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MRCP part 1 > Gastro > Flashcards

Gastro Flashcards

1
Q

Features of Crohn’s Disease

A

Diarrhoea usually non-bloody
Weight loss more prominent
Upper gastrointestinal symptoms, mouth ulcers, perianal disease
Abdominal mass palpable in the right iliac fossa

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2
Q

Features of UC

A

Bloody diarrhoea more common
Abdominal pain in the left lower quadrant
Tenesmus

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3
Q

Extra-intestinal features of Crohn’s disease

A

Gallstones are more common secondary to reduced bile acid reabsorption

Oxalate renal stones*

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4
Q

Extra-intestinal features of UC

A

Primary sclerosing cholangitis more common

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5
Q

Complications of Crohns

A

Obstruction, fistula, colorectal cancer

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6
Q

Pathology of Crohn’s

A

Lesions may be seen anywhere from the mouth to anus

Skip lesions may be present

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7
Q

Pathology of UC

A

Inflammation always starts at rectum and never spreads beyond ileocaecal valve

Continuous disease

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8
Q

Histology of Crohn’s

A

Inflammation in all layers from mucosa to serosa
increased goblet cells
granulomas

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9
Q

Histology of UC

A

No inflammation beyond submucosa (unless fulminant disease) - 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

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10
Q

Crohn’s endoscopy findings

A

Deep ulcers, skip lesions - ‘cobble-stone’ appearance

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11
Q

UC endoscopy findings

A

Widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)

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12
Q

Crohn’s radiology findings

A 
Small bowel enema
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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13
Q

UC radiology findings

A

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

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14
Q

Hep B surface antigen

A

(HBsAg) is the first marker to appear and causes the production of anti-HBs
Usually indicates acute infection 1-6 months
If present >6 months = chronic infection

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15
Q

Anti-HBs

Anti HB surface antigen

A

implies immunity - exposure or immunisation

absent in chronic infection

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16
Q

Anti-HBc

Anti Hep B core antigen

A

previous or current infection

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17
Q

IgM anti-HBc

A

Appears during acute or recent hepatitis B infection and is present for about 6 months.

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18
Q

IgG anti-HBc

A

persistant infection

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19
Q

HbeAg

A

results from breakdown of core antigen from infected liver cells as is, therefore, a marker of infectivity. Marker of HBV replication and infectivity

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20
Q

Hep B

Previous immunisation

A

anti-HBs positive, all others negative

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21
Q

Hep B

previous infection, not a carrier

A

anti-HBc positive, HBsAg negative

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22
Q

previous hepatitis B, now a carrier:

A

anti-HBc positive, HBsAg positive

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23
Q

Wilsons disease

Liver features

A

cirrhosis

hepatitits

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24
Q

Wilsons disease

Neurological features

A

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

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25
Q

Wilson’s disease

Kayser-Fleischer rings

A

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

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26
Q

Wilson’s disease

other

A

renal tubular acidosis
esp Fanconi’s syndrome

Blue nails
haemolysis

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27
Q

Wilson’s disease

Diagnosis

A 
Slit lamp for Kayser-Fleischer rings 
Serum caeruloplasmin - reduced 
Serum total copper - reduced
free copper - increased 
increased 24hr urinary copper secretion
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28
Q

Management of Wilsons disease

A

penicillamine
trientine hydrochloride
tetrathiomolybdate

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29
Q

Complications of coeliac disease

A

hyposplenism
anaemia - iron, folate, B12 deficiency
osteoporosis, osteomalacia
lactose intolerance
T-cell mediated gastric lymphoma
subfertility, unfavourable pregnancy outcomes
rare: oesophageal cancer, other malignancies

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30
Q

Primary biliary cholangitis (prev cirrhosis)

A

interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis which may eventually progress to cirrhosis. The classic presentation is itching in a middle-aged woman

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31
Q

Associations with primary biliary cholangitis

A

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

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32
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

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33
Q

Diagnosis of primary biliary cholangitis

Immunology

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

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34
Q

Diagnosis of primary biliary cholangitis

imaging

A

required before diagnosis to exclude an extrahepatic biliary obstruction (typically a right upper quadrant ultrasound or magnetic resonance cholangiopancreatography (MRCP)

