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MRCP: Gastro > General > Flashcards

General Flashcards

1
Q

Features of peptic ulcer disease?

A

Duodenal ulcers: more common than gastric ulcers, epigastric pain relieved by eating
Gastric ulcers: epigastric pain worsened by eating
Features of upper gastrointestinal haemorrhage may be seen (haematemesis, melena etc)

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2
Q

Features of appendicitis?

A

Pain initial in the central abdomen before localising to the right iliac fossa
Anorexia is common
Tachycardia, low-grade pyrexia, tenderness in RIF
Rovsing’s sign: more pain in RIF than LIF when palpating LIF

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3
Q

Features of pancreatitis?

A

Usually due to alcohol or gallstones
Severe epigastric pain
Vomiting is common
Examination may reveal tenderness, ileus and low-grade fever
Periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign) is described but rare

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4
Q

Features of biliary colic?

A

Pain in the RUQ radiating to the back and interscapular region, may be following a fatty meal.
Obstructive jaundice may cause pale stools and dark urine

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5
Q

Features of acute cholecystitis?

A

Continuous RUQ pain
Fever, raised inflammatory markers and white cells
Murphy’s sign positive (arrest of inspiration on palpation of the RUQ)

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6
Q

Features of diverticulitis?

A

Colicky pain typically in the LLQ
Fever, raised inflammatory markers and white cells

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7
Q

What is the pathophysiology behind achalasia?

A

Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS)
Degenerative loss to Auerbach plexus
LOS remains contracted - oesophagus dilated

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8
Q

Features of achalasia?

A

dysphagia of BOTH liquids and solids
typically variation in severity of symptoms
heartburn
regurgitation of food
may lead to cough, aspiration pneumonia etc
malignant change in small number of patients

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9
Q

Investigations of achalasia?

A

oesophageal manometry - most important diagnostic test
Barium swallow - bird beak
CXR - widened mediastinum - fluid level

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10
Q

Treatment of achalasia?

A

Pneumatic balloon dilation - first line option

Heller cardiomyotomy should be considered if recurrent or persistent symptoms

Drug therapy has a limited role ( calcium channel blockers - nitrates)

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11
Q

Pathogenesis of appendicitis?

A

lymphoid hyperplasia or a faecolith → obstruction of appendiceal lumen → gut organisms invading the appendix wall → oedema, ischaemia +/- perforation

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12
Q

Why does pain change in appendicitis?

A

Peri-umbilcial pain: visceral stretching of appendix lumen and appendix is midgut structure
RIF pain: Localised parietal peritoneal inflammation.

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13
Q

What is the strongest indicator for appendicitis?

A

Lateralisation of pain

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14
Q

Causes of acute liver failure?

A

paracetamol overdose
alcohol
viral hepatitis (usually A or B)
acute fatty liver of pregnancy

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15
Q

Features of acute liver failure?

A

jaundice
coagulopathy: raised prothrombin time
hypoalbuminaemia
hepatic encephalopathy
renal failure is common (‘hepatorenal syndrome’)

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16
Q

What is the pathophysiology of pancreatitis?

A

autodigestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis

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17
Q

Features of acute pancreatitis?

A

severe epigastric pain that may radiate through to the back
vomiting is common
examination may reveal epigastric tenderness, ileus and low-grade fever
periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign) is described but rare

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18
Q

What is a rare ophthalmic complication of pancreatitis?

A

ischaemic (Purtscher) retinopathy - may cause temporary or permanent blindness

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19
Q

Causes of amylase rise?

A

Pancreatic pseudocyst
Mesenteric infarct
Perforated viscus
Acute cholecystitis
Diabetic ketoacidosis

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20
Q

For pancreatitis prognosis what tests need to be scored?

A

age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST

** amylase level is not prognostic

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21
Q

Cause of pancreatitis?

A

GET SMASHED

Gallstones
Ethanol
Trauma

Steroids
Mumps (other viruses include Coxsackie B)
Autoimmune (e.g. polyarteritis nodosa), Ascaris infection
Scorpion venom
Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
ERCP
Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)

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22
Q

Complications of pancreatitis?

A

Acute respiratory distress syndrome
Pseudocyst
Pancreatitic necrosis
Pancreatic abscess
Haemorrhage
Peripancreatic fluid collection

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23
Q

Management of peripancreatic fluid collections?

A

Best leave alone - most resolve. Do not want to introduce infection

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24
Q

Features of pancreatic pseudocyst?

A

collection is walled by fibrous or granulation tissue and typically occurs 4 weeks or more after an attack of acute pancreatitis
Symptomatic cases may be observed for 12 weeks as up to 50% resolve
Treatment is either with endoscopic or surgical cystogastrostomy or aspiration

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25
Q

Features of acute upper GI bleed?

A

Haematemasis
Melena
Raised urea
Diagnosis associated with GI bleed:
- Varices
- Peptic ulcer disease

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26
Q

Characterise bleeding from oesophageal varices?

A

Large volume fresh blood
Likely to rebleed
Associated haemodynamic collapse

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27
Q

Characterise bleeding from oesphagitis?

A

Small volume of fresh blood, often streaking vomit. Malena rare. Often ceases spontaneously. Usually history of antecedent GORD type symptoms.

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28
Q

Characterise bleeding from mallory Weiss tear?

A

Typically brisk small to moderate volume of bright red blood following a bout of repeated vomiting. Malena rare. Usually ceases spontaneously.

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29
Q

How should a UGI bleed be scored?

A

the Glasgow-Blatchford score at first assessment
helps clinicians decide whether patient patients can be managed as outpatients or not

the Rockall score is used after endoscopy
provides a percentage risk of rebleeding and mortality
includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage

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30
Q

In major haemorrhage what parameters for FFP and platelets?

A

If platelets < 50 - transfuse platelets
If fibrinogen < 1 - transfuse FFP
If INR > 1.5 normal - transfuse FFP
Prothrombin complex issue to those on warfarin

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31
Q

Management to non-variceal bleeds?

A

Give PPI after endoscopy

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32
Q

Management of vatical bleeding?

A

terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy)

Surgical options:
band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices
transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures

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33
Q

What is alcoholic ketoacidosis?
Mechanism?

A

non-diabetic euglycaemic form of ketoacidosis. It occurs in people who regularly drink large amounts of alcohol

Once the person becomes malnourished, after an alcohol binge the body can start to break down body fat, producing ketones

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34
Q

Features of alcoholic ketoacidosis?

A

Metabolic acidosis
Elevated anion gap
Elevated serum ketone levels
Normal or low glucose concentration

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35
Q

Treatment of alcoholic ketoacidosis?

A

infusion of saline & thiamine. Thiamine is required to avoid Wernicke encephalopathy or Korsakoff psychosis.

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36
Q

Features of alcoholic related liver disease?

A

gamma-GT is characteristically elevated
the ratio of AST:ALT is normally > 2, a ratio of > 3 is strongly suggestive of acute alcoholic hepatitis

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37
Q

Management of alcoholic hepatitis?

A
  1. Glucocorticoids
    - Maddrey’s discriminant function (DF) is often used during acute episodes to determine who would benefit from glucocorticoid therapy
  2. Pentoxyphylline
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38
Q

Mechanism of 5-ASA?

A

Endogenous production of enterocytes, produce 5-ASA to reduce inflammation
Unclear mechanism

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39
Q

Side effects of sulphasalazine?

A

rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis
see other side effects with mesalazine

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40
Q

Side effects of mesalazine?

A

GI upset, headache, agranulocytosis, pancreatitis*, interstitial nephritis

Pancreatitis 7 time more likely than sulphasalazine

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41
Q

Risk factors for anal cancer?

A

HPV infection - strongest risk factor
Men sex with men
HIV
High number of sexual partners
Women with a history of cervical cancer or cervical intraepithelial neoplasia (CIN) are also at greater risk of anal cancer.
Immunosuppressive drugs used in transplant recipients increase the risk of anal cancer.
Smoking is also a risk factor.

