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Gastroenterology Flashcards

1
Q

Which blood test is the best to screen for hepatitis B infection?

A

HBsAg - surface antigen - implies active infection or chronic disease. In acute - present for 1-6 months. If present >6months - chronic

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2
Q

What is the first marker to appear in acute hepatitis B infection?

A

HBsAg

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3
Q

Will there be anti-HBs in chronic Hepatitis B?

A

No - negative in chronic disease

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4
Q

What does anti-HBs imply?

A

Immunity - either previous exposure or immunisation

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5
Q

What does the presence of anti-HBc signify?

A

Either acute or previous infection - IgM anti-HBc in acute or recent infection, present for 6 months. IgG persists long term

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6
Q

What does HBeAg indicate?

A

Breakdown of core antigen from liver cells - marker of infectivity and viral replication

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7
Q

What will hep B blood tests show in someone who is immunised?

A

Anti-HBs positive, all else negative

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8
Q

What will blood tests show in someone with previous hepatitis B infection who is not a carrier?

A

Anti-HBc positive, anti-HBs negative

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9
Q

What is a recognised complication of TIPSS procedure?

A

exacerbation of hepatic encephalopathy

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10
Q

What are 3 forms of prophylaxis for oesophageal varices?

A
  1. propranolol
  2. endoscopy variceal band ligation- should be done 2 weeks apart until all varices banded
  3. TIPSS if above unsuccessful
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11
Q

What should be done along side prophylactic EVL for varices?

A

PPI cover to prevent EVL-related ulceration

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12
Q

What is melanosis coli?

A

caused by laxative abuse - anthraquinone compounds e.g. senna, cascara result in pigment-laden macrophages in the bowel

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13
Q

When is the carbon isotope 13 (13C) urea breath test not recommended to diagnosis H pylori?

A
  • within 4 weeks of treatment with antibiotics
  • within 2 weeks of antisecretory drug e.g. PPI
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14
Q

How is the urea breath test performed?

A
  • patients consume drink containing carbon isotope 13 (13C) enriched urea
  • broken down by H pylori urease
  • after 30 min patient exhales into glass tube - mass spectrometry analysis calculates amount of 13C CO2
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15
Q

What is the CLO test?

A

rapid urease test for H pylori; bippsy sample mixed with urea and pH indicator, colour change if H pylori urease activity

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16
Q

What is a drawback of using serum antibody to diagnose H pylori?

A

remains positive after eradication

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17
Q

What is the difference between culture of gastric biopsy and gastric biopsy for diagnosing H pylori?

A

culture will provide info on abx sensitivity; gatsric biopsy provides histological evaluation alone, no culture

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18
Q

What are 3 risk factors for giardiasis?

A
  1. foreign travel
  2. swimming / drinking water from a river or lake
  3. male-male sexual contact
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19
Q

What are 3 investigations for giardiasis?

A
  1. stool microscopy for trophozoite and cysts - sensitivity 65%
  2. stool antigen detection assay - greater sensivitiy and quicker
  3. PCR assays being developed
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20
Q

How serioues is hepatitis A?

A

typically a benign, self-limiting disease - serious outcome very rare

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21
Q

What is the incubation period for hepatitis A?

A

2-4 weeks

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22
Q

What are 5 factors associated with NAFLD?

A
  1. obesity
  2. T2DM
  3. hyperlipidaemia
  4. jejunoileal bypass
  5. sudden weight loss/ starvation
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23
Q

What type of virus causes hepatitis A?

A

RNA picornavirus

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24
Q

How is hepatitis A spread?

A

faeco-oral route, often in institutions

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25
Q

What are the clinical features of hepatitis A?

A
  • flu-like prodrome
  • RUQ pain
  • tender hepatomegaly
  • jaundice
  • deranged LFTs
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26
Q

What vaccination is available for hepatitis A?

A

effective vaccine available, booster dose should be given 6-12 months after the initial dose

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27
Q

What are 6 groups of people who should be vaccinated for hepatitis A?

A
  1. people travelling to / going to reside in areas of intermediate - high prevalence if aged >1 year
  2. chronic liver disease
  3. haemophilia
  4. MSM
  5. IVDU
  6. occupational risk: lab worker, staff of large residential institutions, sewage, primates
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28
Q

What is thought to be the main mechanism by whcih obesity leads to NAFLD?

A

insulin resistance

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29
Q

What LFT findings are present in NAFLD?

A

ALT typically greater than AST

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30
Q

What test is used to test for advanced fibrosis in incidentally identified NAFLD (asymptomatic fatty changes on liver US)?

A

ELF blood test (enhanced liver fibrosis) - hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase 1

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31
Q

What is the mainstay of treatment for NAFLD?

A

lifestyle changes (weight loss) + monitoring (research into role of gastric-banding and insulin-sensitising drugs e.g. metformin, pioglitazone)

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32
Q

What is the management of advanced fibrosis in patients with NAFLD?

