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Gastro difficult questions Flashcards

1
Q

MTX induced hepatitis

A

Usually acute onset

High and prolonged doses

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2
Q

Where? When? How?

Approach to LFTs

A

Where?
Australia - elevated AST ?ishcaemic ?toxic
Asia - orofecal transmittable hepatitis virus
Northern European - homozygosity for C282Y mutation HFE gene (haemachromatosis)

When?
Medication related?
Younger - ?Wilson’s ?AIAT def
Older - comorbidities, ?drug induced liver injury, ?right heart failure

How?
Hepatocellular vs cholestatic
- AST and ALT highly concentrated in liver
- AST also in heart, skeletal muscle, kidney, brain and RBC
- ALT has low concentration in skeletal muscle and kidney
- ALT more specific for liver damage
- Half life ALT 47 hours; AST 17 hours
- Decrease in AST/ALT alone does not have prognostic meaning - monitor bilirubin and INR
Magnitude of enzyme alteration
Rate of change (increase/decrease over time)

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3
Q

ALT >1000 Think…

A 
Think
Ischaemic liver injury
Viral liver injury
Drug induced liver injiury
Autoimmune hepatitis
Choledocholithiasis
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4
Q

Mild alteration in aminotransferase levels…

A

History of ETOH/medication use
Risk factors for hepatitis –> hepatitis screen (hep B, C; if acute, hep A, E)
Increased trans sat and ferritin –> test for HFC mutation
Middle aged female +/- concomitant autoimmune disease –> ANA, ASMA, Anti-LKM
Consider also ceruloplasin level (wilson), A1At (esp if lower lobe emphysema), ttg ab (coeliac disease)

If all negative, think fatty liver

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5
Q

Cholestatic LFTs… think…

A

ALP

  • Liver and bone diseases most common cause
  • Also elevated in 3rd trimester of pregnancy and adolescence
  • t1/2 - 1 week (rise late in bile duct obstruction and take a while to get better)
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6
Q

If suspecting hepatic source of ALP rise think…

A

Medications –> check bili and AST/ALT –> liver US (normal)
Female with other autoimmune disease –> check IgM, AMA –> liver US (diffuse disease) –> PBC
UC –> check ANCA, ERCP –> liver US (diffuse disease) –> PSC
RUQ pain, fever –> check bili –> liver (dilated bile ducts) –> biliary obstruction
Other malignancy? –> liver US –> hepatic mets

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7
Q

The primary factor leading to the accumulation in ascites in patients with chronic liver disease is

A

splanchnic vasodilation

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8
Q

Portal HTN when HVPG is

A

> =5mmgHg; clinically significant when >10-12mmHg

Leads to splanchnic vasodilation primarily led by nitric oxide

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9
Q

45M alcoholic
1st oesophageal variceal bleed –> endoscopic band ligation
How do you prevent recurrent bleeding?

A

Non-selective beta blockers (Carvedilol is the best) is superior to banding alone for grade 2-3 varices

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10
Q

How to classify oesophgeal varices?

A

Grade 1 - minimally elevated veins above service (can be flattened)
Grade 2 - medium sized low risk varices –> banded (do not flatten)
Grade 3 - takes up >1/3 of lumen, large varices, red spots over varices (high risk stigmata)
Grade 4 - fibrin plug (white plug) indicates high risk stigmata, Wale signs

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11
Q

New dx of UC
US - nil extrahepatic duct dilatation, nil gallstones
Abnormal LFTs bili 35 ALP 555 GGT 458 ALT 48 albumin 40

Next best investigation for abnormal LFTs?

A

UC is associated with primary sclerosing cholangitis (increases rate of colorectal ca - yearly colonoscopy even without UC)
90% PSC have UC
5% UC develops PSC

MRCP - gold standard
- Multifocal short annular strictures (beading)

Liver bx often not required

ERCP is not needed unless you want to dilate the strictures

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12
Q

What is PSC?

A

Autoimmune
Inflammation, fibrosis + stricturing of medium + large ducts –> cholestasis
Classic: intra + extra hepatic ducts
Small duct: normal cholangiography, but histo consistent

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13
Q

What bloods would you expect in PSC?

