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Medicine - Gastroenterology Flashcards

1
Q

Describe and differentiate the symptoms of mild, moderate and severe flares of ulcerative colitis

A

Mild: <4 stools per day, little blood
Moderate: 4-6 stools per day, varying blood
Severe: >6 stools per day, bloody diarrhoea, systemic upset

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2
Q

What is the name of the criteria used to stage IBD, and what are the 6 criteria?

A 
Truelove and Witts: 
Heart rate
Temperature
Bowel movements 
PR bleeding 
Haemoglobin
ESR
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3
Q

Recall 2 typical histological findings of the gut layer for Crohn’s and then UC

A

Crohn’s: Increased goblet cells, granulomas

UC: Decreased goblet cells, crypt abscesses

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4
Q

What is the most common affected portion of the bowel in Crohn’s vs UC?

A

Crohn’s: terminal ileum (so RIF mass)

UC: rectum

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5
Q

Describe the typical features of inflammation in Crohn’s vs UC

A

Crohn’s: Skip lesions, rose-thorn ulcers, cobblestoning, string sign of kantor (narrow ileum stricture)
UC: ‘lead-pipe’, pseudo-polyps, thumbprinting

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6
Q

Which type of IBD carries the highest risk of colorectal cancer?

A

UC

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7
Q

In which form of IBD are fissures more common and why?

A

Crohn’s - because it affects the full thickness of the bowel wall

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8
Q

Differentiate the appearance of stool in active Crohn’s vs UC

A

Crohn’s: non-bloody diarrhoea

UC: bloody diarrhoea which may contain mucous

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9
Q

Which type of IBD is associated with gallstones and why?

A

Crohn’s

Bile acids are not properly absorbed as terminal ileum is affected

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10
Q

In which form of IBD can surgery be curative?

A

UC

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11
Q

Recall the possible extra-intestinal manifestations of IBD

A 
A PIE SAC
Aphthous ulcers
Pyoderma gangrenosum (skin ulcers)
I (eye) = uveitis, iritis, episcleritis
Erythema nodosum
Sclerosing cholangitis (UC Only) 
Arthritis
Clubbing (Crohn's moreso)
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12
Q

Describe the process of inducing remission in Crohn’s

A

Steroids:
If mild: oral prednisolone
If severe: IV hydrocortisone
If no improvement after 5 days –> infliximab
Oral budesonide can be used in disease between the distal ileum and the ascending colon

Nutritional:
Replace diet with whole protein modular diet - excessively liquid, for 6-8 weeks - this helps to replace lost weight

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13
Q

Describe the process of maintaining remission in Crohn’s

A

First line: DMARDs (eg azothioprine)

Alternatives: infliximab/ aminosalicylates

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14
Q

Describe the management of UC

A

Severe disease:
Fulminant: IV steroids and anti-TNF (ciclosporin/infliximab)
Non-fulminant: oral aminosalicylates and corticosteroids with topical aminosalicylates

Non-severe disease:
1st line:
If distal colitis –> oral + topical aminosalicylates
If extensive colitis (past splenic flexure) –> topical and oral salicylates

2nd line:
Topical –> oral corticosteroids

3rd line:
Oral tacrolimus

4th line: biologics

5th line: surgery

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15
Q

What is the main side effect of aminosalicylates to remember?

A

Acute pancreatitis

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16
Q

In which form of IBD is surgical management most useful?

A

UC

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17
Q

What are the options for surgery in UC?

A

Emergency:
Hartmann’s protosigmoidectomy + end ileostomy –> later IPAA (ileal-pouch ana anastomosis)

Non-emergency:
Protocolectomy + IPAA or
Panprotocolectomy + end ileostomy

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18
Q

What are the criteria used to diagnose IBS?

A

It’s a diagnosis of excusion based on the ROME III criteria:

  • Improvement with defaecation
  • Change in stool frequency
  • Change in stool form/ appearance/ consistency
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19
Q

Recall the grading of haemarrhoids

A

1st: in rectum after defaecation
2nd: prolapse at defaecation, spontaneous reduction
3rd: prolapse at defaecation, manual reduction
4th: persistently prolapsed

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20
Q

What is the first line management of haemorrhoids?

