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Gastroenterology Flashcards

1
Q

Achalasia associated with which cancer

A

SCC (10x risk compared to general population)

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2
Q

Achalasia barium swallow findings

A

Bird’s beak

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3
Q

Which subtype of achalasia is most severe?

A

Type 1

Progression from Type 3 to Type 1

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4
Q

Which subtype of achalasia has the best treatment outcome?

A

Type 2

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5
Q

Oral Tx options for achalasia

A

CCB
Isosorbide dinitrate
(effective in 50-60%)

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6
Q

Complication with Botox injection for achalasia

A

Causes submucosal fibrosis and unable to do subsequent definitive surgical treatment

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7
Q

Efficacy of Balloon dilatation in achalasia

A

60-90% effective
Risk of perforation in 1-6%
Recurrence in 2-3 years

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8
Q

Treatment of choice for achalasia

A

POEM (PerOral Endoscopic Myotomy)

  • Success similar to Lap Myotomy, but less recovery ime
  • SE: Reflux ++
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9
Q

Classic endoscopic features of eosinophilic oesophagitis

A
  • Oedema
  • Longitudinal furrows
  • White exudates
  • Concentric rings
  • Strictures and mucosal tearing
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10
Q

Treatment of eosinophilic oesophagitis

A
  • PPI
  • Aerosolised steroids
  • Diet: Elemental; Eliminate milk, wheat, gluten, eggs, nuts, shellfish, soy
  • Dilatations for strictures
  • Esperimental: Budesonide, montelukast
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11
Q

Mucosa change in Barret’s oesophagus

A

Strafed squamous epithelium replaced by cardiac type mucus secreting columnar epithelium +/- intestinal metaplasia

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12
Q

Medical treatment shown to slow/stop progression of Barrett’s to adenocarcinoma

A

PPI and aspirin therapy

  • AspECT trial
  • Surgical therapy is no more effective than PPI
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13
Q

Survival with Oesophageal Adenocarcinoma

A

5 year survival <20%

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14
Q

Mx recommendation for low grade dysplasia in Barrett’s

A

If LGD confirmed on 2 occasions 6 months apart by two pathologists, then endoscopic RFA is recommended OR close surveillence
-Risk of progression to HGD

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15
Q

Risk of HGD in Barrett’s to progress to Adenocarcinoma

A

~10%

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16
Q

Mx of HGD in Barrett’s

A
  • Oesophagectomy vs endoscopic resection
  • Then RFA to rest of Barrett’s due to risk of transformation
  • Annual Gscope annually for 5 years
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17
Q

Risk of recurrence of Barrett’s post surgical excision/RFA

A

~10%

Greatest in first year

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18
Q

Features suggestive of malignant dysphagia

A 
Shorter duration
Solids > liquids
Constant and progressive
Older age
Accompanying alarm symptoms
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19
Q

Mx of refractory GORD

A

Failed PPI BD trial for 3 months

  • Check compliance and lifestyle modifcations
  • Trial nocte H2 antagonist
  • Repeat scope and perform pH testing
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20
Q

Location of most gastric ulcers and duodenal ulcers

A

Junction of fundus and antrum along the lesser curvature

DU are usually in the 1st or 2nd part

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21
Q

Evidence of PPI therapy in GI bleeding

A

No mortality benefit

Reduction in need for endoscopic therapy compared to placebo

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22
Q

Forrest Ia

A

Spurter

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23
Q

Forrest IIa

A

Non bleeding visible vessel

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24
Q

Forrest IIb

A

Clot at base

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25
Q

Forrest IIc

A

Dot

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26
Q

Forrest III

A

Clean Base

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27
Q

Evidence for post endoscopy PPI for GI bleeds

A

Reduces rebleeding significantly

-IB PPI infusion for 72 hours recommended post procedure

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28
Q

H pylori genes linked to carcinogenesis

A

cagA and vacA

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29
Q

Cancers associated with H. Pylori

A

Gastric cancer

MALT lymphoma

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30
Q

H pylori associated with a decreased risk of what cancer

A

Oesophageal adenocarcinoma

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31
Q

Treatment of H Pylori

A

Quad therapy:
PPI+Amoxy+Metro+Clarythromycin x 14 days
PPI+ Bismuth +Metro+Tetracycline x 14 days

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32
Q

Immune cell associated with MALT Lymphoma

A

Low grade B cell neoplasia

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33
Q

H Pylori association with ITP

A

H pylori eradication improves platelet counts in ~ 50% of ITP

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34
Q

When to do post H pylori eradication testing

A

> 4 weeks after completing treatment

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35
Q

Duration off ABx and PPI to investigate for H pylori

A

> 4 weeks ABx

>2 weeks PPI

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36
Q

Endoscopic features of malignant gastric ulcers

A

Irregular outline with necrotic or haemorrhagic base
Irregular raised margins
Prominent and oedematous rugal folds that usually do not extend to the margins