A

Cholestatic pattern
pANCA 65% positive
AMA PBC 90% positive (F>M)
IgG4 for AI pancreatitis

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14
Q

Azathioprine malignancy risks?

A

Skin cancer

Lymphoma especially in men

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15
Q

What’s the truelove and Witt’s criteria?

A 
Motions/day
Fever
Rectal bleeding
Resting pulse
Hb
ESR/CRP

Defines mild, moderate, severe UC

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16
Q

28F 2 year history of abdo pain and diarrhoea. Smokes 20 cigarettes a day. Small bowel series shows a long stricture in the terminal ileum.
In addition to pred, what is the best initial treatment?

A 
Quit smoking (but this won't reduce the damage that is already done) 
Infliximab = more correct
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17
Q

What are some biologics used in CD?

A

Anti TNF: infliximab, adalimumab (CI in HF, malignancy)
Vedolizumab (anti-integrin inhibitor; very gut specific; stops migration of lymphocytes into the gut)
Ustekinumab (safest; suitable for older patients)

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18
Q

How do the treatment approaches differ between UC and CD?

A

UC - stepwise approach

CD - top down approach (treat aggressively)

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19
Q

What are some immunomodulators used in CD?

A

AZA +/- allopurinol
6MP
MTX

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20
Q

Whats Exclusive Enteral Nutrition (EEN) in CD?

A

Drink resource for 6 weeks = equivalent to steroids

Useful in those who can’t be immunosuppressed

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21
Q

When do you use abx in CD?

A

If confirmed infection only e.g. penetrating disease, perianal disease

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22
Q

What should we check before we start AZA?

A

TMPT mutation

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23
Q

What’s the use of allopurinol in azathioprine?

A

For those who shunt towards producing 6-MMP (inactive) (high TMPT activity). You put them towards the correct pathway and produce more 6-TGN (active).

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24
Q

Risk factors for CD recurrence

A 
Smoking
Genetics 
younger patients with more aggressive phenotype
Disease duration ie shorter pre-op disease duration
Disease extent - UGI, diffuse disease
Prior surgery
Penetrating or fistulating disease
Stricturing disease

Monitor with scope + MRE

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25
Q

Therapies post resection for CD

A

High risk patients - immunosuppressive therapy
If low risk + treatment naive, can consider 3/12 metronidazole
But if they’ve needed surgery they’re going to be high risk of recurrence so in real life, everyone should be on immunosuppressants

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26
Q

58M iron deficiency anaemia requiring blood transfusion (despite oral iron supplements)
Normal gastroscopy and colonoscopy
BM exam normal

What’s the next best investigation?

A

Enteroscopy

- Capsule endoscopy

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27
Q

What’s the most common cause of small bowel bleed?

A

Angioplasia

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28
Q

If you suspect small bowel angioplasia, what next?

A

Double balloon enteroscopy - pass scope into the small bowel and use balloon to stop the bleeding

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29
Q

When do you use CT abdominal angiography and labelled red cell scan?

A

Acute bleed in CT angiography

Labelled red cell scan is done only when CT angiography is not available

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30
Q

25M episode of haematemesis. Nauseous, one large vomitus with fresh blood. No syncope or sizziness.
No past history of PUD
Smokes and heavy ETOH

Obs stable
Tender epigastric region
No melena on PR exam

What are the ddx and most likely dx?

A

Oesophageal varices
- Less likely given no mentioned history of cirrhosis

Gastric ulcer or duodenal ulcer

  • Expect melena
  • Shouldn’t get haematemesis in duodenal ulcer and haemodynamic instability
  • Gastric ulcer should get coffee ground vomit and haemodynamic instability
  • No risk factors

Mallory-Weiss tear***

  • Probably most likely
  • But no mention of repeated vomiting

H. pylori gastritis
- Unlikely

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31
Q

What’s King’s criteria for paracetamol OD?