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35
Q

Management of primary biliary cholangitis

A

ifrst-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

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36
Q

Complications of primary biliary cholangitis

A

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

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37
Q

Boerhaave syndrome

A

Severe vomiting → oesophageal rupture

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38
Q

Mallory-Weiss syndrome

A

Severe vomiting → painful mucosal lacerations at the gastroesophageal junction resulting in haematemesis. Common in alcoholics

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39
Q

Plummer-Vinson syndrome

A

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

Treatment includes iron supplementation and dilation of the webs

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40
Q

where is CCK secreted from

A

I cells in upper small intestine

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41
Q

Action of CCK

A

Increases secretion of enzyme-rich fluid from pancreas, contraction of gallbladder and relaxation of sphincter of Oddi, decreases gastric emptying, trophic effect on pancreatic acinar cells, induces satiety

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42
Q

Stimulation of CCK

A

Partially digested proteins and triglycerides

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43
Q

Source of Gastrin

A

G cells in antrum of the stomach

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44
Q

Stimulation of Gastrin

A

Distension of stomach, vagus nerves (mediated by gastrin-releasing peptide), luminal peptides/amino acids
Inhibited by: low antral pH, somatostatin

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45
Q

Action of Gastrin

A

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

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46
Q

Source of secretin

A

S cells in upper small intestine

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47
Q

Stimulation of secretin production

A

acidic chyme, fatty acids

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48
Q

Action of secretin

A

Increases secretion of bicarbonate-rich fluid from pancreas and hepatic duct cells, decreases gastric acid secretion, trophic effect on pancreatic acinar cells

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49
Q

Source of VIP

A

Small intestine, pancreas

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50
Q

Stimulation of VIP

A

Neural

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51
Q

Action of VIP

A

Stimulates secretion by pancreas and intestines, inhibits acid secretion

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52
Q

Source of somatostatin

A

D cells in the pancreas & stomach

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53
Q

Stimulation of somatostatin

A

Fat, bile salts and glucose in the intestinal lumen

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54
Q

Action of somatostatin

A

Decreases acid and pepsin secretion, decreases gastrin secretion, decreases pancreatic enzyme secretion, decreases insulin and glucagon secretion
inhibits trophic effects of gastrin, stimulates gastric mucous production

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55
Q

Ascending cholangitis

Presenting symptoms

A

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

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56
Q

Management of ascending cholangitis

A

intravenous antibiotics

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

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57
Q

What is whipple’s disease

A

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

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58
Q

Features of whipple’s disease

A

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

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59
Q

Whipple’s disease investigations

A

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

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60
Q

Management of whipple’s disease

A

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

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61
Q

Features of billiary colic

A

Colicky abdominal pain, worse postprandially, worse after fatty foods

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62
Q

Management of billiary colic

A

imaging- gallstones and history compatible then laparoscopic cholecystectomy

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63
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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64
Q

Management of acute cholecystitis

A

Imaging (USS) and cholecystectomy (ideally within 48 hours of presentation)

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65
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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66
Q

Management of gallbladder abscess

A

Imaging with USS +/- CT Scanning
Ideally, surgery although subtotal cholecystectomy may be needed if Calot’s triangle is hostile
In unfit patients, percutaneous drainage may be considered

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67
Q

Features of cholecystitis

A

Patient severely septic and unwell
Jaundice
Right upper quadrant pain

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68
Q

Management of cholecysittis

A

Fluid resuscitation
Broad-spectrum intravenous antibiotics
Correct any coagulopathy
Early ERCP

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69
Q

Features of gallstone ileus

A

Patients may have a history of previous cholecystitis and known gallstones
Small bowel obstruction (may be intermittent)

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70
Q

Management of gallstone ileus

A

Laparotomy and removal of the gallstone from small bowel, the enterotomy must be made proximal to the site of obstruction and not at the site of obstruction. The fistula between the gallbladder and duodenum should not be interfered with.