A

Increased fruit/ fibre
Stool softener
Topical analgesics
Topical steroids (suppository)

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21
Q

Recall some non-operative ways of managing haemorrhoids?

A

Rubber-band ligation
Sclerotherapy
Electrotherapy
Infrared coagulation

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22
Q

Recall 3 surgical options for managing haemorrhoids

A

Haemarrhoidectomy
Haemorrhoidopexy
HALO (haemorrhoidal artery ligation operation)

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23
Q

What is the standard treatment for C diff enterocolitis?

A

Metronidazole –> vancomycin

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24
Q

Which bacteria demonstrates “tumble weed motility”?

A

Listeria monocytogenes

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25
Q

How can listeria gastroenteritis be treated?

A

Amoxicillin/ ampicillin

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26
Q

Which 3 antibiotics are most associated with causing C diff enterocolitis?

A

Cephalosporin
Clindamycin
Ciprofloxacin

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27
Q

Which gastroenteritis-causing pathogen is associated with undercooked seafood?

A

Vibrio parahaemolyticus

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28
Q

Which gastroenteritis-causing pathogen is associated with shellfish handlers?

A

Vibrio vulnificus (in immunocompetent usually causes cellulitis/ nec. fasciitis)

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29
Q

Recal the site of absorption of iron, folate and B12

A

Iron: Duodenum
Folate: Jejunum
B12: Ileum

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30
Q

Which skin condition is pathognomonic for coeliac disease?

A

Dermatitis herpetiformis

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31
Q

Describe the appearance of stool in coeliac disease

A

Waterey, grey, frothy

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32
Q

What system is used to grade coeliac disease?

A

Marsh system

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33
Q

Recall some typical histological findings in coeliac disease

A

Villous atrophy and crypt hyperplasia

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34
Q

Recall the name of the scoring system used to diagnose appendicitis and its components

A

Alvarado score:

Signs:
RLQ tenderness (+2)
Fever
Rebound tenderness

Symptoms:
Anorexia
Nausea/vomiting
Pain migration to RLQ

Lab:
Leucocytosis (WBC > 10,000) (+2)
Left shift (>75% neutrophils)

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35
Q

Recall some eponymous signs on examination that are indicative of appendicitis

A

Rovsing’s sign: Pain greater in RIF than LIF when LIF pressed
Cope’s sign: Pain on passive flexion and internal rotation of the hip

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36
Q

What does rebound tenderness indicate about appendicitis?

A

That it involves peritoneum

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37
Q

What sign can be used to demonstrate a retrocaecal appendix?

A

Pain on extending hip (Psoas sign)

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38
Q

How should an un-perforated appendix be managed?

A

Prophylactic antibiotics followed by laparoscopic appendectomy

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39
Q

How should a perforated appendix be managed?

A

Abdominal lavage

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40
Q

What is “Amirand’s triangle”?

A

Triad of conditions that predisposes to gallstone disease:
Low lecithin
Low bile salts
High cholesterol

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41
Q

How can the symptoms of cholecystitis and cholangitis be differentiated?

A 
Cholecystitis = no jaundice
Cholangitis = obstructive jaundice
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42
Q

How can the symptoms of cholecystitis and biliary colic be differentiated?

A

Biliary colic = RUQ pain

Cholecystitis = RUQ pain + fever

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43
Q

What is Charcot’s triad?

A

Triad of classical symptoms of ascending cholangitis
Jaundice
RUQ pain
fever

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44
Q

What is Reynauld’s pentad?

A 
Pentad of classical symptoms of severe ascending cholangitis 
Jaundice
RUQ pain
Fever
Hypotension
Confusion
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45
Q

Within what time frame should a laparoscopic cholecystectomy be performed for cholecystitis?

A

1 week (use antibiotics whilst waiting)

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46
Q

What is “Mirizzi syndrome”?

A

Impaction of common hepatic duct by a GB stone

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47
Q

What is the pathophysiology of “porcelain gallbladder”?

A

Chronic cholecystitis can –> calcification of GB walls

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48
Q

Recall some complications of acute cholecystitis

A 
Chronic diarrhoea (GB removal --> more bile reaches large intestine --> more water and salt draw into bowel)
Vitamin ADEK malabsorption (can --> bleeding due to less 2,7,9,10 production)
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49
Q

What is a SeHCAT study?