A

referred to liver specialist - likely to have liver biopsy to stage more accurately

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33
Q

What do blood tests typically show in alcoholic liver disease?

A

AST/ALT ratio >2:1, GGT > 2x normal

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34
Q

What distinguishes chronic hep B from acute hep B in blood tests?

A

anti-HBc antibody positive in chronic (not acute)

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35
Q

What is the leading cause of chronic viral infection of the liver in the West?

A

hepatitis C

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36
Q

Which gender is classically affected by AIH?

A

female

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37
Q

What are 4 characteristic blood tests in AIH?

A
  1. high gamma globulins, esp IgG
  2. High transaminases >2000
  3. ANA
  4. SMA
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38
Q

What are 9 features of haemochromatosis?

A
  1. cutaneous hyperpigmentation - bronze
  2. diabetes mellitus
  3. chronic liver disease
  4. dilated cardiomyopathy
  5. cardiac conduction disorders
  6. hypothyroidism
  7. hypogonadism - impotence, loss of libido
  8. arthropathy
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39
Q

What are 4 examples of causes of secondary NAFLD?

A
  1. amiodarone
  2. tamoxigen
  3. hep C
  4. PCOS
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40
Q

What is found on blood tests in NAFLD?

A

ALT raised up to 3x ULN, ALT:AST >1. persistent elevation LFTs for >3 months

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41
Q

What is the inheritance pattern of hereditary haemochromatosis?

A

autosomal recessive

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42
Q

Which race is typically affected by haemochromatosis?

A

caucasian

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43
Q

What type of arthralgias are common in haemochromatosis?

A

pseudogout and chronic arthropathy; small joints of hands commonly affected

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44
Q

What blood tests are key in diagnosing haemochromatosis?

A

transferrin saturation (30% is normal) rises >45% (+ ferritin elevated)

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45
Q

What is the inheritance pattern of Wilson’s disease?

A

autosomal recessive

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46
Q

What is the characteristic blood test finding in Wilson’s disease?

A

reduced serum caeruloplasmin

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47
Q

What type of hyperbilirubinaemia is seen in Gilbert’s syndrome?

A

unconjugated (no bilirubinuria)

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48
Q

What 2 things increase the unconjugated plasma bilirubin in Gilbert’s syndrome?

A
  1. low energy diet
  2. IV injection of nicotinic acid
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49
Q

What are 6 conditions that predispose to Budd-Chiari syndrome?

A
  1. myeloproliferative disorders e.g. PCV, paroxysmal nocturnal haemoglobinuria
  2. pregnancy
  3. tumours
  4. chronic inflammatory diseases
  5. clotting disorders
  6. infections
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50
Q

What are 5 key features of the presentation of Budd Chiari syndrome?

A
  1. hepatomegaly
  2. ascites
  3. abdominal pain
  4. LFTs may be mildly elevated
  5. ascitic fluid has high protein content
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51
Q

What may be present on imaging in Budd-Chiari syndrome?

A
  • CT or MTI may show prominent caudate lobe
  • doppler US may help exclude hepatic venous or inferior vena cava thrombosis
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52
Q

What will liver biopsy show in Budd-Chiari syndrome?

A

centrilobular congestion

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53
Q

What are 3 possible aspects of the treatment of Budd-Chiari syndrome?

A
  1. treat underlying haematological condition
  2. surgical decompression of liver e.g. TIPS, balloon angioplasty/stent for inferior vena caval web
  3. liver transplant
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54
Q

In which part of the pancreas do most pancreatic carcinoma cases occur?

A

head of pancreas (70%)

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55
Q

what is Courvoisier’s law?

A

in the presence of a palpable gallbladder, painless jaundice is unlikely ot be caused by gallstones (gallstones cause shrunken, fibrotic gallbladder)

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56
Q

What is the management of pancreatic carcinoma?

A

surgery (radical pancreaticoduodenectomy aka Whipple’s) - suitable in <10% who present

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57
Q

What is the first line management for mild to moderate C difficile infection?

A

oral vancomycin 10 days

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58
Q

What are 5 complications of Clostridium difficile infection?

A
  1. Pseudomembranous colitis
  2. Toxic megacolon
  3. Perforation of the colon
  4. Sepsis
  5. Death
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59
Q

What is the second line management for mild to moderate C difficile infection?

A

oral fidaxomicin, 10 days

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60
Q

What are the causes of portal hypertension and how can they be divided?

A
  1. Pre-hepatic - portal vein thrombosis, abdo trauma
  2. Intrahepatic - presinusoidal: schistosomiasis, drugs, sarcoid
  3. Intrahepatic - sinusoidal: cirrhosis, polycystic liver, metastatic malignant disease
  4. Intrahepatic - postsinusoidal: veno-occlusive disease
  5. Post-hepatic - Budd-Chiari syndrome
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61
Q

What is the commonest cause of portal hypertension in the Western world?

