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Zero to Finals: Medicine > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

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

A
  • alcoholic fatty liver
  • alcoholic hepatitis
  • cirrhosis
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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
  • Cut down - ever thought you should?
  • Annoyed - when people comment on your drinking?
  • Guilty - ever felt like this over your drinking?
  • Eye-opener - ever drink first thing in the morn?
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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
  • alcoholic liver disease (ALD)
  • cirrhosis
  • HCC
  • wernicke-korsakoff syndrome
  • pancreatitis
  • alcoholic myopathy
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7
Q

signs of ALD? hint: there’s a LOT

A
  • jaundice
  • hepatomegaly
  • spider naevi
  • palmar erythema
  • gynaecomastia
  • bruising (abnormal clotting)
  • ascites
  • caput medusae
  • asterixis (flapping tremor)
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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
  • bloods (lots of things)
  • USS (increased echogenecity)
  • fibroscan (shows degree of cirrhosis)
  • endoscopy (to find and treat oesophageal varices)
  • CT / MRI (fatty changes, HCC, HSM, ascites)
  • liver biopsy (to confirm diagnosis)
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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
  • stop drinking permanently
  • start detox regime
  • thiamine supplements and high protein diet
  • treat complications of cirrhosis
  • liver transplant if severe enough
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12
Q

complications of cirrhosis?

A
  • portal HTN
  • varices
  • ascites
  • hepatic encephalopathy
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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
  • tremor
  • sweating
  • headache
  • craving
  • anxiety
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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
  • acutely confused
  • delusions, hallucinations
  • severe agitation
  • tremor
  • tachycardia
  • HTN
  • hyperthermia
  • ataxia
  • arrhythmias
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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
  • confusion
  • oculomotor disturbances
  • ataxia
  • yes
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24
Q

features of Korsakoff’s syndrome? is it reversible?

A
  • anterograde and retrograde amnesia
  • behavioural changes
  • no
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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
  • amiodarone
  • methotrexate
  • sodium valproate
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28
Q

signs O/E in cirrhosis?

A
  • jaundice
  • hepatosplenomegaly (HSM)
  • spider naevi
  • palmar erythema
  • gynaecomastia and testicular atrophy
  • bruising
  • ascites
  • caput medusae
  • asterixis
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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
  • bilirubin
  • albumin
  • INR
  • ascites
  • encephalopathy
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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
  • malnutrition
  • portal HTN
  • varices, bleeding
  • ascites, SPB
  • hepatorenal syndrome
  • encephalopathy
  • HCC
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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
  • portal venous system has increased pressure (HTN)
  • blood gets backlogged
  • results in swollen, tortuous vessels
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42
Q

common sites for variceal veins?

A
  • gastro-oesophageal junction
  • ileocaecal junction
  • rectum
  • anterior abdominal wall via umbilical vein (caput medusae)
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43
Q

management of stable varices?

A
  • BB (propanolol)
  • elastic band ligation
  • sclerosant injection
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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
  • vasopressin analogue (terlipressin)
  • vit K and FFP to correct any coagulopathy
  • prophylactic broad spectrum ABx
  • endoscopy to inject sclerosant and elastic band ligation
  • Sengstaken-Blakemore tube insertion
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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
  • low Na diet
  • aldosterone antagonist diuretic (spironolactone)
  • paracentesis (ascitic tap or drain)
  • prophylactic ABx against SBP (ciprofloxacin) in pts with low protein
  • TIPS or liver transplant if severe
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49
Q

how might SBP present?

A
  • asymptomatic
  • fever
  • abdo pain
  • deranged bloods
  • ileus
  • hypotension
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50
Q

what might blood tests show in SBP?

A
  • raised WBC
  • raised CRP
  • raised creatinine
  • metabolic acidosis
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51
Q

which 4 organisms most commonly cause SBP?