A

Selenium in Homocholic Acid Taurine - assesses bile acid retention to see if this is cause of diarrhoea

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50
Q

How can diarrhoea post-cholecystectomy be managed?

A

Cholestyramine (binds to bile acids and makes the biologically inactive)

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51
Q

How can ascending cholangitis be managed?

A

IV antibiotics followed by therapeutic ERCP within 48 hours

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52
Q

What are the key symptoms of cholangiocarcinoma?

A

Palpable gallbladder, obstructive jaundice

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53
Q

What is the gold-standard investigation for staging cholangiocarcinoma?

A

ERCP

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54
Q

Recall and compare the symptoms of PBC vs PSC

A

PBC:
Pruritis, obstructive jaundice, RUQ pain in 10%, hyperholesterolaemia

PSC:
Pruritis, obstructive jaundice, steatorrhoea, splenomegaly

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55
Q

Recall and compare the antibodies involved in PBC vs PSC

A

PBC: AMA
PSC: p-ANCA

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56
Q

Recall and compare the best way to investigate PBC vs PSC

A

PBC: cholestatic liver biochemistry and AMA blood test (biopsy is diagnostic but often not carried out)

PSC: MRCP is preferred to start (rosary sign), then p-ANCA + BIOPSY (‘onion skin’ appearance of obliterated cholangitis)

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57
Q

Recall and compare the management approaches for PBS vs PSC

A

PBS: ursodeoxycholic acid + cholestyramine + prednisolone for associated autoimmune disease

PSC: observation –> liver transplant

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58
Q

What % of patients with PSC get cholangiocarcinoma?

A

10%

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59
Q

Which autoimune gallbladder disease is associated with IBD?

A

PSC (ulcerative colitis)

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60
Q

How are the 3 types of autoimmune hepatitis characterised?

A

T1: high titres of ANA or ASMA - adults and children
T2: Anti-LKM-1,2,3 - affects children
T3: Anti-SLA (soluble liver antigen) - middle age

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61
Q

What are the key symptoms of autoimmune hepatitis?

A

Amenorrhoea

Chronic liver disease OR acute hepatitis

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62
Q

Which type of autoimmune gallbladder disease can affect extrahepatic ducts?

A

PSC

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63
Q

How is autoimmune hepatitis managed?

A

Steroids

Eventual liver transplantation

64
Q

What are the 4 signs of portal hypertension?

A 
SAVE
Splenomegaly
Ascites
Varices
Encephalopathy
65
Q

What is the triad of symptoms of Wernicke’s encephalopathy?

A

Ataxia
Confusion
Ophthalmoplegia

66
Q

Recall the mainstay of management for hepatic vs wernicke’s encephalopathy

A

Hepatic encephalopathy: lactulose + rifaximin

Wernicke’s encephalopathy: thiamine, magnesium, folic acid

67
Q

What are the principles of managing ascites?

A

Diet: restrict EtOH and fluids, daily weights

Diuretics: spironolactone (+/- furosemide)

Prophylaxis (for SBP): ciprofloxacin + propranolol

For refractory disease: TIPPS/ transplant

68
Q

What is an abdominal paracentesis procedure used to treat?

A

Tense ascites

69
Q

What is the most common pathogen in SBP?

A

E coli

70
Q

What investigation is used to confirm ascites?

A

USS abdomen

71
Q

How can SBP be confirmed?

A

Ascitic tap with PMN>250 and MC+S

72
Q

What drugs are used to treat vs as prophylaxis for SBP

A

Treatment: piptazobactam/cefotaxime

Prophylaxis: ciprofloxacin + propranolol

73
Q

When should SBP prophylaxis be started?

A

Ascites protein <15g/L

74
Q

What is the screening test for haemachromatosis?

A

Transferrin saturation - >55% in males and >50% in females may indicate further investigation

75
Q

What stain can be used on liver biopsy to identify haemachromatosis?

A

Perl’s stain

76
Q

What is the 1st and 2nd line management for haemachromotosis?

A

1st line: Venesection

2nd line: Desferrioxamine

77
Q

Describe the typical presentation of NAFLD

A

Acute weight loss followed by jaundice

78
Q

Recall the order in which you would order investigations for NAFLD

A

1st: LFTs (ALT will be > AST)
2nd: USS (will show increased echogenicity)
3rd: Enhanced Liver Fibrosis (ELF) panel OR a fibroscan
4th: Liver biopsy

79
Q

What are the components of an ELF panel?

