Gastro difficult questions Flashcards
MTX induced hepatitis
Usually acute onset
High and prolonged doses
Where? When? How?
Approach to LFTs
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)
ALT >1000 Think…
Think Ischaemic liver injury Viral liver injury Drug induced liver injiury Autoimmune hepatitis Choledocholithiasis
Mild alteration in aminotransferase levels…
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
Cholestatic LFTs… think…
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)
If suspecting hepatic source of ALP rise think…
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
The primary factor leading to the accumulation in ascites in patients with chronic liver disease is
splanchnic vasodilation
Portal HTN when HVPG is
> =5mmgHg; clinically significant when >10-12mmHg
Leads to splanchnic vasodilation primarily led by nitric oxide
45M alcoholic
1st oesophageal variceal bleed –> endoscopic band ligation
How do you prevent recurrent bleeding?
Non-selective beta blockers (Carvedilol is the best) is superior to banding alone for grade 2-3 varices
How to classify oesophgeal varices?
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
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?
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
What is PSC?
Autoimmune
Inflammation, fibrosis + stricturing of medium + large ducts –> cholestasis
Classic: intra + extra hepatic ducts
Small duct: normal cholangiography, but histo consistent
What bloods would you expect in PSC?
Cholestatic pattern
pANCA 65% positive
AMA PBC 90% positive (F>M)
IgG4 for AI pancreatitis
Azathioprine malignancy risks?
Skin cancer
Lymphoma especially in men
What’s the truelove and Witt’s criteria?
Motions/day Fever Rectal bleeding Resting pulse Hb ESR/CRP
Defines mild, moderate, severe UC
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?
Quit smoking (but this won't reduce the damage that is already done) Infliximab = more correct
What are some biologics used in CD?
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)
How do the treatment approaches differ between UC and CD?
UC - stepwise approach
CD - top down approach (treat aggressively)
What are some immunomodulators used in CD?
AZA +/- allopurinol
6MP
MTX
Whats Exclusive Enteral Nutrition (EEN) in CD?
Drink resource for 6 weeks = equivalent to steroids
Useful in those who can’t be immunosuppressed
When do you use abx in CD?
If confirmed infection only e.g. penetrating disease, perianal disease
What should we check before we start AZA?
TMPT mutation
What’s the use of allopurinol in azathioprine?
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).
Risk factors for CD recurrence
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
Therapies post resection for CD
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
58M iron deficiency anaemia requiring blood transfusion (despite oral iron supplements)
Normal gastroscopy and colonoscopy
BM exam normal
What’s the next best investigation?
Enteroscopy
- Capsule endoscopy
What’s the most common cause of small bowel bleed?
Angioplasia
If you suspect small bowel angioplasia, what next?
Double balloon enteroscopy - pass scope into the small bowel and use balloon to stop the bleeding
When do you use CT abdominal angiography and labelled red cell scan?
Acute bleed in CT angiography
Labelled red cell scan is done only when CT angiography is not available
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?
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
What’s King’s criteria for paracetamol OD?
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
Basic Autoimmune liver screen
Ana
Anti SM ab
IGG
Cholestatic LFTs
Positive AMA
Primary biliary cholangitis
Which has the shorter half life?
ALT or AST
AST
Causes of AST >ALT
Muscle Wilsons disease NASH HCV with cirrhosis However often not more than 2:1
ETOH (2:1 ratio)
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
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.
Causes of PUD (Ulceration in stomach and duodenum)
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
List 4 testing methods for H pylori
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%
Where do you biopsy for H pylori?
Gastric mucosa
H pylori typically causes duodenal ulceration but increased acid secretion is from stomach.
When do people get infected with H pylori?
Usually in childhood and don’t develop ulcers until later in life
Hence serology will always be positive
How does Prostate radiation result in PR bleed?
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
Common causes of profuse lower GI bleeding
Diverticular bleeding
Ischaemic colitis
Post biopsy/polypectomy
Other forms of colitis
List procedures used for evaluation of lower GI bleed
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
Classic location of pill oesophagitis from doxycycline
Mid-oesophagus - where aortic arch touches the oesophagus and causes indentation
List causes of oesophagela ulcers
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
Eosinophilic oesophagitis
A) Pathophysiology
B) What conditions is it associated with?
