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Med School Finals > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Anatomical boundaries and blood supply of the GI tract?

A

Foregut = oesophagus to proximal half of 2nd part of duodenum (coeliac artery)
Midgut = distal half of 2nd part of duodenum to proximal 2/3rd transverse colon (SMA)
Hindgut = distal 1/3rd transverse colon to rectum (IMA)

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2
Q

Segments of the small vs large bowel?

A

Small = duodenum → jejunum → ileum
Large = caecum → ascending → transverse → descending → sigmoid → rectum → anus

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3
Q

Fat-soluble vitamins?

A

A, D, E and K

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4
Q

Deficiency signs of vitamin A, B1, B3, B12, C, D and K?

A

A = night blindness
B1 (thiamine) = wernicke-korsakoff, dry beri beri, wet beri beri
B3 (niacin) = pellagra (dermatitis, diarrhoea, depression)
B12 = macrocytic anaemia, atrophic glossitis
C = scurvy (gum disease, poor wound healing)
D= rickets, osteomalacia
K = coagulopathy

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5
Q

Gastroenteritis bacteria with short incubation time?

A

Staphylococcus aureus
Bacillus cereus
Clostridium perfringens

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6
Q

Gastroenteritis pathogens which cause bloody diarrhoea?

A

E. Coli O157 (shiga toxin-producing)
Shigella
Salmonella
Campylobacter
Amoebiasis

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7
Q

Gastroenteritis pathogens linked to severe dehydration & rice water diarrhoea, flu-like prodrome, long incubation, most common in UK, most common viral, most common in kids?

A

Severe dehydration/rice water diarrhoea = cholera
Flu-like prodrome = campylobacter
Long incubation = amoebiasis, giardiasis
Most common in UK = campylobacter
Most common viral = norovirus
Most common in kids = rotavirus

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8
Q

Most common cause of Traveller’s diarrhoea and complication?

A

E. Coli O157
Haemolytic uraemic syndrome (AKI, microangiopathic haemaolysis and thrombocytopaenia)

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9
Q

WHO definition of diarrhoea and timescale?

A

≥ 4 loose/watery stools a day
< 14 days = acute
> 14 days = chronic

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10
Q

Common antidiarrhoeal drug and mechanism of action?

A

Loperamide
Opioid agonist

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11
Q

What conditions does IBD cover?

A

Crohn’s disease
Ulcerative colitis (UC)

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12
Q

Extra-intestinal features of IBD?

A

Arthritis
Osteoporosis
Episcleritis, uveitis
Erythema nodosum
Pyoderma gangrenosum

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13
Q

Blood test features of IBD?

A

Anaemia
Vitamin deficiencies
Raised inflammatory markers e.g. CRP/ESR
Raised faecal calprotectin

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14
Q

Bowel section most affected in Crohn’s vs UC?

A

Crohn’s = terminal ileum
UC = rectum (proctitis)

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15
Q

Clinical and histological features of Crohn’s disease?

A

Diarrhoea (non-bloody)
Weight loss
Abdominal pain
Perianal disease
Histology = transmural inflammation, skip lesions, non-caseating granulomas, cobblestoning, lots of goblet cells

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16
Q

Investigations for Crohn’s disease?

A

Colonoscopy + biopsy
Small bowel enema
MRI for small bowel disease

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17
Q

Findings of small bowel enema in Crohn’s disease?

A

“Kantor’s string” sign
“Rose thorn” ulcers

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18
Q

Drug options for inducing remission in Crohn’s disease?

A

1st line = steroid (adults), enteral nutrition (kids)
2nd line = azathioprine or mercaptopurine
3rd line = infliximab

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19
Q

Drugs options for maintaining Crohn’s remission and screening test?

A

Azathioprine or mercaptopurine
→ thiopurine methyltransferase (TPMT)

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20
Q

Drug for isolated perianal vs ileocaecal Crohn’s disease?

A

Perianal = metronidazole
Ileocaecal = budesonide

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21
Q

Investigation and management of perianal fistulae?