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71
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

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72
Q

Management of aculous cholecystitis

A

If patient fit then cholecystectomy, if unfit then percutaneous cholecystostomy

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73
Q

Gilbert’s syndrome

A

autosomal recessive
mild deficiency of UDP-glucuronyl transferase
benign

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74
Q

Crigler-Najjar syndrome, type 1

A

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

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75
Q

Crigler-Najjar syndrome, type 2

A

slightly more common than type 1 and less severe

may improve with phenobarbital

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76
Q

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

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77
Q

Rotor syndrome

A

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

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78
Q

Mechanism of action

Metoclopramide

A

D2 receptor antagonist

it is also a mixed 5-HT3 receptor antagonist/5-HT4 receptor agonist
the antiemetic action is due to its antagonist activity at D2 receptors in the chemoreceptor trigger zone. At higher doses the 5-HT3 receptor antagonist also has an effect
the gastroprokinetic activity is mediated by D2 receptor antagonist activity and 5-HT4 receptor agonist activity

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79
Q

Metoclopramide

Uses

A

Nausea
gastro-oesophageal reflux disease
prokinetic action is useful in gastroparesis secondary to diabetic neuropathy
often combined with analgesics for the treatment of migraine (migraine attacks result in gastroparesis, slowing the absorption of analgesics)

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80
Q

Metoclopramide

adverse features

A

extrapyramidal effects: oculogyric crisis. This is particularly a problem in children and young adults
hyperprolactinaemia
tardive dyskinesia
parkinsonism

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81
Q

Metoclopramide

Ileus vs obstruction

A

Maybe helpful in ileus

Avoid in obstruction

82
Q

Acute management of alcoholic hepatitis

A

glucocorticoids (e.g. prednisolone) are often used during acute episodes of alcoholic hepatitis
Maddrey’s discriminant function (DF) is often used during acute episodes to determine who would benefit from glucocorticoid therapy
it is calculated by a formula using prothrombin time and bilirubin concentration

83
Q

Presenting features 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)

84
Q

Reversible complications of haemochromatosis

A

cardiomyopathy

skin discolouration

85
Q

Irreversible complications of haemochromatosis

A

Liver cirrhosis**
Diabetes mellitus
Hypogonadotrophic hypogonadism
Arthropathy

86
Q

Aminosalicylate drugs

A

5-aminosalicyclic acid (5-ASA) is released in the colon and is not absorbed. It acts locally as an anti-inflammatory. The mechanism of action is not fully understood but 5-ASA may inhibit prostaglandin synthesis

Aminosalicylates are associated with a variety of haematological adverse effects, including agranulocytosis - FBC is a key investigation in an unwell patient taking them.

*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine

87
Q

Sulphasalazine

A

a combination of sulphapyridine (a sulphonamide) and 5-ASA
many side-effects are due to the sulphapyridine moiety: rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis
other side-effects are common to 5-ASA drugs (see mesalazine)

88
Q

Mesalazine

A

a delayed release form of 5-ASA
sulphapyridine side-effects seen in patients taking sulphasalazine are avoided
mesalazine is still however associated with side-effects such as GI upset, headache, agranulocytosis, pancreatitis*, interstitial nephritis

89
Q

Hydatid cysts

A

Hydatid cysts are endemic in Mediterranean and Middle Eastern countries. They are caused by the tapeworm parasite Echinococcus granulosus. An outer fibrous capsule is formed containing multiple small daughter cysts. These cysts are allergens which precipitate a type 1 hypersensitivity reaction.

90
Q

Clinical features of hydatid cysts

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

91
Q

Investigation of hydatid cysts

A

imaging
ultrasound if often used first-line
CT is the best investigation to differentiate hydatid cysts from amoebic and pyogenic cysts
serology
useful for primary diagnosis and for follow-up after treatment
wide variety of different antibody/antigen tests available

92
Q

Peutz-Jagher’s syndrome

A

autosomal dominant condition characterised by numerous hamartomatous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on the lips, face, palms and soles. Although the polyps themselves don’t have malignant potential, around 50% of patients will have died from another gastrointestinal tract cancer by the age of 60 years.

