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YR6 Rotations > Medicine - Gastroenterology > Flashcards

Medicine - Gastroenterology Flashcards

1
Q

How do you differentiate between gastric and duodenal ulcers?

A

After a meal
Gastric = Greater pain
Duodenal = Decrease pain (pain when hungry)

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2
Q

What is associated with the majority of peptic ulcers?

A

H. pylori
95% of duodenal ulcers
75% of gastric ulcers

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3
Q

Name 4 drugs associated with peptic ulcers

A

NSAIDs
SSRIs
corticosteroids
bisphosphonates

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4
Q

Which syndrome is associated with peptic ulcers? What is the pathophysiology?

A

Zollinger Ellison Syndrome
rare cause characterised by excessive levels of gastrin, usually from a gastrin secreting tumour

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5
Q

Which type of peptic ulcer is more common?

A

Duodenal

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6
Q

What is the first line investigation for peptic ulcer disease?

A

H. pylori urea breath test or stool antigen test

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7
Q

Mx of peptic ulcer disease

A

-ve H. pylori: PPIs
+ve H. pylori: eradication therapy- PPI + Amoxicillin BD + Clarithromycin/ Metronidazole BD

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8
Q

What is the only test that can be used to check for H. pylori eradication?

A

Urea breath test

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9
Q

What is the investigation for C. dificile infection?

A

C. difficile toxin (CDT) in stool
C. difficile antigen positivity only shows exposure to the bacteria, rather than current infection

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10
Q

Mx of first episode C. difficile infection

A

1st: Vancomycin PO for 10 days
2nd-line: Fidaxomicin PO
3rd-line: Vancomycin PO +/- Metronidazole IV

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11
Q

Mx of recurrent C. difficile infection

A

<12w of Sx resolution: Fidaxomicin PO
>12w of Sx resolution: Vancomycin OR Fidaxomicin PO

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12
Q

Mx of life-threatening C. difficile infection

A

Vancomycin PO + Metronidazole IV
specialist advice - surgery may be considered

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13
Q

Describe the distribution of UC

A

Starts at Rectum (hence most common site for UC)
Continuous.
Never spreads beyond ileocaecal valve

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14
Q

Differentiate 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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15
Q

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

A 
Truelove + Witts: 
HR
Temperature
Bowel movements 
PR bleeding 
Haemoglobin
ESR
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16
Q

Give 4 gastro symptoms UC presents with

A

bloody diarrhoea
urgency
tenesmus
abdo pain, esp. left lower quadrant

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17
Q

Which 6 extra-intestinal manifestations of UC are related to disease activity?

A

Erythema nodosum
Pauci-articular Arthritis
Apthous ulcers
Episcleritis
Osteoporosis
VTE risk

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18
Q

Which 4 extra-intestinal manifestations of UC are NOT related to disease activity?

A

Axial arthritis: sacroiliitis/ ankylosing spondylitis
Pyoderma gangrenosum
Uveitis
Primary sclerosing cholangitis

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19
Q

Give 3 triggers for a UC flare

A

Stress
Drugs: NSAIDs, Abx
Cessation of smoking

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20
Q

What is seen on barium enema in UC? (3)

A

loss of haustrations
superficial ulceration, ‘pseudopolyps’
long standing disease: colon is narrow + short -‘drainpipe colon’

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21
Q

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

A

Crohn’s: Increased goblet cells, granulomas
UC: Decreased goblet cells, crypt abscesses

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22
Q

When should a diagnostic colonoscopy for UC be avoided? What investigation is preferred?

A

In severe colitis- risk of perforation
Do flexible sigmoidoscopy

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23
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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24
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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25
Q

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

A

UC

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26
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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27
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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28
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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29
Q

In which form of IBD can surgery be curative?

