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MRCP > Gastro > Flashcards

Gastro Flashcards

1
Q

Barretts oesophagus leads to..?

A

oesophageal adenocarcinoma (~50-100x)

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2
Q

Risk factors of Barrett’s oesophagus?

A

GORD - strongest RF
Male (7:1)
Smoking
Central obesity

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3
Q

Management of Barrett’s oesophagus?

A
  • endoscopic surveillance with biopsies: recommended every 3-5 y if metaplasia present
  • high-dose PPI
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4
Q

management of Barrett’s oesophagus if dysplasia identified on biopsy?

A

endoscopic intervention

  • endoscopic mucosal resection
  • radio frequency ablation
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5
Q

Hep B in pregnancy: most appropriate strategy for reducing the vertical transmission rate?

A

if mother HBeAg +ve: give newborn vaccine + Immunoglobulin

  • if not very infective, only vaccine needed
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6
Q

what is the only test recommended for H. pylori post-eradication therapy

A

Urea breath test

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7
Q

What medications should not be taken before urea breath test for H pylori?

A
  • within 4 wks of antibiotics

- within 2 wks of antisecretory drug e.g. PPI

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8
Q

pregnancy:
pruritus, often in the palms and soles +
no rash (although skin changes may be seen due to scratching) +
raised bilirubin

A

Intrahepatic cholestasis of pregnancy

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9
Q

Management of Intrahepatic cholestasis of pregnancy

A
  • ursodeoxycholic acid for symptomatic relief
  • weekly liver function tests
  • women are typically induced at 37 weeks
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10
Q

Features of HELLP?

A

Haemolysis, Elevated Liver enzymes, Low Platelets

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11
Q

Features of Acute fatty liver of pregnancy?

A
  • abdominal pain, nausea & vomiting, jaundice
  • headache
  • hypoglycaemia
  • severe disease may result in pre-eclampsia
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12
Q

Ix of Acute fatty liver of pregnancy?

A

ALT high - typically >500

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13
Q

Mx of Acute fatty liver of pregnancy?

A

supportive care, delivery is definitive management

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14
Q

main risk factor for cholangiocarcinoma?

A

Primary sclerosing cholangitis

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15
Q

Features of cholangiocarcinoma?

A
  • persistent biliary colic symptoms
  • anorexia, jaundice and weight loss
  • palpable mass in RUQ (Courvoisier sign)
  • periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen
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16
Q

most common type of inherited colorectal cancer

A

hereditary non-polyposis colorectal carcinoma (HNPCC, 5%)

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17
Q

most common genes involved with HNPCC?

A

MSH2 (60% of cases)

MLH1 (30%)

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18
Q

Genetics of FAP?

A
  • auto dominant

- APC gene (tumour suppressor) mutation on chromosome 5

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19
Q

Conditions associated with Coeliac disease?

A
  • Autoimmune thyroid disease/ Autoimmune hepatitis
  • Dermatitis herpetiformis
  • Irritable bowel syndrome
  • Type 1 diabetes
  • First-degree relatives (parents, siblings or children) with coeliac disease
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20
Q

HLA assoc with coeliac disease?

A

HLA-DQ2 (95% of patients) and HLA-DQ8 (80%).

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21
Q

IX to diagnose chronic pancreatitis?

A

CT abdo: pancreatic calcification (Sensitivity is 80%, specificity is 85%)
- If imaging inconclusive, faecal elastase to assess exocrine function

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22
Q

Management of chronic pancreatitis?

A

pancreatic enzyme supplements
analgesia
antioxidants: limited evidence base

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23
Q

Diagnosis of Spontaneous bacterial peritonitis

A

paracentesis: neutrophil count > 250 cells/ul

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24
Q

most common organism found on ascitic fluid culture in Spontaneous bacterial peritonitis

A

E coli

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25
Q

Mx of Spontaneous bacterial peritonitis

A

IV cefotaxime

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26
Q

Antibiotic prophylaxis is given to patients w ascites if?

A
  • 1 episode of SBP

- patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome

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27
Q

What antibiotic prophylaxis is given to patients with ascites to prevent SBP?

A

oral ciprofloxacin or norfloxacin

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28
Q

Primary sclerosing cholangitis - assoc w which type of IBD?

A

Ulcerative colitis

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29
Q

genetics of Haemochromatosis

A

auto recessive

- mutations in HFE gene on chromosome 6

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30
Q

Reversible complications of Haemochromatosis

A

Cardiomyopathy (Dilated),
Skin pigmentation

Fatigue
Transaminase elevation

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31
Q

Irreversible complications of Haemochromatosis

A
  • Liver cirrhosis**
  • Arthropathy

Might have some improvement in some:

  • Diabetes mellitus
  • Hypogonadotrophic hypogonadism
  • arthralgia
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32
Q

Mx of Gastric MALT lymphoma?

