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FRACP Shuyu > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Most common cause of peptic ulcers

A

Medications (Previously H. Pylori)

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2
Q

How much blood loss does postural drop reflect

A

>10%

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3
Q

In acute resuscitation of upper GI bleed, when to start bloods

A

Blood after 1-2 L of isotonic fluids

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4
Q

Ongoing upper GI haemorrhage and all else fails

A

Recombinant activated factor VII

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5
Q

Hb treatment aim in acute GI bleed

A

Aim Hb >70

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6
Q

Indication for urgent endoscopy in acute upper GI bleed

A

Ongoing massive bleeding, no response to normal saline

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7
Q

Varices acute bleeding medical therapy

A

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

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8
Q

Secondary prophylaxis for oesophageal varices

A

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

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9
Q

What condition can cause isolated gastric varices without cirrhosis

A

Thrombosed splenic vein - as gastric varices are the anastamoses between short gastric and splenic vein branch

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10
Q

How is endoscopic therapy different in gastric and oesophageal varices

A

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

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11
Q

Nutritional subjective global assessment (SGA) Grade C

A

Muscle wasting, fat wasting, peripheral oedema

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12
Q

What muscle area has high correlation with complications of malnutrition?

A

L3/4 retroperitoneal muscle bulk

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13
Q

Red flags in anorexia - very high refeeding risk likely requiring ICU admission

A

Bradycardia and hypotension

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14
Q

Physiology of refeeding syndrome

A

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

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15
Q

Minimum amount of small bowel (with colon present) required before needing TPN

A

60cm

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16
Q

What effect does bile acid have on the colon

A

Bile acid stimulates water secretion in the colon

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17
Q

What kind of stones can massive small bowel resections lead to

A

Oxalate stones - as steatorrhea loses calcium and calcium normally binds oxalate. Manage with calcium loading and low oxalate diet

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18
Q

Action of glucagon like peptide 2

A

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

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19
Q

What positive antibodies is autoimmuen hepatitis associated with

A

ANA, Anti LKM, anti SMI

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20
Q

What part of the portal triad does autoimmune hepatitis affect

A

peri-portal

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21
Q

Clinical phenotype of viral hepatitis

A

middle-aged women, non-drinker without viral hepatitis

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22
Q

which type of autoimmune hepatitis is worse

A

Type 2 younger onset LKM-1 antibody (liver kidney muscle)

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23
Q

pathonemonic sign of autoimmune hepatitis on histology

A

rosette sign

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24
Q

Treatment of autoimmune hepatitis - first line

A

Pred Azathioprine

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25
Q

What is the biggest sign on histology for relapse in autoimmune hepatitis

A

portal plasma cells

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26
Q

biomarker for primary biliary cholangitis

A

AMA - anti-mitochondrial antibody

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27
Q

What is a marker of disease activity in PBC

A

symptomatic patients (fatiguem pruritis, sicca

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28
Q

What liver function test is elevated the most in PBC

A

ALP - 3-4x ULN AST, ALT <200 Bilirubin rises late HIgh cholesterol (lack of absorption of bile salts)

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29
Q

Medical management of primary biliary cholangitis

A

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)

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30
Q

What is obeticholic acid, what is it used for and what’s its main side effect

A

semi-synthetic analogue of cheno-deoxycholic acid PBC Itch

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31
Q

what other gastro disease is PSC associated with

A

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

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32
Q

What is the appearance of ducts for PSB on imaging and what is the best mode of diagnosis

A

Beading of ducts - inflammation and fibrosis of the intrahepatic duct MRCP

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33
Q

What is more symptomatic out of PBC and PSC

A

PSC - jaundice, itch, ascending cholangitis PBC is generally asymptomatic on presentation and symptoms indicate poor prognosis

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34
Q

What’s a secondary cause of sclerosing cholangitis

A

IgG4 disease

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35
Q

What autoantibodies is associated with PSC

A

p-ANCA 80% AMA <2% ANA 50-60%

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36
Q

Histological feature of PSC

A

Periductal fibrosis - looks like onion peeling Ductpaenia - lack of small bill ducts

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37
Q

Management of PSC

A

Cancer surveillance - reg colonoscopies Pruritis - symptomatic tx: antihistamines, rifampicin, naltrexone no disease specific medical therapy

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38
Q

What is the role of ERCP in PSC

A

to dilate dominant strictures to prevent recurrent infections

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39
Q

How to grade UC

A

Mayo clinic score Stool frequency Rectal bleeding Mucosal appearance at endoscopy Physician rating of disease activity

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40
Q

What is 5-ASA

A

Mesalazine, for UC

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41
Q

How to manage mild to mod flare of UC

A
  • 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
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42
Q

Faecal calprotectin

A

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

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43
Q

Iron deficiency in IBD - how common and why

A

60-80% losses through bleeding, reduced intake, inflammatory mediated side note // if CRP is elevated, cut off for ferritin is 100

