut off for ferritin is 100
What interleukin stimulates hepcidin
IL-6
Side effects of thiopurines
Hepatotoxicity Bone marrow suppression (TMPT; NUDT15 but not available for commercial testing) Pancreatitis - idiosynratic; 4%; avoid all thiopurines Lymphoproliferative disorders (hepatospleno T cell lymphoma) Skin checks
Mechanism of increased gallstones in Crohn’s
Decreased bile reabsorption in terminal ileum
What is the most common stone in crohn’s
calcium oxalate (also the most common in general) Uric acid stones can become mor frequent in colonic resection and ileostomy
Next line when severe UC is not responding fully to steroids
infliximab infusion severe UC = >6 BO in 24hours Oxford.travis criteria is assessing response: Day 3 IV hydrocortisone Stool frequency >8 in 24hours Stool frequency >3 in 24hours with a CRP >45
Pregnancy and IBD treatments
Steroids - cleft lip/palate, gestational diabetes Azathioprine - no inrease in birth defects Infliximab - no increase in brith defects but stop in remission in 3rd trimester as that is when it might cross the placenta Methotrexate - needs to stop atleast 3 months before pregnancy Vedolizumab/ustekiinumab - probably stop not much data
vedolizumab
Monoclonal antibody that binds to integrin α4β7 (LPAM-1, lymphocyte Peyer’s patch adhesion molecule 1, a dimer of Integrin alpha-4 and Integrin beta-7). Blocking the α4β7 integrin results in gut-selective anti-inflammatory activity. Gut selective. //side note another monoclonal antibody that acts on integrin molecules is natalizumab
Ustekinumab
Monoclonal antibody to p40 subunit of IL12/23 Already approved for psoariasis Currently only for use in crohn’s disease
Liver transplant indications
CLD: - MELD score >11-12 indication for referral, usually transpanted when MELD is higher - Hepato-pulmonary syndrome - Porto-pulmonary hypertension - QOL Fulminant liver failure
MELD
dialysis creatinine bilirubin INR Sodium
Biochemical indication for rejection
cholestatic picture
WHat genotypes of HBV does australia have
b/c c is associated with more flares/progression
WHen does E antigen seroconversion occur?
Immune clearance (and subsequently positive in immune control and loss of E antigen immune escape); corresponds with ALT rise
Significant of HBeAg
Marker of active replication and infectivity E antigen loss with a high viral load is a marker of immune escape
Serology post HBV vaccination - when to check and when are they immune
>10mIU/mL anti HBS antibodies <10 exclude HBV infection (see nick’s slides)
Non-responders HBV next step
4th booster
HBV vaccination in ESRD
Increase dose in vaccine
What to do with HBV post exposure prophylaxis in vaccine non responder
HBIG (+/- booster doses)
What to do with HBV post exposure prophylaxis in non vaccinated
HBIG and initiate HB vaccination
When to treat HBV?
Cirrhosis + HCC Without cirrhosis: depends on DNA viral load/surface antigen (see nick’s slides)
What are the pros and cons in HBV treatment with PEG-IFN vs nucleoside reverse transcriptase inhibitors
Peg IFN is finite treatment but more contraindications - also cannot use in cirrhosis Entecavir/tenofovir
What is the serology of HBV core mutant immune escape and ALT
rise in ALT loses core antigen
What timing of HDV transmission in relation to HBV results in lower risk of clearance
When HDV is acquired on top of chronic HBV (as opposed to co-transmission at the same time)
How to test for HCV
anti-HCV serology and RNA Viral load anti-HCV indicates past/current infect Viral load indicates current infection
Interaction between HCV meds and amiodarone
heart block
Which HCV medication is contraindicated in eGFR <30ml/min
see nick’s slides
What is the YMDD mutation in HBV
Lamivudine resistance
Indication for ultrasound surveillance for HBV
(1) cirrhosis; (2) Asian descent plus male sex plus age older than 40 years; (3) Asian descent plus female sex plus age older than 50 years; (4) sub-Saharan African descent plus age older than 20 years; (5) persistent inflammatory activity (defined as an elevated ALT level and HBV DNA levels greater than 10,000 IU/mL for at least a few years); and (6) a family history of hepatocellular carcinoma
NAFLD findings on ultrasound
Hyperechoic liver
Predominant liver enzyme picture in PBC
an increase in serum ALP levels, but a mild to moderate increase in aminotransferase levels is also seen
what is the role of glutathione in paracetamol poisoning
glutathione is able to make non toxic NAPQI conjugated so in malnourishment where there is lower levels of glutathione, there is increased shunting to toxic NAPQI
transplant criteria for paracetanol
pH <7.3 INR >6.5 Creatining 3.4 encephalopathy grades 3/4
pembrolizumab with ALT >5ULN next step
start pred, withhold agent mycophenolate is 2nd line (just like in AIH) biopsy showed autoimmune hepatitis picture
what drug is associated with granulomatous hepatitis
allopurinol
alcoholic hepatitis treatment
NUTRITIONAL SUPPORT +/- pred + NAC (likely via preventing renal dysfunction)
1 cause of death in NASH
CVS disease
Iron poisoning clinical features
GI bleeding, metabolic acidosis
Serum-ascites albumin gradient (SAAG) that is indicative of portal hypertension
>11g/L (seru albumin - ascites albumin)
Treatment of SBP
2g ceftriaxone daily + conc albumin
Secondary prophylaxis of SBP
Bactrim or norflox
Who should get primary prophylaxis of SBP?
