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MRCP: Gastro > MRCP2 > Flashcards

MRCP2 Flashcards

1
Q

Ulcer: Pain relieved by eating

A

Duodenal ulcer

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2
Q

Ulcer: Pain while eating?

A

Gastric ulcer

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3
Q

What is Cullen’s sign?

A

Periumbilical discolouration (Cullen’s sign)

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4
Q

What is grey turner’s sign ?

A

flank discolouration (Grey-Turner’s sign)

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5
Q

Tinkling bowel sounds?

A

Intestinal obstruction

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6
Q

Cause if achalasia?

A

degenerative loss of ganglia from Auerbach’s plexus

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7
Q

Features of achalsia?

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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8
Q

Best investigation for achalasia?

A

LOS manometry

barium swallow
shows grossly expanded oesophagus, fluid level
‘bird’s beak’ appearance
chest x-ray
wide mediastinum
fluid level

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9
Q

Surgery of choice for achalasia?

A

pneumatic (balloon) dilation

If recurrent symptoms: Heller cardiomyotomy

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10
Q

Pancreatitis causes?

A

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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11
Q

Upper GI bleed: 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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12
Q

mall to moderate volume of bright red blood + repeat vomiting

A

Mallory weiss syndrome

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13
Q

NSAID use + haematemesis + epigastric discomfort

A

Diffuse erosive gastritis

Usually haematemesis and epigastric discomfort. Usually there is an underlying cause such as recent NSAID usage. Large volume haemorrhage may occur with considerable haemodynamic compromise

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14
Q

What artery is often implicated in duodenal ulcer ?

A

Gastroduodenal

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15
Q

Previous aortic surgery + major haemorrhage?

A

Aorto-enteric fistula

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16
Q

Constitutional symptoms + dyspepsia +/- major haeemorhage

A

Gastric cancer

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17
Q

How to risk stratify patient with haematemesis?

A

Blatchford scale
helps clinicians decide whether patient patients can be managed as outpatients or not

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18
Q

How to assess mortality of patient AFTER ENDOSCOPY?

A

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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19
Q

When is a platelet transfusion needed in haematemesis?

A

> 50

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20
Q

When is FFP needed in major haemorrhage?

A

fibrinogen level of less than 1 g/litre, or a prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal

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21
Q

Management of non-variceal bleeding?

A

PPIs should be given to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy

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22
Q

Management of variceal bleeding?

A

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

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23
Q

Management of gastric varices?

A

band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices

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24
Q

If varcies are not managed with band ligation or N-butyl-2-cyanoacrylate?

A

transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures

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25
Q

What are the types of alcoholic liver disease?

A

alcoholic fatty liver disease
alcoholic hepatitis
cirrhosis

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26
Q

What is the classic LFT picture for alcoholic liver disease?

A

gamma-GT is characteristically elevated

AST:ALT is normally > 2, a ratio of > 3 is strongly suggestive of acute alcoholic hepatitis

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27
Q

Management of alcoholic liver disease?

A

Prednisolone
pentoxyphylline

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28
Q

What is alkaptonuria?

A

rare autosomal recessive disorder of phenylalanine and tyrosine metabolism
lack of the enzyme homogentisic dioxygenase (HGD)

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29
Q

Features of alkaptonuria?

A

pigmented sclera
urine turns black if left exposed to the air
intervertebral disc calcification may result in back pain
renal stones
Multi-level intervertebral disc calcification with disc space narrowing

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30
Q

Treatment of alkaptonuria?

A

high-dose vitamin C
dietary restriction of phenylalanine and tyrosine

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31
Q

What is the side effect of sulphasalazine?

A

rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis

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32
Q

What is the difference between sulphasalaine and mesalazine?

A

Mesalazine –> delayed release 5 ASA

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33
Q

Side effect of mesalazine?

A

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

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34
Q

Which 5 ASA causes pancreatitis?

A

Mesalazine

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35
Q

Management of angiodysplasia?

A

endoscopic cautery or argon plasma coagulation
antifibrinolytics e.g. Tranexamic acid
oestrogens may also be used

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36
Q

Most common organism to cause ascending cholangitis?

A

E coli

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37
Q

Features of ascending cholangitis?

A

Charcot’s triad of right upper quadrant (RUQ) pain, fever and jaundice occurs in about 20-50% of patients

hypotension and confusion are also common (the additional 2 factors in addition to the 3 above make Reynolds’ pentad)

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38
Q

Management of ascending cholangitis?

A

intravenous antibiotics
endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve any obstruction

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39
Q

What does a SAAG > 11 indicate typically?

A

Portal vein hypertension

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40
Q

Causes of high SAAG ascites?

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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41
Q

Causes of low SAAh ascites?

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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42
Q

What is the risk of drainage of a large volume ascites?

A

paracentesis induced circulatory dysfunction can occur due to large volume paracentesis (> 5 litres). It is associated with a high rate of ascites recurrence, development of hepatorenal syndrome, dilutional hyponatraemia, and high mortality rate

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43
Q

What should be offered to patients as a prophylaxis of ascites > 15G/L

A

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’

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44
Q

HLA type associated with autoimmune hepatitis?

A

HLA B8
HLA DR3.

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45
Q

What are the three types of autimmune hepatitis?

A

Type 1 –> ANA + Smooth muscle antibody
Type 2 –> Anti-liver/kidney microsomal type 1 antibodies (LKM1)
Type 3 –> Soluble liver-kidney antigen

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46
Q

What autimmune hepatitis affects both adults and children?

A

Type 1

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47
Q

What autoimmune hepatitis only affects children?

A

Type 2

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48
Q

What autoimmune hepatitis only affects adults?

A

Type 3

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49
Q

Features of autoimmune hepatitis?

A

acute hepatitis: fever, jaundice etc (only 25% present in this way)
amenorrhoea (common)
liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis

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50
Q

Management of autoimmune hepatitis?