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37
Q

What INR is it safe to do a Gscope at

A

= 2.5

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38
Q

When to restart warfarin post UGIB

A

7-14 days post procedure

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39
Q

Histological Features of Coeliac Disease

A

Intra-epithelial lymphocytes
Crypt hyperplasia
Villous atrophy

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40
Q

Best initial testing for coeliac disease

A

Anti TTG IgA
High sensitivity and specificity
-If weakly positive, then do anti endomysial IgA

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41
Q

Non Responsive Coeliac Disease

A
  • Compliance!
  • Alterative associated issues: SIBO, Microscopic colitis, IBS
  • Diet review
  • Repeat Histo
  • Colonic Bx - ?microscopic colitis
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42
Q

Refractory Coeliac Disease Type 1

A

Steroids +/- steroid sparing agent

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43
Q

Refractory Coeliac Disease Type 2

A

Poorer prognosis
Oligoclonal T cell expansion
High risk of transformation to enteropathy associated T cell lymphoma

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44
Q

PAS positive macrophages in sub mucosa on GI biopsies

A

Whipple’s Disease

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45
Q

Affect of omeprazole on Gastrin Level

A

Omeprazole increases Gastrin levels

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46
Q

Enterchromaffin cells

A

Stimulates gastric acid secretion
Responds to gastrin
Contains Histamine
Stains positive with silver

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47
Q

Hyperplasia of enterochromaffin cells in the gastric mucosa is associated with

A

Atrophic gastritis

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48
Q

Medication effective in preveting gastric ulceration with NSAID use

A

Misoprostol

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49
Q

Immunosuppressed and small discrete ulcers in the oesophagus - cause?

A

HSV

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50
Q

Immunosuppressed and giant ulcers in the oesophagus - cause?

A

CMV

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51
Q

CD117 (c-KIT)

A

GIST

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52
Q

Main mechanism of reflux in majority of episodes

A

Transient LOS relaxation due to vagal stimulation in setting of proximal gastric distension

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53
Q

Side effect of giving folic acid in B12 deficient patients

A

Causes severe neuropathy and worsening B12 deficiency because it will stimulate erythropoesis and further worsen B12

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54
Q

Side effect of giving glucose prior to thiamine in refeeding syndrome

A

Acute Beri Beri

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55
Q

Refeeding Syndrome - Glucose has what effect on insulin

A

Hyperinsulinaemia

  • Which then results in Fluid and salt retention and intracellular K=/PO4 shift
  • Results in dilutional hypoalbuminaemia
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56
Q

Factors which favour intestinal absorption in short bowel syndrome

A

-Length of remaining bowel (>60-90 cm of SB with colon OR >150 cm small bowel)
-Ileum>Jejunum
-Ileocecal valve present
-Absence of mucosal disease
-Presence of colon
-

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57
Q

Benefit of having a retained ileocecal valve in short bowel syndrome

A

Reduces risk of Small bowel bacterial overgrowth

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58
Q

What renal stones are associated with short gut

A

Oxalate

-Treat with calcium

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59
Q

Role of GLP2 in Short gut syndrome

A

Provides feedback to the upper intestine to optimise the nutrient and fluid absorption

  • Mucosal growth
  • Teduglutide
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60
Q

Target Hb for UGIB

A

70-90

-Reduces adverse events, further bleeding and improves 6 week survival

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61
Q

Evidence for IV PPI for 72 hours post endoscopy for UGIB

A

-Improved rate of rebleeding, blood transfusion requirement, duration of hospital stay

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62
Q

Evidence for Octreotide in variceal bleeding

A

Reduction in rebleeding and number of patients failing initial haemostasis

NO reduction in mortality

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63
Q

MOA Terlipressin

A

Synthetic vasopressin analogue

Avoid in significant CAD or PVD

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64
Q

Evidence for ABX in vleeding varices

A

Quinolones/3rd Gen Cephalosporins

  • REduce all cause and infection mortality
  • Reduced rebleeding rates
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65
Q

Evidence for ABX in vleeding varices

A

Quinolones/3rd Gen Cephalosporins

  • REduce all cause and infection mortality
  • Reduced rebleeding rates
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66
Q

Evidence for endoscopic rubber band ligation in acute oesophageal varices

A

Fewer side effects and more effective than sclerotherapy

Reduced mortality and rebleeding

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67
Q

Secondary prophylaxis for oesophageal varices

A

BB - Propanolol - start at Day 3-5 post acute bleed
-Reduce rebleeding and mortality