A

Investigation = MRI
Management = draining seton (high) or fistulotomy (low)

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22
Q

Management of perianal abscess?

A

Incision and drainage + antibiotics

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23
Q

Management of anal fissures?

A

Acute = soften stool (fluids/laxatives), topical treatment
Chronic = topical GTN (1st line) or sphincterotomy (2nd line)

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24
Q

Classic position of haemorrhoids?

A

3, 7 and 11 o’clock position

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25
Q

Management of haemorrhoids?

A

1st line = soften stool (fluids/laxatives), topical treatment
2nd line = surgery e.g. rubber band ligation, haemorrhoidectomy, stapling

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26
Q

Types of UC and where they affect?

A

Proctitis (rectum)
Left sided colitis (rectum + left colon)
Pancolitis (rectum + whole colon)

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27
Q

Clinical and histological features of UC?

A

Diarrhoea (bloody)
Tenesmus
Weight loss
Abdominal pain
Histology = mucosal/submucosal inflammation, continuous, crypt abscesses, loss of goblet cells

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28
Q

Investigations for UC?

A

Sigmoidoscopy/colonoscopy + biopsy
Barium enema

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29
Q

Findings of barium enema in UC?

A

Loss of haustra
Pseudopolyps
“Drainpipe” colon

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30
Q

Drug options for inducing remission in UC?

A

1st line = topical aminosalicylate
2nd line = oral aminosalicylate
3rd line = steroid

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31
Q

Drug options for maintaining remission in UC?

A

1st line = topical aminosalicylate
2nd line = topical + oral aminosalicylate
3rd line = azathioprine or mercaptopurine

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32
Q

Aminosalicylate examples, mechanism of action and side effects?

A

Examples = mesalazine, sulfasalazine
Mechanism of action = inhibits prostaglandin synthesis
Side effects = GI upset, headache, agranulocytosis, pancreatitis (mesalazine), lung fibrosis

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33
Q

Truelove and Witt’s criteria for UC flare?

A

Mild = < 4 stools/day + little blood
Moderate = 4-6 stools/day + varying blood
Severe = > 6 stools/day + systemic upset

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34
Q

Management of severe UC flare?

A

1st line = IV steroids
2nd line = IV ciclosporin
3rd line = surgery

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35
Q

Surgical techniques commonly used for rectosigmoid pathology?

A

Hartmann’s procedure + end colostomy

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36
Q

Cancer linked to IBD and which condition is it more common in?

A

Colorectal cancer
More common in UC

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37
Q

Classification of C. difficile infection by WCC?

A

Normal = mild
< 15 = moderate
> 15 = severe
N.B. life-threatening characterised by hypotension, shock, toxic megacolon etc.

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38
Q

Investigation and management of C. difficile infection?

A

Investigation = stool toxin
First episode = oral vancomycin (1st line) or oral fidoxamin (2nd line)
Recurrent episode = oral fidoxamin (< 12 weeks) or oral vancomycin OR fidoxamin (> 12 weeks)
Life threatening = oral vancomycin + IV metronidazole
N.B. faecal transplant an option if ≥ 2 episodes

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39
Q

Investigation and feature of toxic megacolon?

A

AXR
Transverse colon dilatation > 6cm

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40
Q

Clinical and histological features of coeliac disease?

A

Diarrhoea (non-bloody)
Steatorrhoea
Weight loss
Abdominal pain
Histology = villous atrophy, crypt hyperplasia, intra-epithelial lymphocytes

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41
Q

Conditions associated with coeliac disease?

A

Dermatitis herpetiformis
Hyposplenism
Type 1 diabetes mellitus
Autoimmune thyroid disease e.g. Grave’s

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42
Q

Investigations and management of coeliac disease?

A

Anti TTG IgA antibodies + total IgA
OGD + jejunal biopsy (gold-standard)
Management = gluten-free diet

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43
Q

Vaccination advice for coeliac disease?

A

Pneumococcal booster every 5 years

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44
Q

Cancer linked to coeliac disease?

A

Enteropathy-associated T-cell lymphoma

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45
Q

Features of irritable bowel syndrome?