A
  1. Prednisolone
  2. Liver transplant
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51
Q

What can bile acid malabsorption lead to?

A

Steatorrhea
Malabsorption of vitamins A, D, E, K

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52
Q

Causes of bile acid malabsorption?

A

cholecystectomy
coeliac disease
small intestinal bacterial overgrowth

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53
Q

Investigation of choice for bile acid malabsorption?

A

SeHCAT
- nuclear mediciune scan
- scans are done 7 days apart rto see loss of radioactive isotope

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54
Q

Management of bile acid malabsorption?

A

cholestyramine

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55
Q

What is the triad of budd chiari?

A

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

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56
Q

What does barret’s oesphagus refer to?

A

Metaplasia of LOS from squamous –> columnar
of oesophageal adenocarcinoma, estimated at 50-100 fold

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57
Q

Risk factors for Barret’s oesphagus?

A

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

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58
Q

Is alcohol a risk factor for Barret’s?

A

It is not an independent risk factor

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59
Q

Management of Barret’s?

A

High dose PPI
Endoscopy every 3-5 years

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60
Q

How do you manage dysplasia found in Barret’s?

A

dysplasia of any grade is identified endoscopic intervention is offered. Options include:
radiofrequency ablation:

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61
Q

Identify bleeding source when OGD + colonoscopy fail?

A

Capsule endoscopy

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62
Q

Features of carcinoid tumour?

A

flushing (often the earliest symptom)
diarrhoea
bronchospasm
hypotension
right heart valvular stenosis (left heart can be affected in bronchial carcinoid)

May also secrete:
- ACTH –> Cushings

Pellagra

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63
Q

Investigations for carcinoid tumour?

A

urinary 5-HIAA

plasma chromogranin A y

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64
Q

Management of carcinoid tumour?

A

somatostatin analogues e.g. octreotide

diarrhoea: cyproheptadine may help

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65
Q

Mechanism of cholesytramine?

A

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

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66
Q

What is the main action of cholestyramine ?

A

Reduces LDL cholesterol

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67
Q

What are the 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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68
Q

Crohns disease bowel resection + diarrhoea - how to manage?

A

Cholestryamine

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69
Q

Genetic causes of chronic pancreatitis?

A

genetic: cystic fibrosis, haemochromatosis

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70
Q

Ductal causes of chronic pancreatitis?

A

ductal obstruction: tumours, stones, structural abnormalities including pancreas divisum and annular pancreas

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71
Q

What is the features of chronic pancreatitis?

A

pain is typically worse 15 to 30 minutes following a meal
steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain
diabetes mellitus develops in the majority of patients. It typically occurs more than 20 years after symptom begin

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72
Q

What medication is a risk factor for clostrium difficle?

A

PPI’s

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73
Q

What is the gram stain of c difficle?

A

anaerobic gram-positive, spore-forming, toxin-producing bacillus

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74
Q

Major complication of C difficle?

A

Toxic megacolon

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75
Q

Features of moderate C difficle?

A

↑ WCC ( < 15 x 109/L)
Typically 3-5 loose stools per day

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76
Q

Features of severe C difficle?

A

↑ WCC ( > 15 x 109/L)
or an acutely ↑ creatinine (> 50% above baseline)
or a temperature > 38.5°C
or evidence of severe colitis(abdominal or radiological signs)

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77
Q

Features of life threatening C difficle?

A

Hypotension
Partial or complete ileus
Toxic megacolon, or CT evidence of severe disease

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78
Q

Treatment during first episode of C difficle?

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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79
Q

Treatment during recurrent episode of C difficle?

A

recurrent infection occurs in around 20% of patients, increasing to 50% after their second episode

within 12 weeks of symptom resolution: oral fidaxomicin

after 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin

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80
Q

Management of life threatening C difficile?

A

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

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81
Q

Two episode of recurrent C difficile management?

A

faecal microbiota transplant

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82
Q

Complications of 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

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83
Q

Associated conditions of 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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84
Q

HLA type assocaited with coeliac disease?

A

HLA-DQ2 (95% of patients)
HLA-DQ8 (80%).

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85
Q

What do patients need to be doing before coeliac disease ?

A

Must be eating gluten 6 weeks prior to test

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86
Q

What is the first line serology test for coeliac?

A

Anti TTG (IgA)

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87
Q

What must be tested with other coeliac serology ? And why?

A

endomyseal antibody (IgA)
+
Selective IgA deficiency - may give false positive

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88
Q

What is the gold standard diagnosis of coeliac disease?

A

the ‘gold standard’ for diagnosis - this should be performed in all patients with suspected coeliac disease to confirm or exclude the diagnosis

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89
Q

Findings on biopsy that are consistent with coeliac disease ?

A

villous atrophy
crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes

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90
Q

What are the ways of diagnosis colon cancer - what is gold standard?

A

Goldstandard: Colonoscopy

Other options:
double-contrast barium enema and CT colonography.

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91
Q

How is colon cancer stages?

A

CT chest abdomen pelvis

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92
Q

How is rectal cancer staged?

A

rectal cancer will also undergo evaluation of the mesorectum with pelvic MRI scanning.

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93
Q

Tumour marker for colon cancer?

A

CEA

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94
Q

Gene mutation in HNPCC?

A

Lynch syndrome

MSH2 (60% of cases)
MLH1 (30%)

Affect genes involved in DNA mismatch repair leading to microsatellite instability

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95
Q

Inheritance of HNPCC?

A

Autosomal dominant

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96
Q

Other causes associated in HNPCC ( Lynch) ?

A

Endometrial
Stomach,
Liver,
Kidney,
Brain, and.
Certain types of skin cancers.

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97
Q

Amsterdam criteria for lynch syndrome?

A

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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98
Q

Mutation in FAP ?

