Gastroenterology 2.0

Question 1

What would you see on LFTs for a patient with alcoholic hepatitis

Answer 1

GGT elevated
Elevated AST:ALT, with a ration of > 2:1

a ratio of > 3:1 is strongly suggestive of acute alcoholic hepatitis

ALT > AST for viral hepatitis

Question 2

What investigations should you do for a patient with suspected IBD?

Answer 2

FBC, UEs, LFTs, TFTs, coeliac serology, faecal calprotectin, stool culture

Calproctin >50 abnormal >150 highly suggestive of IBD, can be used as a marker of disease activity

Question 3

Lifestyle advice for patients with IBD

Answer 3

• Smoking cessation (reduces flares/severity in chrohns, reduces overall CVD risk)
• Generally healthy diet (increase omega acids in UC)
• Weight bearing exercise (mood and to prevent osteoporosis from freauent steroid use)
• Psychological coping skillds

Question 4

What are the 4 types of treatment we use to control IBD

What ones do we comomonly use

Answer 4

5-aminosalicylates, corticosteroids, immunomodulatory medicines and biologics

5-ASA’s: sulfasalazine, mesalazine
Steroids: PO prednisone, hydrocortisone acetate enaemas
Immunomodulators: azathioprine, mercaptopurine, MTX (2nd line)
biologics: idalizumab and adalimumab

Question 5

What is the mortality rate from bowel cancer for people with IBD?
How to we monitor for this

Answer 5

10-15%
Monitor with a c-scope at the 10 year mark, then every1-5yrs depending on risk

Question 6

What contraceptives should be avoided in patients with IBD

Answer 6

COCP: may not be absorbed in patients with severe Chrohns
Depo-provera can cause reduced bone density, as can IBD

Question 7

IBD medications and pregnancy

Answer 7

MTX is teratogenic, should be stopped >3/12 prior to trying to concieve

Biologics (inflixumab/adalizumab) can crosss the placenta in the first trimester, however this hasn’t been linked to negative outcomes

Question 8

What test do you need to do prior to starting azathioprine or mercaptopurine and why

Answer 8

Serum thiopurine methyltransferase (TPMT) needs to be checked.
1 out of 150 are TMPT-deficient
TMPT deficient patients develop severe bone marrow toxicity on standard levels of thiopurines

Question 9

How do we use ASA’s for IBD and in what form

Answer 9

Oral 5-ASA’s are often first line for mild-moderate IBD
much more effective in UC then Chrohns
high dose when initiating or during a flare, then slowly taper down
Can use suppositories for rectal disease and enemas for left sided disease

Question 10

What are the most common brand forms of 5-ASA’s
what dose do we use for flares vs maintenance

Answer 10

Pentasa (mesalazine) - releases in the small and large intestine
- 4g for flares, 2g for maintenance

Asacol (mesalazine) - releases in the terminal ileum and colon
- 1.6g TDS for flares, 400-800mg for maintenance

Question 11

Side effects to monitor for pt’s on 5-ASAs

Answer 11

Blood dyscrasisa
- Patients should be advised to report any unexplained bleeding, bruising, fever, malaise, purpura, or sore throat
- monitor FBC, LFTs, UEs

Question 12

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how are steroids (prednisone, hydrocort acetate enema) used in patients with IBD

Answer 12

Used to manage flares / induce remission
- often used if an ASA is ineffective at controlling symptoms
- commonly used initially in pts with severe chrohn
- NOT for IBD maintenance treatment (avoid long-term use)

Monitor risk of osteoporosis and osteonecrosis with oral corticosteroid use

Question 13

dose of steroid in a flare

Answer 13

Pred: initially 40 mg daily for at least two weeks, then reduce dose by 5 mg per week

Hydrocortisone acetate (enema): 1 (approximately 90–100 mg) OD for 2 weeks then once daily on alternate days

Question 14

when do we use immunomodulators (azathioprine, mercaptopurine, MTX)

Answer 14

when ASA’s are ineffective and pts are requiing multiple courses of steroids

Question 15

What should we know about 5-ASA’s and fertility

Answer 15

No affect on female fertility

Sulfasalazine can reduce sperm count and sperm motility.
This is reversible and usually returns to normal 2 to 3 months after you stop taking sulfasalazine.

