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MBBS Y5 > Medicine - Gastroenterology > Flashcards

Medicine - Gastroenterology Flashcards

1
Q

what are the 3 stages of alcohol-related liver disease?

A

NAME?

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2
Q

is alcoholic hepatitis reversible?

A

if mild, it can be reversed with permanent abstinence

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3
Q

what is the recommended alcohol consumption?

A
  • 14 units / week for both men and women| - spread over 3 or more days
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4
Q

what are the CAGE questions?

A

NAME?

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5
Q

what are the 2 screening tools for alcohol misuse?

A
  • CAGE| - AUDIT
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6
Q

complications of alcohol misuse?

A

NAME?

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7
Q

signs of ALD? hint: there’s a LOT

A

NAME?

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8
Q

what are caput medusae?

A

superficial epigastric veins that are engorged

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9
Q

investigations and findings in ALD?

A

NAME?

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10
Q

findings of blood tests in ALD?

A
  • FBC (raised MCV, macrocytic anaemia)- LFT (raised ALT, AST and gamma-GT, low albumin)- clotting (raised PTT) - UEs (deranged)
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11
Q

management of ALD?

A

NAME?

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12
Q

complications of cirrhosis?

A

NAME?

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13
Q

key criterion to be eligible for liver transplant?

A

they must have abstained from alcohol for 3 months prior to referral

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14
Q

alcohol withdrawal symptoms at 6-12 hours?

A

NAME?

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15
Q

alcohol withdrawal symptoms at 12-24 hours?

A

hallucinations

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16
Q

alcohol withdrawal symptoms at 24-48 hours?

A

seizures

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17
Q

what presents 24-72 hours after start of alcohol withdrawal?

A

delirium tremens

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18
Q

mortality rate of untreated delirium tremens?

A

35%

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19
Q

presentation of delirium tremens?

A

NAME?

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20
Q

management of alcohol withdrawal?

A
  • chlordiazepoxide for 7 days - disulfiram (unpleasant reaction to alcohol)- IV pabrinex (B vitamins), then PO thiamine (B1)
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21
Q

what drug class is chlordiazepoxide?

A

benzodiazepine

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22
Q

how does alcohol excess cause Wernicke-Korsakoff syndrome?

A
  • alcohol stops thiamine (B1) absorption| - thiamine deficiency causes WKS
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23
Q

features of Wernicke’s encephalopathy? is it reversible?

A

NAME?

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24
Q

features of Korsakoff’s syndrome? is it reversible?

A

NAME?

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25
Q

4 most common causes of cirrhosis?

A
  • ALD- NAFLD- hepatitis B- hepatitis C
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26
Q

less common causes of cirrhosis?

A
  • autoimmune hep- PBC- haemochromatosis and Wilsons disease - alpha-1 antitrypsin deficiency - cystic fibrosis - drugs
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27
Q

drug causes of cirrhosis?

A

NAME?

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28
Q

signs O/E in cirrhosis?

A

NAME?

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29
Q

what is the tumour marker for hepatocellular carcinoma (HCC)?

A

alpha-fetoprotein

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30
Q

how is HCC screened for in cirrhosis patients?

A

6-monthly AFP levels and liver USS

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31
Q

first line investigation to assess fibrosis in NAFLD?

A

enhanced liver fibrosis (ELF) blood test

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32
Q

USS changes seen in cirrhosis?

A
  • nodular liver surface - “corkscrew” appearance of hepatic arteries (compensating for portal HTN)- enlarged portal vein with reduced flow- fluid- splenomegaly
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33
Q

what does fibroscan measure? how often should it be done in patients at high risk of cirrhosis?

A
  • elasticity of the liver| - every 2 years
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34
Q

risk factors for cirrhosis?

A
  • hep C- hep B- heavy alcohol consumption- existing ALD - existing NAFLD with fibrosis on ELF test
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35
Q

what is the Child-Pugh score?

A

scoring system used to determine the severity and prognosis of cirrhosis

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36
Q

which 5 things are assessed in the Child-Pugh score?

A

NAME?

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37
Q

what is the MELD score? who is it used on? how often is it done?