A

if low grade then 80% respond to H. pylori eradication

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33
Q

Factors in Ulcerative colitis increasing risk of colorectal cancer

A
  • disease duration > 10 years
  • pancolitis
  • onset < 15 years old
  • unremitting disease
  • poor compliance to treatment
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34
Q

Indications for 1 year follow up colonoscopy in UC (due to high risk of developing colorectal ca)

A
  • Extensive colitis with moderate/severe active endoscopic/histological inflammation
  • OR stricture in past 5 years
  • OR dysplasia in past 5 years declining surgery
  • OR primary sclerosing cholangitis / transplant for primary sclerosing cholangitis
  • OR family history of colorectal cancer in first degree relatives aged <50 years
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35
Q

Indications for 3 year follow up colonoscopy in UC (due to intermediate risk of developing colorectal ca)

A
  • Extensive colitis with mild active endoscopy/histological inflammation
    OR post-inflammatory polyps
    OR FHx of colorectal cancer in a first degree relative >/= 50
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36
Q

Indications for 5 year follow up colonoscopy in UC (due to low risk of developing colorectal ca)

A
  • Extensive colitis with no active endoscopic/histological inflammation
  • OR left sided colitis
  • OR Crohn’s colitis of <50% colon
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37
Q

H pylori causes…

A
  • peptic ulcer disease (95% of duodenal ulcers, 75% of gastric ulcers)
  • gastric adenoCa
  • B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
  • atrophic gastritis
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38
Q

findings supportive of coeliac disease on endoscopic intestinal biopsy:

A
  • villous atrophy
  • crypt hyperplasia
  • increase in intraepithelial lymphocytes
  • lamina propria infiltration with lymphocytes
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39
Q

Ix of achalasia: what would you see on oesophageal manometry?

A
  • excessive LOS tone which doesn’t relax on swallowing

- considered the most important diagnostic test

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40
Q

Ix of achalasia: what would you see on barium swallow?

A

shows grossly expanded oesophagus, fluid level

‘bird’s beak’ appearance

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41
Q

Ix of achalasia: what would you see on CXR?

A

wide mediastinum, retrocardiac air-fluid level

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42
Q

Management of achalasia?

A

1st line: pneumatic (balloon) dilatation
If recurrent/ persistent symptoms: Heller cardiomyotomy surgery.
- if high surgical risk: intra-sphincteric injection of botulinum toxin
- medications e.g. nitrates, CCBs

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43
Q

most common cause of HCC in UK/europe?

A

Hep C

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44
Q

most common cause of HCC worldwide?

A

Hep B

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45
Q

Classifying severity of ulcerative colitis?

A
  • mild: < 4 stools/day, only a small amount of blood
  • moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
  • severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
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46
Q

Mx of mild-moderate ulcerative colitis?

A

extensive disease: Rectal + Oral Aminosalicylate
Proctosigmoiditis + left sided UC: rectal only
proctitis: rectal only

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47
Q

Mx of mild-moderate ulcerative colitis if remission not achieved within 4 wks with just rectal aminosalicylate

A

add oral aminosalicylate.

if still not achieved: add topical/ oral steroid

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48
Q

Mx of mild-moderate ulcerative colitis if remission not achieved within 4 wks with just rectal + oral aminosalicylate for extensive disease?

A

stop topical treatments, offer high dose oral aminosalicylate + oral steroid

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49
Q

Mx of severe colitis?

A

IV steroids

  • if steroids CI, IV ciclosporin
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50
Q

Maintaining remission in a flare of mild- mod UC with proctitis/ proctosigmoiditis?

A

Rectal aminosalicylate alone

OR oral + rectal OR oral only

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51
Q

Maintaining remission in a flare of mild- mod UC with left sided and extensive UC?

A

low maintenance dose of an oral aminosalicylate

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52
Q

Maintaining remission in a flare of severe UC or >=2 exacerbations in the past year?

A

oral azathioprine or oral mercaptopurine

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53
Q

what artery may be affected in a posteriorly sited duodenal ulcer?

A

gastroduodenal artery

  • may require laparotomy, duodenotomy and under running of the ulcer
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54
Q

UGIB scoring system to determine need for admission/ timing of endoscopic intervention?

A

Blatchford score

  • 0 is low risk
  • all others are considered high risk and require admission and endoscopy
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55
Q

Screening for cirrhosis: who should be offered transient elastography (Fibroscan)

A
  • people with hepatitis C virus infection
  • men who drink >50u of ETOH/wk + women who drink >35 units of ETOH/wk
  • those diagnosed with alcohol-related liver disease
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56
Q

Ix for those with confirmed liver cirrhosis?

A
  • upper endoscopy to look for varices

- Liver US every 6 mo +/- AFP to screen for HCC

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57
Q

Heyde syndrome?

A

triad of aortic stenosis, an acquired coagulopathy and anaemia due to bleeding from intestinal angiodysplasia

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58
Q

Diagnosis of angiodysplasia if acutely bleeding?

A

mesenteric angiography

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59
Q

Diagnosis of angiodysplasia?

A

colonoscopy

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60
Q

Mx of angiodysplasia?

A

endoscopic cautery or argon plasma coagulation,

antifibrinolytics e.g. TXA, oestrogens

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61
Q

SEs of PPIs?

A

hypoNa, HypoMg
osteoporosis
microscopic colitis
C diff colitis

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62
Q

main foods that contain gluten?

A
  • wheat: bread, pasta, pastry
  • barley: beer
  • rye
  • oats
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63
Q

notable foods which are gluten-free?

A

rice, potatoes, corn (Maize)

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64
Q

mx of NAFLD?

