Gastroenterology Flashcards

1
Q

Substances involved in relaxation of Lower oesophageal sphincter

A

NO (nitrous oxide) & VIP (vasoactive intestinal peptide)

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2
Q

Diagnosis of eosinophilic oesophagitis

A

Biopsy >15 Eos/hpf at mid & prox oesophagus

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3
Q

Mechanism of action of PPI in eosinophilic oesophagitis

A

reduces chemotaxis of eosinophils

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4
Q

Manometry findings in achalasia

A

Incomplete LOS relaxation & aperistalsis

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5
Q

The types of achalasia based on manometry findings

A

Type I: no discernible P increase
Type II: panoesophageal pressurisation –> good prognosis (mostly p/w chest pain)
Type III: early, synchronous contractions (‘spasm’)

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6
Q

Manometry findings in distal oesophageal spasm

A

synchronous, uncoordinated contraction of smooth muscle of oesophageal body

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7
Q

Endoscopic stigmata of peptic ulcer with high risk of rebleeding on medical management

A

Active arterial bleeding (Forrest Ia) - 90%
Non-bleeding visible vessel (Forrest IIa) - 50%
Adherent clot (Forrest IIb) - 25-30%
Oozing without visible vessel (Forrest Ib) - 10-20%

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8
Q

Benefit of high dose PPI infusion for 72hrs for high risk ulcers post-endoscopy

A

Reduction in

  • Re-bleeding
  • Blood transfusion requirements
  • Hospital LOS & mortality
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9
Q

Risk factors of variceal bleeding

A

varix size, presence of red wale mark on varix, CP score, continuous EtOH abuse, HVPG>12mmHg, prev bleed

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10
Q

Benefit of octreotide in variceal bleeding

A

avoid early re-bleeding

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11
Q

Antibiotic choice & benefit of Abx in variceal bleeding

A

Ceftriaxone –> Norflox (total 7/7) - reduces re-bleeding, infection, death

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12
Q

Causes for isolated anti-HBc +ve (-ve HBsAg & anti-HBs)

A
  • Distant quiescent HBV infection (most common, born in HBV endemic areas)
  • False +ve
  • Resolving acute HBV infection
  • Occult HBV infection
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13
Q

When to treat HBV infection?

A
  • When HBeAg +ve & HBV DNA>20k + raised ALT
  • When HBeAg -ve & HBV DNA>2k + raised ALT
  • If fibrosis/cirrhosis
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14
Q

Adverse effect of entecavir in tx of HBV

A

lactic acidosis

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15
Q

Advantages of Tenofovir alafenamide over Tenofovir disoproxil

A

less risk of nephrotoxic & reduced BMD

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16
Q

Drug of choice for tx of HBV during pregnancy

A

Tenofovir disoproxil. not entecavir or pegylated interferon

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17
Q

Adverse effects & contraindication of pegylated interferon

A
  • Rare neuropsychiatric SE, trigger autoimmune dx

- Contraindications: decompensated liver dx, significant comorbidities or pregnancy

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18
Q

Groups with high risk of HCC with HBV infection

A
  1. Cirrhosis
  2. 1st deg relative
  3. Asian men >40 years
  4. Asian women >50 years
  5. ATSI>50 years
  6. African men & women >20 years
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19
Q

Regime for prevention of HBV transmission in pregnancy

A

Tenofovir 3rd trimester (for VL >10^6: start wk 30 to 4-12 wks post-delivery) + vaccination & HBIg for child (reduces risk fr 95% to 10%, tenofovir further reduced it)

  • Not indication for C-section
  • Breastfeeding is not contraindicated
  • Test HBsAg & anti-HBs at 9 months of age
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20
Q

Treatment of Hep D virus infection

A

peg interferon alfa for >48 wks

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21
Q

Hep C genotype most difficult to treat with direct acting antivirals

A

Genotype 3 (most common in Aus)

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22
Q

Extra-hepatic manifestations of HCV infection:-

A
  • MPGN (immune complex),
  • porphyria cutanea tarda
  • Mixed cryoglobulinaemia,
  • lichen planus,
  • arthritis, rash,
  • Neuropathy
  • Lymphoproliferative disorders (NHL, MALT)
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23
Q