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42
Q

Features of anal cancer?

A

Perianal pain, perianal bleeding
A palpable lesion
Faecal incontinence
A neglected tumour in a female may present with a rectovaginal fistula.

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43
Q

Staging for anal cancer?

A

TX primary tumour cannot be assessed
T0 no evidence of primary tumour
Tis carcinoma in situ
T1 tumour 2 cm or less in greatest dimension
T2 tumour more than 2 cm but not more than 5 cm in greatest dimension
T3 tumour more than 5 cm in greatest dimension
T4 tumour of any size that invades adjacent organ(s) - for example, vagina, urethra, bladder (direct invasion of the rectal wall, perirectal skin, subcutaneous tissue, or the sphincter muscle(s) - is not classified as T4)

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44
Q

Definition of anal fissure ?

A

Anal fissures are longitudinal or elliptical tears of the squamous lining of the distal anal canal. If present for less than 6 weeks they are defined as acute, and chronic if present for more than 6 weeks.

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45
Q

Risk factors for anal fissure?

A

constipation
inflammatory bowel disease
sexually transmitted infections e.g. HIV, syphilis, herpes

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46
Q

Features of anal fissure?

A

painful, bright red, rectal bleeding
around 90% of anal fissures occur on the posterior midline.

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47
Q

Management of anal fissure?

A

If < 1 week:
soften stool
dietary advice: high-fibre diet with high fluid intake
bulk-forming laxatives are first-line - if not tolerated then lactulose should be tried
lubricants such as petroleum jelly may be tried before defecation
topical anaesthetics
analgesia

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48
Q

Management of chronic anal fissure?

A

topical glyceryl trinitrate (GTN) is first-line treatment for a chronic anal fissure

If not closed within 8 weeks - for referral for sphincterotomy

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49
Q

Investigation of angiodysplasia?

A

colonoscopy
mesenteric angiography if acutely bleeding

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50
Q

Mnx of angiodysplasia?

A

endoscopic cautery or argon plasma coagulation
antifibrinolytics e.g. Tranexamic acid

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51
Q

Features of ascending cholangitis?

A

Triad:
- Fever
- Jaundice
- RUQ pain

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52
Q

What is Charcot’s pentad?

A

fever is the most common feature, seen in 90% of patients
RUQ pain 70%
jaundice 60%
hypotension and confusion are also common (the additional 2 factors in addition to the 3 above make Reynolds’ pentad)

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53
Q

Cause of ascending cholangitis?

A

Ascending cholangitis is a bacterial infection (typically E. coli) of the biliary tree. The most common predisposing factor is gallstones.

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54
Q

Best investigation for ascneindg cholangitis ?

A

Ultrasound for ? obstruction

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55
Q

How should ascites be classified?

A

serum-ascites albumin gradient (SAAG) <11 g/L or a gradient >11g/L

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56
Q

Causes of ascites > 11 g/l ?

A

Liver disorders are the most common cause
cirrhosis/alcoholic liver disease
acute liver failure
liver metastases

Cardiac
right heart failure
constrictive pericarditis

Other causes
Budd-Chiari syndrome
portal vein thrombosis
veno-occlusive disease
myxoedema

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57
Q

Causes of ascites <11 g/l?

A

Hypoalbuminaemia
nephrotic syndrome
severe malnutrition (e.g. Kwashiorkor)

Malignancy
peritoneal carcinomatosis

Infections
tuberculous peritonitis

Other causes
pancreatitisis
bowel obstruction
biliary ascites
postoperative lymphatic leak
serositis in connective tissue diseases

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58
Q

Management of ascites?

A

Reduce dietary sodium
Spironolactone
Abdominal paracentesis
Prophylactic antibiotic - if qualify

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59
Q

Who would get prophylactic antibiotics with ascites?

A

Protein levle < 15 g/l

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60
Q

Immunology of type 1 autoimmune hepatitis?

A

Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA)

Affects both adults and children

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61
Q

Immunology of type 2 autoimmune hepatitis?

A

Anti-liver/kidney microsomal type 1 antibodies (LKM1)

Affects children only

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62
Q

Immunology of type 3 autoimmune hepatitis?

A

Soluble liver-kidney antigen

Affects adults in middle-age

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63
Q

HLA type association in autoimmune hepatitis?

A

HLA B8, DR3.

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64
Q

Features of autoimmune hepatitis?

A

may present with signs of chronic liver disease
acute hepatitis: fever, jaundice etc (only 25% present in this way)
amenorrhoea (common)
ANA/SMA/LKM1 antibodies, raised IgG levels
liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis

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65
Q

Management of autoimmune hepatitis?

A

Steroids
Liver transplant

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66
Q

What is the pathology in barret’s oesophagus?

A

metaplasia of the lower oesophageal mucosa
ncreased risk of oesophageal adenocarcinoma, estimated at 50-100 fold in cancer

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67
Q

How should barret’s oesophagus be divided?

A

< 3 cm
> 3 cm

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68
Q

Risk factors of Barrett’s oesophagus?

A

gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
male gender (7:1 ratio)
smoking
central obesity

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69
Q

Management of Barrett’s oesophagus?

A

High dose PPI
Endoscopic surveillance every 3-5 years

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70
Q

Management of Barrett’s oesophagus when dysplasia is demonstrated?

A

radiofrequency ablation: preferred first-line treatment, particularly for low-grade dysplasia
endoscopic mucosal resection

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71
Q

How can bile acid malabsorption cause chronic diarrhoea?

A
  1. Excessive bile acid production
  2. Reduced bile acid absorption from Gi tract
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72
Q

What vitamin deficiencies can bile acid malabsorption lead to?

A

A D E K

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73
Q

Secondary causes of bile acid malabsorption?

A

cholecystectomy
coeliac disease
small intestinal bacterial overgrowth

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74
Q

Investigations for bile acid malabsorption?

A

SeHCAT ( Sea cat) test
- nuclear medicine test

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75
Q

Management of bile acid malabsorption?

A

bile acid sequestrants e.g. cholestyramine

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76
Q

What is Budd-chiari syndrome ?

A

Budd-Chiari syndrome, or hepatic vein thrombosis, is usually seen in the context of underlying haematological disease or another procoagulant condition.

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77
Q

Causes of Budd-chiari syndrome?

A

polycythaemia rubra vera
thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies
pregnancy
combined oral contraceptive pill: accounts for around 20% of cases

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78
Q

Features of Budd-chiair syndrome?

A

abdominal pain: sudden onset, severe
ascites → abdominal distension
tender hepatomegaly

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79
Q

Best investigations for Budd Chiari?

A

ultrasound with Doppler flow studies is very sensitive and should be the initial radiological investigation

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80
Q

What are the features of carcinoid syndrome?

A

flushing (often the earliest symptom)
diarrhoea
bronchospasm
hypotension
right heart valvular stenosis (left heart can be affected in bronchial carcinoid)
other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing’s syndrome
pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour

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81
Q

Investigations for carcinoid syndrome?

A

urinary 5-HIAA
plasma chromogranin A y

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82
Q

Management of carcinoid syndrome?

A

Management
somatostatin analogues e.g. octreotide
diarrhoea: cyproheptadine may help

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83
Q

What is carcinoid syndrome?

A

when metastases are present in the liver and release serotonin into the systemic circulation
may also occur with lung carcinoid as mediators are not ‘cleared’ by the liver

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84
Q

Features of cholangiocarcinoma?

A

Bile duct cancer

  • persistent biliary colic symptoms
  • associated with anorexia, jaundice and weight loss
  • a palpable mass in the right upper quadrant (Courvoisier sign)
  • periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen
  • raised CA 19-9 levels
    often used for detecting cholangiocarcinoma in patients with primary sclerosing cholangitis
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85
Q

What eponymous signs are seen in cholangiocarcinoma?

A

Sister Mary Joesph nodule - peeiumbilical lymphadenopathy
Courvioiser sign

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86
Q

Mechanism of cholestyramine and its use?

