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FRACP Shuyu > GIT RPA > Flashcards

GIT RPA Flashcards

1
Q

Which sphincter is implicated in GORD

A

lower oesophageal sphincter transient relaxation

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2
Q

What absorption is impacted by PPI

A

calcium/vitamin D - contributes to osteoporosis

other medications

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3
Q

Alarm symptoms in GORD (3)

A

dysphagia, weight loss, haematemasis

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4
Q

Lifestyle management of GORD

A

weight loss (!!!)
smoking cessation
avoid precipitants (ETOH, coffee, chocolate, spicy food)
Behaviour (nocturnal head elevation)

effective in 20-30%

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5
Q

Classification of Barrett’s

A

short vs long segment

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6
Q

Is malignancy risk high with short or long segment Barrett’s

A

long segment

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7
Q

What is the appearance of Barrett’s in g-scope

A

salmon coloured

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8
Q

What is the pathological change in Barrett’s

A

smoking - squamous
now, mostly adenocarcinoma

change to intestinal mucosa

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9
Q

Management of high grade dysplasia for Barrett’s

A

endoscopic ablative therapy

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10
Q

Barrett’s oesophagus and no dysplasia subsequent management

A

repeat endoscopy in 6 months

maintained on PPIs (but not much evidence)

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11
Q

Barrett’s oesophagus and low grade dysplasia subsequent management

A

Repeat endoscopy in 3 months

Moving towards the same management as high grade dysplasia

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12
Q

G-scope appearance of eosinophilic oesophagitiis

A

Ringed appearance + furrows

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13
Q

What other conditions are eosinophilic oesophagitiis associated with

A

atopic conditions

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14
Q

What is the management of eosinophilic oesophagitis

A

1st line - PPIs
2nd line - topic corticosteroids (ingested fluticasone)

Elimination diets in children (in adults it’s often airborne)

oesophageal dilatation is only performed if there is a single dominant stricture in the oesophagus

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15
Q

Achalasia barium swallow appearance

A

Bird’s beak

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16
Q

Achalasia diagnosis

A

Endoscopy to rule out malignancy

Manometry is for diagnosis

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17
Q

Management of achalasia

A

young patients - pneumatic dilatation of LOS; surgery (laparoscopic Heller’s myotome)

old patients - nitrates, CCB, botox

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18
Q

Portal pressure to develop GO varices

A

> 12mmHg

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19
Q

Portal pressure to have bleeding GO varices

A

> 18 mmHg

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20
Q

Pathogenesis of GO varices

A

Increase portal pressure due to scarred liver

Shunts bleed towards other directions -> spleen (splenomegaly, thrombocytopenia etc)

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21
Q

When is the first endoscopy for cirrhotic patients

A

at diagnosis

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22
Q

Primary prophylaxis for GO varices

A

non-selective BB
- propanolol (decreases risk of first bleed by 50%); need to drop pulse by 25%

Grade 2 +
- banding program
(higher grade do better with banding cf medical therapy)

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23
Q 
Acute haematemesis and varices - which of the following does not improve mortality rates:
A - terlipression
B - octreotide
C - IV antibiotics
D - IV PPIs
E- Early endoscopy
A

IV PPIs

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24
Q

MOA of terlipressin

A

powerful vasopressin

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25
Q

SE of terlipressin (or what conditions should one be more careful with its use or consider octreotide)

A

Strokes, cardiac events, pulmonary oedema due to powerful vasoconstriction of vessels

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26
Q

Management of uncontrolled variceal haemorrhage

A

Danis stent (large self-expanding metal stent that applies direct circumferential pressure) - used if the patient is being bridged to something else

Sengstaken-Blakemore or Linton tube
- more likely to cause ischaemia so can only leave for 48 hr (cf Danis stent which is 7-14 days and a better choice who is being bridged)

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27
Q

TIPSS MOA

A

Decreases portal hypertension

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28
Q

Contraindication for TIPSS

A

encephalopathy as it facilitates increased ammonia to CNS

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29
Q

Secondary prophylaxis to oesophageal varices

A

Beta blockers + band ligation

TIPSS if recurrent bleeding

Await liver transplant

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30
Q

Which condition cannot get TIPSS

A

Primary sclerosis cholangitis

Increased rate of cholangitis due to blocked/dilated ducts

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31
Q

Which is not a risk factor for PUD:

  • enteric coated aspirin
  • alcohol
  • COX-2 inhibitors
  • smoking
  • Helicobacter
A

ETOH

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32
Q

what transplant med causes PUD

A

mycophenolate

and steroids through poor healing - not much evidence

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33
Q

Regimen for people with no allergies for H. Pylori eradiacation

A

amoxicillin 1g bd
clarithromycin 500mg bd
esomeprazole 40mg

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34
Q

most common cause of resistance to H. Pylori

A

Clarithromycin resistance

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35
Q

When should urea breath test be done after treatment H. Pylori

A

8 weeks + after treatment

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36
Q

Urease breath test - what kind of false results can you get

A

only false negatives, can’t get false positives

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37
Q

Pathogenesis of H. Pylori

A

H pylori produces ammonia to survive the gastric acidic environment

The stomach increases gastric pH to compensate and causes ulcers

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38
Q

What kind of ulcers are most frequent in H Pylori

A

duodenum > gastric

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39
Q

H. Pylori eradication treatment in patients with penicillin allergy

A

clarithromycin, metronidazole, PPI

60% successful eradication vs 80% w amoxicillin

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40
Q

Next line in resistant H Pylori

A

Rifabutin, doxycycline, tetracycline PPI

nexium HP7 for 1 week, then levofloxacin based combo therapy for another 10-14 days (din’t se in patients >70 due to risk of C. Diff)

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41
Q

Which NSAID is most likely to cause gastric ulceration

A

aspirin

COX2s are slightly better

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42
Q

MOA of NSAID related ulceration

A

Decreases prostaglandins and inhibition of COX-1 and COX 2
and epithelial proliferation
(see slides)

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43
Q

Management of incidental gastric ulcer, negative for H Pylori and investigations for other causes are negative

A

PPI 40mg bd for 8 weeks then repeat gastroscopy
must biopsy the area if the ulcer is still present

gastric ulcers have malignant potential unlike duodenal ulcers

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44
Q

Approach to anti platelets in PUD

A

only stop for 3-4 days due to increased risk for cardiovascular events

can consider changing aspirin to clopidogrel

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45
Q

Amount of bleeding required to produce melena

A

150mL

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46
Q

Amount of bleeding from upper GI source required to cause bright red PR bleeding

A

high volume >500mL

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47
Q

Management of bleeding duodenal ulcer

A

multiple therapies simultaneously:

- injection w adrenaline, clipping, coagulation w heat probe

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48
Q

Forrest classification in ulcers

A

stigmata in endoscopic appearance to assess risk of rebreeding
Acute hemorrhage

Forrest I a (Spurting hemorrhage)
Forrest I b (Oozing hemorrhage)
Signs of recent hemorrhage

Forrest II a (Non bleeding Visible vessel)
Forrest II b (Adherent clot)
Forrest II c (Flat pigmented haematin (coffee ground base) on ulcer base)
Lesions without active bleeding

Forrest III (Lesions without signs of recent hemorrhage or fibrin-covered clean ulcer base)[2]

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49
Q

Duration of PPI infusion for bleeding ulcer

A

72hr from TIME of endoscopy

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50
Q

Rebleeding after 72hr of PPI infusion after first endoscopy for bleeding ulcer

A

repeat endoscopy and endoscopic therapy and have another PPI infusion

options if ongoing bleeding:
interventional radiology
surgery last line

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51
Q

Insidious presentation of coeliac’s

A

irone deficiency anaemia
osteoporosis
infertility and miscarriages

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52
Q

which family members of coeliac patients to screen

A

first degree relatives

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53
Q

Diagnosis of coeliac’s

A

Small bowel biopsy

antibody testing - tTF and anti-endomysial Ab (>90% sensitivity) not diagnostic however

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54
Q

What autoimmune conditions are associated with coeliac’s

A

autoimmune thyroiditis

dermatitis herpetiformis (80% will have coeliac)

T1DM

and many more..