A

mainstay of tx is lifestyle changes (particularly weight loss) and monitoring

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65
Q

Risk factors for developing eosinophilic oesophagitis?

A
  • Allergies/ asthma: food/ environmental allergies or atopic dermatitis
  • Male sex
  • Family history of eosinophilic oesophagitis or allergies
  • Caucasian race
  • Age between 30-50
  • Coexisting autoimmune disease e.g. coeliac disease
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66
Q

Management of eosinophilic oesophagitis?

A
  • elemental diet/ targeted elimination diet
  • topical steroids (fluticasone/ budesonide) for 8/52 before reassessment
  • oesophageal dilation: 56% will require this at some point due to strictures
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67
Q

Complications assoc with eosinophilic oesophagitis?

A

strictures, impaction, mallory-weirs tears

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68
Q

Lactase breaks down what into what?

A

cleaves disaccharide lactose -> glucose + galactose

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69
Q

Sucrase breaks down what into what?

A

cleaves sucrose into fructose + glucose

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70
Q

Maltase: breaks down what into what?

A

cleaves maltose -> glucose + glucose

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71
Q

what should be assessed before starting azathioprine/ mercaptopurine?

A

TPMT (Thiopurine methyltransferase) activity.

- some have a deficiency -> greater risk of severe side effects

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72
Q

inducing remission in Crohn’s disease?

A
  • steroids 1st line
  • enteral feeding w elemental diet
  • 2nd line: 5-ASA (e.g. mesalazine), azathioprine/ mercaptopurine
  • infliximab (in refractory disease and fistulating Crohn’s)
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73
Q

Inducing remission in Isolated peri-anal crowns disease?

A

metronidazole useful

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74
Q

Maintaining remission in Crohns disease?

A
  • stop smoking
  • 1st line: azathioprine/ mercaptopurine (TPMT activity assessed before starting)
  • 2nd line: methotrexate
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75
Q

Complications of Crohn’s disease?

A
  • strictures/ fistulae
  • small bowel cancer (standard incidence ratio = 40)
  • colorectal cancer (standard incidence ratio = 2, i.e. less than the risk associated with ulcerative colitis)
  • osteoporosis
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76
Q

Genetics of Wilson’s disease?

A

auto recessive, defect in ATP7B gene on chromosome 13

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77
Q

Neurological features of Wilsons disease?

A

basal ganglia degeneration: most copper is deposited in the putamen and globes pallidus
- psych, asterixis, chorea, dementia, Parkinsonism

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78
Q

Diagnosis of Wilson’s disease?

A

reduced serum caeruloplasmin, total serum copper,

Increased 24h urinary copper excretion

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79
Q

Mx of Wilsons disease?

A

penicillamine

Trientine hydrochloride

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80
Q

Genetics of Peutz Jeghers?

A

autosomal dominant

-responsible gene encodes serine threonine kinase LKB1 or STK11

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81
Q

Features of Peutz Jeghers?

A
  • hamartomatous polyps in GI tract (mainly small bowel)
  • pigmented lesions on lips, oral mucosa, face, palms and soles
  • intestinal obstruction e.g. intussusception
  • GI bleeding
  • ~50% will have died from another GI cancer by age 60
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82
Q

what gene mutations increase risk of pancreatic cancer?

A

BRCA2 gene, KRAS gene mutation

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83
Q

Ix of choice of pancreatic cancer?

A

high resolution CT abdomen

- might show “double duct” sign - presence of simultaneous dilatation of the common bile and pancreatic ducts

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84
Q

Mx of pancreatic cancer - palliation?

A

ERCP with stenting

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85
Q

Mx of pancreatic cancer if suitable for surgery?

A

Whipples resection (pancreaticoduodenectomy) +/- adjuvant chemotherapy following surgery.

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86
Q

Liver failure: which clotting factor is paradoxically increased?

A

fVIII
- bc VIII is synthesised in endothelial cells throughout the body, unlike other clotting factors which are synthesised purely in hepatic endothelial cells

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87
Q

Mx of pyloric stenosis

A

Ramstedt pyloromyotomy

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88
Q

1st line management of acute anal fissure?

A

bulk-forming laxatives

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89
Q

1st line mx of chronic anal fissure?

A

Topical GTN

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90
Q

what electrolyte imbalances may cause acute pancreatitis?

A

hypertriglyceridaemia, hyperchylomicronaemia, hyperCa, Hypothermia

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91
Q

what drugs may cause acute pancreatitis?

A

azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate

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92
Q

Histological findings in gastric adenocarcinoma?

A

signet ring cells

  • higher numbers assoc w worse prognosis
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93
Q

Gastric cancer associations?

A
  • H. pylori infection
  • blood group A: gAstric cAncer
  • gastric adenomatous polyps
  • pernicious anaemia
  • smoking
  • diet: salty, spicy, nitrates
  • may be negatively associated with duodenal ulcer
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94
Q

Ix of gastric cancer?

A
  • diagnosis: endoscopy with biopsy

- staging: CT or endoscopic ultrasound - endoscopic ultrasound has recently been shown to be superior to CT

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95
Q

First line for staging of gastric cancer?

A

CT scanning of the chest abdomen and pelvis

  • consider: Laparoscopy to identify occult peritoneal disease, PET CT (particularly for junctional tumours)
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96
Q

Mx of gastric cancers?