A

UC

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30
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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31
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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32
Q

Describe the process of maintaining remission in Crohn’s

A

First line: DMARDs (eg azothioprine)
Alternatives: infliximab/ aminosalicylates

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33
Q

Mx of acute severe UC

A

Admit
1st: IV Hydrocortisone or Methylprednisolone
2nd: anti-TNF (ciclosporin/ infliximab)

If severe intractable colitis: Colectomy

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34
Q

Induction of remission of moderate-severe UC

A

Prednisolone/ Budesonide PO
or
Infliximab/ Adalimumab

+/- Azathioprine

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35
Q

Induction of remission of mild-moderate UC

A

Proctitis: Mesalazine TOP (rectal)
Left sided: Mesalazine TOP + PO +/- Budesonide PO
Extensive: Mesalazine PO +/- Prednisolone/ Budesonide PO

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36
Q

Maintenance of remission in mild-moderate UC

A

Mesalazine TOP alone (daily or intermittent)
or
Mesalazine PO + TOP (daily or intermittent)

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37
Q

Maintenance of remission in mild left sided and extensive UC

A

Mesalazine PO

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38
Q

Maintenance of remission in moderate to severe UC / if >2 flare-ups in 1y

A

Thiopurine: Azathioprine or Mercaptopurine PO
or
Biologic: Infliximab IV or Adalimumab SC

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39
Q

What is the main side effect of aminosalicylates to remember?

A

Acute pancreatitis

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40
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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41
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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42
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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43
Q

What is the first line management of haemorrhoids?

A

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

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44
Q

Recall some non-operative ways of managing haemorrhoids?

A

Rubber-band ligation
Sclerotherapy
Electrotherapy
Infrared coagulation

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45
Q

Recall 3 surgical options for managing haemorrhoids

A

Haemarrhoidectomy
Haemorrhoidopexy
HALO (haemorrhoidal artery ligation operation)

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46
Q

What is the standard treatment for C diff enterocolitis?

A

PO vancomycin
2nd line fidaxomicin
If severe/unresponsive –> IV vanc + met

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47
Q

Which bacteria demonstrates “tumble weed motility”?

A

Listeria monocytogenes

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48
Q

How can listeria gastroenteritis be treated?

A

Amoxicillin/ ampicillin

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49
Q

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

A

Cephalosporin
Clindamycin
Ciprofloxacin

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50
Q

Which gastroenteritis-causing pathogen is associated with undercooked seafood?

A

Vibrio parahaemolyticus

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51
Q

Which gastroenteritis-causing pathogen is associated with shellfish handlers?

A

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

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52
Q

Recal the site of absorption of iron, folate and B12

A

Iron: Duodenum
Folate: Jejunum
B12: Ileum

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53
Q

Which skin condition is pathognomonic for coeliac disease?

A

Dermatitis herpetiformis

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54
Q

Describe the appearance of stool in coeliac disease

A

Waterey, grey, frothy

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55
Q

What system is used to grade coeliac disease?

A

Marsh system

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56
Q

Recall some typical histological findings in coeliac disease

A

Villous atrophy and crypt hyperplasia

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57
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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58
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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59
Q

What does rebound tenderness indicate about appendicitis?

A

That it involves peritoneum

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60
Q

What sign can be used to demonstrate a retrocaecal appendix?

A

Pain on extending hip (Psoas sign)

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61
Q

How should an un-perforated appendix be managed?

A

Prophylactic antibiotics followed by laparoscopic appendectomy

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62
Q

How should a perforated appendix be managed?

A

Abdominal lavage

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63
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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64
Q

How can the symptoms of cholecystitis and cholangitis be differentiated?

A 
Cholecystitis = no jaundice
Cholangitis = obstructive jaundice
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65
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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66
Q

What is Charcot’s triad?

A

Triad of classical symptoms of ascending cholangitis
Jaundice
RUQ pain
fever

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67
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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68
Q

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

A

1 week (use antibiotics whilst waiting)

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69
Q

What is “Mirizzi syndrome”?

A

Impaction of common hepatic duct by a GB stone

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70
Q

What is the pathophysiology of “porcelain gallbladder”?