A

liver cirrhosis

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62
Q

What is the commonest cause of portal hypertension in Africa?

A

schistosomiasis

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63
Q

What evidence may be seen on blood tests of splenomegaly in portal hypertension and why?

A

pancytopenia - reticuloendothelial hyperplasia (not reversible)

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64
Q

What are 4 key investigations in portal hypertension?

A
  1. bloods
  2. portal doppler US - portal vein patency
  3. MRI or CT aniography - portal and hepatic veins
  4. Abdo US (cirrhosis, ascites, splenomegaly)
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65
Q

Is measurement of portal pressure required to diagnose portal hypertension?

A

no - invasive, expensive + complication - can be clinical

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66
Q

What are the direct and indirect methods for portal pressure measurement?

A
  • direct: cannulation of hepatic vein + measuring free hepatic vein pressure
  • indirect: balloon occlusion of hepatic vein + measurement of wedged hepatic vein pressure; calculte hepatic venous pressure gradient from this
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67
Q

What are the key features of PBC (primary biliary cholangitis)?

A

Presents in middle aged females with lethargy, pruritus
- IgM
- Anti-mitochondrial antibodies (M2 subtype)
- obstructive LFTs (raised ALP and GGT)

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68
Q

What vitamin is thiamine also known as?

A

B1

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69
Q

What is the classic triad of Wernicke’s encephalopathy?

A
  1. encephalopathy
  2. ataxia
  3. ophthalmoplegia/nystagmus

(+ peripheral sensory neuropathy)

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70
Q

What are 2 investigations in Wernicke’s encephalopathy?

A
  1. decreased red cell transketolase
  2. MRI
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71
Q

How does Korsakoff’s differ from Wernicke’s encephalopathy?

A

same symptoms, plus anterograde + retrograde amnesia, + confabulations

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72
Q

What process is happening in primary biliary cholangitis (/cirrhosis)?

A

autoimmune disease of the liver with destruction of the bile canaliculi within the liver

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73
Q

What is the treatment of life-threatening C difficile infection?

A

oral vancomycin and IV metronidazole; specialist advice (surgery may be considered)

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74
Q

What are 3 criteria for life-threatening C difficile infection?

A
  1. Hypotension
  2. Partial or complete ileus
  3. Toxic megacolon, or CT evidence of severe disease
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75
Q

What is the management of recurrent C diff?

A
  • if recurs within 12 weeks of symptoms resolution: oral fidaxomicin
  • after 12 weeks: oral vancomycin OR fidaxomicin
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76
Q

Why is spironolactone the diuretic of choice for ascites?

A

patients with cirrhosis develop a secondary hyperaldosteronism

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77
Q

What are 2 adverse effects of spironolactone?

A
  1. hyperkalaemia
  2. gynaecomastia (less common with eplerenone)
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78
Q

What is Curling’s ulcer?

A

acute peptic stress ulcer, complication of severe burns - necrosis of gastric mucosa secondary to hypovolaemia

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79
Q

Of UC and Crohn’s, which one is exacerbated by smoking and which is improved?

A
  • Crohn’s - smoking makes it worse
  • UC - smoking makes it better
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80
Q

What management is used first line to induce remission in Crohn’s disease in adults?

A

glucocorticoids - oral, topical or IV

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81
Q

What alternative to glucocorticoid therapy may be used to induce remission in Crohn’s in some situations?

A

enteral feeding with elemental diet - in addition or instead of other measures, particularly if concern re side effects of steroids (e.g. young children)

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82
Q

What treatment is second-line to glucocorticoids for inducing remission in Crohn’s disease?

A

5-ASA drugs e.g. mesalazine

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83
Q

What drugs may be used as add-on therapy to induce remission in Crohn’s disease?

A

azathioprine or mercaptopurine (methotrexate is alternative to azathioprine) - NOT used as monotherapy

glucocorticoids first line, 2nd line 5-ASAs

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84
Q

What drug may be used for isolated perianal disease in Crohn’s?

A

metronidazole

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85
Q

What is used first line to maintain remission in Crohn’s?

A

azathioprine or mercaptopurine

methotrexate second line

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86
Q

What is the investigation of choice for suspected perianal fistulae?

A

MRI

looks for abscess and whether simple (low) or complex (high fistula)

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87
Q

What is the difference between a simple and complex perianal fistula?

A

simple is a low fistula, complex is a high fistula that passes through or above muscle layers

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88
Q

What are the management options for perianal fistulae in CD?

A
  • oral metronidazole
  • anti-TNF e.g. infliximab - good for closing
  • draining seton - for complex fistulae
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89
Q

When is platelet transfusion indicated in UGIB?

A

active bleeding + platlet count <50

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90
Q

What is an aorto-enteric fistula?

A

in previous abdominal aortic aneurysm surgery, aorto-enteric fistulation is rare but important cause of major haemorrhage

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91
Q

What should be given in UGIB for patient on warfarin?