A
  • to check if pt with compensated cirrhosis needs dialysis| - 6 monthly
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38
Q

how often does a patient with cirrhosis but no known varices need to be endoscopied?

A

every 3 years

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39
Q

complications of cirrhosis?

A

NAME?

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40
Q

management / prevention of malnutrition secondary to cirrhosis?

A
  • regular meals every 2-3 hours - low Na diet (stops fluid retention)- high protein, high kcal diet - avoid alcohol
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41
Q

what causes varices?

A

NAME?

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42
Q

common sites for variceal veins?

A

NAME?

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43
Q

management of stable varices?

A

NAME?

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44
Q

management of portal HTN?

A

transjugular intrahepatic portosystemic shunt (TIPS)

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45
Q

management of bleeding oesophageal varices?

A

NAME?

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46
Q

what is ascites? how does it develop?

A
  • free fluid in the peritoneal cavity| - increased pressure in portal system forces fluid to leak out
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47
Q

what type of ascites does cirrhosis cause?

A

transudative (low protein)

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48
Q

management of ascites?

A

NAME?

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49
Q

how might SBP present?

A

NAME?

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50
Q

what might blood tests show in SBP?

A

NAME?

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51
Q

which 4 organisms most commonly cause SBP?

A

NAME?

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52
Q

management of SBP?

A
  • take ascitic culture| - then IV cephalosporin (cefotaxime)
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53
Q

how does hepatorenal syndrome develop?

A

NAME?

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54
Q

prognosis of hepatorenal syndrome?

A

fatal within a week if no liver transplant

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55
Q

management of hepatorenal syndrome?

A

liver transplant

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56
Q

what is the primary toxin responsible for hepatic encephalopathy? where does it come from? why do cirrhosis patients get a build up of this toxin?

A

NAME?

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57
Q

presentation of hepatic encephalopathy?

A
  • reduced consciousness| - confusion
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58
Q

precipitating factors for hepatic encephalopathy?

A

NAME?

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59
Q

management of hepatic encephalopathy?

A

NAME?

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60
Q

what are the stages of progression from NAFLD to cirrhosis?

A

NAME?

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61
Q

risk factors for NAFLD? (hint: think CVD risk factors)

A

NAME?

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62
Q

what is included in a non-invasive liver screen?

A
  • USS liver- hep B and C serology - autoantibodies - immunoglobulins - caeruloplasmin - alpha-1 antitrypsin - ferritin and transferrin saturation
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63
Q

which conditions might be shown by autoantibodies on a non-invasive liver screen?

A

NAME?

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64
Q

which conditions might be shown by immunoglobulins on a non-invasive liver screen?

A
  • autoimmune hepatitis| - primary biliary cirrhosis
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65
Q

marker of Wilsons disease on a non-invasive liver screen?

A

caeruloplasmin

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66
Q

which condition would cause low alpha-1 antitrypsin on a non-invasive liver screen?

A

alpha-1 antitrypsin deficiency

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67
Q

markers of hereditary haemochromatosis on a non-invasive liver screen?

A

raised ferritin and transferrin saturation

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68
Q

which autoantibodies are on the non-invasive liver screen?

A
  • antinuclear antibodies (ANA)- smooth muscle antibodies (SMA)- antimitochondrial antibodies (AMA)- LKM-1 antibodies
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69
Q

investigations in NAFLD?

A
  • liver USS (very basic, doesn’t show much) - ELF blood test - NAFLD fibrosis score if ELF unavailable- fibroscan is 3rd line
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70
Q

management of NAFLD?

A

NAME?

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71
Q

causes / types of hepatitis?

A
  • alcoholic - NAFLD- viral (A-E)- autoimmune - drug-induced
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72
Q

how might hepatitis present?

A

NAME?

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73
Q

what are the LFT findings in hepatitis?

A
  • AST and ALT rise disproportionately higher than ALP does| - raised bilirubin
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74
Q

which 2 enzymes are transaminases?

A
  • AST| - ALT
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75
Q

what is the most common viral hepatitis worldwide?

A

hep A

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76
Q

what type of organism causes hep A? what is the route of transmission?

A
  • RNA virus| - faeco-oral route
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77
Q

presentation of hep A? (hint: there is cholestasis) signs on examination?

