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FRACP Exam > Gastro > Flashcards

Gastro Flashcards

1
Q

What is the active metabolite of 6-mecap/Aza?

A

6-TGN
6MMP - associated with myelosupression/hepatotoxicity

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2
Q

What does High 6-TGN/High 6MMP mean and what should you do?

A

Thiopurine refractory disease - change to another drug e.f Anti-TNF

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3
Q

What does Low 6-TGN and high 6MMP mean and what should you do?

A

Thiopurine resistance, add allopurinol and reduce thiopurine dose

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4
Q

What is the role of allopurinol administration with Azathioprine?

A

TMPT inhibition to prevent shunt to 6MMP

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5
Q

Which inflammatory bowel disease is methotrexate used in?

A

Chrons, NEVER UC.

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6
Q

Which inflammatory bowel disease gives you strictures and perianal involvement?

A

Chrons

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7
Q

Which IBD is associated with primary sclerosing cholangitis?

A

UC - occurs independent of disease activity and increases CRC risk by x6

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8
Q

What is Vedolizumab?

A

Selectively binds alpha 4 beta 7 intergrin on T cells to inhibit traffiking out of the blood to sites of inflammation - it is gut spefici and used in UC and chrons. Safe side effect profile

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9
Q

What are the things in truelove and Witts criteria

A

For acute severe colitis:
Freq stool Mild - 4 , Mod4-5, Severe - >6
Bloody stool Mild +/- severe +++
Severe features:
Fever >37.5, Tachycardia >90, Anaemia < 100, ESR >30

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10
Q

What are patients high risk for if they have acute severe colitis?

A

DVT/ PE - should have anticoag

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11
Q

How do you treat acute severe colitis?

A

IV Methyl pred, if still >6 BM.day or >3 bloody BM/day by day 3 -0 infliximab

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12
Q

Whst type of IBD is 5ASA used for?

A

UC - rectal suppositories as US always affects the rectum, if thats not enough then move to PO + PR

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13
Q

When do you use anti-TNF in chrons?

A

Inflammatory chrons disease refractory to steroids and refractory fistulising diease

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14
Q

In what scenario would you change Anti-TNF vs change drug class?

A

Therapeutic drug levels but ongoing clinical signs/symptoms = change class
Subtherapeutic levles, and drug antibodies - change Anti-TNF
Subtherapeutic and no antibodies - dose escalate

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15
Q

If have UC AND PSC how often should they have colonoscopy?

A

Annual as high risk of CRC

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16
Q

What is the most common cutaneous extraluminal manifestation of IBD?

A

Erythema nodosum - It presents as tender red nodules on the anterior shins. Less commonly, they affect the thighs and forearms

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17
Q

Whats the second most common skin extraluminal manifestation of IBD?

A

Pyoderma gangrenosum - rapidly enlarging painful ulcer
UC>CD
Ass wiith acitve disease,

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18
Q

What extraluminal disease manifestations of IBD are associated with disease acitivity?

A

Oral ulcers
Erythema nodosum
Large joint arthritis
Episcleritis.

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19
Q

What extraluminal disease manifectations of IBD are NOT associated with disease acitivity?

A
  • Primary sclerosing cholangitis
    • Ankylosing spondylitis
    • Uveitis
    • Pyoderma gangrenosum
    • Kidney stones
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20
Q

Regarding IBD what are the characteristics of High, intermediate and low risk for CRC?

A

High - Extensive colitis UC or >50% CD colitis AND one of PSC, FH of CRC <50, dysplastic polyp in colitis area in last 5 years, colonic stricture
Intermediate: Extensive colitis UR or >50% CD coliting AND Inflammatory polyps, FH CRC >50
Low risk none of above but more than one segment colitis

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21
Q

What are the timeframes of colonoscopy for High Int and low risk IDB patients for CRC?

A

High - annual
Int - 2-3 yearly
Low - 5 yearly

22
Q

What is achalasia?

A

Imparied lower oesophageal sphincter relaxation and peristalsis in the distal oesophagus

23
Q

What is the classic sign on barium swallow in achalasia?

A

Birds beak - cute tapering at the lower esophageal sphincter and narrowing at the gastro-esophageal junction, producing a “bird’s beak” or “rat’s tail” appearance

24
Q

What is type 1 achalasia? + manometry findings

A

No pressure wave in the oesophagus, no muscle tone
They have poor response to treatment

25
Q

What is type 3 achalasia? + manometry findings

A

Hypercontractile, corskrew appearance of barium swallow - poor response to treatment

26
Q

What is the pathophysiology of achalasia?

A

Loss of inhibitory neurons lading to hypercontractility, eventually loss of the stimulatory neurons an dloss of muscle contraction

27
Q

When do you use endoscopic botox in achalasia?

A

If patient is not a surgical/definitive treatment candidate. It causes scarring

28
Q

What is POEM?

A

Peroral endoscopic myotomy - emerging role in treatment of achalasia - would do in someone where heller myotomy is technically difficult

29
Q

What are the outcomes for POEM vs laparoscopic myotomy with fundiplication?