Antiviral for Hep C which can’t be used for decompensated cirrhosis

A

NS3/4a protease inhibitors e.g. Glecaprevir

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24
Q

Antiviral classes for:-

  • Sofusbuvir
  • Velpatasvir, Ledipasvir
  • Glecaprevir, Voxilaprevir
A

Sofusbuvir - NS5b RNA polymerase inhibitors
Velpatasvir/Ledipasvir - NS5a inhibitors
Glecaprevir/Voxilaprevir - NS3/4a protease inhibitors

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25
Q

Medications contraindicated when taking Velatasvir/Sofusbavir (Epclusa)

A

Carbamazepine, Amiodarone

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26
Q

Medications contraindicated when taking Glecaprevir/pibrentasvir (Mavyret)

A

Atorvastatin, simvastatin, carbamazepine

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27
Q

HCV variant most significant for resistance to direct acting antivirals

A

Y93H mutation

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28
Q

Formula for hepatic vein pressure gradient and upper limit pressure causing clinical sequelae

A

HVPG=WHVP-FHVP

>10mmHg likely clinical sequelae (3-5mmHg normal)

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29
Q

Primary mechanism of ascites

A
  • Primarily due to portal HTN (not hypoalbuminaemia)
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30
Q

Criteria to diagnose spontaneous bacterial peritonitis from ascitic fluid

A

leucocytes >500, PMN >250cells/microL

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31
Q

Most common organism in SBP

A

Enterobacteriaceae (E coli & Klebsiella)

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32
Q

Antibiotic for

Spontaneous bacterial peritonitis

A

Ceftriaxone; If on norflox/bactrim -> Tazocin because more likely nosocomial & involves Ceft-res GN

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33
Q

Precipitants of Hepatic Encephalopathy

A
  • Infection
  • Bleeding
  • Constipation/diarrhoea
  • Metabolic/electrolyte derangeement
  • Drugs - opioid
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34
Q

Tx for Hepatorenal syndrome AKI

A

Albumin (1g/kg for D1-2 then 20-40g/day subsequent days + terlipressin

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35
Q

Radiological diagnosis of Hepatocellular Carcinoma

A

arterial enhancement AND portal venous or delayed washout

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36
Q

Why is TACE contraindicated in portal hypertension?

A

TACE blocks hepatic artery, required portal vein to supply liver

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37
Q

Milan Criteria for liver transplant

A
  • Single tumour <5cm OR 3 tumours <3cm each
  • No extrahepatic involvement
  • No major vessel involvement
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38
Q

Patient group to receive Sorafenib in advanced stage HCC

A

CP A cirrhosis, ECOG 0-1

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39
Q

Mechanism of action of Sorafenib

A

Anti VEGF, anti-angiogenesis

40
Q

Adverse effects of Sorafenib

A

fevers, diarrhoea, bleeding risk (need gscope & banding prior), palmar-plantar eryhtrodysesthesia
(Lenvatinib less risk to this)

41
Q

Immunotherapy used in unresectable HCC

A

Atezolizumab (anti-PDL1) & Bevacizumab (anti-VGEF)

42
Q

Genetic variant with high risk of non-alcohol fatty liver disease

A

PNPLA3 genetic risk variants (in Hispanics)

43
Q

Histological findings of NASH

A

> 5% hepatosteatosis wt inflammation & ballooning of hepatocytes with or without fibrosis

44
Q

Gene mutations associated with Hereditary Haemochromatosis

A

C282Y (85%) & H63D (minority of cases & lower likelihood of iron overload)
*only homozygous significant. similar risk to gen ppln if heterozygous

45
Q

indication for therapeutic phlebotomy in Hereditary Haemochromatosis

A

Ferritin>1k OR liver dysfunction (elevated ALT/AST, hepatomegaly) OR cardiac dysfunction (HF, arrhythmia)

46
Q

Components in MEDL score

A

Cr, Bili, INR, Na, HDx

47
Q

Inclusion criteria for liver transplant

A

Chronic liver dx with life-threatening cx
- MELD >15 (Cr, Bili, INR, Na, HDx)
- HCC that fulfill the UCSF criteria
Additional indications:-
▫ 2-yr mortality rate >50% w/out transplant
▫ Diuretic-resistant ascites, recurrent HE, recurrent SBP, recurrent GI haemorrhage
▫ Intractable cholangitis
▫ Hepatopulmo syndrome; portopulmo HTN
▫ Metabolic syndromes (e.g. familial amyloidosis, urea cycle disorders, oxalosis)
▫ Polycycstic liver dx