A

Hyperlipidaemia
Crohn’s disease for treatment diarrhoea following bowel resection.

It decreases bile acid reabsorption in the small intestine, therefore upregulating the amount of cholesterol that is converted to bile acid

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87
Q

Adverse effects of cholestyramine?

A

abdominal cramps and constipation
decreases absorption of fat-soluble vitamins
cholesterol gallstones
may raise level of triglycerides

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88
Q

Causes of chronic pancreatitis?

A

genetic: cystic fibrosis, haemochromatosis
ductal obstruction: tumours, stones, structural abnormalities including pancreas divisum and annular pancreas

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89
Q

Investigation findings for chronic pancreatitis?

A

AXR: Calcifications
CT is better at detecting calcifications

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90
Q

What is the gram stain of C -diff?

A

Gram positive rod

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91
Q

Risk factors for C-difficle?

A

PPI
Cephalosporins
Clindamycin

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92
Q

What are the features of C- diff?

A

Pseudomembraneous colitis

diarrhoea
abdominal pain
a raised white blood cell count (WCC) is characteristic
if severe toxic megacolon may develop

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93
Q

What is the management of clostridium difficult?

A

first-line therapy is oral vancomycin for 10 days
second-line therapy: oral fidaxomicin
third-line therapy: oral vancomycin +/- IV metronidazole

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94
Q

Treatment of life threatening C diff infection?

A

oral vancomycin AND IV metronidazole
specialist advice - surgery may be considered

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95
Q

What monoclonal can be used in C diff? How does it work?

A
  1. bezlotoxumab is a monoclonal antibody which targets C. difficile toxin B
  2. Faecal transplant
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96
Q

What factor levels are high in coagulopathy of liver disease?

A

Factor VIII remains supra-normal
As it is secreted by endothelial cells throughout the body
Normally would be removed by the liver - but as it is not working –> High levels factor VIII

Means: Despite Pt and APTT being raised. MAY STILL BE VERY COAGULABLE
ALSO: reduced synthesis of the purely hepatic derived natural anticoagulants protein c and protein s (vitamin k dependent), and anti-thrombin (non-vitamin k dependent).

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97
Q

What HLA type is associated with coeliac disease?

A

HLA DQ2
HLA DQ8

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98
Q

Signs and symptoms of coeliac disease ?

A

Chronic or intermittent diarrhoea
Failure to thrive or faltering growth (in children)
Persistent or unexplained gastrointestinal symptoms including nausea and vomiting
Prolonged fatigue (‘tired all the time’)
Recurrent abdominal pain, cramping or distension
Sudden or unexpected weight loss
Unexplained iron-deficiency anaemia, or other unspecified anaemia

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99
Q

Complications from coeliac disease?

A

anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
hyposplenism
osteoporosis, osteomalacia
lactose intolerance
enteropathy-associated T-cell lymphoma of small intestine
subfertility, unfavourable pregnancy outcomes
rare: oesophageal cancer, other malignancies

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100
Q

What condition should be screened for in coeliac disease?

A

Autoimmune thyroid disease
Dermatitis herpetiformis
Irritable bowel syndrome
Type 1 diabetes
First-degree relatives (parents, siblings or children) with coeliac disease

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101
Q

Serology for coeliac disease?

A

tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE

endomyseal antibody (IgA)

needed to look for selective IgA deficiency, which would give a false negative coeliac result

anti-gliadin antibody (IgA or IgG) tests are not recommended by NICE
anti-casein antibodies are also found in some patients

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102
Q

Goldstandard investigation for coeliac disease?

A

Endoscopic interstinal biopsy

findings supportive of coeliac disease:
villous atrophy
crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes

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103
Q

Management of coeliac disease?

A
  1. Avoid gluten
  2. Vaccination - due to functional asplenism - offered pneumococcal vaccine

Gluten-containing cereals include:
wheat: bread, pasta, pastry
barley: beer
whisky is made using malted barley. Proteins such as gluten are however removed during the distillation process making it safe to drink for patients with coeliac disease
rye
oats
some patients with coeliac disease appear able to tolerate oats

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104
Q

Genetics of Lynch syndrome (HNPCC) ?

A

Autosomal dominant
Cancers develop in proximal colon
Mutations in DNA mismatch repair genes
Most common genes:
- MSH2
- MLH1

Also at risk of endometrial cancer

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105
Q

Genetics of sporadic colon cancer?

A

more than half of colon cancers show allelic loss of the APC gene
Action of Kras
Deletion of p53 and DCC - lead to invasive disease

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106
Q

Types of colon cancer?

A
  • sporadic
  • FAP ( familial adenomatosis polyposis)
  • HNPCC (Lynch syndrome)
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107
Q

What is the Amsterdam criteria?

A

Used to help diagnose HNPCC

The Amsterdam criteria are sometimes used to aid diagnosis:
at least 3 family members with colon cancer
the cases span at least two generations
at least one case diagnosed before the age of 50 years

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108
Q

What is FAP ?

A

FAP is a rare autosomal dominant condition which leads to the formation of hundreds of polyps by the age of 30-40 years.
Inevitably get cancer

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109
Q

What is the mutation in FAP?

A

Chromosome 5 in APC

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110
Q

What is Gardner’s syndrome?

A

osteomas of the skull and mandible, retinal pigmentation, thyroid carcinoma and epidermoid cysts on the skin

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111
Q

Features of Crohn’s disease

A

Weight loss
diarrhoea: the most prominent symptom in adults. Crohn’s colitis may cause bloody diarrhoea
abdominal pain: the most prominent symptom in children
perianal disease: e.g. Skin tags or ulcers
extra-intestinal features are more common in patients with colitis or perianal disease

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112
Q

Extra-intestinal features of IBD?

A

Unrelated to disease activity:
Arthritis: polyarticular, symmetric
Uveitis
Pyoderma gangrenosum
Clubbing
Primary sclerosing cholangitis

Related to disease activity:
Arthritis: pauciarticular, asymmetric
Erythema nodosum
Episcleritis
Osteoporosis

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113
Q

Histology on Crohn’s disease?

A

inflammation in all layers from mucosa to serosa
goblet cells
granulomas

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114
Q

Features in crohn’s disease seen on small bowel enema?

A

high sensitivity and specificity for examination of the terminal ileum
strictures: ‘Kantor’s string sign’
proximal bowel dilation
‘rose thorn’ ulcers
fistulae

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115
Q

Crohn’s disease management to induce remission?

A

Stop smoking
1. Glucocorticoids
2. 5-ASA drugs - may be used as adjunct, never mono therapy
3. Infliximab - in refractory / fistulating disease

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116
Q

How should patients be kept in remission in crohn’s?

A

Azathioprine or mecaptopurine
Methotrexate is an alternative to azathioprine
May require continued infliximab

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117
Q

Best imaging modality for perianal fistulae?

A

MRI

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118
Q

Treatment of perianal fistulae?

A

Give metronidazole
Anti-TNF inhibitors - infliximab - may be useful to close

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119
Q

What is the function of a Seaton in perianal fissures?

A

seton is a piece of surgical thread that’s left in the fistula for several weeks to keep it open. This is useful because persisting fistula tracks after premature skin closure predispose to abscess formation

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120
Q

What should be tested before starting azathioprine, metcaptopurine or methotrexate?

A

assess thiopurine methyltransferase (TPMT) activity before offering azathioprine or mercaptopurine

Deficiency of TPMT results in significant myelosupression

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121
Q

Most common cause for diarrhoea in children?

A

Rotavirus

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122
Q

Cause of chronic diarrhoea in children?

A

most common cause in the developed world is cows’ milk intolerance
toddler diarrhoea: stools vary in consistency, often contain undigested food
coeliac disease
post-gastroenteritis lactose intolerance

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123
Q

Risk factors for diverticulosis?

A

Increased age
Low fibre diet

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124
Q

Features of diverticulitis?

A

left iliac fossa pain and tenderness
anorexia, nausea and vomiting
diarrhoea
features of infection (pyrexia, raised WBC and CRP)

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125
Q

Complications of diverticulitis?