A

Abdominal pain (relieved by defecation)
Bloating
Change in bowel habit

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46
Q

Management of irritable bowel syndrome?

A

Pain = antispasmodic
Diarrhoea = loperamide
Constipation = bulk-forming laxative

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47
Q

Diverticulosis vs diverticular disease vs diverticulitis?

A

Diverticulosis = diverticula present
Diverticular disease = symptomatic diverticulosis
Diverticulitis = infected diverticulum

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48
Q

Most common site affected by diverticulosis?

A

Sigmoid colon

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49
Q

Feature and management of diverticular disease?

A

Colicky left sided abdominal pain
Management = high-fibre diet

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50
Q

Features and management of diverticulitis?

A

Generally unwell e.g. fever, N&V
Diarrhoea (bloody or non-bloody)
Left iliac fossa pain
Management = oral antibiotic (mild) or IV antibiotics + IV fluids (severe)

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51
Q

Hinchey classification of diverticulitis?

A

I = para-colic abscess
II = pelvic abscess
III = purulent peritonitis
IV = faecal peritonitis

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52
Q

Investigations and management of SBBOS?

A

Hydrogen breath test
Trial of antibiotics
Management = rifaxamin

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53
Q

Jejunal biopsy showing macrophages with Periodic acid-Schiff (PAS) granules and management?

A

Whipple’s disease
Management = co-trimoxazole

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54
Q

Cause of achalasia?

A

Damage to myenteric plexus reducing LOS relaxation

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55
Q

Investigation, feature and management of achalasia?

A

Investigations = barium swallow (bird beak appearance)
Management = balloon dilatation, Heller’s cardiomyotomy

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56
Q

Investigations for GORD?

A

Standard dose PPI trial
Upper GI endoscopy if concerned
Oesophageal pH monitoring

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57
Q

Short-term management of GORD?

A

1st line = high-dose PPI for 1-2 months
2nd line = H. pylori test if still symptomatic

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58
Q

Long-term management of GORD?

A

Ideally an antacid e.g. Gavison
Low-dose PPI if symptoms persist

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59
Q

Histology of Barrett’s oesophagus?

A

Metaplasia of squamous to columnar epithelium

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60
Q

Management of metaplastic vs dysplastic Barrett’s oesophagus?

A

Metaplastic = high-dose PPI + endoscopic surveillance every 3-5 years
Dysplasia = radiofrequency ablation or endoscopic mucosal resection

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61
Q

PPI examples, mechanism of action and side effects?

A

Examples = omeprazole, lanzoprazole
Mechanism of action = blocks H+/K+ ATPase of gastric parietal cells
Side effects = hyponatraemia, hypomagnesia, osteoporosis, increased risk of C. diff

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62
Q

Preferred PPI for patients taking clopidogrel?

A

Lansoprazole

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63
Q

ALARMS features of upper GI malignancy?

A

Anaemia/age > 55
Loss of weight
Anorexia
Recent onset
Masses/malaena/haematemesis
Swallowing issues

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64
Q

Types of oesophageal cancer, where they affect and key risk factor?

A

Adenocarcinoma (lower 1/3rd) = Barrett’s oesophagus
Squamous cell carcinoma (upper 2/3rds) = smoking

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65
Q

Investigation for H. Pylori and rules?

A

Urea breath test
→ not within 4 weeks of antibiotic treatment
→ not within 2 weeks of PPI

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66
Q

H. pylori eradication?

A

No penicillin allergy = PPI + amoxicillin + clarithromycin or metronidazole
Penicillin allergy = PPI + clairithromycin + metronidazole

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67
Q

Complications of H. pylori infection?

A

Duodenal ulcers (95% responsible)
Gastric ulcers (75% responsible)
MALT lymphoma
Atrophic gastritis

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68
Q

Main feature of duodenal vs gastric ulcers?

A

Epigastric pain
Duodenal = worse at night, relieved by eating
Gastric = worse when eating

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69
Q

Drugs associated with peptic ulcer disease?

A

NSAIDs
SSRIs
Corticosteroids
Bisphosphonates

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70
Q

Investigation and management of peptic ulcer disease?