A

tumour suppressor gene called adenomatous polyposis coli gene (APC), located on chromosome 5

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99
Q

Feature of Gardner’s syndrome?

A

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

COlonic polyps
Variant of FAP

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100
Q

Most common type of mutation in sporadic colorectal carcinoma?

A

Loss of APC

Others include loss of P53 and K-ras

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101
Q

FIT test results?

A

5 out of 10 patients will have a normal exam
4 out of 10 patients will be found to have polyps which may be removed due to their premalignant potential
1 out of 10 patients will be found to have cancer

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102
Q

Who is bowel screening done on?

A

ffering screening every 2 years to all men and women aged 60 to 74 years in England, 50 to 74 years in Scotland

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103
Q

Investigation findings in crohn’s?

A

raised inflammatory markers
increased faecal calprotectin
anaemia
low vitamin B12 and vitamin D

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104
Q

Extra-instestinal manifestations related to disease activity in IBD?

A

Arthritis: pauciarticular, asymmetric
Erythema nodosum
Episcleritis
Osteoporosis

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105
Q

Most common extra-intestinal manifestation in crohn’s disease?

A

Arthritis

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106
Q

Extra-instestinal manifestations not related to disease activity in IBD?

A

Arthritis: polyarticular, symmetric
Uveitis
Pyoderma gangrenosum
Clubbing
Primary sclerosing cholangitis

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107
Q

IBD: Uveitis ?

A

UC

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108
Q

IBD: episcleritis

A

Crohn’s

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109
Q

IBD: Primary sclerosis cholangitis ?

A

UC

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110
Q

IBD: Goblet cell + Granuloma?

A

Crohn’s

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111
Q

Histology in crohn’s disease ?

A

inflammation in all layers from mucosa to serosa
goblet cells
granulomas

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112
Q

Small bowel enema for crohn’s disease?

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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113
Q

What marker can be used to correlate disease in crohn’s?

A

CRP

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114
Q

Crohns + smoking

A

Exacerbates

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115
Q

UC + smoking

A

Protects

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116
Q

How to induce remission in crohns’ disease?

A

Firstline: Glucocorticoids or Budesonide

Secondline: 5-ASA drugs (e.g. mesalazine)

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117
Q

What drugs can be added in to help induce remission on crohn’s, but cannot be monotherapy?
Can also be used to maintain remission

A

azathioprine or mercaptopurine
Methotrexate

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118
Q

Disease refractory crohn’s management?

A

Infliximab

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119
Q

Fistulating crohn’s management

A

Infliximab

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120
Q

Management of isolated perianal disease in corhn’s ?

A

Metronidazole

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121
Q

Imaging of choice for suspected perianal disease?

A

MRI

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122
Q

Management of complex fistula in crohn’s disease?

A

draining seton is used for complex fistulae

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123
Q

Management of stricturing iela disease ?

A

ileocaecal resection

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124
Q

What test should be done before starting azathiorpine / metacaptopurine ?

A

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

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125
Q

Signs of decompensated liver disease?

A

Asterixis
Jaundice
Hepatic encephalopathy
Constructional apraxia (ask to draw a clock face)

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126
Q

Causes of decompensated liver disease?

A

Infection - pneumonia, spontaneous bacterial peritonitis, viruses (hepatitis B, C)
Drugs - paracetamol, anaesthetic agents
Toxin - alcohol, Amanita phalloides mushroom
Vascular - Budd-Chiari syndrome, vena-occlusive disease
Haemorrhage - Upper gastrointestinal bleed
Constipation

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127
Q

Management of decompensated liver disease?

A

Enhance nitrate clearance with phosphate enemas

Aim for 3 stools per day

Use lactulose : lactulose to enhance binding of nitrate in the intestine.

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128
Q

Definitions of diarrhoea?

A

Diarrhoea: > 3 loose or watery stool per day
Acute diarrhoea < 14 days
Chronic diarrhoea > 14 days

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129
Q

What is the most common cause of diarrhoea in children?

A

Rotavirus

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130
Q

Most common cause of chroic diarrhoea in infants?

A

cows’ milk intolerance

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131
Q

Undigested food + diarrhoea?

A

Toddler’s diarrhoea

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132
Q

Barium swallow + corkscrew appearance?

A

Diffuse oesphageal spasm

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133
Q

Treatment of diverticulitis?

A

if the symptoms don’t settle within 72 hours, or the patient initially presents with more severe symptoms, the patient should be admitted to hospital for IV antibiotics

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134
Q

Drugs that cause a hepatocellular picture?

A

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

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135
Q

Drug that cause a cholestatic 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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136
Q

Drugs that cause cirrhosis?

A

methotrexate
methyldopa
amiodarone

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137
Q

What is Dubin Johnson syndrome?

A

benign autosomal recessive disorder hyperbilirubinaemia (conjugated, therefore present in urine)

defect in the canillicular multispecific organic anion transporter (cMOAT) protein

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138
Q

Dysphagia: Odonophagia + no weight loss + GORD

A

Oesophagitis

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139
Q

Dysphagia: HIV / steroid use ?

A

Oesophageal candidiasis

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140
Q

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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141
Q

Management for feeding > 4 weeks?

A

Gastric feeding > 4 weeks consider long-term gastrostomy

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142
Q

Complications of enteral feeding?

A

diarrhoea
aspiration
metabolic
hyperglycaemia
refeeding syndrome

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143
Q

Risk factor of developing eosinophilic oesphagitis?

A

Allergies/ asthma: suffering from food/ environmental allergies or atopic dermatitis and asthma increases the risk of diagnosis
Male sex
Family history of eosinophilic oesophagitis or allergies
Caucasian race
Age between 30-50
Coexisting autoimmune disease e.g. coeliac disease

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144
Q

Gold standard diagnosis of eosinophilic oesphagitis?

A

Endoscopy: diagnosis can only be made on the histological analysis of an oesophageal biopsy.