A

IV prothrombin complex concentrate

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92
Q

How is induction of remission done in UC in general?

A

Mild-moderate:
- If distal disease - rectal 5ASA
- If disease more extensive topical + oral 5ASA
( -> oral 5ASA -> steroid)
Severe:
- IV steroid (ciclosporin if CI)

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93
Q

How is remission maintained in UC?

A

Oral 5ASA or oral +-topical (sometimes topical alone)

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94
Q

What is the drug used to maintain remission in UC if there has been a severe relapse or 2 or more in the last year?

A

Azathioprine or mercaptopurine (NOT methotrexate)

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95
Q

How is the severity of a UC flare graded?

A

Truelove and Witts
- mild - <4 stools per day, only small amount of blood
- moderate - 4-6 stools/day, varying blood, no systemic upset
- severe - >6 stools/day, systemic upset

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96
Q

What type of virus is hepatitis C?

A

RNA Flavivirus

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97
Q

Is breastfeeding contraindicated in mothers with hepatitis C?

A

No

98
Q

What proportion of patients develop symptoms after exposure to hepatitis C virus?

A

30%

99
Q

What are the symptoms of hepatitis C virus?

A

Transient rise in serum aminotransferases, jaundice, fatigue, arthralgia

100
Q

What is the investigation for hepatitis C?

A

serum HCV RNA

101
Q

What does the presence of HCV antibodies indicate?

A

Current or previous HCV infection

102
Q

What is the definition of chronic hepatitis C infection?

A

Persistence of HCV RNA for >6 months

103
Q

What are 7 complications of chronic HCV?

A
  1. Rheum: arthralgias, arthritis
  2. Sjögren’s syndrome
  3. Cirrhosis
  4. HCC
  5. Cryoglobulinaemia
  6. Porphyria cutanea tarda
  7. Membranoproliferative glomerulonephritis
104
Q

What is the treatment of chronic HCV?

A

Depends on viral genotype - treated with combination of protease inhibitors (daclatasvir + sofosbuvir or sofosbuvir + simeprevir) +- ribavirin

105
Q

What is the goal of treatment of HCV?

A

Sustained virological response (SVR) - undetectable serum HCV RNA 6 months after end of treatment

106
Q

What are 3 side effects of ribavirin (used to treat HCV)?

A
  1. Cough
  2. Haemolytic anaemia
  3. Teratogenic - shouldn’t conceive within 6 months of stopping treatment
107
Q

What are 5 side effects of interferon alpha (used to treat HCV in the past)?

A
  1. Flu like symptoms
  2. Depression
  3. Fatigue
  4. Leukopenia
  5. Thrombocytopenia
108
Q

What are 5 side effects of interferon alpha (used to treat HCV in the past)?

A
  1. Flu like symptoms
  2. Depression
  3. Fatigue
  4. Leukopenia
  5. Thrombocytopenia
109
Q

What is the presentation of bile-acid malabsorption?

A

chronic diarrhoea - steatorrhoea, and vitamin ADEK malabsorption

110
Q

What are 6 causes of bile-acid malabsorption?

A
  1. Primary: excessive production of bile acid
  2. ileal disease e.g. Crohn’s
  3. cholecystectomy - disturbs cycle of bile release + reabsorption - too much bile progresses to large intestine
  4. coeliac disease
  5. small intestinal bacterial overgorwith
111
Q

What is the test of choice to diagnose bile-acid malabsorption?

A
  • SeHCAT - nuclear medicine test (gamma-emitting selenium molecule in selenium homocholic acid taurine or taroselcholic acid)
  • scans done 7 days apart to assess retention/loss of radiolabelled SeHCAT
112
Q

What is the management of bile-acid malabsorption?

A

bile acid sequestrants e.g. cholestyramine

113
Q

How does cholestyramine work to treat bile-acid malabsorption?

A

binds to bile acids in the small intestine and promotes reabsorption into cycle of bile acid production

114
Q

What are 3 criteria for referral for urgent endoscopy for oesophageal / gastric cancer?

A
  1. dysphagia
  2. upper abdominal mass
  3. age >55y with weight loss AND: upper abdo pain/ reflux / dyspepsia
115
Q

What are 2 criteria for endoscopy for gastric/oesophageal cancer?

A
  1. haematemesis
  2. aged >55y AND: treatment-resistant dyspepsia OR upper abdo pain and low Hb OR raised platelets OR nausea or vomiting + weight loss / reflux / dyspepsia / upper abdo pain
116
Q

What are 3 steps for the management of patients who have undiagnosed dyspepsia but don’t meet the referral criteria for OGD?

A
  1. review medications for cause
  2. lifestyle advice
  3. full dose PPI for 4 weeks OR test and treat for H pylori
117
Q

What is the test for H pylori eradication, if performed?

A

carbon-13 urea breath test

118
Q

What are 4 situations H. pylori re-testing after treatment can be considered?