A

NAME?

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78
Q

what type of organism causes hep B? what is the route of transmission?

A
  • DNA virus| - blood / bodily fluid contact and vertical transmission
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79
Q

what % of hep B cases go on to become chronic? how quickly do the rest recover from it?

A
  • 10-15%| - within 2 months
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80
Q

which viral marker indicates active hep B infection?

A

surface antigen (HBsAg)

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81
Q

which viral marker indicates high infectivity of hep B infection?

A

E antigen (HBeAg)

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82
Q

which viral marker indicates past / current hep B infection?

A

core antibodies (HBcAb)

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83
Q

which viral marker indicates vaccination / past / current hep B infection?

A

surface antibody (HBsAb)

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84
Q

which viral marker is a direct count of hep B viral load?

A

hep B virus DNA (HBV DNA)

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85
Q

which 2 viral markers are tested for in screening for hep B?

A
  • core antibodies (HBcAb) for past infection| - surface antigens (HBsAg) for active infection
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86
Q

management of hep B?

A

NAME?

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87
Q

what are the possible complications of hep B? how can these be screened for?

A
  • cirrhosis (fibroscan)| - HCC (USS)
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88
Q

what type of organism causes hep C? what is the route of transmission?

A
  • RNA virus| - blood / bodily fluid contact
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89
Q

what % of hep C cases become chronic? is it curable?

A
  • 75%| - yes, with direct acting antiviral medication
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90
Q

complications of hep C?

A
  • cirrhosis| - HCC
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91
Q

how is hep C screened for? how is the diagnosis confirmed?

A
  • hep C antibody test to screen| - hep C RNA testing to confirm (shows viral load)
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92
Q

management of hep C?

A
  • screen for other bloodborne viruses and STDs- refer to GI, ID or hepatology for specialist input- notify PHE- stop smoking and alcohol- education on reducing transmission - direct acting antivirals (DAAs) for 12 weeks- liver transplant if end stage disease
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93
Q

what type of organism causes hep D? what is the route of transmission?

A
  • RNA virus| - faeco-oral route
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94
Q

presentation of hep D? management of hep D?

A

NAME?

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95
Q

pathophysiology of autoimmune hepatitis?

A

T cells of immune system recognise liver cells as foreign and attacks them

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96
Q

what age group does type 1 autoimmune hep present in? how might it present?

A
  • adults| - postmenopausal women with fatigue and liver disease signs O/E, less acute presentation
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97
Q

what age group does type 2 autoimmune hep present in? how might it present?

A
  • children| - teens / 20yos with acute hepatitis, raised AST/ALT and IgG, jaundice, very acute presentation
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98
Q

which autoantibodies are found in type 1 autoimmune hep?

A
  • antinuclear antibodies (ANA)- anti-smooth muscle antibodies (anti-actin)- anti-soluble liver antigen (anti-SLA)
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99
Q

which autoantibodies are found in type 2 autoimmune hep?

A
  • anti-liver kidney microsomes-1 (anti-LKM1)| - anti-liver cytosol antigen type 1 (anti-LC1)
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100
Q

how is the diagnosis of autoimmune hep confirmed?

A

liver biopsy

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101
Q

management of autoimmune hep?

A

NAME?

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102
Q

what is haemochromatosis?

A

a genetic iron storing disorder which causes an excess of total body iron

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103
Q

which gene mutation (and chromosome) is associated with haemochromatosis?

A

mutation in the HFE gene on chromosome 6

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104
Q

inheritance pattern for haemochromatosis?

A

autosomal recessive

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105
Q

typically which age would haemochromatosis present at?

A

> 40 years old

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106
Q

why does haemochromatosis present later in females?

A

menstruation actively eliminates iron from the body

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107
Q

presentation of haemochromatosis?

A
  • chronic tiredness - joint pain - bronze pigmentation of skin- hair loss - erectile dysfunction - amenorrhoea - cognitive (memory / mood disturbance)
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108
Q

investigations for haemochromatosis?

A
  • serum ferritin level (diagnostic)- transferrin saturation - to see whether you need to do genetic testing- genetic testing (gold standard)- liver biopsy with Perl’s stain - CT abdo- MRI liver and heart
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109
Q

complications of haemochromatosis?