A
  • Proximally sited disease greater > 5-10cm from the OG junction = sub total gastrectomy
  • Total gastrectomy if tumour is <5cm from OG junction
  • For type 2 junctional tumours (extending into oesophagus) oesophagogastrectomy is usual

+/- Lymphadenectomy +/- pre/post op chemo

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97
Q

Features of Carcinoid syndrome?

A

flushing (often earliest symptom), diarrhoea, bronchospasm, hypotension

  • right heart valvular stenosis
  • ACTH and GHRH may also be secreted–> Cushing’s syndrome
  • pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour
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98
Q

What is carcinoid syndrome?

A
  • usually occurs when mets are present in the liver and release serotonin into the systemic circulation
  • may also occur with lung carcinoid as mediators are not ‘cleared’ by the liver
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99
Q

Ix of carcinoid syndrome?

A

raised urinary 5-HIAA, plasma chromogranin A y

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100
Q

Mx of carcinoid syndrome?

A
  • somatostatin analogues e.g. octreotide

- diarrhoea: cyproheptadine may help

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101
Q

monoclonal antibody which targets Clostridium difficile toxin B- might be used to prevent further recurrence

A

bezlotoxumab

102
Q

Mx of c diff Infection if not responding to normal management? (2nd line)

A

oral fidaxomicin

103
Q

1st line mx of C diff?

A

oral vancomycin for 10 days

104
Q

NICE bariatric referral BMI cut-offs

A

with risk factors (T2DM, HTN etc): > 35 kg/m^2

no risk factors: > 40 kg/m^2

105
Q

first-line bariatric intervention in patients with a BMI of 30-39kg/m^2

A

primarily restrictive: laparoscopic-adjustable gastric banding (LAGB)

  • fewer SEs
106
Q

bariatric intervention in patients with a BMI of >40?

A

consider gastric bypass/ sleeve gastrectomy

107
Q

bariatric intervention in patients with a BMI of >60?

A

primarily malabsorptive: biliopancreatic diversion with duodenal switch

108
Q

features of autoimmune hepatitis?

A
  • may present with signs of chronic liver disease
  • acute hepatitis: fever, jaundice etc (only 25% present in this way)
  • amenorrhoea (common)
  • ANA/SMA/LKM1 antibodies, raised IgG levels
109
Q

liver biopsy of autoimmune hepatitis?

A

inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis

110
Q

mx of autoimmune hepatitis?

A

steroids, other immunosuppressants e.g. azathioprine

- liver transplant

111
Q

most common organism found in pyogenic liver abscesses in children?

A

Staph aureus

112
Q

most common organism found in pyogenic liver abscesses in adults?

113
Q

Management of pyogenic liver abscess?

A

drainage (typically percutaneous) and antibiotics
- amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic: ciprofloxacin + clindamycin

114
Q

first line test for diagnosis of small bowel overgrowth syndrome

A

hydrogen breath test

115
Q

Risk factors for Small bowel bacterial overgrowth syndrome?

A
  • neonates with congenital gastrointestinal abnormalities
  • scleroderma
  • diabetes mellitus
116
Q

management of Small bowel bacterial overgrowth syndrome?

A
  • correct underlying disorder
  • 1st line: Rifaximin
    (2nd line: co-amox/ metronidazole)
117
Q

Oesophageal/Gastric Cancer - What is the best investigation to assess for mural invasion?

A

Endoscopic ultrasound

  • can display all the layers of the wall of the oesophagus and should routinely be performed with CT or MRI scans.
118
Q

most common type of oesophageal ca?

A

adenoca now

119
Q

risk factors of gastro/oesophageal adenocarcinoma?

A 
GORD
Barrett's oesophagus
smoking
achalasia
obesity
120
Q

risk factors of gastro/oesophageal squamous cell carcinoma?

A 
smoking
alcohol
achalasia
Plummer-Vinson syndrome
diets rich in nitrosamines
121
Q

Management of oesophageal cancer?

A

surgical resection - e.g Ivor-Lewis type oesophagectomy.

+/- adjuvant chemo

122
Q

pathophysiology of hepatorenal syndrome?

A

vasoactive mediators cause splanchnic vasodilation -> reduces systemic vascular resistance > less blood going to kidneys

123
Q

Management of hepatorenal syndrome?

A
  • terlipressin - causing vasoconstriction of the splanchnic circulation.
  • volume expansion w 20% albumin
  • Transjugular intrahepatic portosystemic shunt
  • ideal treatment = liver transplant
124
Q

most common site affected in UC

125
Q

Pathophysiology of Zollinger-Ellison syndrome?

A

excessive levels of gastrin, usually from a gastrin secreting tumour usually of the duodenum or pancreas.
~ 30% occur as part of MEN type I syndrome

126
Q

Diagnosis of Zollinger-Ellison syndrome?

A

fasting gastrin levels: the single best screen test

secretin stimulation test

127
Q

features of villous adenomas?

A

characteristically secrete large amts of mucous

  • secretory diarrhoea
  • microcytic anaemia
  • hypokalaemia
128
Q

features of Dubin-Johnson syndrome?