A

Chronic cholecystitis can –> calcification of GB walls

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71
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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72
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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73
Q

How can diarrhoea post-cholecystectomy be managed?

A

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

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74
Q

How can ascending cholangitis be managed?

A

IV antibiotics followed by therapeutic ERCP within 48 hours

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75
Q

What are the key symptoms of cholangiocarcinoma?

A

Palpable gallbladder, obstructive jaundice

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76
Q

What is the gold-standard investigation for staging cholangiocarcinoma?

A

ERCP

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77
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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78
Q

How can features of PBC be remembered?

A

The M rule:
IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females

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79
Q

Recall and compare the antibodies involved in PBC vs PSC

A

PBC: AMA
PSC: p-ANCA

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80
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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81
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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82
Q

What % of patients with PSC get cholangiocarcinoma?

A

10%

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83
Q

Which autoimune gallbladder disease is associated with IBD?

A

PSC (ulcerative colitis)

84
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

85
Q

What are the key symptoms of autoimmune hepatitis?

A

Amenorrhoea

Chronic liver disease OR acute hepatitis

86
Q

Which type of autoimmune gallbladder disease can affect extrahepatic ducts?

87
Q

How is autoimmune hepatitis managed?

A

Steroids + azothioprine

Eventual liver transplantation

88
Q

What are the 4 signs of portal hypertension?

A 
SAVE
Splenomegaly
Ascites
Varices
Encephalopathy
89
Q

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

A

Ataxia
Confusion
Ophthalmoplegia

90
Q

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

A

Hepatic encephalopathy: lactulose + rifaximin

Wernicke’s encephalopathy: thiamine, magnesium, folic acid

91
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

92
Q

What is an abdominal paracentesis procedure used to treat?

A

Tense ascites

93
Q

What is the most common pathogen in SBP?

94
Q

What investigation is used to confirm ascites?

A

USS abdomen

95
Q

How can SBP be confirmed?

A

Ascitic tap with PMN>250 and MC+S

96
Q

What drugs are used to treat vs as prophylaxis for SBP

A

Treatment: piptazobactam/cefotaxime

Prophylaxis: ciprofloxacin + propranolol

97
Q

When should SBP prophylaxis be started?

A

Ascites protein <15g/L

98
Q

What is the screening test for haemachromatosis?

A

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

99
Q

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

A

Perl’s stain

100
Q

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

A

1st line: Venesection

2nd line: Desferrioxamine

101
Q

Describe the typical presentation of NAFLD

A

Acute weight loss followed by jaundice

102
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

103
Q

What are the components of an ELF panel?

A

Hyaluronic acid
Procollagen III
Tissue inhibitor of metalloproteinase 1

104
Q

What is the mainstay of management for NAFLD?

A

Lifestyle changes and wt loss

105
Q

What are the classical symptoms of acute pancreatitis?

A

Severe epigastric pain radiating through to back with nausea and vomiting

106
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

107
Q

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

A

Grey-Turner’s sign = flank bruising

Indicative of acute pancreatitis

108
Q

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

A

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

109
Q

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

A

Serum lipase

110
Q

What criteria are used to grade severity of acute pancreatitis?

A

Glasgow-Imrie

111
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
112
Q

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

A

> 48 hours

113
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

114
Q

Recall some possible early complications of acute pancreatitis

A

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

115
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

116
Q

What % of chronic pancreatitis is due to alcohol excess?

117
Q

What are the signs and symptoms of chronic pancreatitis?

A

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

118
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

119
Q

What is faecal elastase used to measure?

A

Exocrine function

120
Q

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

A

Adenocarcinomas

121
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

122
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

123
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

124
Q

What is the definitive management of pancreatic cancer?

A

Whipple’s procedure

Pancreaticoduodenectomy

125
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
126
Q

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

A

ERCP with stenting

127
Q

What classification is used for diverticular disease?