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145
Q

Oesphagus: epithelial desquamation, eosinophilic microabscesses, and abnormally long papillae

A

Eosinophilic oesphagitis

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146
Q

Management of eosinophilic oesphagitis?

A

Dietary modification
Topical steroids e.g. fluticasone and budesonide
Oesphageal dilitation

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147
Q

Causes of raised calprotectin?

A

bowel malignancy
coeliac disease
infectious colitis
use of NSAIDs

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148
Q

Fever + RUQ pain

A

Acute cholecystitis

149
Q

Fever + RUQ + Jaundice

A

Cholangitis

150
Q

Patients with intercurrent illness + RUQ + Fever ?

A

Acalculous cholecystitis

151
Q

Management of acalculous cholecystitis?

A

cholecystectomy, if unfit then percutaneous cholecystostomy

152
Q

What is dumping syndrome?

A

Complication post gastrectomy

early dumping : food of high osmotic potential moves into small intestine causing fluid shift

late dumping (rebound hypoglycaemia): surge of insulin following food of high glucose value in small intestine - 2-3 hours later the insulin ‘overshoots’ causing hypoglycaemia

153
Q

Comlications of gastrectomy ?

A

Dumping syndrome

Weight loss, early satiety

Iron-deficiency anaemia

Osteoporosis/osteomalacia

Vitamin B12 deficiency

154
Q

Risk factors for gastric cancer?

A

Helicobacer pylori
atrophic gastritis
diet
salt and salt-preserved foods
nitrates
smoking
blood group

155
Q

Lymphatic spread of gastric cancer?

A

left supraclavicular lymph node (Virchow’s node)
periumbilical nodule (Sister Mary Joseph’s node)

156
Q

signet ring cells

A

Gastric cancer

157
Q

H pylori + paraproteinaemia?

A

MALToma

158
Q

Thread worm + pruritus ani

A

Enterobius vermicularis

159
Q

Treatment of enterobius vermiculus

A

Treatment is with mebendazole

160
Q

Features of Ancylostoma duodenale

A

Hookworms that anchor in proximal small bowel
Most infections are asymptomatic although may cause iron deficiency anaemia
Larvae may be found in stools left at ambient temperature, otherwise infection is difficult to diagnose
Infection occurs as a result of cutaneous penetration, migrates to lungs, coughed up and then swallowed

161
Q

Asciariasis?

A

Due to infection with roundworm Ascaris lumbricoides
Infections begin in gut following ingestion, then penetrate duodenal wall to migrate to lungs, coughed up and swallowed, cycle begins again
Diagnosis is made by identification of worm or eggs within faeces
Treatment is with mebendazole

162
Q

What is haemobilia?

A

connection between splanchnic circulation and either the intrahepatic or extrahepatic biliary system
haracterized by right upper quadrant pain, evidence of upper GI bleeding and jaundice.

163
Q

Management of haemochromatosis?

A

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)

164
Q

What are the reversible complications of haemochromatosis?

A

Cardiomyopathy
Skin pigmentation
Transaminitis

165
Q

What are the irreversible complications of haemochromatosis?

A

Liver cirrhosis**
Diabetes mellitus
Hypogonadotrophic hypogonadism
Arthropathy

166
Q

Inheritance of haemocrhomatosis?

A

Autosomal recessive

167
Q

How to screen for haemochromatosis/

A

For proband: Transferin saturation - most useful marker

For family members: HFE mutation

168
Q

Typical iron study for haemochromatosis?

A

transferrin saturation > 55% in men or > 50% in women
raised ferritin (e.g. > 500 ug/l) and iron
low TIBC

169
Q

Treatment for haemochromatosis?

A
  1. Venesection: kept below 50% and the serum ferritin concentration below 50 ug/l
  2. Desferroxime
170
Q

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

171
Q

What is used to determine a postivie heptitis?

A

HbeAG

172
Q

What shows that you have caught hepatitis B ?

A

Anti HBc

173
Q

Features of viral hepatitis

A

nausea and vomiting, anorexia
myalgia
lethargy
right upper quadrant (RUQ) pain

Questions may point to risk factors such as foreign travel or intravenous drug use.

174
Q

Biliary collic + palpable mass in the right upper quadrant (Courvoisier sign), periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node)

A

Cholangiocarcinoma

175
Q

Heart failure + RUQ pain

A

Congestive cardiomyopathy

176
Q

What is the mechanism of hepatorenal syndrome?

A

vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance

results in ‘underfilling’ of the kidneys

177
Q

Features of type 1 hepatorenal syndrome?

A

Rapidly progressive
Doubling of serum creatinine to > 221 µmol/L or a halving of the creatinine clearance to less than 20 ml/min over a period of less than 2 weeks
Very poor prognosis

178
Q

Features of type 2 hepatorenal syndrome?

A

Slowly progressive
Prognosis poor, but patients may live for longer

179
Q

What is hirchsprung disease?

A

Aganglionic segment of bowel

180
Q

Associationed with hirchsprung disease?

A

3 times more common in males
Down’s syndrome

181
Q

Diagnosis of hirchsprung disease?

A

abdominal x-ray
rectal biopsy: gold standard for diagnosis

182
Q

What type of hypersensitivity is hydatid cysts?

A

Type 1 hypersensitivity

183
Q

What causes hydatid cysts in the liver?

A

Echinococcus granulosus.

184
Q

What is the best imaging modality for hydatid liver cysts?

A

ultrasound if often used first-line

CT is the best investigation to differentiate hydatid cysts from amoebic and pyogenic cysts

185
Q

How should hydatid liver cyst be monitored?

A

Serology

186
Q

How best to diagnose hydatid liver cysts?

A

Serology

187
Q

How to differentiate between small or large bowel obstruction?

A

Valvulae conniventes extend all the way across

Haustra extend about a third of the way across

188
Q

Inherited causes of Jaundice:
Conjugated?