A

Investigation = endoscopy + rapid urease test
Management = PPI (H. pylori -ve) or H. pylori eradication (H. pylori +ve)

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71
Q

Main bleeding source in ruptured peptic ulcer?

A

Gastroduodenal artery

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72
Q

Investigation, feature and management of a ruptured peptic ulcer?

A

Investigation = erect CXR (pneumoperitoneum)
Management = endoscopic intervention + IV PPI

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73
Q

Most common causes of acute upper GI bleed and scoring systems?

A

Peptic ulcer disease and oesophageal varices
Glasgow-Blatchford score (pre-endoscopy)
Rockall score (post-endoscopy)

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74
Q

Blood test feature indicating an upper rather than lower GI bleed and why?

A

High urea
Blood proteins are dissolved in stomach

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75
Q

Outline the pathology of pernicious anaemia?

A
  • Anti-intrinsic factor antibodies bind to intrinsic factor blocking vitamin B12
  • Gastric parietal cell antibodies cause atrophic gastritis
  • Decreased intrinsic factor production → low vitamin B12 absorption
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76
Q

Investigation and management of pernicious anaemia?

A

Investigation = anti-intrinsic factor antibodies
Management = IM vitamin B12

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77
Q

Features of Zollinger-Ellison syndrome and association?

A

Duodenal/pancreatic/gastric tumour
Excessive gastrin secretion
Association = MEN 1

78
Q

Most common type of gastric cancer, sub-types and associations?

A

Adenocarcinoma
Intestinal = H. pylori, smoking, chronic gastritis
Diffuse = non-H. pylori

79
Q

Histological feature of diffuse gastric carcinoma?

A

Signet ring cells

80
Q

LFT cholestatic pattern?

A

Raised ALP
Raised GGT
Raised bilirubin

81
Q

LFT hepatitic pattern?

A

Very raised ALT/AST
Raised ALP
Raised bilirubin

82
Q

LFT deranged synthetic function pattern?

A

Raised bilirubin
Raised PT/INR
Low platelets
Low albumin
Low glucose

83
Q

Stool/urine in pre-hepatic, hepatic and post-hepatic jaundice?

A

Pre = both normal
Hepatic = dark urine, normal stool
Post = dark urine, pale stool

84
Q

Explain the stool/urine pattern of post-hepatic jaundice?

A

Blockage forces bile back into liver where it moves into systemic circulation
Stool = less bilirubin absorbed in GI tract to be excreted in faeces
Urine = more bilirubin in blood and filtered by kidneys

85
Q

Features of acute appendicitis?

A

Genrally unwell e.g. fever, N&V
Abdominal pain (central → RIF)
Anorexia, weight loss
Rovsing’s sign (LLQ pressure = RLQ pain)
McBurney’s sign

86
Q

Blood test feature of appendicitis?

A

Neutrophil-dominant leukocytosis

87
Q

Investigation and management of appendicitis?

A

Investigation = clinical diagnosis, abdo USS or CT if unsure
Management = IV prophylactic antibiotics + laparoscopic appendicetomy

88
Q

Causes of acute pancreatitis?

A

GET SMASHED:
Gallstones
Ethanol
Trauma
Steroids
Mumps (and other viruses)
Autoimmune
Scorpion venom
Hypercalcaemia
ERCP
Drugs (e.g. mesalazine)

89
Q

Most common causes of acute pancreatitis in the UK?

A

Gallstones
Alcohol

90
Q

Features of acute pancreatitis?

A

General unwell e.g. fever, N&V
Abdominal pain (epigastric → back)
Pain relieved sitting forward
Periumbilical (Cullen’s) and flank (Grey-Turner’s) discolouration are rare

91
Q

Blood test features of acute pancreatitis?

A

Amylase > 3x normal
Hypocalcaemia
High LDH
Deranged LFTs

92
Q

Scoring system used for acute pancreatitis?

A

Modified Glasgow criteria

93
Q

Investigations and management of acute pancreatitis?