A
  • benign auto recessive
  • hyperbilirubinaemia (conjugated)
  • defective hepatic bilirubin excretion
  • defect in the cannicular multi specific organic anion transporter (cMOAT) protein
129
Q

Associations of primary biliary cirrhosis?

A

Sjogrens (seen in up to 80%),
Rheumatoid arthritis,
systemic sclerosis,
thyroid disease

130
Q

Clinical features of primary biliary cirrhosis?

A 
early: pruritus, fatigue, abnormal LFTs (e.g. raised LFTs)
cholestatic jaundice
hyperpigmentation
RUQ pain in 10%
xanthelasmas, xanthomata
clubbing, hepatosplenomegaly
may progress to liver failure
131
Q

diagnosis of primary biliary cirrhosis?

A

anti-mitochondrial antibodies M2 subtype,
smooth muscle antibodies (in 30%),
raised serum IgM

132
Q

1st line mx of primary biliary cirrhosis?

A

Ursodeoxycholic acid

- slows disease progression and improves symptoms

133
Q

Mx of primary biliary cirrhosis?

A

1st line: ursodeoxycholic acid
pruritus: cholestyramine
fat soluble vitamin supplementation
liver transplant - PBC is a major indication

134
Q

Complications of primary biliary cirrhosis?

A
  • cirrhosis -> portal hypertension -> ascites, variceal haemorrhage
  • osteomalacia, osteoporosis
  • 20 fold increased risk of HCC
135
Q

features of acute liver failure?

A
  • jaundice
  • coagulopathy: raised prothrombin time
  • hypoalbuminaemia
  • hepatic encephalopathy
  • renal failure is common (‘hepatorenal syndrome’)
136
Q

Management of ascites?

A
  • reduce dietary sodium
  • fluid restriction may be recommended (if Na<125)
  • spironolactone +/- furosemide
  • therapeutic abdominal paracentesis
  • prophylactic antibiotics: ciproflox/ norfloxacin (if ascitic protein=15)
  • Transjugular intrahepatic portosystemic shunt may be considered
137
Q

Primary sclerosing cholangitis: associations?

A
  • UC (80% of pts w PSC have UC)
  • Crohn’s
  • HIV
138
Q

Features of primary sclerosing cholangitis?

A
  • cholestasis: jaundice, pruritus, raised bilirubin + ALP
  • RUQ pain
  • fatigue
139
Q

Ix of primary sclerosing cholangitis?

A
  • ERCP/ MRCP: showing multiple biliary strictures giving a ‘beaded’ appearance
  • p-ANCA +ve
140
Q

Complications of primary sclerosing cholangitis?

A
  • cholangiocarcinoma

- increased risk of colorectal ca

141
Q

First-line pharmacological treatment of irritable bowel syndrome?

A

pain: antispasmodic agents
constipation: laxatives but avoid lactulose
diarrhoea: loperamide is first-line

142
Q

Management of patients with constipation in irritable bowel syndrome who are not responding to conventional laxatives?

A

linaclotide

143
Q

Second-line pharmacological treatment of irritable bowel syndrome?

A

low-dose TCAs (e.g. amitriptyline 5-10 mg)

144
Q

Causes of Budd-Chiari syndrome (ie. hepatic vein thrombosis)?

A
  • polycythaemia rubra vera
  • thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies
    pregnancy
  • combined oral contraceptive pill: accounts for around 20% of cases
145
Q

Features of Budd-Chiari syndrome?

A

abdominal pain: sudden onset, severe
ascites → abdominal distension
tender hepatomegaly

146
Q

First line ix of Budd-Chiari?

A

US with doppler flow studies

147
Q

Ix for Haemochroamtosis in general population?

A

transferrin saturation + ferritin

148
Q

Ix for Haemochroamtosis in family members?

A

genetic testing for HFE mutation

149
Q

Diagnostic tests of Haemochromatosis?

A
  • molecular genetic testing for the C282Y and H63D mutations

- liver biopsy: Perl’s stain

150
Q

Mx of haemochromatosis?

A

1st line: venesection

2nd line: desferrioxamine

151
Q

Mx of ascending cholangitis?

A

IV abs

+ ERCP after 24-48h to relieve any obstruction

152
Q

where is gastrin produced?

A

G cells in antrum of the stomach

153
Q

what does gastrin do?

A
  • increases acid secretion by gastric parietal cells

- increases gastric motility, parietal cell maturation, pepsinogen and IF secretion

154
Q

what stimulates gastrin to be released?

A

distension of stomach, vagus nerve, luminal peptides/ amino acids

inhibited by: low pH, somatostatin

155
Q

What does CCK do?

A
  • increases secretion of enzyme-rich fluid from pancreas, contraction of gallbladder and relaxation of sphincter of Oddi
  • decreases gastric emptying
  • induces satiety
156
Q

what produces Cholecystokinin (CCK)?

A

I cells in the upper small intestine

157
Q

what produces secretin?

A

S cells in upper small intestine

158
Q

What does secretin do?

A
  • increases secretion of bicarbonate-rich fluid from pancreas and hepatic duct cells
  • decreases gastric acid secretion
159
Q

What does VIP do?

A

Stimulates secretion by pancreas and intestines

- inhibits acid secretion

160
Q

where is VIP produced?

A

small intestine, pancreas

161
Q

What does somatostatin do?