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55
Q

what malignancy is associated w coeliac disease

A

small bowel lymphoma

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56
Q

first line test to do in compliant coeliac disease who after many years of dietary compliance develops new weight loss and diarrhoea

A

CT abdo pelvis

57
Q

risk factors for NH lymphoma in coeliac patients

A

gluten

refractory disease

58
Q

IgG 4 disease - most common presentation

A

systemic fibroinflammatory condition

autoimmune pancreatitis

mostly affects pancreas and biliary tree

59
Q

Diagnosis of IgG4 disease

A

IgG4 serum levels
Tumefactive lesions
Histology - dense lymhoplasmacytic infiltrate, storiform fibrosis
IgG positive staining on immunohistochemistry

60
Q

Treatment of IgG4 disease

A

Mostly monitoring

Otherwise:
Immunosuppression - steroids, azathioprine methotrexate
Rituximab for refractory disease

61
Q

Prophylaxis for complications of ERCP - pancreatitis

A

indomethacin suppository 100mg

62
Q

ERCP indications

A

These days used for therapeutic not just diagnostic due to high complication rate (except PSC)

1) obstructed bile duct confirmed on CT angio, MRCP, USS
2) gallstone pancreatitis AND cholangitis
3) PSC if inadequate imaging or evidence of biliary obstruction
4) Sphincter of odds dysfunction (Type I; usually don’t perform for type II - biliary colic + 1 of abnormall bloods or imaging)

63
Q

Type 1 sphincter of Oddi dysfunction

A

biliary colic
abnormal LFT/pancreatic enzymes
abnormal dilated ducts

tests should return to normal after 1 week of episode

must satisfy all 3 criteria to get ERCP - as pancreatic rates are +++

64
Q

Investigation for younger patients with recurrent IDA w clear recurrent scopes

A

pill cam

65
Q

Investigation for older patients (80+) with recurrent IDA w clear recurrent scopes

A

Abdo CT scan for malignancy

66
Q

What DAA for HCV is contraindicated in decompensated cirrhosis

A

protease inhibitors

67
Q

What DAA is not recommended in eGFR <30

A

sofosbuvir (oral nucleoside analogue)

68
Q

What genotypes in HBV are associated with better response to IFN

A

A and B respond better than C and D

69
Q

What is genotype F associated with in HBV

A

fulminant liver failure

70
Q

Where is universal screening for HBV performed

A

B cell therapy / immunotherapy for malignancy

antenatal

71
Q

What are the predictors used in most models for HBV cirrhosis/HCC

A

ALT, HbeAg, male, age

72
Q

HbsAg -ve
anti-HBc -ve
anti-HBs -ve

A

susceptible, no current or prior infection

73
Q

HbsAg -ve
anti-HBc +ve
anti-HBs +ve

A

resolved infection but could reactivate

74
Q

HbsAg -ve
anti-HBc -ve
anti-HBs +ve

A

vaccinated

75
Q

HbsAg +ve
anti-HBc +ve
anti-HBs -ve
ImG anti-nbc high titre

A

acute HBV infection

76
Q

Isolated

anti-HBc positive

A

escape mutant or occult infection

77
Q

What phases of HBV should get treatment

A

immune escape
immune clearance

essentially when LFTs are abnormal

78
Q

where in the viral replication cycle does the antivirals work in HBV

A

RNA replication

the cccDNA is not targeted currently
hence why patients remain HbSAg positive
only viral suppression is achieved

79
Q

What antivirals are used in chronic HBV

A

oral nucleotide analogues
entecavir and tenofovir (ETC + TDF)

Peg interferon might sometimes be used as it’s finite therapy for 1 year (more side effects)

80
Q

TAF vs TDF

A

TAF is tenofovir alafenamide - a novel prodrug of tenofovir

TAF has better bone and kidney SE profiles

81
Q

Management of ladies of HbsAG + mothers

A

HBIG + HB Vax x3

82
Q

Management of women planning pregnancy already on antiviral

A

stop prior vs continue - tenofovir ok to continue

83
Q

Who should get antiviral prophylaxis (pregnant women)

A

high viral load >10^6 IU/mL wet 30 to 2-3 months post delivery

84
Q

Extrahepatic manifestation of HEV

A

neurological complications e.g. gillian barre, (see slides)