A

Dubin-Johnson syndrome
Rotor syndrome

189
Q

Inherited causes of Jaundice:
Unconjugated?

A

Gilbert’s syndrome
Crigler-Najjar syndrome

190
Q

Features of Gilbert’s syndrome?

A

autosomal recessive
mild deficiency of UDP-glucuronyl transferase
benign

191
Q

Features of crigler - najjar syndrome type 1?

A

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

192
Q

Features of crigler - najjar syndrome type 2?

A

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

193
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

194
Q

What are the features of rotar syndrome?

A

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

195
Q

Features of intrahpetic cholecystitis in pregnancy?

A

pruritus - may be intense - typical worse palms, soles and abdomen
clinically detectable jaundice occurs in around 20% of patients
raised bilirubin is seen in > 90% of cases

196
Q

Management of intraheptic cholecystitis?

A

Induction of labour at 37-38 weeks
ursodeoxycholic acid
vitamin K supplementation

197
Q

Where is iron absorbed mostly?

A

Duodenum

198
Q

What vitamins can increase iron absorption?

A

Vitamin C
Gastric acid

199
Q

What decreases iron absorption?

A

proton pump inhibitors
tetracycline
gastric achlorhydria
tannin

200
Q

How is iron transported around the body?

A

carried in plasma as Fe3+ bound to transferrin

201
Q

How is iron lost from the body?

A

Lost via intestinal tract following desquamation

202
Q

Diagnostic criteria of IBS?

A

patient has abdominal pain relieved by defecation or associated with altered bowel frequency stool form, in addition to 2 of the following 4 symptoms:

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

203
Q

Suggested blood to complete at GP for IBS?

A

full blood count
ESR/CRP
coeliac disease screen (tissue transglutaminase antibodies)

204
Q

Management of IBS?

A

First-line pharmacological treatment - according to predominant symptom
pain: antispasmodic agents
constipation: laxatives but avoid lactulose
diarrhoea: loperamide is first-line

Linaclotide can be considered if there has been no benefit from different laxatives and the patient has had constipation for at least 12 months.

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

205
Q

Difference between mesenteric ischaemic and ischaemic colitis?

A

Small bowel –> mesenteric colitis
Urgent surgery – mesenteric colitis
Caused by embolism –> mesenteric colitis
large bowel –> ischaemic colitis
Thumb printing –> ischaemic colitis
Bloody diarrhoea –> ischaemic colitis

206
Q

Features of ischaemic hepatitis?

A

increases in aminotransferase levels (exceeding 1000 international unit/L or 50 times the upper limit of normal)

207
Q

Absolute contraindications to laparoscopic surgery?

A

haemodynamic instability/shock
raised intracranial pressure
acute intestinal obstruction with dilated bowel loops (e.g. > 4 cm)
uncorrected coagulopathy

208
Q

Contraindications for 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

209
Q

Causes of liver cirrhosis?

A

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

210
Q

How should cirrhosis of the liver be diagnosed?

A

transient elastography and acoustic radiation force impulse imaging

211
Q

Who need transient elastography testing?

A

people with hepatitis C virus infection

men who drink over 50 units of alcohol per week and women who drink over 35 units of alcohol per week and have done so for several months

people diagnosed with alcohol-related liver disease

212
Q

What investigation do people with liver cirrhosis need regularly?

A

liver ultrasound every 6 months (+/- alpha-feto protein) to check for hepatocellular cancer

213
Q

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

A

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

214
Q

Child + very stable + intermittent intestinal bleeding>?

A

‘Meckel’s scan’ should be considered

215
Q

Presentation of meckel’s 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
secondary to an omphalomesenteric band (most commonly), volvulus and intussusception

216
Q

Imaging for heckles diverticulum?

A

Stable: 99m technetium pertechnetate,

Unstable: mesenteric arteriography

217
Q

Causes of metabolic alkalosis

A

vomiting / aspiration
hypokalaemia
diuretics
liquorice, carbenoxolone
primary hyperaldosteronism
Cushing’s syndrome
Bartter’s syndrome

218
Q

Adverse effects of spironolactone?

A

extrapyramidal effects
acute dystonia e.g. oculogyric crisis
this is particularly a problem in children and young adults
diarrhoea
hyperprolactinaemia
tardive dyskinesia
parkinsonism

219
Q

Mechanism of metaclopramide?

A

D2 receptor antagonist

220
Q

Risk factors for microscopic colitis?

A

smoking
drugs: NSAIDs, PPIs and SSRIs

221
Q

Features of microscopic colitis?

A

watery diarrhoea
faecal urgency
abdominal pain
constitutional symptoms such as weight loss, lethargy and arthralgia may be present
non-specific investigation findings include mild anaemia and raised inflammatory markers. Autoantibodies such as rheumatoid factor and ANA may also be present

222
Q

LFT suggestive of Non-alcoholic fatty liver disease ?

A

ALT is typically greater than AST

223
Q

Types of non-alcoholic fatty liver disease?

A

steatosis - fat in the liver
steatohepatitis - fat with inflammation, non-alcoholic steatohepatitis (NASH), see below
progressive disease may cause fibrosis and liver cirrhosis

224
Q

In an incidental finding of NAFLD, what blood test should be done?

A

enhanced liver fibrosis (ELF) blood test to check for advanced fibrosis

225
Q

Oesphageal cancer + lower third of oesophagus

A

Adenocarcinoma

226
Q

Risk factors for adenocarcinoma of oesophagus?

A

GORD
Barrett’s oesophagus
smoking
obesity

227
Q

Oesophageal cancer + upper two thirds of oesphagus?

A

Squamous carcinoma

228
Q

Risk factors of squamous carcinoma of oesphagus?

A

smoking
alcohol
achalasia
Plummer-Vinson syndrome
diets rich in nitrosamines

229
Q

What is required for local staging of oesophagus?