A
  • E. coli
  • klebsiella pneumoniae
  • staphylococcus
  • enterococcus
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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
  • hypertension in portal system causes vessels to dilate
  • dilatation activates renin-angiotensin system
  • leads to renal vasoconstriction
  • reduced circulation in kidneys
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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
  • ammonia
  • breakdown product from gut bacteria
  • normally the liver can break down ammonia into harmless waste products but cirrhosis impairs this
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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
  • constipation
  • electrolyte disturbance
  • infection
  • GI bleed
  • high protein diet
  • sedating drugs
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59
Q

management of hepatic encephalopathy?

A
  • laxative (lactulose) to stop ammonia being absorbed
  • ABx (rifaximin) to kill off some gut bacteria
  • nutritional support
  • nasogastric feeding
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60
Q

what are the stages of progression from NAFLD to cirrhosis?

A
  • NAFLD
  • NASH
  • fibrosis
  • cirrhosis
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61
Q

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

A
  • obesity
  • poor diet
  • T2DM
  • high cholesterol
  • ageing
  • smoking
  • HTN
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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
  • autoimmune hepatitis
  • primary biliary cirrhosis
  • primary sclerosing cholangitis
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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
  • weight loss
  • exercise
  • stop smoking
  • control DM, BP and cholesterol
  • avoid alcohol
  • if liver fibrosis present then give vit E / pioglitazone
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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
  • asymptomatic
  • abdo pain
  • fatigue
  • pruritis
  • muscle and joint aches
  • nausea and vomiting
  • jaundice
  • fever (if viral)
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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
  • nausea
  • vomiting
  • anorexia
  • jaundice
  • dark urine
  • pale stools
  • moderate hepatomegaly
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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
  • 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
  • antiviral meds
  • liver transplant if end stage disease
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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
  • mild illness, self-resolving within a month
  • notify PHE
  • reassure that no treatment is needed
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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
  • high dose prednisolone initially
  • then azathioprine
  • lifelong drugs
  • can recur in a transplanted liver
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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
  • T1DM (iron in pancreas)
  • liver cirrhosis, HCC (iron in liver)
  • endocrine and sexual problems (hypogonadism, impotence, amenorrhoea, infertility), from iron in pituitary and gonads
  • hypothyroidism (iron in thyroid)
  • cardiomyopathy (iron in heart)
  • chrondocalcinosis, arthritis (iron in joints)
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110
Q

management of haemochromatosis?

A
  • weekly venesection
  • monitor serum ferritin
  • treat complications
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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?

A
  • copper accumulating in the liver
  • this causes chronic hepatitis
  • then cirrhosis
115
Q

neurological symptoms in wilson’s disease?

A
  • concentration and coordination difficulties
  • dysarthria (speech)
  • dystonia (abnormal muscle tone)
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?

A
  • haemolytic anaemia
  • renal tubular acidosis
  • osteopenia
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?

A
  • stop smoking (to stop emphysema progression)
  • symptomatic management
  • organ transplant for end stage liver / lung disease
  • monitor for complications (e.g. HCC)
130
Q

pathophysiology of primary biliary cirrhosis (PBC)?

A
  • immune system attacks the small bile ducts of the liver
  • causes obstruction of bile flow
  • bile acids, bilirubin and cholesterol are not excreted properly so blood levels rise
  • results in pruritus, jaundice, fatty stools etc.
  • eventually: fibrosis, cirrhosis and liver failure
131
Q

what are xanthelasma? what are xanthoma?

A
  • cholesterol deposits in the skin

- same but larger ones

132
Q

presentation of PBC?

A
  • fatigue
  • pruritus
  • abdo pain
  • jaundice
  • pale, greasy stools
  • xanthoma and xanthelasma
  • signs of cirrhosis and liver failure (ascites, splenomegaly, spider naevi etc)
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?

A
  • LFTs
  • autoantibodies
  • liver biopsy
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?

A
  • ursodeoxycholic acid (reduces cholesterol absorption in gut)
  • colestyramine (reduces pruritus by binding to bile acids)
  • liver transplant
  • steroids (immunosuppression)
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?