Further banding sessions 2-4 weeks a part until eradication (3-4 sessions)

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68
Q

NAFL Definition

A

Presence of steatosis without liver injury

Minimal risk of disease progression

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69
Q

NASH Definition

A

Hepatic steatosis and inflammation with hepatocyte injury (ballooning) with or without fibrosis. Can progress to cirrhosis, liver failure and cancer

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70
Q

NASH Cirrhosis Definition

A

Cirrhosis with current or previous evidence of NASH

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71
Q

Cryptogenic Cirrhosis

A

Cirrhosis with no obvious aetiology. Many have metabolic risk factors and likely to have NASH cirrhosis

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72
Q

What percent of Fatty liver progresses to NASH and cirrhosis

A

20% from fatty liver to NASH

4-8% NASH to cirrhosis

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73
Q

Tests used to screen for advanced liver fibrosis in NAFLD

A
  • Presence of T2DM
  • Decreased platelets
  • AST:ALT >1
  • NALFD Fibrosis score
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74
Q

Fibroscan result that correletes well with portal HTN

A

> 25

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75
Q

Most reliable test to rule out advanced hepatic fibrosis (High negative predictive value)

A

Fibroscan

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76
Q

Indications for Liver Bx for NAFLD

A

Abnormal ALT/GGT AND

  • > /=3 features of metabolic syndrome (esp T2DM)
  • NAFLD Fibrosis Score/Fibroscan 8-12
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77
Q

Benefits of weight loss in NAFLD

A

Improves biochemical profile, histo, decreases steatosis, reduces inflammation, decreases fibrosis

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78
Q

HCC surveillance in cirrhosis

A

6 monthly USS in NASH cirrhosis

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79
Q

Haemochromatosis Histo

A

Grade 3 hepatocyte iron accumulation with an acinar distribution pattern
Stains with Perl’s prussian blue

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80
Q

Hereditary Haemachromatosis genetics

A

Autosomal recessive
HFE on chromosome 6
-C282Y mutation

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81
Q

TF Saturation in haemachromatosis

A

> 45%

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82
Q

Classic triad of haemachromatosis

A

Bronze skin
Cirrhosis
Diabetes

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83
Q

Most sensitive screening tool for haemachromatosis

A

Fasting morning transferrin saturation

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84
Q

Hepatitis B in pregnancy - Risk with normal delivery and breast milk

A

No protective effect of C-section

No increased risk with breast milk

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85
Q

Hepatitis E Antigen

A

Correlates with infectivity (marker of active replication) Higher viral load
Anti-HbE important sign of serovconversion of eAg and beginning of clearance

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86
Q

HbsAg -
Anti HBc +
Anti HBs -

A
  • Most often: Distant resolved infection wit hloss of HBsAb
  • Recovering from acute infection before sAb is detected
  • False positive
  • PAssive transfer of maternal anti HBc in children up to 3
  • Occult Hep B

CHECK viral load!

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87
Q

Occult Hepatitis B

A

Presence of HBV DNA without detectable surface antigen

Still at risk of cirrhosis and HCC

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88
Q

Hep B Pre core mutant or Basal core promoter mutant

A

Downregulates HBeAg production: HBeAg negative/Ab positive

Increased rates of advanced disease

Escaping immune control

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89
Q

Risk of death with chronic Hep B

A

15-25% chance of death associated with virus

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90
Q

Chronic Hep B:

Immune Tolerance

A

High HBV DNA
Normal LFTs
HBeAg Positive

Children usually remain in this phase until 20s to 30s

Mx: Monitor 6-12 months

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91
Q

Chronic Hep B:

Immune Clearance

A

Body begins to recognise Hep B and attacks

Viral load begins to drop
Derranged LFTs
Usually HBeAg seroconversion

At risk of progression to cirrhosis and HCC at this stage

Mx: Medications

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92
Q

Chronic Hep B:

Immune Control

A

Inactive virus
Lower HBV DNA
Normal LFTs
HBeAg negative and Ab positive

Mx: Monitor 6-12 months

At this stage: 3 things can happen

  • Clear virus (rare)
  • Remain in immune control long term
  • Immune escape
93
Q

Chronic Hep B:

Immune escape

A

High HBV DNA
Derranged LFTs
HBeAg negative and Ab positive

At risk of cirrhosis and HCC

94
Q

Hep B Surveillance

A

6 monthly Liver USS and AFP
Fibroscan 2 yearly

Patient groups:

  • Cirrhosis
  • Family or PHx of HCC
  • HBV Asian men over 40 or women over 50
  • HBV africans over 20
  • HBV >40 years age with Increased HBV DNA and Increased ALT
95
Q