A
  1. poor compliance to eradication therapy
  2. aspirin or NSAID indicated
  3. family history of gastric malignancy
  4. person requests re-testing
119
Q

If re-testing after H pylori eradication is performed, when should it be done?

A

8 weeks after initial eradication therapy

120
Q

What is the genetic abnormality that causes Wilson’s disease?

A

defect in ATP7B gene on chromosome 13

121
Q

What is usual onset of symptoms of Wilson’s disease?

A

10-25 years

children present with liver disease, young adults - neurological

122
Q
A
123
Q

What are 7 features of Wilson’s disease?

A
  1. hepatitis, cirrhosis
  2. basal ganglia degeneration
  3. speech, behavioural and psychiatric problems
  4. asterixis, chorea, dementia, parkinsonism
  5. Kayser-Fleischer rings
  6. renal tubular acidosis (esp. Fanconi syndrome)
  7. haemolysis
  8. blue nails
124
Q

Where in the brain is most copper deposited in Wilson syndrome?

A

basal ganglia - particularly putamen and globus pallidus

125
Q

What is the cause of Kayser-Fleischer rings?

A

green-brown rings in the periphery of the iris due to copper accumulation in Descemet membrane

126
Q

What will serum caeruloplasmin and total serum copper show in Wilson’s disease?

A
  • caeruloplasmin: reduced
  • copper: reduced (95% of plasma copper carried by caeruloplasmin; free copper increased_
127
Q

What will 24h urinary copper excretion show in Wilson’s?

A

increased copper excretion

128
Q

How is a diagnosis of Wilson’s disease confirmed?

A

genetic analysis of ATP7B gene

129
Q

What are 3 options for the treatment of Wilson’s disease?

A
  1. penicillamine (copper chelator)
  2. trientine hydrochloride - alternative
  3. tetrahiomolybdate - newer, under ix
130
Q

What is the AST:ALT ratio in alcoholic hepatitis?

A

AST:ALT is 2:1

alcoholics sip tequila

131
Q

What are 2 possible aspects of the management of alcoholic hepatitis?

A
  1. steroids
  2. pentoxyphylline
132
Q

How is a decision to use steroids in alcoholic hepatitis made?

A

based on Maddrey’s Discriminant Function (MDF) (based on prothrombin time, bilirubin)

133
Q

Which gene is responsible for hereditary haemochromatosis?

A

HFE gene on both copies of chromosome 6

134
Q

What are the early symptoms of hereditary haemochromatosis?

A

fatigue, erectile dysfunction, arthralgia (often hands)

135
Q

What are 2 complications of hereditary haemochromatsis which are reversible with treatment?

A
  1. cardiomyopathy
  2. skin pigmentation
136
Q

What are 4 features of hereditary haemochromatosis which are not reversible with treatment?

A
  1. liver cirrhosis
  2. diabetes mellitus
  3. hypogonadotrophic hypogonadism
  4. arthropathy
137
Q

What is the inheritance pattern of Peutz-Jeghers syndrome?

A

autosomal dominant

responsible gene encodes serine threonine kinase LKB1 or STK11

138
Q

What are the key features of Peutz-Jeghers syndrome?

A
  • hamartomatous polyps in GI tract (mainly small bowel)
  • pigmented lesions on lips, oral mucosa, face, palms, soles
139
Q

What complications may patients with Peutz-Jeghers syndrome develop?

A
  • GI bleeding
  • small bowel obstruction - commonest presenting complaint (often due to insussusception)
  • malignancy - not from polyps but other forms of GI cancer
140
Q

What is the management of Peutz-Jeghers syndrome?

A

conservative unless complications develop

141
Q

What is the first line abx to treat campylobacter enteritis?

A

clarithromycin

142
Q

What is the first line abx to treat non-typhoid salmonella?

A

ciprofloxacin

143
Q

What is the first line abx to treat shigellosis?

A

ciprofloxacin

144
Q

What imaging may be performed in suspected PBC?

A

RUQ US or MRCP to exclude extrahepatic biliary obstruction

145
Q

What is the commonset cause of travellers’ diarrhoea?

A

E coli

146
Q

What are 4 aspects of the management of PBC?

A
  1. ursodeoxycholic acid - first line
  2. cholestyramine for purutius
  3. fat soluble vitamin supplementation
  4. liver transplant if bili >100
147
Q

What are the features of E coli diarrhoea?

A

watery stools, abdominal cramps and nausea

148
Q

What is the presentation of giardiasis?

A

prolonged, non-bloody diarrhoea

149
Q

What is the presentation of cholera?

A

profuse, watery diarrhoea; severe dehydration resulting in weight loss; (not common amongst travellers)

150
Q

Which 2 bacterial causes of diarrhoea have a short incubation period (1-6h)?

A

Staphylococcus aureus, Bacillus cereus

151
Q

What is the presentation of Staphylococcus aureus GI infection?

A

severe vomiting with short incubation period

152
Q

What are the clinical features of GI campylobacter infection?