A

abscess formation
peritonitis
obstruction
perforation

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126
Q

Drugs that cause hepatocellular driven liver picture?

A

paracetamol
sodium valproate, phenytoin
MAOIs
halothane
anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
statins
alcohol
amiodarone
methyldopa
nitrofurantoin

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127
Q

Drugs that cause cholestatic liver picture?

A

combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
rare reported causes: nifedipine

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128
Q

Drugs that cause liver cirrhosis?

A

methotrexate
methyldopa
amiodarone

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129
Q

Drugs that cause reflux?

A

NSAIDs
bisphosphonates
steroids

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130
Q

Drugs that relax the lower oesophageal sphincter?

A

calcium channel blockers*
nitrates*
theophyllines

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131
Q

What is Dubin Johnston syndrome?

A

Autosomal recessive disorder
Hyperbilirubinaemia - conjugated
THEREFORE DARK URINE
defect in the canillicular multispecific organic anion transporter (cMOAT) protein

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132
Q

Features of pharyngeal pouch?

A

More common in older men
Represents a posteromedial herniation between thyropharyngeus and cricopharyngeus muscles
Usually not seen but if large then a midline lump in the neck that gurgles on palpation
Typical symptoms are dysphagia, regurgitation, aspiration and chronic cough. Halitosis may occasionally be seen

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133
Q

Features of systemic sclerosis ? How does it cause dysphagia?

A

CREST
Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia

Lower oesophageal sphincter is DECREASED

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134
Q

Features of globes hysterics?

A

There may be a history of anxiety
Symptoms are often intermittent and relieved by swallowing
Usually painless - the presence of pain should warrant further investigation for organic causes

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135
Q

Extrinsic causes of dysphagia?

A

Mediastinal masses
Cervical spondylosis

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136
Q

Oesophageal wall causes of dysphagia?

A

Achalasia
Diffuse oesophageal spasm
Hypertensive lower oesophageal sphincter

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137
Q

Intrinsic causes of dysphagia?

A

Tumours
Strictures
Oesophageal web
Schatzki rings (oesophageal ring of tissue)

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138
Q

Neurological causes of dysphagia?

A

CVA
Parkinson’s disease
Multiple Sclerosis
Brainstem pathology
Myasthenia Gravis

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139
Q

What is eosinophilic oesphagitis?

A

Allergic inflammation of the oesophagus
Biopsy demonstrates dense eosinophilic infiltration

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140
Q

Investigations of eosinophilic oesphagitis?

A
  1. PPI trials - if fails GORD is less likely and should consider eosinophilic oesphagitis
  2. Endoscopy
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141
Q

Management of eosinophilic oesphagitis?

A

Topical steroids
Oesophageal dilation - for strictures

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142
Q

Complications from eosinophilic oesphagitis?

A

Strictures of the oesophagus (56%)
Impaction: 55% of patients experience this, and 38% of these require endoscopic removal of the impaction
Mallory-Weiss tears

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143
Q

Increased ferritin + No iron overload?

A

Inflammation (due to ferritin being an acute phase reactant)
Alcohol excess
Liver disease
Chronic kidney disease
Malignancy

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144
Q

Increased ferritin + Iron overload?

A

Primary iron overload (hereditary haemochromatosis)

Secondary iron overload (e.g. following repeated transfusions)

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145
Q

How best to tell if there is iron overload?

A

Look at transferrin saturation
normal values of < 45% in females and < 50% in males exclude iron overload.

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146
Q

Features of acute cholecystitis?

A

Right upper quadrant pain
Fever
Murphys sign on examination
Occasionally mildly deranged LFT’s (especially if Mirizzi syndrome)

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147
Q

Features of gallbladder abscess?

A

Usually prodromal illness and right upper quadrant pain
Swinging pyrexia
Patient may be systemically unwell
Generalised peritonism not present

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148
Q

Features of cholangitis?

A

Patient severely septic and unwell
Jaundice
Right upper quadrant pain

149
Q

Features of Acalculous cholecystitis?

A

Patients with intercurrent illness (e.g. diabetes, organ failure)
Patient of systemically unwell
Gallbladder inflammation in absence of stones
High fever

150
Q

Complications post ERCP?

A

Bleeding 0.9% (rises to 1.5% if sphincterotomy performed)
Duodenal perforation 0.4%
Cholangitis 1.1%
Pancreatitis 1.5%

151
Q

Risk factors for gastric cancer?

A

Helicobacer pylori
- inflammation of the mucosa → atrophy and intestinal metaplasia
Atrophic gastritis
Diet
Salt and salt-preserved foods
Nitrates
smoking
blood group

152
Q

Features of gastric cancer?

A

abdominal pain
typically vague, epigastric pain
may present as dyspepsia
weight loss and anorexia
nausea and vomiting
dysphagia: particularly if the cancer arises in the proximal stomach
overt upper gastrointestinal bleeding is seen only in a minority of patients

if lymphatic spread:
left supraclavicular lymph node (Virchow’s node)
periumbilical nodule (Sister Mary Joseph’s node)

153
Q

Diagnosis of gastric cancer?

A

oesophago-gastro-duodenoscopy with biopsy
- signet ring cells may be seen in gastric cancer. They contain a large vacuole of mucin which displaces the nucleus to one side. Higher numbers of signet ring cells are associated with a worse prognosis
CT

154
Q

Features of MALT lymphoma?

A

paraproteinaemia may be present

associated with H. pylori infection in 95% of cases
good prognosis
if low grade then 80% respond to H. pylori eradication

155
Q

What are the indications for an upper GI endoscopy?

A

age > 55 years
symptoms > 4 weeks or persistent symptoms despite treatment
dysphagia
relapsing symptoms
weight loss

156
Q

What is the gold standard investigation for reflux?

A

If endoscopy is negative consider 24-hr oesophageal pH monitoring (the gold standard test for diagnosis)

157
Q

What produces Gastrin?

A

G cells in antrum of the stomach

158
Q

What stimulates gastrin release?

A

Abdominal distension
Luminal peptides

159
Q

What is the function of gastrin?

A

Increases acid secretion by gastric parietal cells, pepsinogen and IF secretion, increases gastric motility, stimulates parietal cell maturation

160
Q

What inhibits gastrin release?

A

Somatostatin
Low antral pH

161
Q

What secretes cholecystokinin (CCK)?

A

I cells in upper small intestine
Partially digested proteins and triglycerides

162
Q

What stimulates CCK release?

A

Partially digested proteins and triglycerides

163
Q

Function of CCK?

A

Increases secretion of enzyme-rich fluid from pancreas
Contraction of the gallbladder
Relaxation of the sphincter of odd
Induces satiety

164
Q

Where is secretin secreted from?

A

S cells in upper small intestine

165
Q

What stimulates secretin secretion?

A

Acidic chyme

166
Q

Function of secretin ?

A

Increases secretion of bicarbonate-rich fluid from pancreas and hepatic duct cells, decreases gastric acid secretion,

167
Q

What secretes VIP?

A

Small intestine
Pancreas

168
Q

What stimulates VIP secretion?

A

Stimulates secretion by pancreas and intestines, inhibits acid secretion

169
Q

What secretes somatostatin?

A

D cells in the pancreas & stomach

170
Q

What stimulates somatostatin secretion?

A

Fat, bile salts and glucose in the intestinal lumen

171
Q

Function of somatostatin?

A

Decreases acid and pepsin secretion, decreases gastrin secretion, decreases pancreatic enzyme secretion, decreases insulin and glucagon secretion

172
Q

Where in the GI tract is amylase secreted?

A

Mouth

173
Q

What enzymes are found on the brush border?

A

Maltase
Sucrase
Lactase

174
Q

Function of maltase?

A

maltase: cleaves disaccharide maltose to glucose + glucose

175
Q

Function of sucrase?

A

sucrase: cleaves sucrose to fructose and glucose

176
Q

Function of lactase?

A

lactase: cleaves disaccharide lactose to glucose + galactose

177
Q

What are the features of Gilbert’s syndrome?