Treatment of Chronic Hep B:

Polymerase inhibitors

A 
TDF
Entecavir
Lamivudine
Adefovir
TAF

Benefit:

  • Suppress HBV DNA
  • HBeAg seroconversion 10-20%
  • No resistance with Entec and TDF/TAF
  • Safe in deco,pensated disease

Downside:
-Indefinite therapy

96
Q

Treatment of Chronic Hep B:

Immunomodulator

A

Peg Interferon

Benefit:

  • Higher rate of HBeAg loss in 1 year
  • Finite course
  • No resistance

CI:
-Cirrhosis, pregnancy, acute Hep B, immunosuppressed, psych instability

97
Q

What is the normal ULN for ALT

A

25 in females

35 in males

98
Q

HBeAg Positive + non cirrhotic

When to treat?

A

ALT >/= 2xULN
HBV DNA >20,000

If HBV DNA <20,000 and persists for 6 months, then treat

99
Q

HBeAg Negative + non cirrhotic

A

ALT >/= 2xULN

HBV DNA >2,000

100
Q

Choice of Hep B treatment if known previous Lamivudine resistance

A

TDF/TAF

Likely to have Entecavir resistance

101
Q

Choice of Hep B Tx in decompensated cirrhosis

A
  1. Entecavir perferred

2. TDF/TAF

102
Q

Choice of Hep B Tx in Renal insufficiency

A

Entecavir preferred

103
Q

Choice of Hep B Tx in Pregnancy/child bearing age

A

Tenofovir

104
Q

Choice of Hep B Tx in women of child bearing age wishing to eradicate virus prior to pregnancy

A

Peg Interferon alfa 2a or 2b

105
Q

Choice of Hep B Tx in HIV coinfection

A

Tenofovir +Emtricitabine or Lamivudine

106
Q

Pregnant woman + Hep B Viral load in 2nd trimester <10^5 -?Mx

A

Monitor

Infant: HBIG +vaccine at birth w/i 12 hours of birth (efficacy 95%)

107
Q

Pregnant woman + Hep B Viral load in 2nd trimester >10^5

A

Tenofovir at 28-32 weeks

Infant: HBIG +vaccine at birth within 12 hours of birth

108
Q

Hepatitis D

A

Most aggressive Hepatitis
Needs HBsAg to replicate
Treatment Peg interferon for 2 years (30% efficacy)
Check for it if ALT not improving with Hep B treatment

109
Q

Commonest cause for liver transplat

A

Hepatitis C

110
Q

High levels of mutation in Hep C due to what?

A

RNA polymerase can’t proof read

111
Q

Most common genotypes in Australia for Hepatitis C

A

1 and 3

112
Q

Definition of Quasispecies in Hep C

A

Different strains within a host

Importnat in viral persistance, lack of response to IFN based therapy and leads to difficulties in vaccine development

113
Q

How to test for Hepatitis C

A

ELISA
Window period of 6 weeks (ranging 2-26 weeks)

If indeterminate response - Do HCV RNA

114
Q

Most specific test for Hep C

A 
HCV RNA (PCR)
-Can pick up active infection earlier with this

Qualitative: Diagnosis of infection

Quantitative: Viral burden and duration of Tx with IFN

115
Q

Hep C Point of care testing

A

HCV ab mouth swab or fingerprick
HCV viral load in 105 mins
Same day result

116
Q

What are the perinatal transmission risks for Hep C

A

2-8% risk of vertical transmission if RNA + (Higher if HIV +)
No increased risk of transmission with breast feeding
No evidence for CS

Baby: Can only check HCV ab after 15-18 months due to passive transfer from mum

117
Q

Factors related to spontaneous clearance of Hep C

A

Younger age
Female
MHC genes, IL28B

118
Q

Extrahepatic Manifestations of Hepatitis C

A
  • Rh Factor postive
  • T2DM 11x increase risk
  • Cryo
  • Membranoproliferative GN 7x risk
  • PCT
  • Lichen planus
  • Lymphoma
  • Keratoconjunctivitis sicca
119
Q

APRI Test

A

Used to assess for Fibrosis

  • AST to Platelet Ratio Index
  • > 1 result is suggestive of cirrhosis

Equation: AST/ULN AST all divided by platelet count x100

120
Q

SVR -Sustained virological response in Hep C definition

A

HCV RNA negative 12 weeks after completion of treatment

121
Q

Direct Acting Antivirals MOA

A

Target specific non structural proteins of HCV to disrupt viral replication
-4 classes

122
Q

Nucleoside NS5B polymerase inhibitors

A
  • Buvirs

- Sofosbuvir

123
Q

Non Nucleoside NS5B polymerase inhibitors

A

-Dasabuvir

124
Q

NS3/4 Serine protease inhibitors

A

-Previrs

125
Q

NS5A replication inhibitors

A

-Asvirs

126
Q

Pangenotypic Hep C treatment

A

Sofosbuvir/Velpatasvir

-Add ribavirin for Child pugh B and C

127
Q

Hep C treatment duration

A

Varies with regimes and if cirrhotic

  • Cirrhosis: 12 weeks
  • Sometimes less if non cirrhotic
128
Q

Hep C Treatment Adverse effects

A

Fatigue/Insomnia
Headache
GI Sx

Can Reactivate Hep B!