A

Hinchey classification

128
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)

129
Q

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

A

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

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

130
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

131
Q

What is the gold standard test for diagnosis of GORD?

A

24 hour oesophageal pH monitoring

132
Q

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

A

H pylori –> ulcers –> dyspepsia

GORD –> dyspepsia

133
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
134
Q

What is the mainstay of management for H pylori?

A

Clarithromycin, amoxicillin, PPI

135
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

136
Q

What is the surgical management option for refractory GORD?

A

Nissen fundoplication

137
Q

What are the most common complications of nissen fundoplication?

A

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

Dysphagia (if wrap is too tight)

138
Q

What is Maddrey’s discriminant function?

A

For alcoholic hepatitis:

Predicts prognosis and who will benefit from steroids

139
Q

What score is used to stage liver cirrhosis?

A

Childs Pugh

140
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

141
Q

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

A

Abdominal pain, ascites, tender hepatomegaly

142
Q

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

A

Abdominal USS with doppler

143
Q

What are the 3 best investigations when suspecting achalasia?

A

LOS manometry
Barium swallow
CXR

144
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

145
Q

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

A

Urinary 5-HIAA

Plasma chromogranin A y

146
Q

What is the first line management for the carcinoid syndrome?

A

Somatostatin analogues eg octreotide

147
Q

Recall some antibiotics that may predispose to C diff infection

A 
Amoxicillin
Ampicillin
Cephalosporin (eg cefuroxime, ceftriaxone) 
Clindamycin
Co-amoxiclav 
Quinolones
148
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

149
Q

Recall 3 risk factors for small bowel overgrowth

A

Neonates with congenital abnormalities
Diabetes mellitus
Scleroderma

150
Q

Recall the signs and symptoms of small bowel overgrowth

A

Very similar to IBS
Chronic diarrhoea
Bloating and flatulence
Abdominal pain

151
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

152
Q

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

153
Q

What is Mackler’s triad?

A

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

154
Q

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

A

Gastroduodenal artery

155
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

156
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

157
Q

How long does autoimmune hepatitis need to be treated for?

A

At least 2 years after blood results normalise before discontinuing therapy

158
Q

How should benign peptic strictures be managed?

A

PPI to treat underlying GORD

Balloon dilatation following benign biopsy

159
Q

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

A

Oesophageal rupture (which may cause mediastinitis)

160
Q

How can oesophageal rupture be imaged best?

A

CT with oral contrast

161
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)

162
Q

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

A

IV hydrocortisone

163
Q

How can blood glusose be used to assess liver function?

A

Assesses synthetic function

164
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

165
Q

What is the best surgical management for bleeding varices?

A

Band ligation or sclerotherapy

166
Q

What is the most appropriate long term management of varices?

A

Non-cardioselective beta blocker

167
Q

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

A

Insertion of Sengstaken Blakemore tube

168
Q

What are the 5 components of the Childs Pugh score?

A 
Serum bilirubin
Serum albumin
Prothrombin time
Presence of ascites 
Presence of encephalopathy
169
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

170
Q

If someone has a diagnostic ascitic 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
171
Q

Which 2 investigations are best for imaging chronic pancreatitis?

172
Q

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

A

Roziglitazone
Flucloxacillin
Macrolides
Statins

173
Q

When is mesenteric angiography used?

A

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

174
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

175
Q

What is BAM?

A

Bile acid malabsorbption
Bile acids enter colon –> too many bile acids in colon –> profuse waterey diarrhoea
Should be halted by fasting

176
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

177
Q

Recall 3 examples of inflammatory diarrhoea

A

UC
Crohn’s
Shigella

178
Q

Recall 4 examples of diarrhoea due to abnormal motility

A

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

179
Q

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

180
Q

What is Zollinger Ellison syndrome?

A

A rare digestive disorder caused by a neuroendocrine tumour that produces gastrin which leads to excess gastric acid. This excess gastric acid can cause peptic ulcers in the stomach and intestine

181
Q

How should autoimmune hepatitis be treated (broadly)?