A

Investigations = abdo US, CT, MRCP
Management = IV fluids + IV analgesia + surgery dependent on cause e.g. ERCP

94
Q

Persistent elevated amylase following acute pancreatitis?

A

Pseudocyst

95
Q

Most common cause of chronic pancreatitis?

A

Alcohol excess

96
Q

Features of chronic pancreatitis and tests used to assess them?

A

Exocrine dysfunction = faecal elastase
Endocrine dysfunction = fasting glucose/OGTT

97
Q

Investigations and management of chronic pancreatitis?

A

Investigations = AXR, CT
Management = treat complications, pancreatic supplements e.g. creon

98
Q

Courvoisier’s law?

A

Patients with painless jaundice + RUQ mass are unlikely to have simple gallstones
Treat as a pancreatic or biliary neoplasm until proven otherwise

99
Q

Features of pancreatic cancer?

A

Painless jaundice
Weight loss
Palpable mass
Atypical back pain
Trousseau syndrome (migratory thrombophlebitis)
Steatorrhoea/diabetes

100
Q

Investigation and feature of pancreatic cancer?

A

Abdo US, CT abdo/pelvis, endoscopic US
“Double-duct” sign (dilated CBD + pancreatic duct)

101
Q

Management options for pancreatic cancer?

A

Surgery e.g. Whipple’s resection
Chemotherapy
ERCP with stenting

102
Q

Tumour marker for pancreatic cancer?

A

CA 19-9

103
Q

Outline the production of bile salts?

A
  • Liver makes the primary bile acids (cholic acid and chenodeoxycholic acid)
  • Excreted into bowel where gut flora coverts them into secondary bile acids (deoxycholic acid and lithocholic acid)
  • Primary/secondary acids return to liver and are conjugated with taurine or glycine to form the 8 principal bile salts
104
Q

Risk factors for gallstones?

A

Fat/female/fertile/forty
Crohn’s disease
Diabetes mellitus
Drugs e.g. COCP

105
Q

Blood test features of biliary colic vs acute cholecystitis vs ascending cholangitis?

A

Biliary colic = normal
Acute cholecystitis = raised inflammatory markers, normal/slightly raised LFTs
Ascending cholangitis = raised inflammatory markers and deranged LFTs

106
Q

Features, investigation and management of biliary colic?

A

Colicky abdominal pain (RUQ → shoulder)
Investigation = abdo US, MRCP
Management = avoid triggers, elective lap chol

107
Q

Most common pathogens associated with biliary infection?

A

E.Coli
Klebsiella

108
Q

Areas affected by cholecystitis vs cholangitis?

A

Cholecystitis = inflammation of the gallbladder and cystic duct
Cholangitis = inflammation of the biliary tree

109
Q

Features, investigation and management of acute cholecystitis?

A

Generally unwell e.g. fever, N&V
Abdominal pain (RUQ → shoulder)
NO JAUNDICE
Investigation = abdo US, MRCP/ERCP
Management = IV antibiotics + lap chol

110
Q

Small bowel obstruction following acute cholecystitis. AXR shows air in the biliary tree?

A

Gallstone ileus

111
Q

Features of ascending cholangitis?

A

Charcot’s triad:
→ RUQ pain, fever, jaundice
Reynold’s pentad:
→ above, hypotension, confusion

112
Q

Investigations and management of ascending cholangitis?

A

Investigation = abdo US, MRCP
Management = IV antibiotics + ERCP

113
Q

Complications of ERCP?

A

Bleeding
Duodenal perforation
Pancreatitis
Cholangitis

114
Q

Features of primary sclerosing cholangitis (PSC)?

A

Abdominal pain (RUQ)
Jaundice, pruritis
PMH of ulcerative colitis

115
Q

Blood test feature of primary sclerosing cholangitis (PSC)?

A

p-ANCA +ve

116
Q

Investigation, finding and management of primary sclerosing cholangitis (PSC)?

A

Investigation = MRCP (multiple biliary strictures)
Management = ERCP, cholestyramine

117
Q

Cancer linked to PSC vs PBC?