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44
Q

What interleukin stimulates hepcidin

A

IL-6

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45
Q

Side effects of thiopurines

A

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

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46
Q

Mechanism of increased gallstones in Crohn’s

A

Decreased bile reabsorption in terminal ileum

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47
Q

What is the most common stone in crohn’s

A

calcium oxalate (also the most common in general) Uric acid stones can become mor frequent in colonic resection and ileostomy

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48
Q

Next line when severe UC is not responding fully to steroids

A

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

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49
Q

Pregnancy and IBD treatments

A

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

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50
Q

vedolizumab

A

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

51
Q

Ustekinumab

A

Monoclonal antibody to p40 subunit of IL12/23 Already approved for psoariasis Currently only for use in crohn’s disease

52
Q

Liver transplant indications

A

CLD: - MELD score >11-12 indication for referral, usually transpanted when MELD is higher - Hepato-pulmonary syndrome - Porto-pulmonary hypertension - QOL Fulminant liver failure

53
Q

MELD

A

dialysis creatinine bilirubin INR Sodium

54
Q

Biochemical indication for rejection

A

cholestatic picture

55
Q

WHat genotypes of HBV does australia have

A

b/c c is associated with more flares/progression

56
Q

WHen does E antigen seroconversion occur?

A

Immune clearance (and subsequently positive in immune control and loss of E antigen immune escape); corresponds with ALT rise

57
Q

Significant of HBeAg

A

Marker of active replication and infectivity E antigen loss with a high viral load is a marker of immune escape

58
Q

Serology post HBV vaccination - when to check and when are they immune

A

>10mIU/mL anti HBS antibodies <10 exclude HBV infection (see nick’s slides)

59
Q

Non-responders HBV next step

A

4th booster

60
Q

HBV vaccination in ESRD

A

Increase dose in vaccine

61
Q

What to do with HBV post exposure prophylaxis in vaccine non responder

A

HBIG (+/- booster doses)

62
Q

What to do with HBV post exposure prophylaxis in non vaccinated

A

HBIG and initiate HB vaccination

63
Q

When to treat HBV?

A

Cirrhosis + HCC Without cirrhosis: depends on DNA viral load/surface antigen (see nick’s slides)

64
Q

What are the pros and cons in HBV treatment with PEG-IFN vs nucleoside reverse transcriptase inhibitors

A

Peg IFN is finite treatment but more contraindications - also cannot use in cirrhosis Entecavir/tenofovir

65
Q

What is the serology of HBV core mutant immune escape and ALT

A

rise in ALT loses core antigen

66
Q

What timing of HDV transmission in relation to HBV results in lower risk of clearance

A

When HDV is acquired on top of chronic HBV (as opposed to co-transmission at the same time)

67
Q

How to test for HCV

A

anti-HCV serology and RNA Viral load anti-HCV indicates past/current infect Viral load indicates current infection

68
Q

Interaction between HCV meds and amiodarone

A

heart block

69
Q

Which HCV medication is contraindicated in eGFR <30ml/min

A

see nick’s slides

70
Q

What is the YMDD mutation in HBV

A

Lamivudine resistance

71
Q

Indication for ultrasound surveillance for HBV

A

(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

72
Q

NAFLD findings on ultrasound

A

Hyperechoic liver

73
Q

Predominant liver enzyme picture in PBC

A

an increase in serum ALP levels, but a mild to moderate increase in aminotransferase levels is also seen

74
Q

what is the role of glutathione in paracetamol poisoning

A

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

75
Q

transplant criteria for paracetanol

A

pH <7.3 INR >6.5 Creatining 3.4 encephalopathy grades 3/4

76
Q

pembrolizumab with ALT >5ULN next step

A

start pred, withhold agent mycophenolate is 2nd line (just like in AIH) biopsy showed autoimmune hepatitis picture

77
Q

what drug is associated with granulomatous hepatitis

A

allopurinol

78
Q

alcoholic hepatitis treatment

A

NUTRITIONAL SUPPORT +/- pred + NAC (likely via preventing renal dysfunction)

79
Q

1 cause of death in NASH

A

CVS disease

80
Q

Iron poisoning clinical features

A

GI bleeding, metabolic acidosis

81
Q

Serum-ascites albumin gradient (SAAG) that is indicative of portal hypertension

A

>11g/L (seru albumin - ascites albumin)

82
Q

Treatment of SBP

A

2g ceftriaxone daily + conc albumin

83
Q

Secondary prophylaxis of SBP

A

Bactrim or norflox

84
Q

Who should get primary prophylaxis of SBP?

A

Low protein <10g/L ascites or bilirubin >50 with impaired renal function

85
Q

How often to do variceal screening in cirrhosis?

A

Annual if small varices 2nd yearly if no varices

86
Q

How to calculate the hepatic venous pressure gradient?