Question 16

Extra intestinal side effects or complications of coeliacs disease

Answer 16

headache, fatigue
dermatitis herpatiformis
Loss of dental enamel , angular stomatitis
Iron b12, folate deficiency
Elevated liver enzymes
osteoporosis
GI malignancy or T-cell lymphoma

Question 17

Genes associated with coeliacs

Serology ?

Answer 17

HLA DQ2 and HLA DQ8
Anti-TTG, do with IgA (need to be having >5g/day for 4 weeks prior)
- if above high > will reflex due EMA -TTG
- if IgA low > will do DGP-TTG

IgA deficient pts will give you a false neg, when they are actually high

Question 18

Red flags for dyspepsia

Answer 18

First presentation >50yrs ( or >40 years if Māori, Pacific, Asian descent)
FHX gastric cancer (especially if <50yrs)
Severe or persistent dyspepsia despite treatment
Coughing spells or nocturnal aspiration
Dysphagia
Weight loss
IDA
bleeding (haemtemesis, malaena
Palpable abdominal mass
Persistent or protracted vomiting

Question 19

Medications that can cause dyspepsia

Answer 19

NSAIDs
Aspirin, clopidogrel, other anticoagulants
bisphosphonates
steroids

Question 20

H.pylori serology is not available in NZ, what do we use instead

Answer 20

Faecal (antigen) test:
- requires a fresh stool sample (must arrive within 48 hours, otherwise freeze the sample).
- demonstrates active infection, so suitable for diagnosis and follow-up testing.

False negative results occur if recent antibiotics (1 month) or proton pump inhibitor (PPI) (2 weeks) before testing.

only do test of cure if ongoing symptoms at 3/12 or known complications

Question 21

difference between a femoral and inguinal hernia on exam

Answer 21

Inguinal: medial and above pubic tubercle
Femoral: lateral and below pubic tubercle (under inguinal ligmaent next to femoral vessels)

Question 22

hepatitis B bloods

Answer 22

HbsAg: surface antigen (active infection)
HbcAg: core antigen (active infection)
HbeAg: Envelope antigen (active infection) indicates greater infectivity and increased risk of chronic liver disease.
viral DNA (active infection)

Hb core IgM antibodies: immediate immune response (active infection or recovery)
Hb core IgG antibodies: later immune reaction (chronic infection)

Anti-HbS: recovery (post infection or immunisation)

Question 23

Antibodies for autoimmune hepatitis

Answer 23

Antinuclear antibody (ANA), anti‑smooth muscle antibody (ASMA), anti‑mitochondrial antibody (AMA)

Question 24

What is needed to calculate a Fib4 score
how do we use the score

Answer 24

ALT, AST, PLT, age

Do fibro scan if
≤ 60 years and score ≥ 1.3
> 60 years and score ≥ 2

otherwise, recheck score in 2 yrs

25% have NAFL, 5-15% develop fibrosis

Question 25

What causes HCC

Answer 25

most HCC arises in patients with cirrhosis.
50% Hep B
30% Hep C
20% alcoholic cirrhosis, NAFL, Haemochromatosis

Question 26

chronic liver disease (and/or HCC) signs/sx on exam

Answer 26

Palmar erythema
Spider naevi
Jaundice
Liver tenderness, hepatomegaly, splenomegaly
Masses or irregularity
Abdominal pain or distention
Flapping tremor
Fever
Jaundice
Ascites
Peripheral oedema
Gynaecomastia
Caput medusae

liver usually breaks down oestrogen, high blood oestrogen levels > gynaecomastia + spider naevi + palmar erythema

Question 27

complications of cirrhosis

Answer 27

Portal hypertension (driver of other complications)
GI bleeding
Splenomegaly
Oedema and ascites
Encephalopathy
Liver cancer / HCC
Sepsis - especially SBP