129
Q

Drug interactions with Hep C treatments

A

Statins
Omeprazole - Reduces absorption
Amiodarone (Bradycardia)
Potent P-gp inducers (rifampicin, St. Johns wort)

130
Q

MELD scores for HEP C treatment guidance

A

MELD < 15 -treat
MELD 15-20/25 - Treat cautiously
MELD >20/25 -Defe Tx until post Transplant - If not a transplant candidate - discuss with patient as may worsen liver failure

131
Q

HCC screening after SVR in Hep C

A

Mild fibrosis - none

F3-F4 fibrosis: USS and AFP 6 monthly

132
Q

MOA of Cirrhosis

A
  • Primarily due to activation of hepatic stellate cells (liver macrophages)
  • Involved in healing and repair after biliary or hepatocellular injury
  • Chronic activation results in increased collagen & extracellular matrix
133
Q

Fibroscan Scores

A

F0-1: <7.5 = absent/mild disease
F2-3: 7.5-13 = unclear
F4: >13 = Cirrhosis

134
Q

Factors assessed in Child Pugh Score

A
  • Encephalopathy
  • Ascites
  • INR
  • Albumin
  • Bilirubin
135
Q

MOA of cirrhotic portal HTN

A

-Increased vascular resistance due to structure (liver vasc architecture by fibrosis) and Dynamic (increased hepatic vascular tone due to endothelial dysfunction and decreased NO bioavailability

136
Q

Ascites

A
  • Reflects renal Na+ and H2O retention via activation of RAAS
  • Portal HTN is primary driver, not hypoalbuminaemia
137
Q

SAAG Score

A

Serum Albumin - Ascites albumin

> 11 suggestive of portal HTN

138
Q

SBP Leucs and PMN in ascitic fluid

A

Leucs >500
PMN >250

If significantly higher leucs and polys, may need to consider alternative cause - ?perforation

139
Q

SBP Mx

A
  • 3g Ceftriaxone for 5-7 days
    (Tazocin if on norflox/bactrim)
    -IV Conc Albumin load and >2 bottles/day for >3 days
    -Repeat tap 48 hours post tratment
140
Q

Hepatic Hydrothorax

A

Ascitic fluid leaking into pleural space, usually right sided

141
Q

Ascites Mx

A
  • Spiro 100mg
  • Frusemide 20 mg
  • Aim 1 kg weight loss/day
  • Restrict salt to 5 g/day (more important than fluid restriction)
  • AVOID Normal Saline, leads to salt retention and worsening ascites
142
Q

Albumin with paracentesis

A

20% conc albumin 100 ml over 1/24 for each 2L ascites drained

  • Colloid osmotic effect 4x that of plasma
  • Prevents large plasma volume drainage - renal failure/hypotension
143
Q

Ascites refractory to diuretics

A
  • Weekly Albumin infusion shown to improve mortality
  • TIPS; Terlipressin infusions as outpatient
  • Transplant consideration
144
Q

Hepatic Encephalopathy

West Haven Criteria

A

Grade 1: Trivial lack of awareness; euphoria or anxiety; shortened attention span; impaired performance of addition or subtraction

Grade 2: Lethargy or apathy; minimal disorientation for time/place; personality change, inappropriate behavior

Grade 3: somnloence to semistupor but responsive to verbal stimuli; confusion; gross disorientation

Grade 4: Coma

145
Q

Hepatic encephalopathy Mx

A

Lactulose
Rifaximin add on
-Reduced recurrence of HE, not mortality

146
Q

Mx of VAriceal bleeding

A
  1. SBP >90
  2. Hb >70
  3. Blood/ albumin preferable - avoid saline
  4. IV thiamine if drinker
  5. Blood cultures and empical IV Ceftriaxone
  6. Terlipressin
  7. Scope
147
Q

TIPS Indications

A
  • Variceal bleeding unable to be treated endoscopically
  • Diuretic refractory ascites or hepatic hydrothorax
  • Budd Chiari
148
Q

TIPS Contrindications

A

Increased Risk of HE!