A

wedge hepatic venous pressure (WHVP) - free hepatic venous pressure (FHVP)

87
Q

MOA of terlipressin

A

Long-acting vasopressin analog Reverses splanchnic vasodilation

88
Q

Criteria for acute liver failure liver transplantation

A

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

89
Q

Which IBD do you get goblet cell deletion?

A

Ulcerative colitis (also crypt distortion, cryptitis, cryp abscesses)

90
Q

What metabolites of azathioprine can be measured for therapeutic drug monitoring

A

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

91
Q

Next step in loss of response to anti-TNF in inflammatory bowel disease

A

Measure trough drug levels and anti-drug antibodies

92
Q

Ultrasound appearance of NAFLD

A

Increased hepatic echogenicity (increased sensitivity with increased steatosis)

93
Q

What test to distinguish steatosis from NASH

A

Liver biopsy for histology

94
Q

What are the pathological features of NASH

A
  1. Steatosis - greated in zone 3 (peri-central vein) 2. Lobular inflammation 3. Fibrosis Summation of above in a scoring system indicates NASH
95
Q

Factors in calculating NAFLD fibrosis score

A

Age BMI IGF/diabetes AST ALT Platelets Albumin

96
Q

What is the biggest predictor of NASH/progression to fibrosis in NAFLD?

A

Diabetes

97
Q

Should statins be used in NAFLD

A

Yes even for patients with moderately abnormal liver tests

98
Q

What genes are responsible for HFE hereditary haemochromatosis

A

C282Y and H63D on HFE gene (chromosome 6) autosomal recessive w incomplete penetrance

99
Q

What is the most sensitive initial screening tool for haemochromatosis?

A

>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)

100
Q

What is the window period for anti-HCV Ab ELISA?

A

6 weeks

101
Q

Breast feeding in HCV risk of transmission

A

HCV RNA detected in breast milk but no increased risk with breast feeding

102
Q

What percentage of acute hep C progress to chronic hep C?

A

75-80% More chance of clearing if jaundiced initially

103
Q

What are extrahepatic manifestation of HCV?

A

Immune dysregulation: - Essential mixed cryoglobulinaemia 11x - membranoproliferative GN 7x - PCT 12x (photosensitive and blistering skin rash) - Lymphoma Also 11x increased risk of T2DM

104
Q

Can you treat HCV in pregnancy?

A

No

105
Q

HCV polymerase inhibitor antiviral ending

A

buvir

106
Q

HCV proteasome inhibitor antiviral ending

A

previr

107
Q

What antiviral regimens can be used for HCV in Child-Pugh B&C?

A

Sofosbuvir/velpatasvir ADD ribavirin

108
Q

What HCV antiviral should not be used for eGFR <30ml/min

A

Sofosbuvir

109
Q

How does cirrhosis affect the HCV DAA treatment?

A

Need to increase duration (normally from 8 to 12 weeks)

110
Q

How does MELD score affect HCV DAA treatment

A

MELD 15-20 treat cautiously MELD >20 defer treatment post transplant

111
Q

What drugs interact with DAAs in HCV

A

Amiodarone (can precipitate heart block) St John’s Wart Statins Digoxin Anticonvulsants PPIs ART

112
Q

Factors in Child Pugh Scoring

A

Encephalopathy

Ascites

INR

Albumin

Bilirubin

113
Q

What is the primary driver of ascites?

A

Portal hypertension

(not hypoalbuminaemia)

114
Q

Treatment of SBP if already on norfloxacin or bactrim prophylaxis

A

Piptaz

115
Q

What are high risk features in cirrhotic varices?

A
  • Size
  • Red wale marks
  • Advanced liver disease
116
Q

Indications for TIPS

A
  • Variceal bleedig unable to be treated endoscopically
  • Diuretic refractory ascites or hepatic hydrothorax
  • Budd-chiari
117
Q

Quad/triple phase CT appearance of HCC

A
  • Arterial enhancement
  • Porta vein washout
118
Q

Indications for HCC screening

A
  1. Cirrhotic patients, CP A and B
  2. Cirrhotic patients CP C awaiting liver transplantation
  3. Non-cirrhotic HBV carriers with active hepatitis or family history of HCC
  4. Non-cirrhotic patients with chronic hep C and advanced liver fibrosis F3
  5. Chronic HBV med >40, women >50 and african origin patients on diagnosis
119
Q

Treatment of stage C HCC (portal invasion

A

Sorafenib or lenvatinib (oral multi-kinase inhibitor)

se: palmar-plantar erythrodysesthesia

120
Q

What is a negative risk factor for GORD?

A

H. Pylori

121
Q

What is the main mechanism of reflux?

A

Transient lower oesophageal sphincter relaxation

122
Q

Surveillance of Barrett’s oesophagus

A
123
Q

Dysphagis and food impaction with following picture

  1. Diagnosis
  2. Treatment
A
  1. Eosinophilic oesophagitis
  2. PPI + topical steroid (fluticasone puffer)
124
Q
A

FRACP Shuyu (65 decks)

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