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BPT Written > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Early dumping syndrome

A
  • Rapid onset - 15 minutes
  • Colicky abdominal pain, diarrhoea, nausea, tachycardia
  • Sympathetic nervous response - due to rapid emptying of food into bowel causing fluid shifts
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2
Q

Late dumping syndrome

A
  • Onset 2-3 hours post meal
  • Dizziness, fatigue, diaphoresis, weakness
  • Postprandial (reactive) hypoglycaemia - following insulin peak
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3
Q

Hepatitis B serology - Previous infection

A

HBsAg-
HBsAb+
HBcAb+
HBeAg-

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4
Q

Hepatitis B serology - Previous vaccination

A

HBsAg-
HBsAb+
HBcAb-
HBeAg-

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5
Q

Hepatitis B serology - Chronic infection

A

HBsAg+
HBsAb-
HBcAb+
HBeAg+

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6
Q

Hepatitis B serology - Acute infection

A

HBsAg+
HBsAb-
HBcAb+
HBeAg+

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7
Q

Hepatitis B serology - Precore mutant infection

A

HBsAg+
HBsAb-
HBcAb+
HBeAg-

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8
Q

Indications for infliximab and adalimumab in Crohn’s disease

A
  • Refractory to steroids and AZA/MP/MTX

- Refractory fistulising Crohn’s disease

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9
Q

Indications for H. pylori eradication

A

MALT lymphoma
Active peptic ulcer disease
PHx of documented peptic ulcer

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10
Q

Common cause of portal hypertension

A

Cirrhosis - 90%
Portal vein thrombosis
Hepatic schistosomiasis

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11
Q

Portal hypertension - diagnosis

A

Hepatic venous pressure gradient (HVPG) = wedged hepatic venous pressure (WHVP) - free hepatic venous pressure (FHVP)

PHT = HVPG greater than 5
Clinically significant PHT = HVPH greater than 10

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12
Q

Cirrhosis - predictors of 3 month mortality

A

MELD score

  • INR
  • Creatinine
  • Bilirubin
  • Haemodialysis
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13
Q

Cirrhosis - predictors of 1-2 year mortality

A

Child-Pugh score

  • Encephalopathy
  • Ascites
  • Bilirubin
  • Albumin
  • Prothrombin time / INR
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14
Q

Site of folic acid absorption

A

Proximal jejunum

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15
Q

Site of fat absorption

A

Duodenum

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16
Q

Site of bile salt absorption

A

Terminal ileum

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17
Q

Site of vitamin B12 (cobalamin) absorption

A

Terminal ileum

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18
Q

Alpha-1 antitrypsin deficiency (AAT) - liver pathophysiology

A

Toxic gain of function - accumulation in hepatocyte of unsecreted variant AAT protein

19
Q

Site of vitamin C absorption

A

Proximal jejunum

20
Q

Site of iron absorption

A

Duodenum

21
Q

Site of calcium absorption

A

Proximal jejunum

22
Q

Serology - primary biliary cirrhosis (PBC)

A

AMA +ve
ANA +ve
ALP elevated
Lipids elevated

23
Q

Serology - primary sclerosing cholangitis

A

P-ANCA +ve
Serum IgM elevated
Hypergammaglobulinaemia
ALP elevated

24
Q

Serology - autoimmune hepatitis type-1 (AIH-1)

A

Anti-SMA +ve
ANA +ve
P-ANCA +ve

25
Q

Serology - autoimmune hepatitis type-2 (AIH-2)

A

Anti-LKM +ve

ANA +ve

26
Q

Paracetamol poisoning - indications for N-acetyl cysteine (NAC)

A
  • Concentration above treatment line in normogram at ≥4 hours
  • Single ingestion more than 150mg/kg (or 7.5g total), if concentration unavailable
  • Unknown time of ingestion and concetration more than 10mg/L
  • Evidence of liver injury and past history of paracetamol ingestion
27
Q

Eosinophilic oesophagitis - presentation

A 
Oesophageal dysfunction / dysphagia
Food bolus obstruction
Corrugated iron rings, longitudinal furrows
Young males
History of atopy
28
Q

Eosinophilic oesophagitis - treatment

A

PPI - sufficient up to 80%
Topical corticosteroid (eg. fluticasone)
Oesophageal dilatation

29
Q

Barrett’s oesophagus - treatment

A
  • Surveillance - until high grade dysplasia
  • PPI - reduces progression
  • Oesophagectomy - young patients
  • Endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) - preferred treatment
30
Q

Achalasia - treatment

A
  • Dilatation - treatment of choice, younger patients
  • Botox - 70% success, elderly patients
  • Myotomy - surgical division of LOS
  • GTN / CCB - less effective
31
Q

Most common pharmacological cause of gastric ulceration

A 
Aspirin - 45%
Ibuprofen - 25%
Indomethacin - 25%
Diclofenac - 15%
Meloxicam - less ulcers, but not completely benign
32
Q

H.pylori associated ulcers - treatment

A

Triple therapy

  • Amoxycillin
  • Clarithromycin
  • PPI
33
Q

Most likely Hepatitis C genotype to progress to cirrhosis / HCC

A

Genotype 3

  • Associated with steatosis
  • Increased progression to cirrhosis / HCC
  • Lower response rates to treatment
34
Q

Hepatitis C - treatment

A 
Genotype:
1 – sofosbuvir, ledipasvir
2 – sofosbuvir, ribavirin
3 – sofosbuvir, daclatasvir
4, 5, 6 – sofosbuvir, peg-interferon, ribavirin
(usually 12 weeks duration)
35
Q

Hepatitis C direct acting antivirals (DAA) - mechanism of action

A

Sofosbuvir - nucleoside NS5B polymerase inhibitor
Ledipasvir - NS5a inhibitor
Daclatasvir - NS5a inhibitor

36
Q

Chronic hepatitis B - treatment

A

Entecavir
OR Tenofovir
OR Pegylated interferon

(until 6 months after HBeAg seroconversion and undetectable HBV DNA; if HBeAg -ve chronic hepatitis, treat until HBsAg clearance)

37
Q

Hepatocellular carcinoma (HCC) - treatment

A

Resection - very early stage, less than 2 cm
Transplantation - early stage, 3 nodules ≤3cm
Chemoembolisation (TACE) - larger tumours
Sorafenib - advanced stage, slows progression

38
Q

Hepatocellular carcinoma (HCC) - surveillance

A

6-monthly liver US and AFP

39
Q

Spontaneous bacterial peritonitis - treatment

A

IV Ceftriaxone

Prophylaxis - norfloxacin, Bactrim DS

40
Q

Ulcerative colitis - treatment (induction)

A

Sulfasalazine or 5-aminosalicylate - in mild to moderate

Corticosteroids - in severe

41
Q

Ulcerative colitis - treatment (maintenance)

A

Sulfasalazine

5-aminosalicylate

42
Q

Crohn’s disease - treatment (induction)

A

Corticosteroids - eg. budesonide

43
Q

Crohn’s disease - treatment (maintenance)

A

Thiopurine - eg. azathioprine

Infliximab - in refractory or fistulising disease

BPT Written (20 decks)

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