A
  • decreases acid and pepsin secretion
  • decreases gastrin + pancreatic enzyme + insulin/ glucagon secretion
  • stimulates gastric mucous production
162
Q

Where is somatostatin produced?

A

D cells in the pancreas & stomach

163
Q

What hormone is useful to test for in chronic pancreatits/ pancreatic insufficiency?

164
Q

gold standard test for diagnosis of GORD?

A

24h oesophageal pH monitoring

165
Q

GORD: indications for upper GI endoscopy?

A
  • age > 55 years
  • symptoms > 4 weeks or persistent symptoms despite treatment
  • dysphagia
  • relapsing symptoms
  • weight loss
166
Q

what laxative to avoid in management of irritable bowel syndrome?

167
Q

most common complication of ERCP?

A

acute pancreatitis

168
Q

common complication of TIPSS procedure?

A

exacerbation of hepatic encephalopathy

169
Q

Red flag features that suggest smth apart from IBS?

A
  • rectal bleeding
  • unexplained/unintentional weight loss
  • family history of bowel or ovarian cancer
  • onset after 60 years of age
170
Q

Which laxative is shown to have carcinogenic potential?

A

co-danthramer

  • should only be prescribed to palliative patients due to its carcinogenic potential.
171
Q

score for likelihood of acute appendicitis?

A

Alvarado score

172
Q

features of Plummer-Vinson syndrome?

A

triad of

  • dysphagia (secondary to oesophageal webs)
  • glossitis
  • iron deficiency anaemia

tx includes iron supplementation and dilation of the webs

173
Q

Drugs associated with cholestasis?

A
  • COCP
  • abx: flucloxacillin, co-amoxiclav, erythromycin
  • anabolic steroids, testosterones
  • chlorpromazine, prochlorperazine
  • sulphonylureas e.g. gliclazide
  • fibrates
  • rare: nifedipine
174
Q

what is monitored in haemochromatosis to assess for adequacy of treatment?

A

transferrin saturation should be <50%

serum ferritin <50 ug/l

175
Q

features of post-cholecystectomy syndrome?

A

dyspepsia, vomiting, pain, flatulence, diarrhoea

- in up to 40% post surgery

176
Q

Management of post-cholecystectomy syndrome?

A

low fat diet,
bile acid sequestrants e.g. Cholestyramine
dyspepsia - PPIs

177
Q

Management of hepatic encephalopathy?

A

tx underlying cause

  • Lactulose 1st line: increases excretion of ammonia
  • +/- Rifaximin: modulate gut flora to decrease ammonia production
178
Q

cotton wool spots on fundoscopy post head trauma and in conditions such as acute pancreatitis, fat embolisation, amniotic fluid embolisation and vasculitic diseases?

A

Purtscher retinopathy

179
Q

multikinase inhibitor used in management of HCC?

180
Q

drugs that may lead to liver cirrhosis

A

methotrexate
methyldopa
amiodarone

181
Q

malabsorption of ____ is a common cause of diarrhoea following ileal resection?

A

bile salts

182
Q

management of malabsorption of bile salts post ileal resection?

A

cholestyramine

183
Q

Pathophysiology of Whipple’s disease?

A

rare multi-system disorder caused by Tropheryma whippelii infection.

  • most often affects joints/ digestive system
  • chronic, curable, systemic bacterial infection
184
Q

features of Whipple’s disease?

A

malabsorption: diarrhoea, weight loss,
- large joints arthralgia
- lymphadenopathy
- skin: hyperpigmentation and photosensitivity
- pleurisy, pericarditis
- ophthalmoplegia, dementai, seizures, ataxia, myoclonus

185
Q

Ix of Whipple’s disease?

A

jejunal biopsy: deposition of macrophages containing Periodic acid-Schiff (PAS) granules

186
Q

Mx of Whipple’s disease?

A

oral co-trimoxazole for a year, sometimes preceded by course of IV penicillin

187
Q

histological features of Crohn’s disease?

A
  • inflammation of all layers from mucosa to serosa
  • increased goblet cells
  • granulomas
188
Q

histological features of Ulcerative colitis?

A
  • no inflammation beyond submucosa- inflammatory cell infiltrate in lamina propria
  • crypt abscesses
  • depletion of goblet cells and mucin
  • granulomas are infrequent
189
Q

Intestinal causes of malabsorption

- e.g. villous atrophy

A
  • coeliac disease
  • Crohn’s disease
  • tropical sprue
  • Whipple’s disease
  • Giardiasis
  • brush border enzyme deficiencies (e.g. lactase insufficiency)
190
Q

pancreatic causes of malabsorption?

- due to deficiency of pancreatic enzyme production/ secretion

A

chronic pancreatitis, pancreatic ca, cystic fibrosis

191
Q

Biliary causes of malabsorption?

- deficiency of bile salts needed for emulsification of fats

A

biliary obstruction, primary biliary cirrhosis

192
Q

Other causes of malabsorption?

A

bacterial overgrowth e.g. systemic sclerosis, diverticula, blind loop

  • short bowel syndrome
  • lymphoma
193
Q

autoimmune hepatitis is assoc with raised Ig of which subtype?

194
Q

Primary biliary cirrhosis is assoc with raised Ig of which subtype?

195
Q

Alcoholic liver disease is assoc with raised Ig of which subtype?