A

Hyaluronic acid
Procollagen III
Tissue inhibitor of metalloproteinase 1

80
Q

What is the mainstay of management for NAFLD?

A

Lifestyle changes and wt loss

81
Q

What are the classical symptoms of acute pancreatitis?

A

Severe epigastric pain radiating through to back with nausea and vomiting

82
Q

What is Cullen’s sign and what diagnosis does it support?

A

Cullen’s sign = “superficial oedema with bruising in the subcutaneous fatty tissue around the peri-umbilical region”
Indicative of acute pancreatitis

83
Q

What is Grey Turner’s sign and what diagnosis does it support?

A

Grey-Turner’s sign = flank bruising

Indicative of acute pancreatitis

84
Q

How raised is serum amylase likely to be in acute pancreatitis?

A

> 3 times the upper limit of normal (in 75% of patients)

85
Q

What is the most specific marker for acute pancreatitis that will be raised in the blood?

A

Serum lipase

86
Q

What criteria are used to grade severity of acute pancreatitis?

A

Glasgow-Imrie

87
Q

What criteria are used to estimate prognosis in acute pancreatitis?

A 
PANCREAS
PaO2 <8 
Age >55
Neutrophils >15
Calcium <2
Renal urea >16
Enzymes (LDH>600, AST/ALT >200) 
Albumin <32
Sugar >10
88
Q

How long does an acute episode of pancreatitis have to last for to be considered ‘severe’?

A

> 48 hours

89
Q

Recall and differentiate between the management of acute pancreatitis vs necrotising pancreatitis?

A

For both:
Fluids, analgesia (stat boluses of IV morphine until comfortable), enteral feeding maintained, correct the cause
Only if necrotising: antibiotics

90
Q

Recall some possible early complications of acute pancreatitis

A

Haemorrhage
SIRS/ARDS
Hyperglycaemia (see pancreas critera)
Hypocalcaemia (see pancreas criteria)

91
Q

Recall some possible late complications of acute pancreatitis

A

25% –> peri-pancreatic fluid collection
Pseudocysts (appear at around 4w)
Pancreatic abscess (infected pseudocyst)
Pancreatic necrosis

92
Q

What % of chronic pancreatitis is due to alcohol excess?

A

80%

93
Q

What are the signs and symptoms of chronic pancreatitis?

A

Symptoms: epigastric pain, typically worse 15-30 mins post-prandially
Signs: Steatorrhoea, diabetes

94
Q

What investigations can be done in suspected chronic pancreatitis?

A

USS for gallstones
Contrast-enhanced CT
Faecal elastase (measures exocrine function)
Screen for diabetes and osteoporosis

95
Q

What is faecal elastase used to measure?

A

Exocrine function

96
Q

What histological type of cancer are 80% of pancreatic cancers?

A

Adenocarcinomas

97
Q

What is the classical presentation of pancreatic cancer?

A

Painless obstructive jaundice, painless palpable gallbladder (courvoisier’s law), FLAWS
Symptoms of lost exocrine/endocrine function

98
Q

What is trousseau’s sign of malignancy, and in which types of cancer is it sometimes observed?

A

Migratory superficial thrombophlebitis (moves from one leg to the other)
Strongly associated with adenocarcinoma of the pancreas and lung

99
Q

What is the pathognemonic sign on High Resolution CT for head of the pancreatic/bile duct cancer?

A

“Double duct” sign

Shows simultaneous dilation of CBD and pancreatic duct

100
Q

What is the definitive management of pancreatic cancer?

A

Whipple’s procedure

Pancreaticoduodenectomy

101
Q

What are the common complications of Whipple’s procedure?

A 
Dumping syndrome (gastric emptying of contents into duodenum too fast) 
PUD (if delayed gastric emptying instead of dumping syndrome) 
Bile/pancreatic link
102
Q

What is the non-surgical management of pancreatic cancer (eg if metastatic/ unsuitable for resection)?

A

ERCP with stenting

103
Q

What classification is used for diverticular disease?

A

Hinchey classification

104
Q

What is the investigation of choice for:

a) acute diverticulitis
b) chronic diverticular disease?