A
  • flu-like prodrome (headache, malaise) followed by crampy abdo pains, fever, diarrhoea - may be bloody
  • abdo pain - may mimic appendicitis
153
Q

What are the 2 types of illness seen with GI Bacillus cereus?

A
  1. vomiting within 6 hours, stereotypically due to rice
  2. diarrhoeal illness occurring after 6h
154
Q

```

~~~

What is the typical presentation of amoebiasis?

A

gradual onset bloody diarrhoea, abdominal pain and tenderness which may last for several weeks

155
Q

What are 2 types of diarrhoeal illness with an incubation period >7days?

A
  • giardiasis (non bloody)
  • amoebiasis (bloody)
156
Q

What molecular genetic testing may be performed for haemochromatosis?

A

C282Y and H63D

157
Q

What are 4 further tests in addition to transferrin saturation and ferritin that may be used to investigate hereditary haemochromatosis?

A
  1. liver function tests
  2. molecular genetic testing
  3. MRI - to quantif liver and/or cardiac iron
  4. liver biopsy - only if suspected cirrhosis
158
Q

Which 2 blood tests are most important in monitoring hereditary haemochromatosis?

A
  1. transferrin saturation - aiming for <50%
  2. ferritin - aiming <50 ug/L
159
Q

What is the first and second-line treatment of hereditary haemochromatosis?

A
  1. first line: venesection
  2. 2nd: desferrioxamine
160
Q

What is Barrett’s oesophagus?

A

metaplasia of lower oesophageal mucosa, usual squamous epithelium is replaced by columnar epithelium

Simple to Cancer

161
Q

What is the risk associated with Barrett’s oesophagus?

A

risk of oesphageal adenocarcinoma 50-100x

162
Q

How is Barrett’s oesophagus subdivided and WHY?

A

short (<3cm) and long (>3cm) - correlates with chances of identifying metaplasia

163
Q

What are 4 risk factors for Barrett’s oesophagus?

A
  1. GORD
  2. male gender
  3. smoking
  4. central obesity
164
Q

What are 3 aspects of the management of Barrett’s oesopahgus?

A
  1. High-dose PPI
  2. Endoscopic surveillance with biopsies
  3. If dysplasia identifies: radiofrequency ablation / endoscopic mucosal resection
165
Q

How often is endoscopic surveillance of Barrett’s oesophagus recommended in patients with metaplasia (but no dysplasia)?

A

every 3-5 years

166
Q

What is the chemical name for vitamin A and what are the symptoms of a deficiency state?

A
  • retinoids
  • night-blindness (nyctalopia)
167
Q

What is the chemical name for vitamin B1 and what are the symptoms of a deficiency state?

A
  • thiamine
  • beriberi: polyneuropathy, Wernicke-Korsakoff’s syndrome, heart failure
168
Q

What is the chemical name for vitamin B3 and what are the symptoms of a deficiency state?

A
  • niacin
  • pellagra - dermatitis, diarrhoea, dementia
169
Q

What is the chemical name for vitamin B6 and what are the symptoms of a deficiency state?

A
  • pyridoxine
  • deficiency state: anaemia, irritability, seizures
170
Q

What is the chemical name for vitamin B7 and what are the symptoms of a deficiency state?

A
  • biotin
  • dermatitis, seborrhoea
171
Q

What is the chemical name for vitamin B9 and what are the symptoms of a deficiency state?

A
  • folic acid
  • megaloblastic anaemia, neural tube defects (pregnancy)
172
Q

What is the chemical name for vitamin B12 and what are the symptoms of a deficiency state?

A
  • cyanocobalamin
  • megaloblastic anaemia, peripheral neuropathy
173
Q

What is the chemical name for vitamin C and what are the symptoms of a deficiency state?

A
  • ascorbic acid
  • scurvy: gingivitis, bleeding e.g. gums
174
Q

What is the chemical name for vitamin D and what are the symptoms of a deficiency state?

A
  • ergocalciferol, cholecalciferol
  • rickets, osteomalacia
175
Q

What is the chemical name for vitamin E and what are the symptoms of a deficiency state?

A
  • tocopherol, tocotrienol
  • mild haemolytic anaemia in newborns, ataxia, peripheral neuropathy
176
Q

What is the chemical name for vitamin K and what are the symptoms of a deficiency state?

A
  • naphthoquinone
  • haemorrhagic disease of newborn, bleeding diathesis
177
Q

When is drug treatment indicated in campylobacter infection?

A
  • severe symptoms - high fever, bloody diarrhoea, >8 stools / day
  • symptoms > 1 week
  • immunocompromised patient
178
Q

What are the BMI categories?

A
  • Underweight < 18.5
  • Normal 18.5 - 25
  • Overweight: 25-30
  • Obese I: 30-35
  • Clinically obese (II): 35-40
  • Morbidly obese (III): >40
179
Q

What is the most common organism found on ascitic fluid culture in SBP?