196
Q

Features of VIPoma?

A
  • 90% arise from pancreas
  • large volume diarrhoea, dehydration
  • weight loss
  • hypoK, low levels of HCl stomach acid
197
Q

antibiotics associated w c diff?

A
  • clindamycin: RR = 31.8
  • cephalosporins: RR = 14.9
  • ciprofloxacin: RR = 5.0
198
Q

Management of HCC with Child-Pugh A cirrhosis without signs of portal hypertension, who have single lesion <2cm in size?

A

surgical resection

199
Q

Management of HCC with Child Pugh A and B cirrhosis, and 2-3 tumours <=3cm or 1 tumour <=5cm WITHOUT vascular invasion or extra hepatic spread?

A

Liver transplantation

- as a bridge to liver transplantation: Transarterial chemoembolization (TACE) or Radio Frequency ablation (RFA)

200
Q

Management of HCC with Child Pugh A or B cirrhosis, good performance status and evidence of vascular, lymphatic or extra hepatic spread?

A

Sorafenib (multiple tyrosine kinase inhibitor) has been shown to prolong survival

201
Q

Management of Child-Pugh C cirrhosis with end stage liver disease?

A

supportive/ palliative care

202
Q

Mx of alcoholic ketoacidosis?

A

IV saline + thiamine

203
Q

causes of jejunal villous atrophy? (apart from coeliac disease)

A
  • coeliac disease
  • tropical sprue
  • hypogammaglobulinaemia
  • GI lymphoma
  • Whipple’s disease
  • cows milk intolerance
204
Q

what vitamin supplementations are required in gastric bypass operations?

A
  • all bypass the duodenum

- need iron supplementation

205
Q

Ix that can confirm diagnosis of Gilbert’s syndrome?

A

rise in bilirubin following prolonged fasting or IV nictotinic acid (nicotinic acid test)

206
Q

what elements make up the Child-Pugh score

A

Bilirubin, Albumin, INR, Ascites, encephalopathy

207
Q

Ix of choice for bile acid malabsorption?

A

SeHCAT

- scan to assess retention/ loss of radiolabelled SeHCAT

208
Q

Mx of bile acid malabsorption?

A

Bile acid sequestrants e.g. cholestyramine

209
Q

Ix of suspected severe acute flare of Ulcerative colitis?

A

flexi sig

- for biopsies to confirm diagnosis and exclude CMV

210
Q

what Ix is recommended if metastases are not seen on initial staging CT scans? (for oesophageal cancer)

A

FDG-PET CT scans

- to detect occult metastases

211
Q

US scan showing ‘sand sign’ (debris within hepatic cyst moving freely) and neighbouring sister cysts?

A

characteristic of hydatid disease

- echinococcus granulosus

212
Q

3rd line management of c diff infection (1st episode)?

ie. after oral vancomycin course, oral fidaxomicin

A

oral vancomycin +/- IV metronidazole

213
Q

management of life threatening c Diff infection

ie. hypotension, partial/ complete ileus, toxic megacolon or CT evidence of severe disease

A

oral vancomycin AND IV metrondiazole

- may need to consider surgery

214
Q

management of recurrent episode of c diff infection?

A

within 12 wks of symptom resolution: oral fidaxomicin

after 12 wks: oral vancomycin OR fidaxomicin

215
Q

what type of autoimmune hepatitis ONLY affects children?

A

type 2

- Anti-liver/kidney microsomal type 1 antibodies (LKM1)

216
Q

management of pruritus in primary biliary cirrhosis?

A

cholestyramine

217
Q

primary biliary cirrhosis: what management slows disease progression and improves symptoms?

A

ursodeoxycholic acid

218
Q

investigation of occult GI bleeding if scopes normal?

A

repeat OGD or capsule endoscopy

> If capsule is negative then either a second capsule or enteroscopy is indicated.

219
Q

what management is useful in inducing remission in patients who have refractory (and fistulating) Crohn’s disease?

A

infliximab

220
Q

NICE recommended screening tool for inflammatory bowel disease?

A

faecal calprotectin

  • can also be used to monitor the response to treatment
  • In adults, sensitivity of 93% and specificity of 96% for IBD. In children, the specificity falls to around 75%.
221
Q

other causes of raised faecal cal protection apart from IBD?

A
  • bowel malignancy
  • coeliac disease
  • infectious colitis
  • use of NSAIDs
222
Q

what additional risk comes with dual immunomodulator and biological therapy e.g. azathioprine + infliximab compared to biological therapy (e.g. azathioprine) alone?

A

increased risk of non-melanoma skin cancer (standardised incidence ratio 3.46) and other cancers (standardised incidence ratio 2.82)

223
Q

Ulcerative colitis acute flare: management if no improvement seen after 72 hours of IV steroids or pt deteriorates despite steroids?

A

Urgent surgical review

+ IV ciclosporin (2mg/kg/day)

224
Q

features of alkaptonuria?

- build up of toxic homogentisic acid

A
  • homogentisic acid accumulates in cartilage and other tissues
    > pigmented sclera
    > urine turns black if exposed to air
    > intervertebral disc calcification –> back pain
    > renal stones
225
Q

alkaptonuria: management?