A

a) CT abdomen

b) barium enema (can’t do in acute phase as may cause perforation)

105
Q

How does the management of mild and severe diverticular disease differ?

A

Medical:
Mild: PO antibiotics
Severe: IV antibiotics + drip and suck (due to BO) + soluble, high-fibre diet

Surgical (only if severe)
Hartmann’s –> primary anastomosis

106
Q

Recall some indications for an urgent (2ww) OGD on suspicion of gastric/oesophageal malignancy?

A

Dyspepsia
Upper abdominal mass
Age >55 AND weight loss AND any of dyspepsia/GORD/upper abdo pain
nb if no weight loss –> NON-urgent OGD

107
Q

What is the gold standard test for diagnosis of GORD?

A

24 hour oesophageal pH monitoring

108
Q

What is the mechanism by which H pylori vs GORD produce dyspepsia?

A

H pylori –> ulcers –> dyspepsia

GORD –> dyspepsia

109
Q

What are the 3 ways in which you can test for H pylori?

A
  1. Carbon-13 urea breath test
  2. Stool antigen test
  3. Lab-based serology
110
Q

What is the mainstay of management for H pylori?

A

Clarithromycin, amoxicillin, PPI

111
Q

How does the medical management differ between endoscopically-proven vs endoscopically-negative GORD?

A

Proven: 2 months PPI trial followed by 1 month trial of double dose, 2nd line = add H2-RA

Negative: 1 month trial of PPI, 2nd line = H2-RA

112
Q

What is the surgical management option for refractory GORD?

A

Nissen fundoplication

113
Q

What are the most common complications of nissen fundoplication?

A

Gas-bloat syndrome (can’t belch/vomit)

Dysphagia (if wrap is too tight)

114
Q

What is Maddrey’s discriminant function?

A

For alcoholic hepatitis:

Predicts prognosis and who will benefit from steroids

115
Q

What score is used to stage liver cirrhosis?

A

Childs Pugh

116
Q

What is Budd Chiari syndrome and how is it classified?

A

Syndrome caused by blockage of the hepatic vein
Type 1 = thrombosis
Type 2 = tumour occlusion

117
Q

What are the possible signs and symptoms of Budd-chiari syndrome?

A

Abdominal pain, ascites, tender hepatomegaly

118
Q

What is the gold standard investigation for budd-chiari syndrome?

A

Abdominal USS with doppler

119
Q

What are the 3 best investigations when suspecting achalasia?

A

LOS manometry
Barium swallow
CXR

120
Q

Recall some signs and symptoms of the carcinoid syndrome, and recall which hormone is responsible for these symptoms

A

Flushing, diarrhoea, bronchospasm, hypotension, pulmonary stenosis, pellagra, endocrine over-function
Serotonin

121
Q

What 2 investigations can be used to investigate the carcinoid syndrome?

A

Urinary 5-HIAA

Plasma chromogranin A y

122
Q

What is the first line management for the carcinoid syndrome?

A

Somatostatin analogues eg octreotide

123
Q

Recall some antibiotics that may predispose to C diff infection

A 
Amoxicillin
Ampicillin
Cephalosporin (eg cefuroxime, ceftriaxone) 
Clindamycin
Co-amoxiclav 
Quinolones
124
Q

Recall the management of C diff colitis

A

1st episode: oral metronidazole
2nd episode/ severe 1st: oral vancomycin
Life-threatening/ ileus: oral vancomycin + IV metronidazole
ALL antibiotics over 10-14 day period

125
Q

Recall 3 risk factors for small bowel overgrowth

A

Neonates with congenital abnormalities
Diabetes mellitus
Scleroderma

126
Q

Recall the signs and symptoms of small bowel overgrowth

A

Very similar to IBS
Chronic diarrhoea
Bloating and flatulence
Abdominal pain

127
Q

Recall 3 ways of investigating for a small bowel overgrowth

A

Hydrogen breath test
Folate (will be high as bacteria produce it)
Diagnostic course of antibiotics

128
Q

What is the usual first line antibiotic for small bowel overgrowth?

A

Rifamixin

129
Q

What is Mackler’s triad?