A

Autosomal recessive disorder
unconjugated hyperbilirubinaemia (i.e. not in urine)
jaundice may only be seen during an intercurrent illness, exercise or fasting

178
Q

How is Gilbert’s syndrome investigated?

A

investigation: rise in bilirubin following prolonged fasting or IV nicotinic acid
no treatment required

179
Q

What is the anatomy of a direct inguinal hernia?

A

Protrudes through Hesselback triangle
Passes medial to the inferior epigastric artery

180
Q

What is the anatomy of a indirect inguinal hernia?

A

Protrudes through the inguinal ring
Passes lateral to the inferior epigastric artery

181
Q

What is the anatomy of the femoral hernia?

A

Protrudes below the inguinal ligament, lateral to the pubic tubercle

182
Q

Why does a indirect inguinal hernia occur? Who typically gets it?

A

Failure of the processus vaginalis to close
Children

183
Q

What hernia carries the highest risk of strangulation?

A

Femoral

184
Q

Features of haemochromatosis?

A

Autosomal recessive - chromsome 6
HFE gene mutation
Results in iron accumulation

Early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)
‘bronze’ skin pigmentation
diabetes mellitus
liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
cardiac failure (2nd to dilated cardiomyopathy)
hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
arthritis (especially of the hands)

185
Q

Reversible complications of haemochromatosis?

A

Cardiomyopathy
Skin pigmentation

186
Q

Irreversible complications of haemochromatosis?

A

Liver cirrhosis**
Diabetes mellitus
Hypogonadotrophic hypogonadism
Arthropathy

187
Q

what is the most useful marker to monitor haemochromatosis?

A

Transferrin saturations

188
Q

What are the most common haemochromatosis mutations?

A

molecular genetic testing for the C282Y and H63D mutations
liver biopsy: Perl’s stain

189
Q

What is the management of haemochromatosis?

A
  1. Venesection
  2. Desferrioxime
190
Q

What is the pathophysiology of H pylori?

A
  1. chemotaxis away from low pH areas, using its flagella to burrow into the mucous lining to reach the epithelial cells underneath
  2. secretes urease → urea converted to NH3 → alkalinization of acidic environment → increased bacterial survival
191
Q

Associations with H pylori infection?

A

Peptic ulcer disease
Gastric cancer
B cell lymphoma - MALT
Atrophic gastritis

192
Q

What is the management of H pylori?

A

eradication may be achieved with a 7-day course of
a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)
if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin

193
Q

Test for H pylori?

A
  1. Urea breath test
  2. Rapid urease test ( CLO test)
  3. Serum antibody
  4. Culture gastric biopsy
  5. Gastric biopsy
  6. Stool antigen
194
Q

What test should be done to test for H pylori eradication?

A

Urea breath test

195
Q

When can a urea breath test not be carried out?

A

4 weeks of treatment with an antibacterial or within 2 weeks of an antisecretory drug (e.g. a proton pump inhibitor)

196
Q

What is the suspected mechanism of hepatic encephalopathy?

A

excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut.

197
Q

Features of alcoholic encephalitis?

A

confusion, altered GCS (see below)
asterix: ‘liver flap’, arrhythmic negative myoclonus with a frequency of 3-5 Hz
constructional apraxia: inability to draw a 5-pointed star
triphasic slow waves on EEG
raised ammonia level (not commonly measured anymore)

198
Q

How should alcoholic encephalitis be measured?

A

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

199
Q

Precipitating factors of alcoholic encephalitis ?

A

infection e.g. spontaneous bacterial peritonitis
GI bleed
post transjugular intrahepatic portosystemic shunt
constipation
drugs: sedatives, diuretics
hypokalaemia
renal failure
increased dietary protein (uncommon)

200
Q

Treatment of alcoholic encephalitis?

A
  1. Lactulose + rifaximin
201
Q

Can hepatitis B be transmitted by breast feeding?

A

No!

202
Q

Management for babies with mothers with chronic hepatitis B infection?

A

should receive a complete course of vaccination + hepatitis B immunoglobulin
Vertical transmission is rare

203
Q

What is the first hepatitis B marker to appear? What does it suggest?

A

surface antigen (HBsAg)
HBsAg normally implies acute disease (present for 1-6 months)

204
Q

What implies chronic hepatitis B infection?

A

HBsAg present for > 6 months

205
Q

Hepatitis B: What does Anti-Hbs mean?

A

Implies immunity (either exposure or immunisation). It is negative in chronic disease

206
Q

Hepatitis B: What does Anti-Hbc mean?

A

Anti-HBc implies previous (or current) infection. IgM anti-HBc appears during acute or recent

anti-HBc = caught, i.e. negative if immunized

207
Q

What does the HbeAg result from in hepatitis B?

A

Breakdown of the core antigen

208
Q

What does presence of HbeAg mean?

A

Marker of HBV replication and infectivity

209
Q

Causes of hepatosplenomegally?

A

chronic liver disease* with portal hypertension
infections: glandular fever, malaria, hepatitis
lymphoproliferative disorders
myeloproliferative disorders e.g. CML
amyloidosis

210
Q

What is hirschprung disease?

A

aganglionic segment of bowel due to a developmental failure of the parasympathetic Auerbach and Meissner plexuses.

211
Q

How does hirschprung disease present?

A

neonatal period e.g. failure or delay to pass meconium
older children: constipation, abdominal distension

212
Q

Management of hirschprung disease?

A

initially: rectal washouts/bowel irrigation
definitive management: surgery to affected segment of the colon

213
Q

What is the most common cause of hepatobilliary disease in HIV patients?

A

Sclerosing cholangitis - from CMV, cryptosporidium

214
Q

Features of hydatid disease?

A

Up to 90% of cysts occur in the liver and lungs
Can be asymptomatic, or symptomatic if cysts > 5cm in diameter
Morbidity caused by cyst bursting, infection and organ dysfunction (biliary, bronchial, renal and cerebrospinal fluid outflow obstruction)
In biliary rupture, there may be the classical triad of; biliary colic, jaundice, and urticaria

215
Q

Features of hydatid cyst burst?

A

classical triad of; biliary colic, jaundice, and urticaria

216
Q

What causes hydatid disease?

A

tapeworm parasite Echinococcus granulosus

217
Q

Best investigations for hydatid cyst?

A

ultrasound if often used first-line
CT is the best investigation to differentiate hydatid cysts from amoebic and pyogenic cysts
serology

218
Q

What are the 4 inherited jaundice disorders?

A

Gilbert’s
Dubin-Johnson Syndrome
Crigler- Najjar syndrome 1
Criggler - Najjar syndrome 2
Rotar syndrome

219
Q

Features of Gilbert’s syndrome?

A

autosomal recessive
mild deficiency of UDP-glucuronyl transferase
benign

220
Q

Features of Dubin-Johnson Syndrome?

A

autosomal recessive. Relatively common in Iranian Jews
mutation in the canalicular multidrug resistance protein 2 (MRP2) results in defective hepatic excretion of bilirubin
results in a grossly black liver
benign

221
Q

Features of Crigler- Najjar syndrome 1

A

autosomal recessive
absolute deficiency of UDP-glucuronosyl transferase
do not survive to adulthood

222
Q

Features of Crigler- Najjar syndrome 2

A

Autosomal recessive
slightly more common than type 1 and less severe
may improve with phenobarbital

223
Q

Features of Rotar syndrome?

A

autosomal recessive
defect in the hepatic uptake and storage of bilirubin
benign

224
Q

Genetic jaundice disorders that cause conjugated hyperbilirubinaemia ?

A

Dubin-Johnson syndrome
Rotor syndrome

225
Q

Genetic jaundice disorders that cause unconjugated hyperbilirubinaemia ?

A

Gilbert’s syndrome
Crigler-Najjar syndrome

226
Q

Features of IBS?