A
  • high dose vitamin C

- dietary restriction of phenylalanine and tyrosine

226
Q

Why are there valve abnormalities in carcinoid syndrome?

A

Serotonin induced fibrosis of the valvular endocardium, usually tricuspid and pulmonary
- usually results in right heart failure

227
Q

Management of acute alcoholic hepatitis?

A

Prednisolone (improves survival at 28 days)

- can sometimes use pentoxyphylline but this does not improve survival

228
Q

in severe alcoholic hepatitis, how long to continue prednisolone for?

A

7 days then reassess

229
Q

Maddrey Discriminant Score

A
  • used in Alcoholic hepatitis
    > Prednisolone has been shown in meta-analyses to confer a significant reduction in 28-day mortality in patients with an MDS >32 or hepatic encephalopathy, however, there was no demonstrable benefit at 90 days or at one year.
230
Q

primary indications for TIPSS (transjugular intrahepatic portosystemic shunt)?

A

uncontrolled variceal haemorrhage
refractory ascites
hepatic pleural effusion

231
Q

Absolute contraindications for TIPSS?

A
  • Severe and progressive liver failure (Child-Pugh score >12 is associated with a high risk of early death)
  • Uncontrolled hepatic encephalopathy
  • Right-sided heart failure
  • Uncontrolled sepsis
  • Unrelieved biliary obstruction
232
Q

endoscopic management of oesophageal varices?

A

band ligation

233
Q

endoscopic management of gastric varices?

A

injections of N-butyl-2-cyanoacrylate

234
Q

what is the best marker to determining the risk of developing liver cirrhosis in patients with Hepatitis B?

A

Hepatitis B DNA levels

ie. viral load

235
Q

Venesection regime for haemochromatosis?

A

initially 500ml every 1-2 weeks
then once ferritin levels ~50-100, transition to maintenance of once every 2-4 months.
aim ferritin <50

236
Q

Following successful treatment of Barretts oesophagus with low grade dysplasia, how often should endoscopic surveillance be offered?

A

every 6 months for the first year and then annually thereafter

237
Q

Following successful treatment of Barretts oesophagus with high-grade dysplasia or intra-mucosal carcinoma, how often should endoscopic surveillance be offered?

A

every 3 months for the first year, every 6 months for the second year and then annually thereafter.

238
Q

Fabry disease

A

X-linked recessive lipid storage disorder > deficiency in the fat enzyme alpha-galactosidase

accumulation of alpha-galactosyl-lactosyl-ceramide in various tissues, including kidney, liver, blood vessels and nerve ganglion cells

239
Q

Clinical features of Fabry disease

A
  • acroparaesthesia: tingling, burning pain in the hands and feet triggered by stress such as emotion, extreme temperatures, or exercise
  • Angiokeratoma corporis diffusum: lightly verrucous, deep-red to blue-black papules on the trunk (in the bathing trunk distribution)
  • Cardiac: mitral valve prolapse or regurgitation usually, but any valvular heart defect can occur
  • Strokes: including young strokes/TIAs
  • Chronic Kidney Disease: proteinuria usually, can present late in fulminant renal failure needing dialysis
240
Q

Haemobilia?

A

bleeding into the biliary tree following connection between splanchnic circulation and either the intrahepatic or extrahepatic biliary system. E.g. post biopsy

Characterized by RUQ pain, upper GI bleeding and jaundice.

241
Q

Should you continue azathioprine in pregnancy?

242
Q

Investigation of choice for suspected perianal fistulae?

A

MRI

  • can be used to determine if there (is an abscess and if the fistula is simple (low fistula) or complex (high fistula that passes through or above muscle layers)
243
Q

radiological appearance of autoimmune pancreatitis?

A

diffuse enlargement, giving the appearance of a ‘sausage-shaped’ pancreas

244
Q

Causes of high SAAG ascites > 11g/L?

A

High SAAG: (indicates portal hypertension)

Liver disorders: cirrhosis, acute liver failure, liver mets

Cardiac:
right heart failure
constrictive pericarditis

Other causes:
Budd-Chiari syndrome
portal vein thrombosis
veno-occlusive disease
myxoedema
245
Q

Causes of low SAAG ascites (<11)?

A

Low albumin:
Hypoalbuminaemia
nephrotic syndrome
severe malnutrition (e.g. Kwashiorkor)

Malignancy: peritoneal carcinomatosis

Infections: tuberculous peritonitis

Other: pancreatitis
bowel obstruction
biliary ascites
postoperative lymphatic leak
serositis in connective tissue diseases
246
Q

what is Zieve’s syndrome?

A

haemolytic anaemia, cholestatic jaundice, and hyperlipidaemia.

247
Q

2nd line tx of pyoderma gangrenosum if not responding to oral steroids?

A
  • antiTNF e.g. infliximab, adalimumab

- topical or oral tacrolimus

248
Q

best management for patient with recurrent hepatic hydrothorax not responsive to medical mx?

A

liver transplant

249
Q

Anti-Saccharomyces cerevisiae antibodies

- Assoc with which IBD?

A

Crohns Disease

250
Q

Treatment of H Pylori in Penicillin allergic patients or as a second line after triple therapy?

A

Quadruple therapy:
bismuth subsalicylate, tetracycline, metronidazole, and a proton pump inhibitor for 14 days

MRCP (21 decks)

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