A

PSC = cholangiocarcinoma
PBC = hepatocellular carcinoma

118
Q

Tumour marker for cholangiocarcinoma?

A

CA 19-9

119
Q

Stages of liver disease?

A

Steatosis (NAFLD or alcoholic)
Steatohepatitis
Cirrhosis

120
Q

Investigations for liver cirrhosis?

A

ELF blood test
FibroScan (liver USS)
Biopsy

121
Q

Monitoring of cirrhosis?

A

Liver USS every 6 months +/- AFP

122
Q

LFT features indicative of alcoholic hepatitis?

A

AST:ALT > 2
Raised GGT

123
Q

Alcohol intake guidelines?

A

No more than 14 units/week
If around 14 units, spread over 3 days

124
Q

Management of acute alcoholic hepatitis?

A

High dose steroid

125
Q

Management of alcoholic ketoacidosis?

A

IV saline + IV thiamine

126
Q

Features and complications of liver failure?

A

Low albumin → ascites → SBP
High ammonia → hepatic encephalopathy → cerebral oedema
High oestrogen → palmar erythema, gynaecomastia, spider naevi etc.
Low clotting factors → coagulopathy → bleed
Shunts → varices → bleed
Release of vasodilators → hepatorenal syndrome

127
Q

Outline the pathophysiology of hepatic encephalopathy?

A
  • Liver failure leads to ammonia build-up
  • Ammonia crosses BBB and converted into glutamine
  • Glutamine disturbs osmotic pressure and causes astrocyte swelling
128
Q

Management and prophylaxis of hepatic encephalopathy?

A

Management = lactulose + IV mannitol
Prophylaxis = rifaxamin

129
Q

Outline the pathophysiology of hepatorenal syndrome?

A
  • Portal hypertension causes release of vasodilators
  • Splanchnic vasodilation and decreased SVR
  • Kidneys activate RAAS in response to hypovolaemia leading to vasoconstriction and decreased eGFR
130
Q

Management of hepatorenal syndrome?

A

Terlipressin + IV albumin

131
Q

Serum-ascites albumin gradient (SAAG) categories and causes?

A

> 11g/L = portal hypertension
< 11g/L = malignancy, infection e.g. TB

132
Q

Management options for ascites?

A

Low sodium intake
Fluid restriction
Aldosterone antagonist
Therapeutic paracentesis

133
Q

NICE spontaneous bacterial peritonitis (SBP) prophylaxis guidelines?

A

Offer oral ciprofloxacin or norfloxacin to those with cirrhosis and ascites with a SAAG < 15g/L

134
Q

Blood test feature, most common pathogen and management of SBP?

A

Neutrophil count > 250 + ≥ 90% polymorphs
E.Coli
Management = IV tazocin

135
Q

Management of acute variceal haemorrhage?

A

ABCDE
Terlipressin + IV antibiotics
Band ligation (1st line), sclerotherapy (2nd line)
Sengstaken-Blakemore tube if uncontrolled
TIPS procedure if all above fails

136
Q

Drug prophylaxis of variceal bleeding?

A

Propanolol

137
Q

What is TIPS procedure, indications and key side effect?

A

Transjugular intrahepatic portosystemic shunt (channel between hepatic vein and portal vein)
Severe portal hypertension, refractory ascites, hepatorenal syndrome, secondary prophylaxis of variceal bleed
Can worsen or cause hepatic encephalopathy

138
Q

Features of hepatitis?

A

Abdominal pain (RUQ)
Hepatomegaly
Jaundice
Fatigue

139
Q

Hepatitis most associated with chronic infection, IVDUs, co-infection, mum to baby, tropical travel and acute/flu-like disease?

A

Chronic = hepatitis C
IVDUs = hepatitis C
Co-infection = hepatitis B & D
Mum to baby = hepatitis B
Tropical travel = hepatitis E
Acute/flu-like disease = hepatitis A

140
Q

First serum marker to appear after hepatitis B infection?

A

HBsAg (surface antigen)

141
Q

Hepatitis B significance of HBsAg, anti-HBs, anti-HBc (IgM/IgG), HbeAg and anti-HBeAg?