A

If pain is alleviated on defecation

Plus –> Two from the following:
- altered stool passage (straining, urgency, incomplete evacuation)
- abdominal bloating (more common in women than men),
- distension, tension or hardness
- symptoms made worse by eating
- passage of mucus

227
Q

Management of IBS?

A

pain: antispasmodic agents
constipation: laxatives but avoid lactulose
diarrhoea: loperamide is first-line

For patients with constipation who are not responding to conventional laxatives linaclotide may be considered, if:
optimal or maximum tolerated doses of previous laxatives from different classes have not helped and
they have had constipation for at least 12 months

Second-line pharmacological treatment
low-dose tricyclic antidepressants (e.g. amitriptyline 5-10

228
Q

Risk factor for mesenteric ischaemia?

A

increasing age
atrial fibrillation - particularly for mesenteric ischaemia
other causes of emboli: endocarditis, malignancy
cardiovascular disease risk factors: smoking, hypertension, diabetes
cocaine: ischaemic colitis is sometimes seen in young patients following cocaine use

229
Q

What are the features of mesenteric ischaemia?

A

abdominal pain - in acute mesenteric ischaemia this is often of sudden onset, severe and out-of-keeping with physical exam findings
rectal bleeding
diarrhoea
fever
bloods typically show an elevated white blood cell count associated with a lactic acidosis

230
Q

What is the pathophysiology of acute mesenteric ischaemia?

A

Acute mesenteric ischaemia is typically caused by an embolism resulting in occlusion of an artery

231
Q

What is the pathophysiology of ischaemic colitis?

A

ransient compromise in the blood flow to the large bowel
More likely to occur at watershed areas e.g. scenic flexure
borders of the territory supplied by the superior and inferior mesenteric arteries.

232
Q

Investigations in ischaemic colitis?

A

‘thumbprinting’ may be seen on abdominal x-ray due to mucosal oedema/haemorrhage

233
Q

Causes of jejunal villous atrophy ?

A

coeliac disease
tropical sprue
hypogammaglobulinaemia
gastrointestinal lymphoma
Whipple’s disease
cow’s milk intolerance

234
Q

Examples of stimulant laxatives?

A

Senna
docusate
bisacodyl
glycerol

235
Q

What stimulant laxatives can only be used in palliative patients

A

co-danthramer should only be prescribed to palliative patients due to its carcinogenic potential

236
Q

Bulk forming laxatives?

A

Ispaghula husk and methylcellulose

237
Q

Faecal softeners laxatives?

A

include arachis oil enemas
not commonly prescribed

238
Q

Contraindications to liver biopsy?

A

deranged clotting (e.g. INR > 1.4)
low platelets (e.g. < 60 * 109/l)
anaemia
extrahepatic biliary obstruction
hydatid cyst
haemoangioma
uncooperative patient
ascites

239
Q

Causes of liver cirrhosis?

A

alcohol
non-alcoholic fatty liver disease (NAFLD)
viral hepatitis (B and C)

240
Q

How should liver cirrhosis be diagnosed?

A
  1. Ultrasound
  2. Fibroscan
241
Q

Once cirrhosis has been diagnosed, how else should patients be investigated?

A
  1. upper endoscopy to check for varices in patient’s with a new diagnosis of cirrhosis
  2. liver ultrasound every 6 months (+/- alpha-feto protein) to check for hepatocellular cancer
242
Q

Intestinal causes of malabsorption?

A

coeliac disease
Crohn’s disease
tropical sprue
Whipple’s disease
Giardiasis
brush border enzyme deficiencies (e.g. lactase insufficiency)

bacterial overgrowth (e.g. systemic sclerosis, diverticulae, blind loop)
short bowel syndrome
lymphoma

243
Q

Pancreatic causes of malabsorption?

A

chronic pancreatitis
cystic fibrosis
pancreatic cancer

244
Q

Biliary causes of malabsorption?

A

biliary obstruction
primary biliary cirrhosis

245
Q

What is the rule of 2’s for heckles diverticulum?

A

occurs in 2% of the population
is 2 feet from the ileocaecal valve
is 2 inches long

246
Q

Pathology of the meckles diverticulum?

A

contains ectopic ileal, gastric or pancreatic mucosa.

247
Q

Presentation of meckles diverticulum?

A

abdominal pain mimicking appendicitis

rectal bleeding
- Meckel’s diverticulum is the most common cause of painless massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years

intestinal obstruction
- volvulus and intussusception

248
Q

How should a meckles be investigated?

A

Meckel’s scan’ should be considered
uses 99m technetium pertechnetate, which has an affinity for gastric mucosa

249
Q

What is melanosis coli?

A

Melanosis coli is a disorder of pigmentation of the bowel wall. Histology demonstrates pigment-laden macrophages

associated with Senna

250
Q

What is the profession of fatty liver disease?

A
  1. steatosis - fat in the liver
  2. steatohepatitis - fat with inflammation, non-alcoholic
  3. steatohepatitis (NASH),
  4. progressive disease may cause fibrosis and liver cirrhosis
251
Q

What are the features of adenocarcinoma of the oesophagus?

A

Located lower third of oesophagus

Features:
GORD
Barrett’s oesophagus
smoking
achalasia
obesity

252
Q

What are the features of squamous cell carcinoma of the oesophagus?

A

Located upper third of oesophagus

smoking
alcohol
achalasia
Plummer-Vinson syndrome
diets rich in nitrosamines

253
Q

What is the best investigation to diagnose oesophageal cancer?

A

Endoscopy

254
Q

What is the best investigation to stage oesophageal cancer?

A

Endoscopic ultrasound is the preferred method for locoregional staging

255
Q

What is the most common surgical procedure for removal of oesphageal cancer?

A

Ivor-Lewis

256
Q

What is the triad of Plummer Vinson syndrome?

A

Triad of:

dysphagia (secondary to oesophageal webs)
glossitis
iron-deficiency anaemia

257
Q

What is boerhave syndrome?

A

Severe vomiting → oesophageal rupture

258
Q

Features of pancreatic cancer?

A

Classically painless jaundice
- pale stools, dark urine, and pruritus
Cholestatic liver function tests

Courvoisier’s law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
however, patients typically present in a non-specific way with anorexia, weight loss, epigastric pain

Loss of exocrine function (e.g. steatorrhoea)
Loss of endocrine function (e.g. diabetes mellitus)
Atypical back pain is often seen
Migratory thrombophlebitis (Trousseau sign) is more common than with other cancers

259
Q

Best investigation for pancreatic cancer?

A

high-resolution CT scanning is the investigation of choice if the diagnosis is suspected
‘double duct’ sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts

260
Q

Management of pancreatic cancer?

A

Whipple’s resection (pancreaticoduodenectomy
adjuvant chemotherapy is usually given following surgery
ERCP with stenting is often used for palliation

261
Q

What is the pathophysiology of pernicious anaemia

A

Antibodies to intrinsic factor +/- gastric parietal cells

intrinsic factor antibodies → bind to intrinsic factor blocking the vitamin B12 binding site
gastric parietal cell antibodies → reduced acid production and atrophic gastritis. Reduced intrinsic factor production → reduced vitamin B12 absorption

262
Q

Associations of pernicious anaemia?

A

thyroid disease, type 1 diabetes mellitus, Addison’s, rheumatoid and vitiligo

263
Q

Features of pernicious anaemia?

A

Anaemia features
- lethargy
- pallor
- dyspnoea

Peripheral neuropathy
Subacute cord degeneration

264
Q

what is peutz jeuger syndrome?

A

Autosomal dominant
numerous hamartomatous polyps in the gastrointestinal tract
Increased colonic cancer risk - 50% die of cancer

265
Q

Clinical features of peutz jeuger?

A

hamartomatous polyps in the gastronintestinal tract (mainly small bowel)
small bowel obstruction is a common presenting complaint, often due to intussusception
gastrointestinal bleeding
pigmented lesions on lips, oral mucosa, face, palms and soles

266
Q

What are the genetics of peutz jeuger?

A

autosomal dominant
responsible gene encodes serine threonine kinase LKB1 or STK11

267
Q

What is post cholecystectomy syndrome?