A

NAME?

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110
Q

management of haemochromatosis?

A

NAME?

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111
Q

what is wilson’s disease?

A

excessive accumulation of copper in body tissues

112
Q

which gene mutation (and on which chromosome) causes wilson’s disease?

A

“Wilson disease protein” on chromosome 13

113
Q

inheritance pattern of wilson’s disease?

A

autosomal recessive

114
Q

how does wilson’s disease affect the liver?

115
Q

neurological symptoms in wilson’s disease?

116
Q

how could wilson’s disease cause parkinsonism?

A

copper deposits in the substantia nigra (basal ganglia)

117
Q

psychiatric symptoms of wilson’s disease?

A
  • depression| - psychosis
118
Q

describe copper deposits in the eyes. how are these investigated?

A
  • Kayser-Fleischer rings in cornea| - slit lamp examination
119
Q

other than liver / neuro / psych, what are the other features of wilson’s disease?

120
Q

initial investigation in wilson’s disease?

A

serum caeruloplasmin

121
Q

what is caeruloplasmin?

A

a protein which carries copper in the blood

122
Q

gold standard investigation in wilson’s disease?

A

liver biopsy

123
Q

other than serum caeruloplasmin and liver biopsy, which other investigations can be done for wilson’s disease?

A
  • 24H urine copper assay - serum copper (low) - MRI brain (nonspecific changes)
124
Q

management of wilson’s disease?

A

copper chelation:- penicillamine - trientene

125
Q

what is alpha-1 antitrypsin (A1AT) deficiency?

A

inherited deficiency of alpha-1 antitrypsin (a protease inhibitor)

126
Q

which chromosome carries the gene for A1AT?

A

chromosome 14

127
Q

what are the 2 main organs affected by A1AT deficiency? what happens to them?

A
  • liver (cirrhosis)| - lungs (pulmonary basal emphysema)
128
Q

investigations in A1AT deficiency?

A
  • serum A1AT blood test (low), screening test- liver biopsy (acid-Schiff-positive globules)- genetic testing for A1AT gene - high res CT thorax (emphysema)
129
Q

management of A1AT deficiency?

130
Q

pathophysiology of primary biliary cirrhosis (PBC)?

131
Q

what are xanthelasma? what are xanthoma?

A
  • cholesterol deposits in the skin| - same but larger ones
132
Q

presentation of PBC?

133
Q

risk factors for PBC?

A
  • middle aged women - other autoimmune disease (thyroid, coeliac etc)- rheumatoid disease (systemic sclerosis, sjogren’s, RA etc)
134
Q

investigations in PBC?

135
Q

blood results in PBC?

A
  • LFT shows raised ALP early on - anti-mitochondrial antibodies present, most specific to PBC, diagnostic if present- anti-nuclear antibodies present in 35% - raised ESR- raised IgM
136
Q

management of PBC? how do each of them help?

137
Q

2 most important complications of PBC?

A
  • cirrhosis| - portal hypertension
138
Q

pathophysiology of primary sclerosing cholangitis?

A

intrahepatic / extrahepatic bile ducts get strictured and fibrotic

139
Q

which other condition is PSC associated with?

A

ulcerative colitis

140
Q

risk factors for PSC?

A
  • male - age 30-40- PMHx of UC- FHx
141
Q

presentation of PSC?

142
Q

LFT findings in PSC?

A
  • “cholestatic” picture - raised ALP early- then other enzymes and bilirubin rise later
143
Q

are antibody tests useful in PSC investigation?

A
  • only in finding out if there is an autoimmune element| - none are sensitive / specific to PSC so not useful in diagnosing it
144
Q

which autoantibodies are found in PSC?

A
  • antineutrophil cytoplasmic antibody (p-ANCA), seen in up to 94%- antinuclear antibodies (ANA) in 77%- anticardiolipin antibodies (aCL) in 63%
145
Q

gold standard investigation for PSC? what does it show in PSC?

A
  • magnetic resonance cholangiopancreatography (MRCP)- it’s an MRI of liver, bile ducts and pancreas - shows bile duct lesions and strictures
146
Q

complications in PSC?