A

Endoscopic ultrasound

230
Q

Diagnostic test for oesophageal carcinoma?

A

Upper GI endoscopy

231
Q

Best test for staging of oesophagus?

A

CT scanning of the chest, abdomen and pelvis is used for initial staging

FDG-PET CT may be used for detecting occult metastases if metastases are not seen on the initial staging CT scans.

Laparoscopy is sometimes performed to detect occult peritoneal disease

232
Q

Plummer vinson syndrome?

A

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

233
Q

Management of Plummer Vinsons syndrome?

A

Treatment includes iron supplementation and dilation of the webs

234
Q

Double duct sign?

A

Pancreatic carcinoma

235
Q

Associations of pancreatic cancer?

A

increasing age
smoking
diabetes
chronic pancreatitis (alcohol does not appear an independent risk factor though)
hereditary non-polyposis colorectal carcinoma
multiple endocrine neoplasia
BRCA2 gene
KRAS gene mutation

236
Q

What is trousseau sign?

A

migratory thrombophlebitis (Trousseau sign)

237
Q

Features of pancreatic cancer?

A

classically painless jaundice
pale stools, dark urine, and pruritus
cholestatic liver function tests
the following abdominal masses may be found (in decreasing order of frequency)
hepatomegaly: due to metastases
gallbladder: Courvoisier’s law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
epigastric mass: from the primary tumour
many patients 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

238
Q

When is a whipples procedure required?

A

a Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas.

239
Q

Side effect of whipples procedure?

A

dumping syndrome and peptic ulcer disease

240
Q

Palliative management of pancreatic carcinoma?

A

ERCP stenting

241
Q

Pathophysiology 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

242
Q

Features of pernicious anaemia?

A

anaemia features
lethargy
pallor
dyspnoea

peripheral neuropathy: ‘pins and needles’, numbness. Typically symmetrical and affects the legs more than the arms
subacute combined degeneration of the spinal cord: progressive weakness, ataxia and paresthesias that may progress to spasticity and paraplegia
neuropsychiatric features: memory loss, poor concentration, confusion, depression, irritabiltiy

mild jaundice: combined with pallor results in a ‘lemon tinge’
glossitis → sore tongue

243
Q

Investigation findings for pernicious anaemia?

A

full blood count
macrocytic anaemia: macrocytosis may be absent in around of 30% of patients
hypersegmented polymorphs on blood film
low WCC and platelets may also be seen

antibodies
anti intrinsic factor antibodies: sensivity is only 50% but highly specific for pernicious anaemia (95-100%)
anti gastric parietal cell antibodies in 90% but low specificity so often not useful clinically

244
Q

Management of pernicious anaemia?

A

Vitamin B12 replacement:
- no neurological features: 3 injections per week for 2 weeks followed by 3 monthly treatment of vitamin B12 injections
- Given IM

245
Q

Complication of pernicious anaemia?

A

Gastric cancer

246
Q

Phenotype of peutzjeghers syndrome?

A

pigmented freckles on the lips, face, palms and soles.
numerous hamartomatous polyps in the gastrointestinal tract.

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

247
Q

Inheritance of peutz joggers syndrome?

A

autosomal dominant
responsible gene encodes serine threonine kinase LKB1 or STK11

248
Q

Where is most likely place for a pharyngeal pouch ?

A

posteromedial diverticulum through Killian’s dehiscence

Killian’s dehiscence is a triangular area in the wall of the pharynx between the thyropharyngeus and cricopharyngeus muscles

249
Q

Features of pharyngeal pouch?

A

dysphagia
regurgitation
aspiration
neck swelling which gurgles on palpation
halitosis

250
Q

What is the best investigation for pharyngeal pouch?

A

Barium swallow

251
Q

How to different between Intrahepatic cholestasis of pregnancy and acute fatty liver?

A

Acute fatty liver –> third trimester / after delivery
Hypoglycaemia –> acute fatty liver
Pre-eclampsia –> acute fatty liver
ALT 500 –> acute fatty liver

252
Q

associations between primary billiary sclerosis ?

A

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

253
Q

Features of primary billiard sclerosis?

A

early: may be asymptomatic (e.g. raised ALP on routine LFTs) or fatigue, pruritus
cholestatic jaundice
hyperpigmentation, especially over pressure points
right upper quadrant pain
xanthelasmas, xanthomata

also: clubbing, hepatosplenomegaly
late: may progress to liver failure

254
Q

Antibodies associated primary billiary sclerosis?

A

Raised IgM
anti-mitochondrial antibodies (AMA) M2 subtype

255
Q

What is the best investigation for primary billiary sclerosis?

A

MRCP

256
Q

Management of primary billiary sclerosis?

A
  1. first-line: ursodeoxycholic acid

Puritis: cholestyramine

257
Q

Complications of primary billiary sclerosis?

A

cirrhosis → portal hypertension → ascites, variceal haemorrhage

osteomalacia and osteoporosis

significantly increased risk of hepatocellular carcinoma (20-fold increased risk)

258
Q

What conditions are associated with primary sclerosing 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

259
Q

Features of primary sclerosing cholangitis?

A

cholestasis
jaundice, pruritus
raised bilirubin + ALP
right upper quadrant pain
fatigue

260
Q

How is primary sclerosing cholangitis diagnosed?

A

ERCP
MRCP

Shows multiple biliary strictures giving a ‘beaded’ appearance

261
Q

What serological test may be positive in primary sclerosing cholangitis?

A

p-ANCA

262
Q

Onion skin?

A

Primary sclerosing cholangitis

263
Q

Complications of primary scerlosing cholangitis?

A

cholangiocarcinoma (in 10%)
increased risk of colorectal cancer

264
Q

What is pseudomyxoma peritoni?

A

rare mucinous tumour most commonly arising from the appendix

265
Q

What is the treatment for pseudomyoxoma peritoni?