A

dyspepsia, vomiting, pain, flatulence and diarrhoea

Pain is often due to sphincter of Oddi dysfunction and the development of surgical adhesions.

268
Q

Management of intraheptic cholecystitis in pregnancy?

A

ursodeoxycholic acid is used for symptomatic relief
weekly liver function tests
women are typically induced at 37 weeks

** increase rate of still birth

269
Q

What is HELLP syndrome?

A

Haemolysis, Elevated Liver enzymes, Low Platelets

270
Q

Associations with primary biliary cholangitis?

A

Sjogren’s syndrome (seen in up to 80% of patients)
rheumatoid arthritis
systemic sclerosis
thyroid disease

271
Q

Pathophysiology in primary biliary cholangitis?

A

Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis which may eventually progress to cirrhosis.

272
Q

Clinical features of primary biliary cholangitis?

A

early: may be asymptomatic (e.g. raised ALP on routine LFTs) or fatigue, pruritus
cholestatic jaundice
hyperpigmentation, especially over pressure points
around 10% of patients have right upper quadrant pain
xanthelasmas, xanthomata
also: clubbing, hepatosplenomegaly
late: may progress to liver failure

273
Q

Immunology in PBC?

A

anti-mitochondrial antibodies (AMA) M2 subtype are present in 98% of patients and are highly specific
smooth muscle antibodies in 30% of patients
raised serum IgM

274
Q

Management of PBC?

A

First-line: ursodeoxycholic acid
- slows disease progression and improves symptoms
pruritus: cholestyramine
fat-soluble vitamin supplementation
liver transplantation
e.g. if bilirubin > 100 (PBC is a major indication)
recurrence in graft can occur but is not usually a problem

275
Q

Complications of PBC?

A

cirrhosis → portal hypertension → ascites, variceal haemorrhage
osteomalacia and osteoporosis
significantly increased risk of hepatocellular carcinoma (20-fold increased risk)

276
Q

Associations with primary sclerosis cholangitis?

A

ulcerative colitis: 4% of patients with UC have PSC, 80% of patients with PSC have UC
Crohn’s (much less common association than UC)
HIV

277
Q

Investigations for primary sclerosing cholangitis?

A

ERCP
MRCP

P ANCA may be positive

278
Q

Mechanism of PPI?

A

irreversible blockade of H+/K+ ATPase of the gastric parietal cell.

279
Q

Complications of PSC?

A

cholangiocarcinoma (in 10%)
increased risk of colorectal cancer

280
Q

What is primary sclerosis cholangiits?

A

characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts.

281
Q

Complications of PPI?

A

hyponatraemia, hypomagnasaemia
osteoporosis → increased risk of fractures
microscopic colitis
increased risk of C. difficile infections

282
Q

Features of pyloric stenosis?

A

‘projectile’ vomiting, typically 30 minutes after a feed
constipation and dehydration may also be present
a palpable mass may be present in the upper abdomen
hypochloraemic, hypokalaemic alkalosis due to persistent vomiting

283
Q

Organisms implicated in liver abscess?

A

Staph aureus
E coli

284
Q

Management of liver abscess?

A

drainage (typically percutaneous) and antibiotics
amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic: ciprofloxacin + clindamycin

285
Q

Features of refeeding syndrome?

A

hypophosphataemia
hypokalaemia
hypomagnesaemia: may predispose to torsades de pointes
abnormal fluid balance

286
Q

What are the features of smallbowel overgrowth syndrome?

A

xcessive amounts of bacteria in the small bowel resulting in gastrointestinal symptoms.

287
Q

Treatment in small bowel overgrowth syndrome?

A

antibiotic therapy:rifaximin is now the treatment of choice due to relatively low resistance. Co-amoxiclav or metronidazole are also effective in the majority of patients.

288
Q

Features of spontaneous bacterial peritonitis?

A

ascites
abdominal pain
fever

289
Q

Diagnosis of SBP?

A

paracentesis: neutrophil count > 250 cells/ul
the most common organism found on ascitic fluid culture is E. coli

290
Q

Treatment of SBP?

A

intravenous cefotaxime is usually given

291
Q

Who should receive antibiotic prophylaxis for SBP?

A
  1. patients who have had an episode of SBP
  2. patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
  3. NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’
292
Q

Treatment for thread worms?

A

mebendazole is used first-line for children > 6 months old

293
Q

Features of ulcerative colitis?

A

bloody diarrhoea
urgency
tenesmus
abdominal pain, particularly in the left lower quadrant
extra-intestinal features (see below)

294
Q

Ulcerative colitis findings on endoscopy?

A

red, raw mucosa, bleeds easily
no inflammation beyond submucosa (unless fulminant disease)
widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)
inflammatory cell infiltrate in lamina propria
neutrophils migrate through the walls of glands to form crypt abscesses
depletion of goblet cells and mucin from gland epithelium
granulomas are infrequent

295
Q

UC findings on imaging?

A

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

296
Q

Criteria for 5 year colonoscopy follow up for UC?

A

5 year follow up colonoscopy
Extensive colitis with no active endoscopic/histological inflammation
OR left sided colitis
OR Crohn’s colitis of <50% colon

297
Q

Critieria for 3 year colonoscopy follow up for UC?

A

3 year colonoscopy
Extensive colitis with mild active endoscopy/histological inflammation
OR post-inflammatory polyps
OR family history of colorectal cancer in a first degree relative aged 50 or over

298
Q

Criteria for 1 year colonoscopy follow up ?

A

1 year follow up colonoscopy
Extensive colitis with moderate/severe active endoscopic/histological inflammation
OR stricture in past 5 years
OR dysplasia in past 5 years declining surgery
OR primary sclerosing cholangitis / transplant for primary sclerosing cholangitis
OR family history of colorectal cancer in first degree relatives aged <50 years

299
Q

Criteria for severity of UC ?

A

mild: < 4 stools/day, only a small amount of blood
moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

300
Q

Management of proctitis - UC?

A

topical (rectal) aminosalicylate
if remission is not achieved within 4 weeks, add an oral aminosalicylate
If remission still not achieved - steroid

301
Q

Management of proctosigmoid and left sided colitis?

A

topical (rectal) aminosalicylate
if remission is not achieved within 4 weeks, add an oral aminosalicylate
If remission still not achieved - steroid

302
Q

Management of extensive UC disease ?

A

topical (rectal) aminosalicylate and a high-dose oral aminosalicylate:
if remission is not achieved within 4 weeks, stop topical treatments and offer a high-dose oral aminosalicylate and an oral corticosteroid

303
Q

Following > 2 relapses of UC or a severe relapse, treatment?

A

oral azathioprine or oral mercaptopurine

methotrexate is not recommended for the management of UC (in contrast to Crohn’s disease)

304
Q

Management of variceal bleed?

A

ABC: patients should ideally be resuscitated prior to endoscopy
correct clotting: FFP, vitamin K
Terlipressin
prophylactic IV antibiotics
Sengstaken-Blakemore tube if uncontrolled haemorrhage
Endoscopy: band ligation

Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail
connects the hepatic vein to the portal vein
exacerbation of hepatic encephalopathy is a common complication

305
Q

Prophylaxis for variceal haemorrhage?

A

Propanolol

306
Q

Features of VIPoma?

A

VIP (vasoactive intestinal peptide)
source: small intestine, pancreas
stimulation: neural
actions: stimulates secretion by pancreas and intestines, inhibits acid and pepsinogen secretion

large volume diarrhoea
weight loss
dehydration
hypokalaemia, hypochlorhydia

307
Q

What is whipples disease?

A

multi-system disorder caused by Tropheryma whippelii infection. It is more common in those who are HLA-B27 positive and in middle-aged men.

308
Q

Features of whipples disease?

A

malabsorption: diarrhoea, weight loss
large-joint arthralgia
lymphadenopathy
skin: hyperpigmentation and photosensitivity
pleurisy, pericarditis
neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus

309
Q

Best investigation and its findings for whipples disease?