147
Q

management of PSC?

148
Q

what does ERCP stand for? where does it go through? what happens?

149
Q

what are the 2 types of primary liver cancer?

A
  • hepatocellular carcinoma (HCC), 80%| - cholangiocarcinoma, 20%
150
Q

risk factors for HCC?

A
  • hep B / C infection- alcohol- NAFLD- any other cause of cirrhosis- A1AT deficiency- being male - metabolic syndrome (e.g. DM)
151
Q

which condition is associated with cholangiocarcinoma?

A

PSC (10% of cholangiocarcinoma patients have it)

152
Q

presentation of liver cancer?

153
Q

investigations in liver cancer?

154
Q

tumour marker for HCC?

A

alpha-fetoprotein (AFP)

155
Q

tumour marker for cholangiocarcinoma?

156
Q

management of HCC?

A
  • if caught before mets, transplant is curative| - kinase inhibitors (all end in -fenib)
157
Q

prognosis of HCC?

158
Q

management of cholangiocarcinoma?

A
  • if caught before mets, surgical resection is curative| - ERCP to stent bile duct being compressed by tumour, relieves obstructive symptoms
159
Q

prognosis of cholangiocarcinoma?

A
  • poor| - resistant to chemo and radiotherapy
160
Q

what is a hemangioma?

A
  • a common benign liver tumour| - found incidentally
161
Q

what are the chances of a hemangioma becoming cancerous? how are they monitored and treated?

A
  • nil| - no monitoring or treatment needed
162
Q

what is a focal nodular hyperplasia?

163
Q

how are focal nodular hyperplasias monitored and treated?

A
  • no monitoring or treatment needed| - no malignant potential
164
Q

most common acute indications for a liver transplant?

A
  • acute viral hepatitis| - paracetamol OD
165
Q

factors making a liver transplant unsuitable?

A
  • significant other comorbid conditions (CKD, HF)- excessive weight loss / malnutrition - active hep B or C infection - end stage HIV - active alcohol use
166
Q

how long does a patient need to be abstinent for before a liver transplant?

167
Q

management post-liver transplant?

168
Q

why is it important to monitor for cancer in liver transplant patients?

A

they’re immunosuppressed which increases risk of malignancy significantly

169
Q

signs of liver transplant rejection?

170
Q

what is the histology of the oesophagus lining?

A

squamous epithelium

171
Q

what is the histology of the stomach lining?

A

columnar epithelium

172
Q

presentation of GORD?

173
Q

which investigation can be used in GORD? which patients need this done urgently?

A
  • endoscopy, to assess for ulcers and malignancy| - urgent if evidence of an UGIB or cancer
174
Q

evidence of UGIB?

A
  • melaena| - coffee ground vomiting
175
Q

red flags of cancer which warrant an urgent endoscopy referral?

176
Q

lifestyle advice given in GORD?

177
Q

medication classes used in GORD? give examples

178
Q

surgical management of GORD? how does it work?

A
  • laparoscopic fundoplication| - tying the fundus up, making the LOS narrower
179
Q

what type of bacteria is H. pylori?

A

gram -ve aerobic bacteria

180
Q

how does H. pylori affect the stomach?

181
Q

who gets offered H. pylori testing?

A

anyone with dyspepsia

182
Q

what needs to be done prior to H. pylori testing to ensure accuracy?

A

no PPI use in the last 2 weeks

183
Q

3 methods of testing for H. pylori?

A
  • urea breath test- stool antigen test (1st choice method, easiest to do)- rapid urease test (CLO test), done in endoscopy
184
Q

which substance is needed for the urea breath test?

A

radiolabelled carbon 13

185
Q

what happens in a CLO test?

186
Q

eradication therapy for H. pylori? how long for?

A
  • “triple therapy”- 1 PPI (e.g. omeprazole)- 2 ABx (e.g. amoxicillin and clarithromycin) - 7 days
187
Q

what is barretts oesophagus?

A

metaplasia of lower oesphageal mucosa from squamous to columnar epithelium

188
Q

is barretts oesophagus dangerous?

A
  • not by itself| - premalignant for adenocarcinoma in some
189
Q

monitoring of barretts oesophagus?