A

The triad of symptoms seen in Boerhaave’s syndrome:
Chest pain
Vomiting
Subcutaneous emphysema

130
Q

In PUD, which artery is most likely to be a major source of bleeding?

A

Gastroduodenal artery

131
Q

When should opioid analgesia NOT be used following major abdominal surgery, and what alternative should be used?

A

In respiratory disease eg COPD

Alternative is epidural anaesthesia

132
Q

How should autoimmune hepatitis be treated?

A

30mg prednisolone PO, followed by introduction of azothioprine
MUST have confirmation of diagnosis from biopsy first unless there is a CI to biopsy

133
Q

How long does autoimmune hepatitis need to be treated for?

A

At least 2 years after blood results normalise before discontinuing therapy

134
Q

How should benign peptic strictures be managed?

A

PPI to treat underlying GORD

Balloon dilatation following benign biopsy

135
Q

What is the most common complication of balloon dilatation of a peptic stricture?

A

Oesophageal rupture (which may cause mediastinitis)

136
Q

How can oesophageal rupture be imaged best?

A

CT with oral contrast

137
Q

Recall some extra-articular manifestations of UC - saying which are related to disease activity and which are not

A 
Examples of extra-intestinal conditions related to activity of colitis:
Erythema nodosum
Aphthous ulcers
Episcleritis
Anterior uveitis
Acute arthropathy

Not related to activity of colitis:
Sacroiliiitis /Ankylosing spondylitis
Primary sclerosing cholangitis

(info from capsule case 202)

138
Q

What is the 1st line management for acute severe ulcerative colitis?

A

IV hydrocortisone

139
Q

How can blood glusose be used to assess liver function?

A

Assesses synthetic function

140
Q

How should variceal bleeds be managed when there is haemodynamic instability?

A
  1. Fluid resuscitation with blood transfusion
  2. IV vasopressin analogue eg terlipressin
  3. IV antibiotics
  4. Refer to endoscopy

nb. No IV PPI given prior to endoscopy

141
Q

What is the best surgical management for bleeding varices?

A

Band ligation or sclerotherapy

142
Q

What is the most appropriate long term management of varices?

A

Non-cardioselective beta blocker

143
Q

If variceal bleeding cannot be stopped with ligation, how can it be managed?

A

Insertion of Sengstaken Blakemore tube

144
Q

What are the 5 components of the Childs Pugh score?

A 
Serum bilirubin
Serum albumin
Prothrombin time
Presence of ascites 
Presence of encephalopathy
145
Q

Recall some differentials for the cause of ascites depending on whether the SAAG is low or high

A

High: portal HTN secondary to cirrhosis/ alcoholic hepatitis/ heart failure/ portal vein thrombosis

Low: peritoneal cause eg. malignancy, infections, pancreatitis and nephrotic syndrome

146
Q

If someone has a diagnostic ascigtic tap, what 7 tests should the fluid be sent for?

A 
Culture and sensitivity 
Cytology 
LDH 
Glucose 
Total protein content 
Albumin concentration 
Cell count and differential
147
Q

Which 2 investigations are best for imaging chronic pancreatitis?

A

CT

MRCP

148
Q

Recall 2 drugs and 2 drug classes that can cause drug-induced liver damage

A

Roziglitazone
Flucloxacillin
Macrolides
Statins

149
Q

When is mesenteric angiography used?

A

To find the source of a GI bleed when endoscopy cannot do so

150
Q

What is the programme for screening for hepatocellular carcinoma?

A

In patients with cirrhosis, ultrasound every 6 months with additional CT/MRI if focal lesions seen on USS

151
Q

What is BAM?

A

Bile acid malabsorbption
Bile acids enter colon –> profuse diarrhoea (look this up)
Should be halted by fasting

152
Q

Recall some examples of secretory diarrhoea

A

C diff
E coli 157
Cholera
Neuroendocrine tumours eg vasointestinal peptide-oma –> profound hypokalaemia without being fasted

153
Q

Recall 3 examples of inflammatory diarrhoea

A

UC
Crohn’s
Shigella

154
Q

Recall 4 examples of diarrhoea due to abnormal motility

A

Hyperthyroidism
Autonomic neuropathy (in DM)
Stimulant laxatives eg senna
IBS

155
Q

What is the histological finding of “owl’s eyes” pathognemonic for?

A

CMV

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