48
Q

King’s College Hospital Criteria for acute liver failure (paracetamol-induced)

A
- pH of ABG <7.3 OR
All 3 of the following:-
- INR>6.5
- Cr>300
- Grade III/IV encephalopathy
49
Q

King’s College Hospital Criteria for acute liver failure (not paracetamol-induced)

A
- INR >6.5 OR
3 out of 5:-
- Age <10 or >40
- Bili >300
- Jaundice-to-Coma time of >7/7
- Drug toxicity
- INR>3.5
50
Q

UCSF Criteria for liver transplant in HCC

A
  • Single nodule <6.5cm or

- Up to 3 nodules, largest <4.5cm or Cumulative tumour size<8cm

51
Q

Immune cells involved in coeliac disease

A

CD4 T cells

52
Q

Coeliac ab serology testing

A

Either request tTG-IgA + Total IgA level (2-3% coeliac Ig A def) OR tTG-IgA + DGP-IgG (de-amidated gliadin)

53
Q

Findings from small bowel biopsy in coeliac

A

intraepithelial lymphocytes, crypt hyperplasia & villous atrophy

54
Q

HLA a/w coeliac disease which can be used to exclude diagnosis

A

HLA-DQ2, HLA-DQ8

55
Q

susceptibility genes ininflammatory bowel disease

A

NOD2/CARD15

56
Q

Histological findings in :-

UC vs Crohn’s

A

UC: Confined to mucosa & submucosa, Lymphocytic infiltrate & goblet cell depletion, Crypt distortion, cryptitis & crypt abscesses

Crohn’s: Transmural inflamm with lymphocytic infiltrate & macrophages. Granulomas can be present

57
Q

Antibodies a/w UC vs Crohn’s

A

UC - ANCA

Crohn’s - ASCA (anti-saccharomyces cerevisiae ab)

58
Q

Extra-intestinal Manifestations

of UC a/w active disease

A

Oral ulcers
Erythema nodosum
Large joint arthritis
Episcleritis

59
Q

Extra-intestinal Manifestations

of UC independent of disease

A
Primary sclerosing cholangitis
Ankylosing spondylitis
Uveitis
Pyoderma gangrenosum
Kidney stones, gallstones
60
Q

thiopurine + anti-TNF in young males is a/w which malignancy?

A

hepatosplenic T-cell lymphoma

61
Q

Indications for Anti-TNF alpha antibodies in IBD

A

i. Inflammatory CD refractory to steroid & AZA/MP/MTX
ii. Refractory fistulizing CD
iii. Acute severe UC failing IV steroid
iv. Mod-severe chronic UC failing 5-ASA/thiopurine

62
Q

What to do if loss of response to TNF blocker?

A

check trough drug level & anti-drug ab (ADA)

  • if therapeutic drug level -> switch out of class
  • if subtherapeutic & ADA +ve, switch to another TNF blocker
63
Q

Mechanism of action of Vedolizumab

A

Inhibitor of α4β7 integrin on T lymp surface –> blocks MAdCAM-1 on intestinal endothelium –> inhibits trafficking of leukocytes to sites of inflamm

64
Q

Mechanism of action of Ustekinumab

A

mAb to p40 subunit of IL12/IL23

65
Q

Definition of acute severe colitis for UC

A

bloody stool freq >6/day + one of these (HR>90, temp>37.8C, Hb<105, ESR>30)

66
Q

Surgical indication for UC

A
  • Fulminant dx
  • Failed medical tx
  • Dysplasia/cancer
67
Q

Surgical indication for Crohn’s

A

Failed medical tx (ineffective, poorly tolerated) with complications - stricture, fistula, abscess, perforation

68
Q

When to perform annual surveillance colonoscopy in IBD?