Genetics
autosomal dominant
responsible gene encodes serine threonine kinase LKB1 or STK11

93
Q

Peutz-Jeghers syndrome

Features

A

hamartomatous polyps in GI tract (mainly small bowel)
pigmented lesions on lips, oral mucosa, face, palms and soles
intestinal obstruction e.g. intussusception
gastrointestinal bleeding

94
Q

What is carcinoid syndrome

A

usually occurs 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

95
Q

Features of carcinoid syndrome

A

flushing (often 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

96
Q

Investigations of carcinoid syndrome

A

urinary 5-HIAA

plasma chromogranin A y

97
Q

Management of carcinoid syndrome

A

somatostatin analogues e.g. octreotide

diarrhoea: cyproheptadine may help

98
Q

Primary causes of bile acid malabsorption

A

excessive production of bile acid, or secondary to an underlying gastrointestinal disorder causing reduced bile acid absorption. It can lead to steatorrhoea and vitamin A, D, E, K malabsorption.

99
Q

Secondary causes of bile acid malabsorption

A

ileal disease e.g. Crohn’s
cholecystectomy
coeliac disease
small intestinal bacterial overgrowth

100
Q

Investigations of bile acid malabsorption

A

the test of choice is SeHCAT
nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT)
scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCAT

101
Q

Management of bile acid malabsorption

A

bile acid sequestrants e.g. cholestyramine

102
Q

Threadworms

A

Enterobius vermicularis

103
Q

Management of enterobius vermicularis

A

CKS recommend a combination of anthelmintic with hygiene measures for all members of the household
mebendazole is used first-line for children > 6 months old. A single dose is given unless infestation persists

104
Q

Crigler-Najjar syndrome, type 1

A

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

105
Q

Crigler-Najjar syndrome type 2

A

slightly more common than type 1 and less severe
may improve with phenobarbitol
unconjugated hyperbilirubinaemia

106
Q

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
Conjugated hyperbilirubinaemia

107
Q

Rotor syndrome

A

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

108
Q

Gilbert’s syndrome

A

autosomal recessive
mild deficiency of UDP-glucuronyl transferase
benign
unconjugated hyperbilirubinaemia

109
Q

Wilson’s disease - genetics

A

Defect in the ATP7B gene

110
Q

adverse effects of sulfasalazine

A

sulphapyridine moiety: rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis, GI upset, headache, agranulocytosis, pancreatitis*, interstitial nephritis

111
Q

Typical history of Whipple’s disease

A

a 45-year-old man is being investigated for diarrhoea, weight loss and arthralgia. Jejunal biopsy shows deposition of macrophages containing PAS-positive granules

112
Q

What is whipple’s disease

A

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

113
Q

Features of Whipple’s disease

A

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

114
Q

Investigation findings of Whipple’s disease

A

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

115
Q

Management of Whipple’s disease

A

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

116
Q

Bile acid malabsorption: causes

A

primary, due to excessive production of bile acid, or secondary to an underlying gastrointestinal disorder causing reduced bile acid absorption. It can lead to steatorrhoea and vitamin A, D, E, K malabsorption.

Secondary causes are often seen in patients with ileal disease, such as with Crohn’s. Other secondary causes include:
cholecystectomy
coeliac disease
small intestinal bacterial overgrowth

117
Q

Bile acid malabsorption investigations

A

the test of choice is SeHCAT
nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT)
scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCA

118
Q

Bile acid malabsorption management

A

bile acid sequestrants e.g. cholestyramine

119
Q

Hormones that decrease gastric H+ secretion

A

secretin
VIP
somatostatin

120
Q

familial adenomatous polyposis chromosome

A

chromosome 5

121
Q

Genetic causes of colorectal cancer

A

sporadic (95%) ( half of colon cancers show allelic loss of the APC gene) further series of gene abnormalities e.g. activation of the K-ras oncogene, deletion of p53 and DCC tumour suppressor genes lead to invasive carcinoma
hereditary non-polyposis colorectal carcinoma (HNPCC, 5%)
familial adenomatous polyposis (FAP, <1%)