A

Recommends who should be immediately referred for liver transplant

Arterial pH <7.3

INR >6.5 (PT >100s)

Creatinine >300micromol/L

Grade III or IV hepatic encephalopathy

  • III: marked confusion, incoherent speech, sleeping most of the time but arousable to vocal stimuli
  • IV: comatose, unresponsive to pain; decorticate or decerebrate posturing

Meet 2+ criteria = transfer for transplant

Other predictors of poor prognosis without transplant
Lactate >3.5mmol/L after fluid resus (<4h) or Lactate >3 mmol/L after full fluid resus (12h)

Phosphate >1.2mmol/L at 48-96h

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32
Q

Basic Autoimmune liver screen

A

Ana
Anti SM ab
IGG

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33
Q

Cholestatic LFTs

Positive AMA

A

Primary biliary cholangitis

34
Q

Which has the shorter half life?

ALT or AST

A

AST

35
Q

Causes of AST >ALT

A 
Muscle
Wilsons disease
NASH
HCV with cirrhosis 
However often not more than 2:1

ETOH (2:1 ratio)

36
Q 
Which of the following confers worst prognosis in non-alcoholic fatty liver disease?
A) CV disease
B) Hypertriglyceridaemia
C) Impaired glucose tolerance
D) T2DM
E) Obesity
A

T2DM is the worst in terms of disease progression
CV disease is the worst in terms of mortality

Prognostic markers in NAFLD/NASH

  • Histological subtype most important - NASH vs NAFLD. NASH is much worst and has higher risk of cirrhosis.
  • Metabolic factors - DM is the strongest metabolic factor of progression of NAFLD to cirrhosis.
37
Q

Causes of PUD (Ulceration in stomach and duodenum)

A

Duodenal ulcer more likely H. pylori
Gastric ulcer more likely NSAIDs

NSAIDs (especially high dose, 2 weeks more) and H pylori (20-25% in Australia, up to 70% in Africa and Asia) are the most common causes

Others

  • Medications - steroids (more co-factor), bisphosphonates, clopidogrel (more co-factor), sirolimus, 5-FU
  • Crohn’s
  • Sarcoidosis
  • TB, HSV, CMV
  • Gastrinoma - increased acid secretion
  • Smoking and ETOH cofactors
38
Q

List 4 testing methods for H pylori

A

Urea breath test

Faecal H.pylori antigen

H pylori serology - does not discriminate between past and present infection - 95%+ sensitivity. Results are satisfactory if no history of eradication.

Biopsies for gastric mucosa - reduced sensitivity in context of GI bleeding and high dose PPIs - NPV about 55%, sensitivity <70%

39
Q

Where do you biopsy for H pylori?

A

Gastric mucosa

H pylori typically causes duodenal ulceration but increased acid secretion is from stomach.

40
Q

When do people get infected with H pylori?

A

Usually in childhood and don’t develop ulcers until later in life
Hence serology will always be positive

41
Q

How does Prostate radiation result in PR bleed?

A

Acute radiation proctopathy - often occurring during radiotherapy or 1-2 months after due to inflammation

Chronic radiation proctopathy - often occurs 18 months after - due to ischaemia and subsequent telangiectasia (friable blood vessels are prone to bleeding). Tend to ooze more rather than bleeding profusely.
Rx: colonoscopy and argon photo-coagulation (APC) is gold standard

42
Q

Common causes of profuse lower GI bleeding

A

Diverticular bleeding
Ischaemic colitis
Post biopsy/polypectomy
Other forms of colitis

43
Q

List procedures used for evaluation of lower GI bleed

A

1) Red cell scan
Need minimum 0.5ml/min bleeding
Only gives 2D picture. Not as good for localising site of bleeding

2) CT angiogram +/- embolisation
Need minimum 1ml/min bleeding or 3 units of blood/day

3) Angiogram
4) Colonoscopy

44
Q

Classic location of pill oesophagitis from doxycycline

A

Mid-oesophagus - where aortic arch touches the oesophagus and causes indentation

45
Q

List causes of oesophagela ulcers

A

Reflux oesophagitis typically affects lower oesophagus

Pill oesophagitis - typically at level of arotic arch (extrinsic compression)
- Tetracyclines, bisphopshonates

Other causes

  • CMV, HSV, candida oesophagitis (in immunocompromised)
  • Cancer
  • Crohn’s
46
Q

Eosinophilic oesophagitis

A) Pathophysiology

B) What conditions is it associated with?

C) What demographic?

D) What do you see on endoscopy?