A
  • jaundice
  • chronic RUQ pain
  • pruritus
  • fatigue
  • hepatomegaly
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?

A
  • acute bacterial cholangitis
  • cholangiocarcinoma
  • colorectal cancer
  • cirrhosis and liver failure
  • biliary strictures
  • fat soluble vitamin (ADEK) deficiencies
147
Q

management of PSC?

A
  • ERCP to dilate and stent strictures
  • ursodeoxycholic acid to stop cholesterol absorption
  • cholestyramine to help with pruritus
  • liver transplant
148
Q

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

A
  • endoscopic retrograde cholangio-pancreatography
  • through the mouth and oesophagus etc down to the sphincter of Oddi
  • then into ampulla or Vater and into bile ducts
  • any strictures are stented
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?

A
  • asymptomatic for years initially
  • weight loss
  • abdo pain
  • anorexia
  • N+V
  • jaundice - painless in cholangiocarcinoma
  • pruritus
153
Q

investigations in liver cancer?

A
  • alpha-fetoprotein (AFP)
  • CA19-9
  • USS liver
  • CT, MRI to stage
  • ERCP to take biopsies or diagnose cholangiocarcinoma
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?

A
  • poor because presents late
  • resistant to chemo and radiotherapy
  • kinase inhibitors extend lifespan by months
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?

A
  • a benign liver tumour made of fibrotic tissue
  • found incidentally
  • linked to oestrogen so more common in women on COCP
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?

A
  • lifelong immunosuppression with steroids, azathioprine and tacrolimus
  • avoid alcohol and smoking
  • treat any opportunistic infections
  • monitor for new disease (hepatitis, PBC, cancer)
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?

A
  • abnormal LFTs
  • fatigue
  • fever
  • jaundice
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?

A
  • heartburn
  • acid regurg
  • retrosternal / epigastric pain
  • bloating
  • nocturnal cough
  • hoarse voice
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?

A
  • dysphagia at any age
  • aged >55
  • weight loss
  • upper abdo pain and reflux
  • Tx-resistant dyspepsia
  • N+V
  • low Hb
  • raised platelets
176
Q

lifestyle advice given in GORD?

A
  • reduce tea, coffee, alcohol
  • weight loss
  • avoid smoking
  • smaller, lighter meals
  • avoid heavy meals before bed
  • sit upright after meals
177
Q

medication classes used in GORD? give examples

A
  • acid neutralisers (gaviscon, rennie)
  • PPIs (omeprazole, lansoprazole)
  • H2 receptor antagonist (ranitidine)
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?

A
  • damages the gastric lining
  • causes gastritis
  • increases risk of stomach cancer
  • produces ammonia which also damages the lining
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?

A
  • biopsy of stomach taken in endoscopy
  • urea added to it
  • if H. pylori present, ammonia produced
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?

A
  • stress
  • alcohol
  • caffeine
  • smoking
  • spicy foods
194
Q

presentation of peptic ulcers?

A
  • epigastric discomfort / pain
  • N+V
  • dyspepsia
  • haematemesis (coffee ground)
  • melaena
  • Fe def anaemia (from constant bleeding)
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?

A
  • endoscopy to Dx
  • CLO test done at same time to check for H. pylori
  • consider biopsy to rule out malignancy
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?

A
  • oesophageal varices
  • Mallory-Weiss tear
  • peptic ulcers
  • stomach / duodenal cancers
201
Q

presentation of UGIB?

A
  • haematemesis (fresh blood in vomit)
  • coffee ground vomit (digested blood)
  • melaena (tarry stools)
  • haemodynamic instability
  • signs of underlying disease (e.g. pain, jaundice)
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?

A
  • oesophagogastroduodenoscopy (OGD) to do interventions
  • variceal banding
  • cauterisation of bleeding vessels
211
Q

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

A
  • No blood or mucus in stools (less common)
  • Entire GI tract affected
  • Skip lesions on endoscopy, Smoking is RF
  • Terminal ileum affected most, Transmural inflamm
  • others: weight loss, strictures, fistulas
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?