122
Q

HNPCC- hereditary non-polyposis colorectal carcinoma

A

an autosomal dominant condition, is the most common form of inherited colon cancer. Around 90% of patients develop cancers, often of the proximal colon, which are usually poorly differentiated and highly aggressive. Currently seven mutations have been identified, which affect genes involved in DNA mismatch repair leading to microsatellite instability. The most common genes involved are:
MSH2 (60% of cases)
MLH1 (30%)

123
Q

Typical history of Plummer-Vinson syndrome

A

a 60-year-old woman presents with dysphagia and lethargy. On examination she has a smooth, swollen tongue and pale conjunctivae

124
Q

What is Plummer-Vinson syndrome

A

dysphagia (secondary to oesophageal webs)
glossitis
iron-deficiency anaemia- managed with iron replacement and dilatation of the webs

125
Q

Stereotypical history of Meckle’s diverticulum

A

a 1-year-old boy with a recent history of rectal bleeding presents with intestinal obstruction. During surgery he is found to have a omphalomesenteric band

126
Q

What is Meckle’s diverticulum

A

congenital diverticulum of the small intestine. It is a remnant of the omphalomesenteric duct (also called the vitellointestinal duct) and contains ectopic ileal, gastric or pancreatic mucosa

127
Q

Rule of 2 - Meckle’s diverticulum

A

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

128
Q

Presentation of Meckle’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

129
Q

Management of Meckle’s diverticulum

A

removal if narrow neck or symptomatic. Options are between wedge excision or formal small bowel resection and anastomosis.

130
Q

Pathophysiology of Meckle’s diverticulum

A

normally, in the foetus, there is an attachment between the vitellointestinal duct and the yolk sac. This disappears at 6 weeks gestation
the tip is free in the majority of cases
associated with enterocystomas, umbilical sinuses, and omphaloileal fistulas.
arterial supply: omphalomesenteric artery.
typically lined by ileal mucosa but ectopic gastric mucosa can occur, with the risk of peptic ulceration. Pancreatic and jejunal mucosa can also occur.

131
Q

Actions of somatostatin

A

Decreases acid and pepsin secretion, decreases gastrin secretion, decreases pancreatic enzyme secretion, decreases insulin and glucagon secretion
inhibits trophic effects of gastrin, stimulates gastric mucous production

132
Q

Wilson’s disease chromosome

A

Chromosome 13

133
Q

Prophylaxis of variceal haemorrhage

A

propranolol, endoscopic banding and ligation

134
Q

Treatment of variceal haemorrhage

A

Telipressin, IV abx (quinolones), ABCDE, banding

135
Q

Kantor’s string sign

A

gastrointestinal string sign (also known as the string sign of Kantor) refers to the string-like appearance of a contrast-filled bowel loop caused by its severe narrowing

136
Q

Stereotypical history of Gardener’s syndrome

A

multiple colonic polyps, osteomas, epidermoid cysts

137
Q

What is Gardener’s syndrome

A

sub-type of familial colorectal polyposis

138
Q

stereotypical history of Gilbert syndrome

A

a young man is noted to have an elevated unconjugated bilirubin level on a fasting blood sample

139
Q

Stereotypical history of Dubin-Johnson syndrome

A

a 20-year-old man of Iranian Jewish descent is investigated for jaundice and found to have an elevated conjugated bilirubin level

140
Q

Haemochromatosis chromosomal abnormalities

A

Haemochromatosis is an autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by inheritance of mutations in the HFE gene on both copies of chromosome 6

141
Q

Management of Hepatorenal syndrome

A

vasopressin analogues, for example terlipressin, have a growing evidence base supporting their use. They work by causing vasoconstriction of the splanchnic circulation
volume expansion with 20% albumin
transjugular intrahepatic portosystemic shun

142
Q

pathophysiology of hepatorenal syndrome

A

pathophysiology of HRS is that vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance. This results in ‘underfilling’ of the kidneys. This is sensed by the juxtaglomerular apparatus which then activates the renin-angiotensin-aldosterone system, causing renal vasoconstriction which is not enough to counterbalance the effects of the splanchnic vasodilation.