A

endoscopy to check for adenocarcinoma changes

190
Q

management of barretts oesophagus?

A
  • PPI| - surgical ablation in those with dysplasia
191
Q

what are peptic ulcers? most common type?

A
  • includes gastric and duodenal ulcers| - duodenal more common
192
Q

pathophysiology of peptic ulcers?

A

2 main causes:- breakdown of gastric / duodenal mucosa by drugs or H. pylori- increased stomach acid

193
Q

causes of increased stomach acid?

194
Q

presentation of peptic ulcers?

195
Q

how does eating affect gastric ulcers?

A

worsens the pain

196
Q

how does eating affect duodenal ulcers?

A

eases the pain

197
Q

investigations for peptic ulcers?

198
Q

management of peptic ulcers?

A
  • same as GORD| - high dose PPIs
199
Q

complications of peptic ulcers?

A
  • bleeding, can be life-threatening- perforation, causing peritonitis and “acute abdomen”- scarring and strictures of mucosa, can lead to pyloric stenosis
200
Q

causes of UGIB?

201
Q

presentation of UGIB?

202
Q

what is the Glasgow-Blatchford score?

A

risk of having an UGIB looking at various risk factors

203
Q

why does urea rise in UGIB?

A

it is a breakdown product in the digestion of blood

204
Q

what is the Rockall score?

A

risk of rebleeding and mortality after an endoscopy

205
Q

management of UGIB?

A
  • ABCDE- IV fluid bolus- Bloods- Access (IV, 2 large bore cannulas)- Transfuse blood- Endoscopy, urgent within 24h- Drugs, stop NSAIDs and anticoags
206
Q

which bloods are requested in UGIB?

A
  • FBC (Hb, platelets)- UEs- coagulation (INR)- LFTs- crossmatch 2 units of blood
207
Q

management in UGIB with a massive haemorrhage?

A

transfuse blood, platelets and clotting factors (FFP)

208
Q

when is prothrombin complex concentrate used in UGIB management?

A

patients on warfarin who are actively bleeding

209
Q

additional management of suspected oesophageal varices in UGIB? (e.g. an alcoholic with a bleed)

A
  • terlipressin| - broad spectrum ABx (prophylaxis)
210
Q

definitive management of UGIB?

211
Q

crows NEST: features of crohn’s disease? (hint: 2S and 2T), any others?

212
Q

uc CLOSEUP: features of UC?

A
  • Continuous inflamm on endoscopy - Limited to colon and rectum - Only superficial mucosa affected- Smoking is protective!!!- Excreting blood and mucus- Use aminosalicylates - PSC is an association
213
Q

overall presentation of IBD?

214
Q

investigations in IBD?

215
Q

screening for IBD?

A

faecal calprotectin

216
Q

what is the diagnostic test for IBD?

A

endoscopy (OGD and colonoscopy) with biopsy

217
Q

potential complications of IBD?

218
Q

management of crohn’s?

A
  • induce remission: steroids (pred or IV hydrocortisone)- 2nd line is azathioprine - maintaining remission: azathioprine, methotrexate, infliximab- surgery
219
Q

when can surgery be used to manage crohn’s?

A
  • when disease only affects the distal ileum| - to treat strictures and fistulas secondary to crohn’s
220
Q

3 principles of IBD management?

221
Q

management of UC?

A
  • inducing remission in mild-mod disease: mesalazine, 2nd line is pred- inducing remission in sev disease: IV hydrocortisone, 2nd line is IV ciclosporin - maintaining remission: mesalazine, azathioprine - surgery
222
Q

which drug class is mesalazine?

A

aminosalicylate

223
Q

surgical management of UC?

A
  • total removal of colon and rectum| - patient left with permanent ileostomy or J-pouch
224
Q

what is IBS?

225
Q

which demographic are more likely to get IBS?

A

young females

226
Q

symptoms of IBS?

227
Q

diagnostic criteria for IBS?

228
Q

advice given in management of IBS?

229
Q

medical management of IBS?

A
  • trial probiotics for 4 weeks- loperamide if diarrhoea - laxatives if constipated - buscopan for cramps - 2nd line: amitriptyline - 3rd line: SSRI - CBT if distress
230
Q

why is lactulose avoided in IBS management?