RHF

149
Q

Type 1 HRS

A
  • Acute deterioration
  • Poor outcome if untreated (50% survival at 11 days)
  • Mx: Terlipressin infusion and Albumin, and ultimately need transplant or will ide
150
Q

Type 2 HRS

A
  • Slow progression
  • A/W refractory ascites
  • 6 month transplant free survival 40-50%
151
Q

HCC CT Quad phase finding

A

Arterial enhancement, portal vein washout

152
Q 
HCC Mx (BCLC Staging)
-Single HCC <2 cm, normal Portal pressure
A

Resection

153
Q 
HCC Mx (BCLC staging)
-Single HCC <2 cm, Increased Portal pressure
A

Transplant

154
Q 
HCC Mx (BCLC staging)
-3 nodules <3 cm and no associated diseases
A

Transplant

155
Q 
HCC Mx (BCLC staging) Early stage
-3 nodules <3 cm and no associated diseases
A

RFA

156
Q 
HCC Mx (BCLC staging) Intermediate
-Multinodular and no portal HTN
A

TACE (palliative)

  • Transarterial chemo embolisation
  • Can decompensated CLD if portal HTN is present
157
Q 
HCC Mx (BCLC staging) Advanced
-Portal invasion, metastatic disease
A 
Sorafenib (palliative)
-Multi kinase inhibitor
(VEGF and platelet derived growth factor receptors), RAF
-Only suitable for compensated cirrhosis
-ECOG 0-1

SE: Palmar-plantar erythrodysesthesia, Fatigue, fevers, diarrhea, increased bleeding risk (so banding prior)

  • Lenvatinib (non inferior and also first line)
  • Can change between the two if there is intolerance
158
Q 
HCC Mx (BCLC staging)
-Child Pugh C
A

Terminal, symptomatic

159
Q

SBP Prophylaxis indication

A 
low protein (<10g/L) or Bilirubin >50 with impaired renal function
-Norflox 400 mg daily or Bactrim reduces mortality and SBP
160
Q

Variceal screening frequency if small varices

A

annual

161
Q

Variceal screening frequency if no varices

A

2 yearly

162
Q

Calculating Hepatic Venous Pressure Gradient (HVPG)

A

HVPG = WHVP - FHVP

WHVP = Wedged Hepatic Venous Pressure

FHVP = Free Hepatic Venous pressure

163
Q

HVPG suggesting Portal HTN

A

> 5

If >10, then increased likelihood of varices, decompensation and HCC

Gives you pressure over the sinusoids

164
Q

MOA of propanolol with varices

A

Reduction in cardiac output and splanchnic blood flow

Allow unopposed alpha-1 adrenergic receptor activity which results in splanchnic vasoconstriction and reduction in portal pressure

165
Q

Kings college criteria for ALF (paracetamol Induced)

A
  • pH <7.3 OR all of the following:
  • INR >6.5
  • Cr >300 micromol/L
  • Grade 3 or 4 HE
166
Q

Kings college criteria for ALF (non paracetamol induced)

A
  • INR >6.5 OR 3 out of 5 of the following:
  • Age <11 or >40
  • Bilirubin >300 micromol/L
  • Jaundice to coma time >7 days
  • INR >3.5
  • Drug toxicity
167
Q

MELD Score for Transplantation

A

> 15

168
Q

Early (<3/12) Liver Tx morbidity/mortality

A

Graft failure (rare)
Infection
Biliary stricture
Renal/diabetes/cosmetic

169
Q

Findings of acute Rejection in Liver Transplant and time period

A
  • Portal Based inflammation (cholestatic LFTs)
  • Usually at days 7-10
  • Occurs in 1/3
  • No chronic sequelae
  • Mx: Bolus steroids
170
Q

Findings of chronic Rejection in Liver Transplant

A

Rare

  • Vanishing bile duct syndrome (cholestatic LFTs)
  • Increase Tacrolimus dose for Mx
171
Q

Milan Criteria for HCC Transplantation

A 

Single lesion ≤ 5cm, and/or

Up to 3 separate lesions, all < 3cm

No evidence of gross vascular invasion

No evidence of regional nodal or distal metastases
172
Q

UCFS Criteria for HCC Transplantation

A


A single nodule ≤ 6.5cm, or

Up to 3 nodules, the largest of which is ≤ 4.5cm

Cumulative tumoursize (sum of all diameters) ≤ 8cm

173
Q

Most specific LFT parameter for liver

A

ALT

174
Q

LFTs in Pregnancy:

Hyperemesis Gravidarum

A

1st Trimester
Vomiting and weight loss
ALT/AST Increase

175
Q

LFTs in Pregnancy:

HELLP

A

2nd/3rd Trimester/Postpartum
HTN, RUQ/epigastric pain, N+V, Headache, visual changes
AST >2x ULN; Plt <100,000; LDH >600; Pr:Cr >0.3 mg
Mx - Delivery

176
Q

LFTs in Pregnancy:

Preeclampsia

A

2nd/3rd Trimester/Postpartum
HTN, Headache, visual change, RUQ/epigastric pain
AST/ALT >2xULN, Plt <100,000
Mx - antihypertensives, MgSO4

177
Q

LFTs in Pregnancy:

Intrahepatic Cholestasis

A

2nd/3rd trimester
Pruritis, steatorrhea, RUQ pain
Usually AST/ALT <2xULN
Mx - Ursodeoxycholic acid or cholestyramine

178
Q

LFTs in Pregnancy:

Acute Fatty Liver in Pregnancy

A

3rd Trimester
N+V, abdo pain, acute liver failure
AST and ALT elevations up to 500
Mx- Delivery

179
Q

Cause of Increased AST:ALT

A

Alcoholic hepatitis
NASH
Chronic HCV cirrhosis
Wilson’s disease

180
Q

Role for Maddrey Score

A

In Alcoholic Hepatitis
Prognostication
Uses PT and Bilirubin
Score >32 suggests poor prognosis and may benefit from steroids

181
Q

Drug of choice for agitation in patients with hepatic encephalopathy

A

Haloperidol

182
Q

PBC Histo

A

shows periportal inflammation, periductal granulomas, and biliary inflammation and necrosis

183
Q

What percent of the liver blood supply is from the hepatic portal vein

A

75%

184
Q

New Mx in IBS

A

IBS-D

  • Ondans - 65% Sx relief
  • Rifaximin - 40% Sx relief
  • Eluxadoline

IBS - C
-Linaclotide - guanylate cyclase c receptor

Chronic constipation

  • Elobixibat - inhibitor of bile acid transporter
  • Tanapenor - increases intestinal fluid and improves transit
185
Q

Eluxadoline MOA and SE

A

For IBS-D
29% effective
Peripherally acting mixed mu-opioid receptor agonist, gamma opioid receptor antagonist, Kappa opiod receptor agonist

SE: Rare sphincter of Oddi Spasm, pancreatitis

186
Q

CAPS - Centrally mediated abdominal pain syndrome

A

Severe continuous abdominal pain, impacting daily function, chronic, usually associated with psych issues

187
Q

Favorable factor in Hep C treatment

A

-Genotype 1 (IL-28B polymorphism)

188
Q

USe of amiodarone when starting Hep C Treatment

A

NEed 3 months off amiodarone as it can precipitate heart block

189
Q

Tx of Hep C genotype 3 and decompensated liver disease

A

Add riboviran to increase treatment success from 50% to 85%

190
Q

HEp C treatment in pregnacy

A

Contraindicated in pregnancy

If on ribviran therapy, need to wait 6 months before getting pregnant

191
Q

Sofosbuvir CI

A

egfr <30

192
Q

Hep C regime for renal impairment

A

ombitasvir
paritaprevir
Ritonivir

193
Q

Hep C Tx protease inhibitor CI

A

Child Pugh B or C OR portal HTN

194
Q

Ribavirin precautions

A

PRegnant women
Men whose partners are pregnant
Haemoglobinopathies
Preexisting cardiac disease

195
Q

NAFL Histo

A

Steatosis with lobular or portal inflammation, with or without hepatocyte ballooning

196
Q

NASH Histo

A

presence of hepatic steatosis in association with hepatocyte ballooning degeneration and hepatic lobular inflammation

197
Q

Pioglitazone in NAFLD

A

shown to improve fibrosis, inflammation, and steatosis

198
Q

NAC MOA

A

replenishing body stores of the antioxidant glutathione.

Glutathione reacts with the toxic NAPQI metabolite so that it does not damage cells and can be safely excreted.

199
Q

Alcoholic Hepatitis Histo

A

Neutrophil infiltration
MAllory Dank bodies (eosinophilic accumulations of intracellular protein aggregates within the cytoplasm of hepatocytes)
• Fibrosis with a perivenular, perisinusoidal, and pericellular distribution

200
Q

Liver histo piecemeal necrosis

A

chronic viral hepatits/AI hepatitis

201
Q

SIBO features

A

macrocytic anaemia
B12 deficiency
fecal fat

Histopathological findings associated with SIBO include villous blunting, cryptitis, intraepithelial lymphocytosis, and eosinophilia.

202
Q

Diagnosing SIBO

A

positive carbohydrate breath test or jejunal aspirate culture

lactulose/glucose results in an early peak (w/i 90 mins) in breath hydrogen/methane levels due to metabolism by small bowel bacteria.