A

surgical and consists of cytoreductive surgery (and often peritonectomy) combined with intra-peritoneal chemotherapy with mitomycin C

266
Q

What pH abnormality is seen in pyloric stenosis?

A

hypochloraemic, hypokalaemic alkalosis due to persistent vomiting

267
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

268
Q

What is the most likely organism to cause liver abscess?

A

Staphylococcus aureus in children and Escherichia coli in adults.

269
Q

Management of liver abscess?

A

Drainage
Amoxicillin + Ciprofloxacin + Metronidazole

if penicillin allergic: ciprofloxacin + clindamycin

270
Q

Riglers / Double wall sign?

A

Pneumoperitoneum

271
Q

What is the biochemistry of refeeding syndrome?

A

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

272
Q

What is the test for small bowel overgrowth syndrome?

A

Hydrogen breath test

273
Q

Risks of small bowel overgrowth syndrome?

A

neonates with congenital gastrointestinal abnormalities
scleroderma
diabetes mellitus

274
Q

What is antibiotic of choice for small bowel overgrowth syndrome?

A

Rifaxamin

275
Q

Fever + Ascites + Abdominal pain ?

A

Spontaneous bacterial peritonitis

276
Q

Paracentesis results from SBP?

A

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

277
Q

Management of SBP?

A

IV cefotaxime

278
Q

How to prevent SBP?

A

Give antibiotic prophylaxis if:
- Previous SBP
- fluid protein < 15

Offer ciprofloxacin or norfloxacin

279
Q

What is the treatment for threadworms?

A

mebendazole

280
Q

Mild UC?

A

mild: < 4 stools/day, only a small amount of blood

281
Q

Moderate UC?

A

moderate: 4-6 stools/day, varying amounts of blood, no systemic upset

282
Q

Severe UC?

A

severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

283
Q

Treatment of proctitis?

A

topical (rectal) aminosalicylate

If no remissino in 4 weeks then add an oral aminosalicylate

If remission still not achieved add oral corticosteroid

284
Q

Management of left sided UC?

A

topical (rectal) aminosalicylate

If no remissino in 4 weeks then:
- high-dose oral aminosalicylate OR switch to a high-dose oral aminosalicylate and a topical corticosteroid

If remission still not achieved add oral corticosteroid

285
Q

Severe colitis management?

A

IV steroids

286
Q

How to maintain remission of proctitis and proctosigmoiditis?

A

topical (rectal) aminosalicylate alone (daily or intermittent)

an oral aminosalicylate plus a topical (rectal) aminosalicylate (daily or intermittent)

an oral aminosalicylate by itself:

287
Q

How to maintain remission if > 2 exacerbations in a year?

A

oral azathioprine or oral mercaptopurine

288
Q

Varices: antibiotic prophylaxis?

A

Offer prophylactic intravenous antibiotics for people with cirrhosis who have upper gastrointestinal bleeding

289
Q

Prophylaxis of variceal bleeds?

A

Propanolol

290
Q

What is a villous adenoma?

A

secrete large amounts of mucous

non-specific lower gastrointestinal symptoms
secretory diarrhoea may occur
microcytic anaemia
hypokalaemia

291
Q

What is vitamin A (retinol) used for?

A

converted into retinal, an important visual pigment

292
Q

What is the consequences of Vitamin A deficiency?

A

night blindness

293
Q

Consequences of thiamine deficiency?

A

Wernicke’s encephalopathy: nystagmus, ophthalmoplegia and ataxia
Korsakoff’s syndrome: amnesia, confabulation
dry beriberi: peripheral neuropathy
wet beriberi: dilated cardiomyopathy

294
Q

Functions of vitamin D?

A

increases plasma calcium and plasma phosphate

increases renal tubular reabsorption and gut absorption of calcium

increases osteoclastic activity

increases renal phosphate reabsorption

295
Q

Sigmoid volvulus associations?

A

older patients
chronic constipation
Chagas disease
neurological conditions e.g. Parkinson’s disease, Duchenne muscular dystrophy
psychiatric conditions e.g. schizophrenia

296
Q

Caecal volvulous associations ?

A

all ages
adhesions
pregnancy

297
Q

Management of sigmoid volvulus?

A

sigmoid volvulus: rigid sigmoidoscopy with rectal tube insertion

298
Q

Management of caecal volvulus?

A

Right hemicolectomy is often needed

299
Q

HLA association of whipples disease?

A

HLA B 27

300
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

301
Q

Investigation findings of whipples disease?

A

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

302
Q

Gene defect in Wilsons disease?

A

defect in the ATP7B gene located on chromosome 13.

303
Q

Management of Wilsons disease?

A

Penicillamine

304
Q

Features of Wilson’s disease ?

A

liver: hepatitis, cirrhosis
neurological:
basal ganglia degeneration
Kayser-Fleischer rings
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails

305
Q

Biochemistry for Wilsons disease/

A

reduced serum caeruloplasmin

reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)

increased 24hr urinary copper excretion

306
Q

What is Zollinger Ellison syndrome associated with?

A

MEN1

307
Q

Features of Zollinger Ellison syndrome?

A

multiple gastroduodenal ulcers
diarrhoea
malabsorption

308
Q

Single best screening test for Zollinger Ellison syndrome?

A

fasting gastrin levels: the single best screen test

Secretin stimulation test

309
Q

Cirrhosis + Grade 1varices?

A

Rescope 1 year

310
Q

Cirrhosis + Grade 2 varices?

A

Non-cardio selective beta blocker

311
Q

Difference ebwteen type 1 and type 2 hepatorenal syndrome?

A

Type 2 slow rising of creatinine
Type 1 rapid doubling of creatine - dies quickly

312
Q

Management of diffuse oesphageal spasm?

A

Chest pain: Calcium channel blocker

dysphagia resistant to pharmacological therapies require more invasive or surgical treatments.