A

Both as effective as each other - both risk of post procedure reflux 10-50%

30
Q

What are the endoscopic findings of eosinophilic oesophagitis?

A
  • Long furrows
    • Concentric rings
    • Strictures with fragile mucosa
      • White exudates
31
Q

How do you treat eosinophilic oesophagitis?

A

PPI for 8 weeks
If no improvement then swallowed MDI steroids, dietary therapy 6-8 weeks, 6 food eliminatoin , if no improvement, prednisone and endoscopic dilation in case of stenosis

32
Q

How do you treat barrets oesophagus?

A

High dose PPI + aspirin ( aspirin addition by reduce risk fo cancer progression )

33
Q

What is the risk of oesophageal carcinoma in barrets?

A

annual risk of progression 0.38% compared to 0.07% without.
7 x increase if have reflux sx 1/week

34
Q

If there is high grade dysplasia in barrets oesophagus what is the management??

A

Endoscopic mucosal resection (EMR) of the nodule and then RFA of the rest of the Barrett’s. RFA of the whole Barret’s to prevent more high grade dysplasia developing.

35
Q

What is the risk of progression to oesophageal carcinoma if high grade dysplasia found?

A

Annual risk 10% - needs intervention.

36
Q

What is T1a vs T1b in oesophageal cacinoma?

A

T1 - intramucosal, T1b - invasive carcinoma - cant be treated with radiofrequency ablation therapy

37
Q

What makes up glutin?

A

50% gliadin, 50% glutenin. Gliadin has high immunogenicity.

38
Q

What is the histology seen on biopsy in coeliac disease?

A

Villous atrophy, crypt hyperplasia, raised intraepithelial lymphocytes based on multiple biopsies from the 1st and 2nd part of the duodenum.

39
Q

What HLA is highly specific for coeliacs ( i.e, if you don’t have it you probably don’t have coeliac)

A

HLA-DQ2.5, DQ2.2, and DQ8 can exclude the diagnosis of coeliac disease

40
Q

How can you tell different help C drugs actions?

A

All proteasome inhibitors end with “previr” eg Simeprevir. All NS5a inhibitors end with ‘asvir’ eg Daclatasvir. All NS5B inhibitors end with ‘buvir’

41
Q

What is in the Kings college criteria for acute liver failure?

A

Paracetamol related:
- pH on ABG < 7.3 OR
All 3 of : INR >6.5 + Cr > 300 + grade III or IV encephalopathy
Non-paracetamol induced acute liver failure
- INR >6.5 OR
Three of:
- Age <11 or > 40
- Serum bilirubin > 300
- Jaundice-to-coma time of > 7 days
- INR > 3.5
- Drug toxicity

42
Q

At what MELD score should people be considered for transplant?

A

MELD 10-15 ( and above)

43
Q

How does acute liver transplant cellular rejection present?

A

occurs in ~30% - cholestatic LFT secondary to potal based inflammation, occurs at day ~7-10

44
Q

What is the Milan criteria for transplant in HCC?

A

1 lesion < 5cm or 3 < 3cm
UCSF criteria ( used in Aus)
- Single nodule < 6.5cm OR
- Up to 3 nodlues, no greater than < 4.5cm
- AND cumulative tumour size ( sum of all diameters < 8cm)
1 year survival in this group is 90% and 5 year is 75%

45
Q

How does rifaximin reduce recurrence of encephalopathy in cirrhosis?

A

Rifaximin is a poorly absorbed antibiotic that is thought to reduce ammonia production by eliminating ammonia-producing colonic bacteria

46
Q

What is the treatemnt for PSC?

A

There are no provem medical therapies that alter disease progression and need for transplant.
Transplant is the only proven treatment of benefit, with recurrence of up to 20% at 5 years

47
Q

What is the pathogenesis of primary biliary cholangitis?

A

T-lymphocyte-mediated attack on small intralobular bile ducts. A continuous assault on the bile duct epithelial cells leads to their gradual destruction and eventual disappearance

48
Q

What antibodies are found in primary biliary cholangitis?

A

AMA (anti-mitochondrial antibody) are the serologic hallmark of PBC. They are present in approximately 95 percent of patients with PBC. Can also get ANA

49
Q

What conditions are associated with PBC?

A

Sjrogens, autoimmune thyroid disease, RA

50
Q

How do you diagnose PBC?

A

A diagnosis of PBC is established if there is no extrahepatic biliary obstruction, no comorbidity affecting the liver, and at least two of:
ALP >1.5 times ULN
Presence of antimitochondrial antibodies (AMA) at a titre of 1:40 or higher
Histologic evidence of PBC (nonsuppurative destructive cholangitis and destruction of interlobular bile ducts) - Biopsy not required for diagnosis however

51
Q

How do you treat PBC?

A

Ursodeoxycolic acid
(1) protection of injured cholangiocytes against toxic effects of bile acids, (2) stimulation of impaired biliary secretion, (3) stimulation of detoxification of hydrophobic bile acids, and (4) inhibition of apoptosis of hepatocytes

52
Q

melanosis coli on colonbiopsy indicates what?

A

Laxatice abuse

FRACP Exam (15 decks)

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