203
Q

Colonic pseudo-obstruction

A

appearance of mechanical obstruction without demonstrable evidence of such an obstruction in the intestine

in the elderly with serious concurrent medical and surgical/post-operative conditions

Risk of perforation if not decompressed

204
Q

UC Histo

A 
Mucosal/submucosal
Lymphocytic infiltrateGoblet cell depletion
Cryptitis
Crypt abscesses
NO GRANULOMAS
205
Q

Crohns histo

A 
•
Transmural inflammation
•
Infiltrate of lymphocytes and macrophages
•
Granulomas in ~ 50% of cases
206
Q

NOD1/Card15 in Crohns

A

Younger onset of disease
Small bowel involvement
Stricturing phenotype
Early initial surgery and surgical recurrence

207
Q

ASCA

A

Anti saccaromyces cervisiae antibodies

Associated with crohns

208
Q

pANCA and IBD

A

Associatted with UC

209
Q

Extraintestinal IBD manifestations associated with active GI disease

A 
•
Oral ulcers
•
Erythema nodosum
•
Large-joint arthritis
•
Episcleritis
210
Q

IBD Mx: Sulfaslazine and 5 aminosalicylates MOA and SE

A

Mechanism of action unclear

SE
Diarrhea (3%), headache (2%), nausea (2%), rash (1%)

Main role in UC.

  • Reduces risk of CRC
  • Induce and maintain remission in mild-mod UC
211
Q

IBD Mx: Thiopurines MOA

A

Inhibit purine synthesis
Inhibit T and B cell proliferation
Induce T-cell apoptosis

212
Q

Low/Absent 6-TGN/

Low/Absent 6-MMP

A

Non adherence

213
Q

Low 6-TGN/

Low 6-MMP

A

Underdosing

214
Q

High 6-TGN/

High 6-MMP

A

Thiopurine refractory

Trial another drug

215
Q

Low 6-TGN/

High 6-MMP

A

Thiopurine resistance

Add allopurinol and reduce thiopurine dose

216
Q

IBD Mx: Cyclisporine MOA and SE

A

Calcineurin antagonist
•
Potent inhibitor of cell-mediated immunity
•
Rescue therapy for severe steroid refractory UC

SE:
Nephrotoxicity, hypertension, neurotoxicity, infections

217
Q

IBD Mx: Vedolizumab MOA

A

Selectively binds α4β7 integrin on surface of T lymphocytes
•
Blocks interaction with MAdCAM-1 on intestinal endothelium
•
Inhibits trafficking of leukocytes to sites of inflammation
•
Approved for treatment UC and Crohn’s
•
Excellent safety profile

218
Q

IBD Mx Ustekinumab MOA and indication

A

Monoclonal antibody to p40 subunit of IL-12 / IL-23

Indications: Crohns

219
Q

Risk for hepatosplenic T cell lymphoma in IBD

A

Highest risk in men <35 on Infliximab and thiopurine

220
Q

Definition of acute severe colitis in IBD`

A 
Bloody stool frequency >6/day plus >1 of:
•
Pulse >90bpm
•
Temp >37.8oC
•
Hb<10.5g/dL
•
ESR >30mm/hr
221
Q

Autoimmune hepatitis histo

A

predominantly periportal hepatitis

Interface hepatitis with lymphoplasmacytic infiltrate

Hepatic rosettes

222
Q

Type 1 AIH

A

Any age

Antibodies:
ANA, SMA, Anti F-actin

223
Q

Type 2 AIH

A

Childhood/young adult

Antibodies:
LKM-1, Anti LC1

USually severe and treatment failure common

224
Q

PRedictor of relapse in AIH at end of therapy and rescue options

A

End of therapy histo

-TAc, Cyc, MMF, Ritux

225
Q

PBC Histo

A

Non‐suppurative
lymphocytic destructive
cholangitis on biopsy
• Periportal fibrosis

226
Q

Biochemistry findings in PBC

A

 Serum ALP almost always elevated (typically 3‐4x ULN)
 AST, ALT < 200 U/L (unless an overlap syndrome)
 Bilirubin ‐ usually rises late
 Cholesterol elevated in 85%
 IgM ‐ commonly elevated

AMA Positive!

227
Q

Mx of PBC

A

UDCA
• Improves liver biochemistries and overall survival

Second line:
Obeticholic acid (OCA) is a semi‐synthetic analogue of  cheno‐deoxycholic acid
• Selectively activates the
nuclear hormone receptor
farnesoid X receptor (FXRagonist)
228
Q

Non specific auto antibody that may be present in PSC

A

pANCA

Bpt (15 decks)

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