A
  • active disease
  • PSC
  • Family hx of 1st deg relatives
69
Q

Risk of absent ileocecal valve

A

small intestinal bacterial overgrowth

70
Q

Signs of zinc deficience

A

oligospermia, hair loss, growth retardation, hypogonadism in males, delayed wound healing, bullour-pustular dermatitis, alopecia

71
Q

Stool tests for:-

  • inflammation
  • protein-losing enteropathy
  • lack pancreatic enzymes
A
  • inflammation -> calprotectin
  • protein-losing enteropathy -> A1AT
  • lack pancreatic enzymes - elastase
72
Q

Medications causing cholestatic picture in DILI

A

Augmentin, cephalosporin, fluclox, OCP

73
Q

Medications causing hepatocellular picture in DILI

A

paracetamol, statins, isoniazid

74
Q

Causes of markedly elevated ALT & AST (>25 ULN)

A
  • Ischaemic hepatitis (hypotension, renal failure, elevated LDH)
  • Viral hepatitis
  • Drug induced (paracetamol)
  • Hepatic vein thrombosis
75
Q

Causes with AST:ALT >2

A

EtOH/NAFLD, Hep C cirrhosis or Wilson’s(if in acute liver failure)

76
Q

Histology findings in Alcohol-related liver damage

A

globular red hyaline material within hepatocytes

77
Q

Histology findings in Alcoholic hepatitis

A

neutrophil infiltrate

78
Q

Mechanism of action of acamprosate vs naltrexone

A

acamprosate - reduces neuronal hyperexcitability of withdrawal
naltrexone - blocks effects of endogenous opioids to reduce cravings

79
Q

Histological findings in primary sclerosing cholangitis

A

degeneration of small bile ducts with periductal sclerosis/fibrosis - onion skin pattern

80
Q

Histological findings in primary biliary cholangitis

A

bile duct degeneration with periductal granulomatous inflammation - florid bile duct lesion

81
Q

difference between osmotic vs secretory diarrhoea

A

secretory - large volume watery stool despite fasting (consider carcinoid syndrome)

82
Q

tests for carcinoid syndrome

A

urinary 24-hr 5-HIAA (metabolite of serotonin), chromogranin A

83
Q

diagnosis of irritable bowel syndrome

A

recurrent abdo pain, at least one day per week in last 3/12 + at least 2:-
1. relieved with defecation, 2. assoc wt change in freq & 3. changeform/appearance of stool

84
Q

Mechanism of action of PPI

A

Selectively inhibit H-K ATPase in gastric parietal cells –> suppress gastric acid secretion

85
Q

Types of adenoma with the highest oncogenic potential

A

Tubular adenoma, tubulovillous adenoma

> sessile > hyperplastic

86
Q

Amsterdam Criteria –> refer for genetic counselling/testing for risk of CRC/Lynch

A
  • 3 relatives w CRC, 1 of whom is 1st deg relative of the other 2
  • At least 2 successive generations involved
  • At least 1 of the ca dx
87
Q

Malignancy related to familial adenomatous polyposis

A
  • colorectal ca
  • ampullary/duodenal ca - 5 yearly duodenoscopy
  • desmoid tumours
88
Q

When to perform prophylactic colectomy in classical FAP?

A

age 15-25 once adenomas observed

89
Q

Screening colonoscopy for

Peutz-jeghers syndrome

A

Screening colonoscopy at 8 y/o then every 3 yrs fr 18 +/- capsule endoscopy/MR enterography

90
Q

Effects of Cholecystokinin production (produced from D cell)

A
  • slow down gastric emptying
  • Pancreatic enzyme release
  • Smooth muscle contraction
91
Q

what happens with

loss of interstitial cells of Cajal

A

motility disorder of the GI

92
Q

Histology of autoimmune hepatitis

A

lymphoplasmocytic infiltrate in portal tract that extends into the lobule causing hepatic necrosis with rosetting of liver cells

93
Q

Drugs precipitating Autoimmune hepatitis

A

Minocycline, nitrofurantoin, INH, PTU, Methyldopa

94
Q

antibodies a/w autoimmune hepatitis type 1

A

anti-SMA, ANA

95
Q

antibodies a/w autoimmune hepatitis type 2

A

anti-LKM1, anti-LKM3

96
Q

Initial tx for autoimmune hepatitis

A

prednisolone & azathioprine

97
Q

Blood test findings in primary biliary cholangitis

A

Elevated IgM, high lipids, AMA (95%), ANA (30%)