A

it causes bloating

231
Q

which drug class is buscopan?

A

antispamodic

232
Q

specialist laxative offered in IBS?

A

linaclotide

233
Q

what is coeliac disease?

A

autoimmune condition where exposure to gluten causes inflammation in the small bowel

234
Q

when does coeliac disease typically develop?

A

early childhood

235
Q

autoantibodies found in coeliac disease?

A
  • anti-tissue transglutaminase (anti-TTG)| - anti-endomysial (anti-EMA)
236
Q

which part of the GI tract is affected by coeliac disease?

A

jejunum (middle of small intestine)

237
Q

pathophysiology of coeliac disease?

A

reaction to gluten causes atrophy of jejunal villi

238
Q

presentation of coeliac disease?

239
Q

which dermatological sign is seen in coeliac disease?

A

dermatitis herpetiformis

240
Q

describe dermatitis herpetiformis

A
  • itchy blistering rash| - typically abdominal
241
Q

rare neurological signs of coeliac disease?

242
Q

which condition is strongly associated with coeliac disease? how is this managed?

A
  • T1DM| - all type 1 diabetics are screened for coeliac disease
243
Q

which gene is strongly associated with coeliac disease?

A

HLA-DQ2 (90% have it)

244
Q

why is it important to test for total IgA in coeliac disease?

A

the autoantibodies (anti-TTG, anti-EMA) are IgA themselves, so if the patient is IgA deficient, these 2 will come back falsely negative

245
Q

investigations to diagnose coeliac disease?

A
  • all must be carried out whilst patient has gluten in their diet- total IgA, then anti-TTG (1st), then anti-EMA- endoscopy and biopsy
246
Q

findings on endoscopy in coeliac disease?

A
  • crypt hypertrophy| - villous atrophy
247
Q

which conditions are associated with coeliac disease?

A

autoimmune ones:- T1DM- thyroid disease- autoimmune hepatitis - PBC- PSC

248
Q

complications of untreated coeliac disease?

249
Q

management of coeliac disease?

A

lifelong gluten free diet

250
Q

risk factors for hepatocellular carcinoma (HCC)?

251
Q

prophylaxis of bleeding from oesophageal varices?

A

propanolol

252
Q

management of a variceal bleed during endoscopy?

A

terlipressin

253
Q

presentation of C. jejuni infection?

254
Q

which bacteria is associated with reheated rice?

A

bacillus cereus

255
Q

eye signs of IBD?

A
  • anterior uveitis (more in UC)- episcleritis (more in crohn’s)- conjunctivitis
256
Q

joint signs of IBD?

257
Q

skin signs of IBD?

A
  • erythema nodosum| - pyoderma gangrenosum
258
Q

which malignancies could raised AFP indicate?

A
  • liver| - testicular / yolk sac
259
Q

which malignancy could raised hCG indicate?

A

testicular cancer

260
Q

which malignancy could raised immunoglobulins indicate?

A

multiple myeloma

261
Q

which malignancy could raised CA-19-9 indicate?

A

pancreatic cancer

262
Q

which malignancies could raised CEA indicate?

A
  • colon| - stomach
263
Q

what is cullen’s sign? hint: seen in pancreatitis

A

bruising around umbilicus in pancreatitis with retroperitoneal haemorrhage

264
Q

triad seen in mesenteric anaemia?

265
Q

key condition associated with gastroparesis?

266
Q

features of gastroparesis?

267
Q

how can gastroparesis be diagnosed?

A

solid meal gastric scintigraphy

268
Q

management of gastroparesis?

269
Q

features of vit C def?

270
Q

RFs for vit C def?

271
Q

RFs for vit B1 (thiamine) def?

A
  • chronic alcohol use| - any cause of malabsorption
272
Q

features of thiamine def?

A
  • wernicke’s encephalopathy| - wet or dry beriberi
273
Q

features of vit A def?

274
Q

RFs for C. difficile infection?

275
Q

which underlying diseases can predispose to a C. diff infection?

276
Q

management of c. diff?

A
  • 1st line: PO vancomycin

MBBS Y5 (27 decks)

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