143
Q

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

144
Q

Type 2 hepatorenal syndrome

A

Slowly progressive

Prognosis poor, but patients may live for longer

145
Q

Stereotypical history of Peutz-Jeghers syndrome

A

a man who presents with intussusception is noticed to have multiple polyps on colonoscopy. These are later shown to be hamartomatous. He also has pigmented lesions on his lips and palms

146
Q

Stereotypical history of Villous adenoma

A

a 75-year-old man presents with passing large amounts of a mucous-like diarrhoea. Bloods demonstrate hypokalaemia

147
Q

What is Peutz-Jeghers syndrome

A

Autosomal dominant condition characterised by numerous hamartomatous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on the lips, face, palms and soles. Although the polyps themselves don’t have malignant potential, around 50% of patients will have died from another gastrointestinal tract cancer by the age of 60 years.

148
Q

Genetics of Peutz-Jeghers syndrome

A

autosomal dominant

responsible gene encodes serine threonine kinase LKB1 or STK11

149
Q

Features of Peutz-Jeghers syndrome

A

hamartomatous polyps in GI tract (mainly small bowel)
pigmented lesions on lips, oral mucosa, face, palms and soles
intestinal obstruction e.g. intussusception
gastrointestinal bleeding

150
Q

Aetiology of Dubin-Johnson syndrome

A

Mutation in the canalicular multidrug resistance protein 2 (MRP2) results in defective hepatic excretion of bilirubin

151
Q

Stereotypical history of biliary colic

A

an obese 50-year-old woman presents with pain in the RUQ which radiates to the interscapular region. She is apyrexial and not jaundiced

152
Q

Tropheryma whippelii

A

Jejunal biopsy shows periodic acid-Schiff positive macrophages

153
Q

Anatomy of direct inguinal hernia

A

Protrudes through Hesselback triangle

Passes medial to the inferior epigastric artery

154
Q

Anatomy of indirect inguinal hernia

A

Protrudes through the inguinal ring

Passes lateral to the inferior epigastric artery

155
Q

Anatomy of femoral hernia

A

Protrudes below the inguinal ligament, lateral to the pubic tubercle
more common in women

156
Q

Contra indications of 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
157
Q

What is Whipple’s disease

A

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

158
Q

Features of Whipple’s disease

A

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

159
Q

Autoimmune hepatitis- features

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

160
Q

Types of autoimmune hepatitis - type 1

A

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

Affects both adults and children

161
Q

Types of autoimmune hepatitis - type 2

A

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

Affects children only

162
Q

Types of autoimmune hepatitis - type 3

A

Soluble liver-kidney antigen

Affects adults in middle-age

163
Q

Second line management of C. diff

A

oral fidaxomicin

164
Q

Features of c.diff

A

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

165
Q

Metabolic consequences of re-feeding syndrome

A

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

166
Q

How to prevent vertical transmission of Hep B

A

give baby Hep B vaccine and immunoglobulin after birth

167
Q

Bile malabsorption investigations

A

is SeHCAT
nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT)
scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCAT

168
Q

Monoclonal antibody for treatment of c.diff

A

Bezlotoxumab is a monoclonal antibody which binds to Clostridium difficile toxin B and neutralises it to prevent recurrence of infection.

169
Q

Features of severe pancreatitis

A 
age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST
170
Q

Plummer Vinson Syndrome

A

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

Treatment includes iron supplementation and dilation of the webs

171
Q

Gilbert syndrome

A

isolated hyperbilirubinaemia in relation to physiological stress- student revising for exams

172
Q

Features 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)

173
Q

Genetics of Haemochromatosis

A

inheritance of mutations in the HFE gene on both copies of chromosome 6*. It is often asymptomatic in early disease and initial symptoms often non-specific e.g. lethargy and arthralgia

Epidemiology
1 in 10 people of European descent carry a mutation in the genes affecting iron metabolism, mainly HFE
prevalence in people of European descent = 1 in 200, making it more common than cystic fibrosis