A

jejunal biopsy shows deposition of macrophages containing Periodic acid-Schiff (PAS) granules

310
Q

Treatment of whipples disease?

A

oral co-trimoxazole for a year is thought to have the lowest relapse rate, sometimes preceded by a course of IV penicillin

311
Q

Genetics in Wilson disease?

A

Autosomal recessive
ATP7B gene located on chromosome 13.

312
Q

Treatment of Wilson’s disease ?

A

liver: hepatitis, cirrhosis
neurological:
basal ganglia degeneration: in the brain, most copper is deposited in the basal ganglia, particularly in the putamen and globus pallidus
speech, behavioural and psychiatric problems are often the first manifestations
also: asterixis, chorea, dementia, parkinsonism
Kayser-Fleischer rings
green-brown rings in the periphery of the iris
due to copper accumulation in Descemet membrane
present in around 50% of patients with isolated hepatic Wilson’s disease and 90% who have neurological involvement
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails

313
Q

Management of Wilson’s disease?

A

Penicillamine

314
Q

What is Zollinger-Ellison syndrome?

A

excessive levels of gastrin, usually from a gastrin secreting tumour
Associated with MEN 1

315
Q

Features of zollinger- Ellison syndrome?

A

multiple gastroduodenal ulcers
diarrhoea
malabsorption

316
Q

How is zollinger-ellison syndrome diagnosed?

A

fasting gastrin levels: the single best screen test
secretin stimulation test

317
Q

Causes of liver cirrhosis exaggeration ?

A

Constipation

318
Q

What is the test for small bowel bacterial overgrowth syndrome?

A

Hydrogen breath test

319
Q

Management of Wilson’s disease?

A

Penacillamine

320
Q

Where do VIPoma arrive from mostly?

A

pancreas

321
Q

With venesection what is reversible in haemochomatosis ?

A

cardiomyopathy and skin pigmentation are reversible with treatment

322
Q

Diarrhoea, weight, arthralgia, lymphadenopathy, ophthalmoplegia ?

A

Whipples disease

323
Q

Area most likely to be affected by ischaemic colitis?

A

splenic flexure is the most likely area to be affected by ischaemic colitis

324
Q

How to test for cirrhosis?

A

Transient elastography

325
Q

Investigation findings for Wilson’s disease?

A

slit lamp examination for Kayser-Fleischer rings
reduced serum caeruloplasmin
reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
free (non-ceruloplasmin-bound) serum copper is increased
increased 24hr urinary copper excretion
the diagnosis is confirmed by genetic analysis of the ATP7B gene

326
Q

Management of Wilson’s disease?

A
  1. Penacillamine
327
Q

Prophylaxis for alcoholic liver disease?

A
  1. Lactulose
  2. Rifaxamin
328
Q

What is the most severe factor in pancreatic scoring?

A

Hypocalcaemia

329
Q

Bariatric surgery known to cause malabsorption?

A

Biliopancreatic diversion with duodenal switch is a primarily malabsorptive procedure and reserved for patients who are very obese

330
Q

Scoring for liver cirrhosis severity?

A

Child Pugh classification
Bilirubin (µmol/l)
Albumin (g/l)
Prothrombin time
Encephalopathy
Ascites

331
Q

Jejunal biopsy shows PAS positive granules?

A

Whipples disease

332
Q

what type of immunoglobulin is elevated in autoimmune hepatitis?

A

IgG

333
Q

What is the side effect of a transjugular hepatic shunt?

A

Transjugular Intrahepatic Portosystemic Shunt commonly causes an exacerbation of hepatic encephalopathy

334
Q

If IBS symptoms have not improved in 12 months, consider doing what?

A

low dose tricyclic antidepressant

335
Q

Barret oesphagus biopsy report?

A

Non-dysplastic columnar-lined oesophagus

336
Q

What does PAS positive stand for?

A

Periodic acid-Schiff (PAS) granules

337
Q

Biopsy of gastric cancer shows?

A

signet ring cells

338
Q

In duodenal ulcers what is the vessels that bleed?

A

Gastroduodenal artery

339
Q

What is the reversal agent for dabigatron?

A

Idarucizumab

340
Q

What is the first line treatment of primary billiard cholangitis?

A

Ursodeoxycholic acid

341
Q

What should is the antibiotic of choice for ascites prophylaxis in alcoholic liver disease?

A

Ciprofloxacin

342
Q

What is the most common genetic colonic cancer?

A

Hereditary nonpolyposis colorectal carcinoma (HNPCC)

343
Q

Best monitoring for haemochromatosis?

A

Transferrin saturation + ferritin

344
Q

How should a jejunal biopsy be done for coeliac?

A

Patients must eat gluten for at least 6 weeks before they are tested

345
Q

Features of acute fatty liver of pregnancy?

A

Features
abdominal pain
nausea & vomiting
headache
jaundice
hypoglycaemia
severe disease may result in pre-eclampsia

346
Q

Investigation findings for acute fatty liver of pregnancy?

A

ALT is typically elevated e.g. 500 u/l

347
Q

Mother hep b positive gives birth. manage?

A

course of vaccination + hepatitis B immunoglobulin

348
Q

How can PPI cause diarrhoea?

A

PPIs are a cause of microscopic colitis, which can present with chronic diarrhoea, colonoscopy and biopsy should be considered when patients present in this way and are taking a PPI

349
Q

Why is the rectosigmoid junction affected in ischaemic colitis?

A

Watershed area
Inferior mesenteric artery

350
Q

Patient with incidental NAFLD - management?

A

Send a enhanced liver fibrosis blood test

351
Q

What drug should be avoided in IBS?

A

Lactulose - bloating

352
Q

How should IBS be managed?

A

First line:
pain: antispasmodic agents
constipation: laxatives but avoid lactulose
diarrhoea: loperamide is first-line

Second line:
low-dose tricyclic antidepressants (e.g. amitriptyline 5-10 mg) are used in preference to selective serotonin reuptake inhibitors

353
Q

How should IBS be managed?

A

First line:
pain: antispasmodic agents
constipation: laxatives but avoid lactulose
diarrhoea: loperamide is first-line

Second line:
low-dose tricyclic antidepressants (e.g. amitriptyline 5-10 mg) are used in preference to selective serotonin reuptake inhibitors

354
Q

T2DM with abnormal LFTs - ?

A

non-alcoholic fatty liver disease

355
Q

Diarrhoea + hypokalaemia?

A

→ villous adenoma

356
Q

Goblet cell depletion

A

Ulcerative colitis

357
Q

pathological process seen in the hepatocytes of such patients with fulminant hepatitis?

A

Necrosis

358
Q

Scleroderma + Diarrhoea?

A

Malabsorptive syndrome

358
Q

Scleroderma + Diarrhoea?

A

Malabsorptive syndrome

359
Q

Pathophysiology behind hepatorenal syndrome?

A

Hepatorenal syndrome is primarily caused by splanchnic vasodilation

360
Q

What antibodies are seen in PBC?

A

Primary biliary cholangitis - the M rule
IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females

361
Q

What is Heyde’s syndrome?

A

aortic stenosis and angiodysplasia resulting in chronic gastrointestinal blood loss

362
Q

If IDA + negative OGD and colonoscopy - management

A

Capsule endoscopy for ? Heyde’s syndrome

363
Q

What type of bleed gives a high urea?

A

Upper GI bleed

364
Q

gold standard test for GORD?

A

24hr oesophageal pH monitoring is gold standard investigation in GORD

364
Q

gold standard test for GORD?

A

24hr oesophageal pH monitoring is gold standard investigation in GORD

365
Q

Crypt abscesses?

A

Ulcerative colitis

366
Q

Most common causes of hepatocellular carcinoma?

A

Hepatocellular carcinoma
hepatitis B most common cause worldwide
hepatitis C most common cause in Europe

367
Q

Terlipressin mechanism?

A

Terlipressin - method of action = constriction of the splanchnic vessels

MRCP: Gastro (2 decks)

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