A

E. coli

180
Q

What is diagnostic of SBP?

A

ascitic paracentesis neutrophils >250

181
Q

What is the management of SBP?

A

IV cefotaxime

182
Q

What is given as prophylaxis for SBP?

A

ciprofloxacin or norfloxacin

183
Q

What are the indications for SBP prophylaxis?

A
  1. previous episode SBP
  2. fluid protein < 15 g/L and Child Pugh at least 9 or HRS
184
Q

hat are the

What is achalasia?

A

failure of oesophageal peristalsis and relaxation of LOS due to degenerative loss of ganglia from Auerbach’s plexus - LOS contracted and oesophagus above dilated

185
Q

What will barium swallow show in achalasia?

A

grossly expanded oesophagus, fluid level, ‘bird’s beak’ appearance

186
Q

What is the most important diagnostic test for achalasia?

A

oesophageal manometry - excessive LOS tone which doesn’t relax on swallowing

187
Q

What is the first-line treatment for achalasia?

A

pneumatic (balloon) dilation

188
Q

What treatments are available for achalasia if a) they have recurrent or persistent symptoms despite pneumatic dilation b) they are high surgical risk?

A
  • a) Heller cardiomyotomy
  • b) intra-sphincteric injection of botulinum toxin
189
Q

What is acrodermatitis enteropathica?

A

recessively inherited partial defect in intestinal zinc absorption.

190
Q

Which patients may develop zinc deficiency?

A

patients with anorexia nervosa

191
Q

What is likely to cause a bloody infectious diarrhoea after a barbecue?

A

Campylobacter

192
Q

What are the blood test features of alcohol ketoacidosis?

A
  • metabolic acidosis
  • raised anion gap
  • ketonaemia
  • normal capillary blood glucose
193
Q

What is the management of alcoholic ketoacidosis?

A

IVF and thiamine infusion

194
Q

What are 4 extraintestinal IBD features that are related to disease activity?

A
  1. Arthritis: pauciarticular, asymmetric
  2. Episcleritis
  3. Erythema nodosum
  4. Osteoporosis
195
Q

What are 5 extraintestinal features of IBD that are unrelated to disease activity?

A
  1. Arthritis: polyarticular, symmetrical
  2. Uveitis
  3. Pyoderma gangrenosum
  4. Clubbing
  5. Primary sclerosing cholangitis
196
Q

Of episcleritis / uveitis which is more common in CD / UC?

A
  • Episcleritis - more common in CD
  • Uveitis - more common in UC
197
Q

What is the most common extraintestinal feature in IBD?

A

arthritis

198
Q

Is PSC more common in CD or UC?

A

UC

199
Q

What are the 3 types of autoimmune hepatitis (antibodies + age)?

A
  • Type I: ANA and/or SMA, affects both adults and children
  • Type II: anti-liver/kidney microsomal type 1 antibodies (LKM1) , affects children
  • Type III: soluble liver-kidney antigen, affects adults in middle age
200
Q

What are 4 features common in autoimmune hepatitis?

A
  1. signs of CLD
  2. acute hepatitis: fever, jaundice (25%)
  3. amenorrhoea - common
  4. ANA / SMA / LKM1 antibodies, raised IgG
201
Q

What will be seen on biopsy in autoimmune hepatitis?

A

inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis

202
Q

What are the management options for autoimmune hepatitis?

A
  • steroids
  • other immunsuppressants e.g. azathioprine
  • liver transplant
203
Q

Which neurotransmitters are involved in the alcohol withdrawal response?

A

decreased inhibitory GABA and increased NMDA glutamate transmission (normally chronic alcohol consumption enhances GABA mediated inhibition in CNS and inhibits glutamate receptors)

204
Q

What is the peak incidence of seizures during alcohol withdrawal?

A

36 hours

205
Q

What is the peak incidence of delirium tremens after alcohol withdrawal?

A

48-72h

206
Q

Which patients withdrawing from alcohol should be admitted to hospital?

A

complex withdrawals e.g. delirium tremens, seizures, blackouts

207
Q

Which benzodiazepine for alcohol withdrawal may be needed in liver failure?

A

lorazepam

208
Q

What are 5 causes of raised ferritin without iron overload?

A
  1. inflammation
  2. alcohol excess
  3. liver disease
  4. chronic kidney disease
  5. malignancy
209
Q

What is the best way to assess whether iron overload is present with increased ferritin?

A

transferrin saturation

210
Q

What are 2 standard diagnostic investigations for PSC and what will they show?

A
  • ERCP or MRCP
  • multiple biliary strictures - beaded appearance
211
Q

Which blood test may be positive in PSC?

A

p-ANCA

212
Q

Waht may be seen on liver biopsy in PSC?

A

fibrous, obliterative cholangitis - onion skin

213
Q

What are 2 complications of PSC?

A
  1. cholangiocarcinoma
  2. colorectal cancer
214
Q

What are 2 types of hiatus hernia?