85
Q

Lipophilic vs hydrophilic statin in HCC

A

lipophilic statins reduce HCC (simvastatin + atorvastatin)

86
Q

Liver nodule <1cm in cirrhotic patient on screening next step

A

Repeat US at 4 months

87
Q

Liver nodule >1cm in cirrhotic patient on screening

A

Multiphasic contrast-enhanced CT or multiphase contrast-enhanced MRI

If classic features on imaging, don’t need biopsy, can treat as HCC

classic features:
- 4 phase multi-slice CT: arterial enhancement, washout on portal and delayed phase

88
Q

Early stage HCC w 2-3 nodules <3cm treatment

A

transplant (or ablation if not transplant candidate)

89
Q

Intermediate stage HCC w multi nodular unresectable + preserved liver function treatment

A

chemoembolization (considered palliative)

90
Q

Small solitary HCC in resectable patients <5cm treatment

A

resection or transplant

resection has better long term survival
recurrence rate is 50-60% at 5 years with probably a new tumour

91
Q

SIRT for HCC

A

selective internal radiation therapy

very small beads delivered into the tumour selectively

92
Q

Systemic therapies for HCC - 2 first lines on PBS

A

sorafenib (kinase inhibitor drug)

lenvatinib

93
Q

Acute liver failure key features (4)

A

severe acute failure
liver injury AST/ALT >2-3 ULN
and impaired liver function

must have hepatic encephalopathy within 12 weeks of onset of jaundice

if there is no hepatic encephalopathy, it’s just acute liver injury

94
Q

King’s college criteria for paracetamol ALF and transplantation

A

pH < 7.3

or

In a 24h period, all 3 of:

INR > 6 (PT > 100s) +
Cr > 300mmol/L +
grade III or IV encephalopathy

95
Q

Child pugh scoring

A

ascites, encephalopathy, bilirubin, serum albumin, INR

96
Q

Higher mortality out of decompensation w ascites vs decompensation w bleeding

A

decompensation w bleeding

97
Q

Acute-on-chronic liver failure

A

characterised by acute decompensation of chronic liver disease associated with organ failures and high short-term mortality. Alcohol and chronic viral hepatitis are the most common underlying liver diseases. Up to 40%–50% of the cases of ACLF have no identifiable trigger; in the remaining patients, sepsis, active alcoholism and relapse of chronic viral hepatitis are the most common reported precipitating factors. An excessive systemic inflammatory response seems to play a crucial role in the development of ACLF.

98
Q

Management of ascites

A

1st line
dietary manipulation (low salt)
spiro
up to 400mg/day

2nd line
diuretics large volume paracentesis + IV albumin

refractory ascites
2nd line
TIPSS
Transplant

Nutritional support for all

99
Q

Non transplant treatment that improves survival for refractory ascites

A

TIPSS

100
Q

Ascites PMN for SBP

A

> 250/mcL

101
Q

Type 1 vs 2 HRS

A

type 1 is a form of AKI - really poor early survival
creatinine doubles to >220

type 2 is a form of acute on chronic kidney injury of chronic kidney disease (patients w declining renal function over 6 to 12 months)
Cr >133

102
Q

Management of AKI in cirrhosis

A

Withdrawal diretics
treat infection
plasmave volume expansion w diuretics
vasoconstriction

dialysis
transplant

103
Q

what BB is preferred for primary prophylaxis of variceal bleeding

A

carvedilol

cancel 2019 paper carvedilol prevents deaths in ascites

104
Q

Which pulmonary complication is a contraindication to liver transplant in cirrhosis

A

Portopulmonary hypertension

compared with hepatopulmonary syndrome which is an indication for transplantation

105
Q

what type of diet (aside from low salt) in liver disease

A

high protein high energy

106
Q

what are the histological manifestations of NASH

A

hepatic steatosis w either lobular inflammation, hepatocyte ballooning with or without fibrosis

107
Q

PNPLA3

A

genetic driver of NAFLD in hispanics

108
Q

Most important determinant of outcome in NAFLD

A

fibrosis (can only be determined by biopsy)

109
Q

What other malignancies are associated with NALFD (Aside from HCC)