A
  • diarrhoea
  • abdo pain
  • passing blood (UC)
  • weight loss
214
Q

investigations in IBD?

A
  • bloods: FBC, TFT, LFT, UEs
  • faecal calprotectin
  • endoscopy with biopsy
  • USS, CT, MRI to look for complications
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?

A
  • fistulas
  • abscesses
  • strictures
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?

A
  • inducing remission
  • maintaining remission
  • surgery
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?

A
  • irritable bowel syndrome
  • abnormal functioning of an otherwise healthy bowel
  • diagnosis of exclusion
225
Q

which demographic are more likely to get IBS?

A

young females

226
Q

symptoms of IBS?

A
  • diarrhoea
  • constipation
  • mucus in stools sometimes
  • fluctuating bowel habit
  • abdo pain, worse after eating
  • bloating
  • symptoms improve on opening bowels
227
Q

diagnostic criteria for IBS?

A
  • must exclude other pathology
  • normal FBC, ESR and CRP
  • negative faecal calprotectin (IBD)
  • negative anti-TTG antibodies (coeliac)
  • cancer not suspected / excluded
228
Q

advice given in management of IBS?

A
  • reassurance
  • adequate fluid intake
  • regular small meals
  • reduce processed foods
  • limit caffeine and alcohol
  • low FODMAP diet
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?

A
  • often asymptomatic
  • FTT in young children
  • diarrhoea
  • fatigue
  • weight loss
  • mouth ulcers
  • anaemia (Fe, B12 or folate def)
  • dermatitis herpetiformis
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?

A
  • peripheral neuropathy
  • cerebellar ataxia
  • epilepsy
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?

A
  • vitamin def
  • anaemia
  • osteoporosis
  • ulcerative jejunitis
  • enteropathy-assoc T-cell lymphoma (EATL) of the intestine
  • non-hodgkin lymphoma
  • adenocarcinoma of small bowel (rare)
249
Q

management of coeliac disease?

A

lifelong gluten free diet

250
Q

risk factors for hepatocellular carcinoma (HCC)?

A
  • cirrhosis secondary to any cause
  • A1AT def
  • drugs (COCP, anabolic steroid use)
  • being male
  • metabolic syndrome (e.g. DM)
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?

A
  • prodrome of generally feeling unwell
  • abdo pain (mimics appendicitis)
  • bloody diarrhoea
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?

A
  • arthralgia
  • ankylosing spondylitis (UC)
  • sacroiliitis
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?

A
  • Hx of CVD
  • raised lactate
  • soft but tender abdomen
265
Q

key condition associated with gastroparesis?

266
Q

features of gastroparesis?

A
  • N+V
  • feeling full despite after a few bites
  • abdo pain
  • bloating
  • poor HbA1C management if diabetic
267
Q

how can gastroparesis be diagnosed?

A

solid meal gastric scintigraphy

268
Q

management of gastroparesis?

A
  • dietary modification
  • domperidone
  • metoclopramide / erythromycin (both aid motility)
269
Q

features of vit C def?

A
  • spontaneous bleeding / bruising
  • gingivitis
  • coiled hairs
  • tooth loss
270
Q

RFs for vit C def?

A
  • famine
  • war
  • refugees
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?

A
  • night blindness
  • xeropthalmia (collection of eye signs)
  • complete blindness
274
Q

RFs for C. difficile infection?

A
  • broad-spectrum ABx
  • healthcare settings incl. care homes
  • age >65
  • PPI use
  • underlying diseases
  • immunosuppression (e.g. HIV, chemo)
275
Q

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

A
  • IBD
  • cancer
  • renal disease
276
Q

management of c. diff?

A
  • 1st line: PO vancomycin

Zero to Finals: Medicine (11 decks)

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