A

HBsAg = current infection
Anti-HBs = immunity
Anti-HBc = IgM (acute infection) and IgG (chronic infection)
HbeAg = high infectivity
Anti-HBeAg = low infectivity
N.B. those immune via vaccine only WILL NOT be positive for anti-HBc

142
Q

Anti-HBs level criteria following immunisation programme?

A

> 100 = good response, booster every 5 years
10-100 = suboptimal response, give 1 more dose then re-check levels
< 10 = no response, test for current/past infection, give 3 more doses then re-check levels

143
Q

Drug used to treat hepatitis B and indications?

A

Peginterferon alfa-2a
→ liver disease, pregnant, kids

144
Q

Most common group affected by autoimmune hepatitis vs primary biliary cirrhosis?

A

AH = young women
PBC = middle-aged women

145
Q

Blood test features of autoimmune hepatitis?

A

ANA, SMA
Raised IgG

146
Q

Blood test features of primary biliary cholangitis (PBC)?

A

AMA, ANA
Raised IgM

147
Q

Main drugs for primary biliary cholangitis (PBC)?

A

Ursodeoxycholic acid
Cholestyramine

148
Q

What is Budd-Chiari syndrome and causes?

A

Hepatic vein thrombosis
→ blood disease e.g. polycythaemia, thrombophilia
→ pregnancy
→ COCP

149
Q

Investigation for Budd-Chiari syndrome?

A

Liver US with doppler flow studies

150
Q

Outline the pathophysiology of bilirubin metabolism?

A
  • Heme is broken down into biliverdin and iron
  • Biliverdin is oxidised to UCB and released into blood
  • UCB taken into hepatocytes and conjugated
  • CB moved into bile then digestive tract
  • Most removed in faeces, some in urine
151
Q

Bilirubin level at which jaundice becomes noticeable?

A

35umol/l

152
Q

Gilbert’s syndrome deficiency and blood test feature?

A

UDP glucuronosyltransferase
Unconjugated hyperbilirubinaemia

153
Q

Features of Wilson’s disease?

A

Liver disease
Neurological deficit
Psychiatric changes
Kayser-Fleischer rings

154
Q

Most common place of copper deposition in the brain?

A

Basal ganglia (especially putamen and globus pallidus)

155
Q

Blood test features of Wilson’s disease?

A

Low/normal serum caeruloplasmin
Low/normal serum copper
Raised free and urinary copper

156
Q

Management of Wilson’s disease?

A

1st line = D-penicillamine
2nd line = trientine

157
Q

Features of haemochromatosis?

A

Fatigue
Bronze skin
Liver disease
Arthritis/arthralgia (hands)
Erectile dysfunction
Dilated cardiomyopathy

158
Q

Iron study features of haemochromatosis?

A

Raised transferrin saturation
Raised ferritin
Raised iron
Low TIBC

159
Q

Management of haemochromatosis?

A

1st line = venesection
2nd line = desferrioxamine

160
Q

Monitoring of haemachromatosis and target values?

A

Transferrin saturation < 50%
Serum ferritin < 50ug/l

161
Q

Most common liver tumours?

A

Metastatic (95%)
Hepatocellular carcinoma
Chlolangiocarcinoma

162
Q

Most common cause of hepatocellular carcinoma?

A

Chronic hepatitis B or C

163
Q

Location of inguinal vs femoral hernias, which is more common and which has a higher risk of strangulation?

A

Inguinal = superomedial to pubic tubercle
Femoral = inferolateral to pubic tubercle
Inguinal are more common
Femoral have a higher risk of strangulation

164
Q

Cough test for inguinal hernia?

A

Press over deep inguinal ring and ask to cough
Direct hernias will reappear
Indirect hernias will not

165
Q

Surgical management of femoral vs inguinal hernia?

A

Femoral = laparoscopic or laparotomy
Inguinal = open (unilateral) or laparoscopic (bilateral/recurrent)

166
Q

Incarcerated vs strangulated hernia?