A

breast ca

colorectal ca

110
Q

HCC surveillance in NASH

A

6 monthly US in NASH cirrhosis

111
Q

Hyperferritinaemia in NAFLD

A

Not a marker of iron overload - rather of inflammation
Associated w fibrosis in NAFLD
phlebotomy is not associated w improvement

112
Q

liver enzynes pattern in alcoholic hepatitis

A

AST>ALT
<1000

> 1000 more likely paracetamol, ischaemic etc

113
Q

treatment of alcoholic hepatitis

A

pred

114
Q

Autoimmune hepatitis type I vs II

A

type I - ANCE, ANA, Anti Smooth muscle, anti-actin anti soluble liver antigen

type II - anti LKM, anti-liver cytosol

115
Q

Autoimmune hepatitis treatment

A

Pred

Azathioprine

116
Q

Primary biliary cholangitis serological findings

A

positive AMA >95%
+ANA

AMA titre does not correlate to disease stage

117
Q

Which IBD has preserved goblet cells

A

crohn’s has preserved goblet cells where as UC has depleted goblet cells

118
Q

mechanism of action of faecal calprotectin

A

calcium binding protein found in cytosol of neutrophils
released w cell damage in GI tract
good for distinguishing IBD and IBS
role in following disease course

119
Q

Anti-Saccharomyces cerevisiae antibody (ASCA) in IBD

A

specific but not very sensitive in Crohn’s

120
Q

when to consider thiopurines in crown’s and UC

A

Crohn’s: at diagnosis

UC: use 5ASA first and if it doesn’t work then aza

121
Q

Use of cyclosporin in IBD

A

rescue therapy in UC (not crown’s)

122
Q

What has been proven to stop post op recurrence in crohn’s disease

A

metronidazole
aza
TNF-alpha
stopping smoking

123
Q

Not responding to first line immunomodulator in IBD

A

combination therapy with biologic

124
Q

how long to wait to immunosuppress after live vaccine

A

3 weeks before starting immunosuppression

have to wait 3 months after immunosuppression before giving live vaccines

125
Q

Colon cancer screening if have both PSC and UC

A

yearly C-scopes

126
Q

Who/when to screen for colon cancer in UC and Crohn’s

A

UC beyond sigmoid colon
CD >1/3 colon involved

from 8 yr after diagnosis
start earlier if strong FHx of CRC

yearly in active disease, strong 1st degree relative family history

3 yearly in inactive UC/CD or 1st degree relative >50yr

127
Q

what’s greatest risk to pregnancy in IBD

A

flare of IBD

128
Q

Follow up of PUD - gastric and duodenal

A

8 weeks of PPI should heal any ulcer - EXCEPT if it’s malignant

If gastric, should rescope after to look for malignancy

If duodenal don’t need to rescope

Also do not ned to continue PPI

129
Q

What ulcers are more associated with H Pylori

A

duodenal (90% caused by H Pylori)

130
Q

Second line for H Pylori after 1st line failed

A

Amoxycillin 1g
Levofloxacin 500mg bd
PPI

10 days

131
Q

HCV SVR rates for pan genotypic agents

A

95%

132
Q

Options for HCV treatment failure

A

Sofosbuvir/velpatasvir/voxilaprevir (VOSEVI)

133
Q

pathophysiology of hepatorenal syndrome

A

due to marked splanchnic arterial vasodilatation causing markedly decreased effective arterial blood volume
overcoming the RAS system
causing renal perfusion

hence why there is no intrinsic renal disease

134
Q

terlipressin in hepatorenal syndrome

A

for transplant candidates as it only causes a temporary constriction in the splanchnic arteries

hence as bridging therapy

135
Q

least common side effect of lenvatinib

A

rash

136
Q

lenvatinib

A

multi-kinase inhibitor
rash is much less than sorafenib

for advanced metastatic disease + child pugh A

137
Q

advanced metastatic disease HCC + child pugh B/C

A

palliate

138
Q

pathophysiology of alpha1-antitrypsin deficiency

A

There are different types of alpha1-antitripsin mutations

z mutation results in the production of an abnormal protein which is trapped in the endoplasmic reticulum of hepatocytes. The protein is toxic to the hepatocytes.

the null null mutation results in no liver disease because there’s no abnormal protein in hepatocytes

FRACP Shuyu (65 decks)

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