Low protein <10g/L ascites or bilirubin >50 with impaired renal function
How often to do variceal screening in cirrhosis?
Annual if small varices 2nd yearly if no varices
How to calculate the hepatic venous pressure gradient?
wedge hepatic venous pressure (WHVP) - free hepatic venous pressure (FHVP)
MOA of terlipressin
Long-acting vasopressin analog Reverses splanchnic vasodilation
Criteria for acute liver failure liver transplantation
Paracetamol vs non-paracetamol Paracetamol: - pH <7.3 or - INR >6.5 AND creatinine >300 AND grade III/IV encephalopathy Non-paracetamol: - INR>6.5 OR - 3 of 5: age <11 or >40, serum bilirubin >300, jaundice to coma >7 days, INR >3.5 and drug toxicity
Which IBD do you get goblet cell deletion?
Ulcerative colitis (also crypt distortion, cryptitis, cryp abscesses)
What metabolites of azathioprine can be measured for therapeutic drug monitoring
6-MMP (TMPT pathway metabolite) 6-TGN Both low/absent = non adherence/under-dosing Both high = thiopurine refractory 6-MMP high and 6-TGN low = thiopurine resistance -> add allopurinol which inhibits XO and TPMT and creates more 6-TGN to cause more immunosuppression But don’t use allopurinol normally cos it can increase toxicity
Next step in loss of response to anti-TNF in inflammatory bowel disease
Measure trough drug levels and anti-drug antibodies
Ultrasound appearance of NAFLD
Increased hepatic echogenicity (increased sensitivity with increased steatosis)
What test to distinguish steatosis from NASH
Liver biopsy for histology
What are the pathological features of NASH
- Steatosis - greated in zone 3 (peri-central vein) 2. Lobular inflammation 3. Fibrosis Summation of above in a scoring system indicates NASH
Factors in calculating NAFLD fibrosis score
Age BMI IGF/diabetes AST ALT Platelets Albumin
What is the biggest predictor of NASH/progression to fibrosis in NAFLD?
Diabetes
Should statins be used in NAFLD
Yes even for patients with moderately abnormal liver tests
What genes are responsible for HFE hereditary haemochromatosis
C282Y and H63D on HFE gene (chromosome 6) autosomal recessive w incomplete penetrance
What is the most sensitive initial screening tool for haemochromatosis?
>45% in fasting morning transferrin saturation NEXT step is HFE genotype (but can go straight to this step is there is an affected family member)
What is the window period for anti-HCV Ab ELISA?
6 weeks
Breast feeding in HCV risk of transmission
HCV RNA detected in breast milk but no increased risk with breast feeding
What percentage of acute hep C progress to chronic hep C?
75-80% More chance of clearing if jaundiced initially
What are extrahepatic manifestation of HCV?
Immune dysregulation: - Essential mixed cryoglobulinaemia 11x - membranoproliferative GN 7x - PCT 12x (photosensitive and blistering skin rash) - Lymphoma Also 11x increased risk of T2DM
Can you treat HCV in pregnancy?
No
HCV polymerase inhibitor antiviral ending
buvir
HCV proteasome inhibitor antiviral ending
previr
What antiviral regimens can be used for HCV in Child-Pugh B&C?
Sofosbuvir/velpatasvir ADD ribavirin
What HCV antiviral should not be used for eGFR <30ml/min
Sofosbuvir
How does cirrhosis affect the HCV DAA treatment?
Need to increase duration (normally from 8 to 12 weeks)
How does MELD score affect HCV DAA treatment
MELD 15-20 treat cautiously MELD >20 defer treatment post transplant
What drugs interact with DAAs in HCV
Amiodarone (can precipitate heart block) St John’s Wart Statins Digoxin Anticonvulsants PPIs ART
Factors in Child Pugh Scoring
Encephalopathy
Ascites
INR
Albumin
Bilirubin
What is the primary driver of ascites?
Portal hypertension
(not hypoalbuminaemia)
Treatment of SBP if already on norfloxacin or bactrim prophylaxis
Piptaz
What are high risk features in cirrhotic varices?
- Size
- Red wale marks
- Advanced liver disease
Indications for TIPS
- Variceal bleedig unable to be treated endoscopically
- Diuretic refractory ascites or hepatic hydrothorax
- Budd-chiari
Quad/triple phase CT appearance of HCC
- Arterial enhancement
- Porta vein washout
Indications for HCC screening
- Cirrhotic patients, CP A and B
- Cirrhotic patients CP C awaiting liver transplantation
- Non-cirrhotic HBV carriers with active hepatitis or family history of HCC
- Non-cirrhotic patients with chronic hep C and advanced liver fibrosis F3
- Chronic HBV med >40, women >50 and african origin patients on diagnosis
Treatment of stage C HCC (portal invasion
Sorafenib or lenvatinib (oral multi-kinase inhibitor)
se: palmar-plantar erythrodysesthesia
What is a negative risk factor for GORD?
H. Pylori
What is the main mechanism of reflux?
Transient lower oesophageal sphincter relaxation
Surveillance of Barrett’s oesophagus
Dysphagis and food impaction with following picture
- Diagnosis
- Treatment
- Eosinophilic oesophagitis
- PPI + topical steroid (fluticasone puffer)