C) What demographic?
D) What do you see on endoscopy?
E) Rx
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)
List biologics in Crohn’s
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
Is CRP good at detecting active inflammation in IBD?
No
Only has 70% sensitivity
CRP can also normalise when there is no objective change to inflammation
Do symptoms correlate with improvement in IBD?
Symptoms correlate poorly with inflammation
Rx UC refractory to treatment with azathioprine
Infliximab better than adalimumab
Vedolizumab is good too but takes time to work
Rx CD with perianal fistula
Infliximab
Has evidence in this specific setting
What is Pouchitis?
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.
What is fulminant UC?
> 6 bowel actions/day
Tachycardia
Anaemia
Raised inflammatory markers
Toxic megacolon (transverse colon typically) or features of sepsis
Rx: infliximab
Surgery is often needed
Atezolizumab + bevacizumab for …
HCC
Tofacitinib for …
Moderate-severe UC
GLP2 agonist (teduglutide) for …
Short bowel syndrome
Which micronutrient deficiency is common in coeliac? A) Iron B) B12 C) Selenium D) Zinc
Iron deficiency
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
Ferroportin-1
Terminal ileum absorbs
Bile acid –> portal system –> liver (recycled)
B12
Duodenum absorbs
Fe - classically deficiency in Coeliac disease
If you lose terminal ileum, can get…
Don’t get bile salt reabsorption
Bile salt diarrhoea (acts as osmotic agent)
Fat malabsorption = steatorrhoea
B12 deficiency
How does hepcidin work to reduce iron?
Removes ferroportin-1
Iron trapped inside enterocytes of duodenum then every few days, these enterocytes get sloughed off –> lose iron through the gut
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?
Small bowel Lymphoma!
Due to increased turning on and off of lymphocytes
Others: small bowel adenocarcinoma (rare), NHL, refractory coeliac disease (very rare)
How does refractory coeliac disease present? How to differentiate from lymphoma?
Less weight loss
Also get diarrhoea
Lack of B symptoms
This is very rare
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
Repeat endoscopy in 3 years if no dysplasia
What is Barrett’s? What does it look like on endoscopy?
Intestinal metaplasia
Squamous –> columnar (intestinal) mucosa
Appears as salmon-coloured tongues of mucosa seen on endoscopy
When to treat Barrett’s?
Presence of dysplasia, doesn’t matter if low grade
If can’t treat in dysplasia for whatever reason, then yearly endoscopic surveillance
Treatment options for Barrett’s
Radiofrequency ablation
Endoscopic mucosal resection or endoscopic sub-mucosal dissection
Surgery
Everyone gets PPI
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
Liver transplant
NOT
Surgical resection
CI in portal hypertension (varices, ascites in the stem)
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
Atezolizumab + bevacizumab
Now first line therapy and PBS covered
Superior to levatinib/sorafenib
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 =
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
What is achalasia?
Failure of lower oesophgeal sphincter relaxation and no peristalsis
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
Modified barium swallow
What are the 2 types of dysphagia?
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
What’s the difference between modified barium swallow and barium swallow?
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
Eosinophilic oesophagitis Rx
30% respond to PPI
If no response, then topical steroids (ingested flixotide inhaler, budesonide slurry)
Food elimination diet
Occasionally, need dilatation for strictures
Autoimmune hepatitis is associated with which autoantibodies?
Most common: Raised ANA, SMA, LKM-1, IgG
Others:
LC-1
pANCA
SLA - highly specific for AIH
All of the following are reported side effects of Tofacitinib except A) gastrointestinal perforation B) VTE C) Shingles D) Bell's palsy
Bell’s palsy
Used in IBD
Oral preparation
AE
- Serious infections
- Shingles (common)
- Rare: VTE, GI perforation, non-melanoma skin ca
Tofacinitib is what kind of biologic in IBD?
JK inhibitor
How does vedolizumab vs adalimumab in mod-severe UC?
First head to head study
Vedolizumab is superior
To prevent vertical transmission, treat with …
tenofovir 3rd trimester + 3 months post partum
PSC and UC
Multifocal dysplasia in the colon. Lesions on the right hand side have been successfully removed.
What’s the management?
Total colectomy due to big field area