A

Prednisolone and azothioprine

182
Q

How to choose ERCP vs MRCP?

A

ERCP is only now used as a therapeutic test - do this if worried about cancer (to take samples) or if there is something you can stent

MRCP is purely diagnostic (eg for PSC, see beading)

183
Q

Recall 3 GI causes of clubbing

A

GI malignancy
IBD
Chronic liver disease

184
Q

What is the cause of leukonychia?

A

Hypoalbuminaemia

185
Q

Recall 3 differentials for hepatomegaly

A

Hepatitis
NAFLD
Haematological malignancy

186
Q

How can you tell the spleen and kidney apart on palpation, apart from location?

A 
Spleen: 
Moves down with inspiration 
You cannot get above it 
Has a notch 
Dull to percussion 
Not ballotable
187
Q

Recall 3 differentials for splenomegaly

A

Haematological malignancies
Alcohol misuse
Primary sclerosing cholangitis

188
Q

Recall 3 differentials for enlarged kidneys

A

Renal vein thrombosis (usually UL)
Obstructive uropathy
PCKD

189
Q

Recall 3 causes of ascites

A

Portal hypertension
Constrictive pericarditis
Ovarian malignancy

190
Q

Recall some causes of cholestasis

A

Pancreatic cancer physically obstructing the gut
PBC (nb AMA pos, high IgM)
Chronic active hepatitis (anti-nuclear factor pos, high IgG)

191
Q

What drugs must be stopped to make a carbon13 Urea breath test reliable?

A

Amoxicillin 4w prior

PPI 2w prior

192
Q

What is the difference in the metabolic derangement that can be caused by diarrhoea vs vomiting?

A

Diarrhoea: normal anion gap acidosis
Vomiting: alkalosis

193
Q

What vaccine is given every 5 years in coeliac disease?

A

Pneumococcal

194
Q

How should a mild-moderate flare of UC be managed?

A

In a mild-moderate flare of ulcerative colitis extending past the left-sided colon, oral aminosalicylates should be added to rectal aminosalicylates, as enemas only reach so far (Passmed)

195
Q

What medication change is required for gastroscopy?

A

Stop PPI (eg omeprazole) 2w before procedure

196
Q

How should nutrition be managed in acute pancreatitis?

A

All patients with moderate to severe acute pancreatitis should be offered enteral nutrition (eg normal feeding or ng tube if needed) within 72 hours. They should only be offered parenteral nutrition if they cannot tolerate food (eg profuse vomiting).

197
Q

How can Crohn’s increase the risk of gallstones?

A

Terminal ileitis can reduce bile salt resorption

198
Q

In which patients with sigmoid volvulus would you NOT treat with a therapeutic flexible sigmoidoscopy?

A

In patients with sigmoid volvulus who have bowel obstruction with symptoms of peritonitis

199
Q

If mild/mod C difficile does not respond to oral vancomycin, what should be used 2nd line?

A

Oral fidaxomicin

If more severe infectiom = oral vancomycin + IV metronidazole

200
Q

How should high grade dysplasia in Barret’s oesophagus be managed?

A

Endoscopic ablation

201
Q

What are the grades of hepatic encaphalopathy?

A

Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma

202
Q

How might subcutaneous emphysema appear on examination?

A

Mild crepitus in the epigastric region

203
Q

What are the 2 most important blood tests for monitoring haemachromatosis?

A

Ferritin and transferrin saturation

204
Q

How is alcoholic ketoacidosis managed?

A

Infusion of thiamine and saline

205
Q

What is the limit of protein concentration in ascites for giving antibiotic prophylaxis, and what antibiotic is used?

A

Give antibiotics if protein concentration <15g/L

Abx of choice = ciprofloxacin

206
Q

If coeliac needs to be confirmed by biopsy, what is biopsied?

YR6 Rotations (22 decks)

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