A
  1. sliding (95%) - GOJ moves above diaphragm
  2. rolling (paroesophageal): GOJ remains below diaphragm but separate part of stomach herniates through
215
Q

What are 2 risk factors for hiatus hernia?

A
  • obesity
  • increased intraadominal pressure - ascites, multiparity
216
Q

What is the most sensitive test for hiatus hernia? What is often done first line?

A

barium swallow - many patients have endoscopy on 2ww first due to symptoms

217
Q

What is the approach to management of hiatus hernias?

A
  • conservative management - weight loss
  • medical: PPI
  • surgical: fundoplication only has role in symptomatic paraoesophageal (rolling) hernias
218
Q

What is the period from infection to developing symptoms of norovirus?

A

15 - 50 hours

219
Q

Is norovirus a notifiable disease in the UK?

A

no

220
Q

How is a diagnosis of norovirus made?

A

clinical history and stool culture viral PCR

221
Q

What are 3 differences between E coli and norovirus gastroenteritis?

A
  • E coli has longer incubation period (3-4 days, up to 10 days)
  • E coli commonly causes severe abdo cramping
  • E coli frequently causes bloody diarrhoea, noro does not
222
Q

How long do norovirus symptoms typically resolve after?

A

72h

223
Q

What is an association with cyclical vomiting syndrome?

A
  • migraines - also present in 80% of children and 25% adults
224
Q

What is the typical history in cyclical vomiting syndrome?

A
  • severe nausea and sudden vomiting lasting hours to days
  • prodromal intense sweating and nausea
  • well in between episodes
225
Q

How is a diagnosis of cyclical vomiting syndrome made?

A
  • clinical diagnosis
  • pregnancy test in women
  • routine blood tests to exclude other aetiologies
226
Q

What are 3 drugs which can be given as prophylaxis in cyclical vomiting syndrome?

A
  1. amitriptyline
  2. propranolol
  3. topiramate
227
Q

What are 3 drugs which can be used in cyclical vomiting syndrome?

A
  1. ondansetron
  2. prochlorperazine
  3. triptans
228
Q

What are 6 complications of hepatitis B infection?

A
  1. chronic hepatitis
  2. fulminant liver failure
  3. hepatocellular carcinoma
  4. glomerulonephritis
  5. polyarteritis nodosa
  6. cryoglobulinaemia
229
Q

What are 5 risk factors for responding poorly to 3 doses of the hepatitis B vaccine?

A
  1. age > 40 years
  2. obesity
  3. smoking alcohol excess
  4. immunosuppression
230
Q

What should be done in someone who has had a course of 3 doses of hepatitis B vaccine and anti-HBs level is 10-100?

A

one additional vaccine dose should be given

231
Q

What should be done in someone who has had a course of 3 doses of hepatitis B vaccine and anti-HBs level is < 10?

A
  • non-responder - test for current or past infection
  • give further course (i.e. further 3 doses) with testing following
  • if fails to resopnd, HBIG would be required for protection if exposed to the virus
232
Q

What are 4 types of drugs which can be used first-line to treat hepatitis B?

A
  1. pegylated interferon-alpha
  2. tenofovir
  3. entecavir
  4. telbivudine
233
Q

What are 6 infectious causes of bloody diarrhoea?

A
  1. salmonella
  2. shigella
  3. campylobacter jejuni
  4. Yersinia enterocolitica
  5. E. coli
  6. Entamoeba histolytica
234
Q

What is the guidance regarding antibiotics in acute pancreatitis?

A

Should NOT give prophylactic antibiotics - could cause infected pancreatic necrosis

235
Q

What products should be avoided by patients with coeliac disease?

A
  • wheat
  • barley
  • rye
  • spelt
  • kamut
  • triticale

maize is OK

236
Q

What is the first line antibiotic management of acute uncomplicated diverticulitis?

A

co-amoxiclav

237
Q

What are 2 drug options for achalasia and what limits their use?

A
  • nitrates, CCBs
  • side-effects
238
Q

What are 7 features of zinc deficiency?

A
  1. acrodermatitis - red, crusted lesions periorally and perianally
  2. alopecia
  3. short stature
  4. hypogonadism
  5. hepatosplenomegaly
  6. geophagia (ingesting clay/soil)
  7. cognitive impairment
239
Q

What will CXR show in achalasia?

A

wide mediastinum, fluid level

240
Q

What is the classical presentation of achalasia?

A

dysphagia of BOTH liquids and solids at same time; heartburn, regurgtation

241
Q

What are 5 risk factors for squamous cell oesophageal cancer?

A
  1. smoking
  2. alcohol
  3. achalasia
  4. Plummer-Vinson syndrome
  5. diets rich in nitrosamines
242
Q

What options are available if ELF testing is not available to investigate NAFLD (diagnosis + monitoring)?

A

FIB4 score or NAFLD fibrosis scan +- FibroScan

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