174
Q

Function of luminal peptide

A

trigger secretion of Gastrin

175
Q

Features of Whipple’s disease

A

HLA-B27 positive
malabsorption: diarrhoea, weight loss
large-joint arthralgia
lymphadenopathy
skin: hyperpigmentation and photosensitivity
pleurisy, pericarditis
neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus

176
Q

Investigations of Whipple’s disease

A

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

177
Q

Conditions associated with H Pylori

A

peptic ulcer disease (95% of duodenal ulcers, 75% of gastric ulcers)
gastric cancer
B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
atrophic gastritis

178
Q

Histology of Barrett’s oesophagus

A

the columnar epithelium may resemble that of either the cardiac region of the stomach or that of the small intestine (e.g. with goblet cells, brush border)

179
Q

Secondary haemochromatosis

A

iron overload from multiple transfusions
Tan
New onset DM

180
Q

Features of carcinoid tumours

A

flushing (often 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

181
Q

Primary biliary cholangitis

A 
the M rule
IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females
Commonly presents with itching
182
Q

Complications of primary biliary cirrhosis

A

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

183
Q

Management of primary biliary cirrhosis

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

184
Q

Diagnosis of primary biliary cirrhosis

A

immunology
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
imaging
required before diagnosis to exclude an extrahepatic biliary obstruction (typically a right upper quadrant ultrasound or magnetic resonance cholangiopancreatography (MRCP)

185
Q

Features of Child Pugh score

A 
bilirubin 
albumin
prolonged prothrombin
encephalopathy 
ascites
186
Q

Drugs causing dyspepsia

A 
NSAIDs
bisphosphonates
steroids
calcium channel blockers*
nitrates*
theophyllines
187
Q

Post-cholecystectomy syndrome

A

dyspepsia, vomiting, pain, flatulence and diarrhoea
Pain related to sphincter of oddi dysfunction
low fat diet and cholestyramine

188
Q

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

189
Q

Features of primary sclerosing cholangitis

A 
cholestasis
jaundice, pruritus
raised bilirubin + ALP
right upper quadrant pain
fatigue
190
Q

Investigations of primary sclerosing cholangitis

A

endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopancreatography (MRCP) are the standard diagnostic investigations, showing multiple biliary strictures giving a ‘beaded’ appearance
p-ANCA may be positive
there is a limited role for liver biopsy, which may show fibrous, obliterative cholangitis often described as ‘onion skin’

191
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)
192
Q

pancreatic causes of malabsorption

A

chronic pancreatitis
cystic fibrosis
pancreatic cancer

193
Q

Diagnosis of small bowel overgrowth

A

hydrogen breath test
small bowel aspiration and culture: this is used less often as invasive and results are often difficult to reproduce
clinicians may sometimes give a course of antibiotics as a diagnostic trial

194
Q

Features of small bowel overgrowth

A

Chronic diarrhoea
bloating, flatulence
abdominal pain

195
Q

Peutz-Jeghers syndrome

A

hamartomatous polyps in GI tract (mainly small bowel)
pigmented lesions on lips, oral mucosa, face, palms and soles
intestinal obstruction e.g. intussusception
gastrointestinal bleeding

196
Q

VIP - vasoactive intestinal peptide

A

source: small intestine, pancreas
stimulation: neural
actions: stimulates secretion by pancreas and intestines, inhibits acid and pepsinogen secretion

197
Q

VIPoma

A 
90% arise from pancreas
large volume diarrhoea
weight loss
dehydration
hypokalaemia, hypochlorhydia
198
Q

Zollinger-Ellison syndrome

A 
Excessive gastrin production
usually from a gastrin secreting tumour usually of the duodenum or pancreas. Around 30% occur as part of MEN type I syndrome
multiple gastroduodenal ulcers
diarrhoea
malabsorption
199
Q

Melanosis coli

A

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

It is associated with laxative abuse, especially anthraquinone compounds such as senna

200
Q

Autoimmune hepatitis

A

young women
amennorrhoea
derranged LFTs

201
Q

Purtscher retinopathy

A

cotton wool spots on fundoscopy

associated with acute pancreatitis

MRCP part 1 (15 decks)

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