A

Incarcerated = can’t be reduced
Strangulated = ischaemic hernia

167
Q

Types of hiatus hernia, anatomy and which is more common?

A

Sliding = GOJ moves above diaphragm
Rolling = GOJ stays below diaphragm but another section of stomach herniates through oesophageal hiatus
Sliding are 95% of all hiatus hernias

168
Q

Investigations and management of hiatus hernia?

A

Investigations = barium swallow, endoscopy
Management = weight loss, PPI, surgery

169
Q

Big 3 of bowel obstructions?

A

Adhesions (small bowel)
Hernias (small bowel)
Tumours (large bowel)

170
Q

Features of bowel obstruction?

A

Abdominal pain (central)
Bilious vomiting
No stools or flatulence
Abdominal distension
Tinkling bowel sounds

171
Q

Investigations and findings of bowel obstruction?

A

AXR, CT (dilated bowel, pneumoperitoneum)

172
Q

Management of bowel obstruction?

A

1st line = nasogastric tube + IV fluids (“drip and suck”)
2nd line = surgery

173
Q

Investigations, finding and management of sigmoid volvulus?

A

Investigation = AXR, CT (coffee bean sign)
1st line = therapeutic sigmoidoscopy
2nd line = laparotomy (1st line if necrosis/perforation/peritonitis)

174
Q

Diffuse abdominal pain following an URTI?

A

Mesenteric adenitis

175
Q

Hamartomatous polyps and pigmented lesions on lips, face, palms and soles?

A

Peutz-Jeghers syndrome

176
Q

Most common cause of inherited colon cancer?

A

HNPCC (Lynch syndrome)

177
Q

Affected genes in HNPCC vs FAP?

A

HNPCC = mismatch repair e.g. MSH2
FAP = APC

178
Q

Most common site of colorectal cancer?

A

Rectum

179
Q

Outline colorectal cancer screening?

A
  • FIT test every 2 years between 60-74 (England) and 50-74 (Scotland)
  • If result abnormal, offered a colonoscopy
180
Q

Duke’s staging for colorectal cancer?

A

A = limited to bowel wall
B = extends beyond bowel wall
C = local lymph node involvement
D = distant metasases

181
Q

Tumour marker used to monitor colorectal cancer?

A

Carcinoembryonic antigen (CEA)

182
Q

What is removed in a hemicolectomy, subtotal colectomy, proctocolectomy, panproctocolectomy, anterior resection, AP resection and Hartmann’s procedure?

A

Hemicolectomy = right or left side of colon
Subtotal colectomy = whole colon but rectum and anus remain
Proctocolectomy = whole colon + rectum
Panproctocolectomy = whole colon + rectum + anus
Anterior resection = sigmoid + part or all of rectum
Abdomino-perineal resection = sigmoid + rectum + anus
Hartmann’s = sigmoid

183
Q

Ileostomy vs colostomy?

A

Ileostomy = spouted, discharges small bowel liquid
Colostomy = level with skin, discharges formed stools

184
Q

Bowel surgery technique used alongside proctocolectomy?

A

Ileo-anal pouch (J pouch)

185
Q

Acute management of abdominal wound dehiscence?

A

Cover with saline-soaked gauze
IV broad-spectrum antibiotics
Analgesia
Return to theatre

186
Q

List some classes and examples of anti-emetics?

A

H1 antagonists = cyclizine
D2 antagonists = domperidone, metoclopramide
5HT3 antagonists = ondansetron
Anti-muscarinics = hyoscine butylbromide

187
Q

Preferred route of total parenteral nutrition (TPN) and why?

A

Via a central vein e.g. PICC line
Peripheral veins are at risk of thrombophlebitis

188
Q

Bilious vomit and absent bowel sounds post-abdominal surgery?

A

Ileus (small bowel paralysis)

189
Q

Central colicky pain after eating and abdominal bruit on examination?

A

Chronic mesenteric ischaemia

190
Q

Mallory-Weiss vs Boerhaave syndrome?

A

Mallory-Weiss = GOJ lacerations
Boerhaave = oesophageal rupture

Med School Finals (18 decks)

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