  1. Endoscopic Botox is beneficial but may require multi-level injections and repeat treatments
  2. Significant weight loss –> Consider pneumatic dilation
313
Q

What is better: Banding or sclerotherapy?

A

Banding

314
Q

Vitamin deficiency + adult ?

A

Osteomalacia

315
Q

Non-variceal UGI bleed: do you give high dose PPI?

A

Give if PPI is not going to be given within 24 hours

316
Q

Thumb print

A

Specific for nothing
Doesn ot mean ischaemic colitis
Just colitis in general

317
Q

What is considered diagnostic of bile acid malabsorption?

A

A 7-day SeHCAT retention value of less than 15% is generally considered indicative of bile salt malabsorption

318
Q

What pregnancy drug can cause hepatitis?

A

Labetalol

319
Q

Coffee bean shape

A

Sigmoid volvulus

320
Q

Zieves syndrome?

A

Zieve syndrome is a triad of symptoms: haemolytic anemia, cholestatic jaundice, and transient hyperlipidemia

Occur during withdrawal from prolonged alcohol abuse.

321
Q

Features of pouchitis?

A

30 % of patients develop pouchitis

increased stool frequency, urgency, incontinence and nocturnal seepage.

322
Q

Treatment of pouchitis?

A

Metronidazole

323
Q

Hydatid cyst + hypotension +/- wheeze ?

A

Think type 1 hypersensitivity reaction

324
Q

Differentiate between acute fatty liver of pregnancy and obstetric cholestasis?

A

Increased bile salts –> cholestasis

325
Q

What can a TIPS procedure exacerbate?

A

hepatic encephalopathy

326
Q

Criteria for 5 yearly check up colonoscopy?

A

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

327
Q

Criteria for 3 yearly check up colonoscopy?

A

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

328
Q

Criteria for yearly check up colonoscopy?

A

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

329
Q

Ascitic tap: Mixed growth

A

Think perforation

330
Q

Antibiotic that causes cholestasis ?

A

Flucloxacillin

331
Q

In haemodynamically stable patients, what Hb is require in upper go bleeding?

A

70-80
Do not over transfuse

332
Q

In incomplete bowel obstruction, how can this be managed?

A

Metoclopramide
Make sure they pass flatus

333
Q

Alternative to prednisolone in UC?

A

Budesonide
It is less good

334
Q

Barrets oesphagus + low grade dysplasia?

A

Radiofrequency ablation

335
Q

IBD + pANCA?

A

Ulcerative colitis

336
Q

IBD + Anti-Saccharomyces cerevisiae antibodies

A

Crohn’s

337
Q

lymphocytic infiltrate large bowel

A

microscopic colitis

338
Q

Biologic therapy is considered in treatment of an acute flare of Crohn’s disease when symptoms don’t improve after 5 days of IV hydrocortisone

A

Biologic therapy is considered in treatment of an acute flare of Crohn’s disease when symptoms don’t improve after 5 days of IV hydrocortisone

339
Q

What is the diagnostic test for Wilsons?

A

Gene test for ATP7B

340
Q

light bright on use?

A

fat –> steatosis

341
Q

What causes whipples disease?

A

Tropheryma whippelii infection

342
Q

What is the treatment for whipples disease?

A

IV penicilline

343
Q

High grade dysplasia + Barrets?

A

Endoscopic resection

344
Q

Gallstone ileum may have pneumobillia?

A

Stone fistulas through into bowel

345
Q

When can penacillamine not be used?

A

Penicillin allergy
Alternative: trientine

346
Q

Screening for hepatocellular carcinoma in cirrhosis?

A

6 monthly

347
Q

Ulcerative colitis + cholestatis (e.g. jaundice, raised ALP)

A

primary sclerosing cholangitis

348
Q

Venesection regimen for haemochromatosis?

A

400-500 ml every 1-2 week

349
Q

Surveillance for barrels with no risk factors?

A

3 years

350
Q

Primary biliary cholangitis - the M rule
IgM

A

anti-Mitochondrial antibodies, M2 subtype
Middle aged females

351
Q

Hyperemesis can lead to…?

A

Thiamine deficiency
Wernickes

352
Q

pellagra is deficiency of what?

A

Niacin

353
Q

Test for autoimmune pancreatitis?

A

IgG4

354
Q

burning pain and tingling in the hands and feet, particularly after exertion or when weather temperatures are extremely hot or cold.

A

fabrys

355
Q

Low B12 + high follate?

A

Small bowel bacterial overgrowth

356
Q

UC drug that causes heinz bodies?

A

Sulphasalazine
Heinz bodies indicate oxidative damage

357
Q

Carcinoid syndrome - heart changes?

A

Fibrous endocardial thickeing

358
Q

Can you take azathioprine in pregnancy ?

A

Yes

359
Q

CT findings of poor visualization of the hepatic veins with hypoattenuation of the peripheral zones

A

Budd chiari

360
Q

Hepatits B: Best level for determining if going to develope cirrhosis?

A

Hepatitis B DNA level

361
Q

Complete bowel obstruciton secondary to metastasis?

A

Steroids

362
Q

If a patient has a low TPMT test - what does this mean?

A

Do not treat with azathiprine
or
mercaptopurine

363
Q

Carcinoid: What is the better test 24 urinary 5HIAA or plasma chromogranin?

A

24 urinary 5HIAA

364
Q

Hepatic encephalopathy: Steroids?

A

Review use of steriods at 7 days

If not improving consider stopping

365
Q

Acute dystonic reaction treatment - reaction from metoclopramide?

A

IV procyclidine

366
Q

Sjorgans is associated with PBC

A

Sjorgans is associated with PBC

367
Q

Joint complication related to haemocromatosis?

A

pseudogout

368
Q

How to manage hepatorenal syndrome?

A

Terlipressin + Albumin

369
Q

Diarrhoea, fatigue, osteomalacia

A

coeliac

MRCP: Gastro (2 decks)

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