E) Rx

A

A) Eosinophils infiltration of oesophagus –> oedema –> fibrosis with ongoing long-term inflammation

B) History of asthma and other atopy

C) Affects younger people; M > F

D) Endoscopy - narrowing or burrows, micro-abscesses, rings (trachelisation of the oesophagus)
Does not cause frank ulceration

E) Rx: topical steroids, PPI +/- dietary elimination (dairy, wheat can typically contribute, also soy, eggs)

47
Q

List biologics in Crohn’s

A

Anti-TNF agents
Infliximab
Adalimumab

Ustekinumab - anti IL 12/23 P40 agents - very effective in CD. Promising results in UC but still in clinical trials

Vendolizumab - anti-integrin (alpha4beta7) and inhibits WBC transfer to gut lumen from gut vasculature - more effective in UC than CD

48
Q

Is CRP good at detecting active inflammation in IBD?

A

No
Only has 70% sensitivity
CRP can also normalise when there is no objective change to inflammation

49
Q

Do symptoms correlate with improvement in IBD?

A

Symptoms correlate poorly with inflammation

50
Q

Rx UC refractory to treatment with azathioprine

A

Infliximab better than adalimumab

Vedolizumab is good too but takes time to work

51
Q

Rx CD with perianal fistula

A

Infliximab

Has evidence in this specific setting

52
Q

What is Pouchitis?

A

Inflammation of residual J pouch in someone with total proctocolectomy (turn ileum on itself and connect the bottom of the J to the anus). Bottom of J acts as a reservoir to hold stool. Pouch is very prone to inflammation.

53
Q

What is fulminant UC?

A

> 6 bowel actions/day
Tachycardia
Anaemia
Raised inflammatory markers

Toxic megacolon (transverse colon typically) or features of sepsis

Rx: infliximab
Surgery is often needed

54
Q

Atezolizumab + bevacizumab for …

A

HCC

55
Q

Tofacitinib for …

A

Moderate-severe UC

56
Q

GLP2 agonist (teduglutide) for …

A

Short bowel syndrome

57
Q 
Which micronutrient deficiency is common in coeliac?
A) Iron
B) B12
C) Selenium
D) Zinc
A

Iron deficiency

58
Q 
In the absorption of iron, which of the following is situated on the basolateral membrane of duodenal enterocytes?
A) Tf
B) Divalent metal transporter-1
C) Ferroportin 1
D) Hepcidin
A

Ferroportin-1

59
Q

Terminal ileum absorbs

A

Bile acid –> portal system –> liver (recycled)

B12

60
Q

Duodenum absorbs

A

Fe - classically deficiency in Coeliac disease

61
Q

If you lose terminal ileum, can get…

A

Don’t get bile salt reabsorption
Bile salt diarrhoea (acts as osmotic agent)
Fat malabsorption = steatorrhoea

B12 deficiency

62
Q

How does hepcidin work to reduce iron?

A

Removes ferroportin-1
Iron trapped inside enterocytes of duodenum then every few days, these enterocytes get sloughed off –> lose iron through the gut

63
Q

60F - diagnosed with coeliac at 20 years old and has been adherent to GFD since.
She now has new onset profound watery diarrhoea and LOW 15kg over 6 months. What is the most likely diagnosis?

A

Small bowel Lymphoma!
Due to increased turning on and off of lymphocytes

Others: small bowel adenocarcinoma (rare), NHL, refractory coeliac disease (very rare)

64
Q

How does refractory coeliac disease present? How to differentiate from lymphoma?

A

Less weight loss
Also get diarrhoea
Lack of B symptoms

This is very rare

65
Q

50M GORD
Endoscopy - 5cm Barrett’s mucosa in the lower part of the oesophagus
Biopsies confirm intestinal metaplasia without dysplasia. What next?
A) No follow up
B) repeat endoscopy in 3 years
C) Radiofrequency ablation
D) Endoscopic mucosal resection

A

Repeat endoscopy in 3 years if no dysplasia

66
Q

What is Barrett’s? What does it look like on endoscopy?

A

Intestinal metaplasia
Squamous –> columnar (intestinal) mucosa

Appears as salmon-coloured tongues of mucosa seen on endoscopy

67
Q

When to treat Barrett’s?

A

Presence of dysplasia, doesn’t matter if low grade

If can’t treat in dysplasia for whatever reason, then yearly endoscopic surveillance

68
Q

Treatment options for Barrett’s

A

Radiofrequency ablation

Endoscopic mucosal resection or endoscopic sub-mucosal dissection

Surgery

Everyone gets PPI

69
Q

45M cirrhosis due to hep C complicated by varices and ascites

Triple phase CT finds a solitary 2cm lesion, high washout (from arterial to venous)

What's the most appropriate action?
A) surgical resection
B) Liver transplant
C) locoregional therapy
D) Sorafenib
A

Liver transplant

NOT
Surgical resection
CI in portal hypertension (varices, ascites in the stem)

70
Q 
63M child pugh A cirrhosis 
Diagnosed with multifocal HCC - 7 tumours
What is the most appropriate treatment?
A) Liver transpalnt
B) CST 
C) Levatinib
D) Atezolizumab + bevacizumab
A

Atezolizumab + bevacizumab

Now first line therapy and PBS covered
Superior to levatinib/sorafenib

71
Q 
HCC management
If no portal HTN = 
If within criteria = 
If non transplant candidate = 
If advanced/metastatic disease + Child pugh A = 
If metastatic disease + child pugh B/C =
A

If no portal HTN = resect
If within criteria = transplant
If non transplant candidate = locoregional therapy (TACE/ablation)
If advanced/metastatic disease + Child pugh A = atezolizumab + beacizumab > sorafenib/lenvatinib
If metastatic disease + child pugh B/C = palliate

72
Q

What is achalasia?

A

Failure of lower oesophgeal sphincter relaxation and no peristalsis

73
Q 
80M from RACF
Dysphagia and LOW. Localises issue to this throat. Obstructive symptoms that take a number of swallows to clear. 
Occasionally coughs and chokes on liquids. 
Which is the most useful diagosis?
A) Barium swallow
B) modified barium swallow
C) oesophageal manometry
D) gastroscopy
A

Modified barium swallow

74
Q

What are the 2 types of dysphagia?

A

1) Oropharyngeal dysphagia
Problem getting food from oral cavity into oesophagus
Post stroke, dementia, neurological disorder
Ix: speech, modified barium swallow (looks at the top part)
Key sx: repetitive swallows, cough when trying to swallow, nasal regurgitation, delayed/absent swallow initiation

2) Oesophageal dysphagia
Problem getting food down the oesophagus 
mechanical things (strictures, ca) or dysmotility (achlasia, spasm) or both (eosinophil oesophagitis)
Ix: barium swallow, manometry, gastroscopy
75
Q

What’s the difference between modified barium swallow and barium swallow?

A

Modified barium swallow - done by speech path, looks at neurological and pharyngeal function

Barium swallow - looks at structure of oesophagus, done in radiology, looks at propagation of contrast

76
Q

Eosinophilic oesophagitis Rx

A

30% respond to PPI

If no response, then topical steroids (ingested flixotide inhaler, budesonide slurry)
Food elimination diet
Occasionally, need dilatation for strictures

77
Q

Autoimmune hepatitis is associated with which autoantibodies?

A

Most common: Raised ANA, SMA, LKM-1, IgG

Others:
LC-1
pANCA
SLA - highly specific for AIH

78
Q 
All of the following are reported side effects of Tofacitinib except
A) gastrointestinal perforation
B) VTE
C) Shingles
D) Bell's palsy
A

Bell’s palsy

Used in IBD
Oral preparation

AE

  • Serious infections
  • Shingles (common)
  • Rare: VTE, GI perforation, non-melanoma skin ca
79
Q

Tofacinitib is what kind of biologic in IBD?

A

JK inhibitor

80
Q

How does vedolizumab vs adalimumab in mod-severe UC?

A

First head to head study

Vedolizumab is superior

81
Q

To prevent vertical transmission, treat with …

A

tenofovir 3rd trimester + 3 months post partum

82
Q

PSC and UC
Multifocal dysplasia in the colon. Lesions on the right hand side have been successfully removed.
What’s the management?

A

Total colectomy due to big field area

Gastro (9 decks)

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